Acute Poisonings

Emergency Care of Acute Poisonings

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Most cases of acute poisoning are self-inflicted but not all. Poisoning can be caused by pharmaceuticals or illegal drugs but also by gases, chemicals, mushrooms and many other types of biological toxins. A primary assessment should try to determine whether the poisoning is intentional or inadvertent and if it is self-inflicted or caused by another, this should be documented and recorded and it also affects the diagnosis classification. Here are general guidelines for care of acute poisoning, but treatment may vary and each case must be assessed based on the severity of poisoning and patient condition.

Patients with acute poisoning must be treated with careful monitoring, which is of great importance for a good prognosis. In most cases, the main treatment is symptomatic. Most importantly, adequate monitoring of breathing, circulation and alertness is required. Emergency care includes securing of vital functions by establishing and securing free airway and optimization of breathing and circulation.

At the same time, careful care is given on the identification of intake of poison, alcohol, pharmaceutical or illegal drugs. Which medicines have been taken and when did this happen? Adequate antidote treatment is given in specific severe cases.

The most important issue in most cases of poisoning is to:

  • Carefully monitor alertness and breathing
  • Assist breathing and circulation when needed
  • Treat acute confusion and mental anxiety calmly and safely
  • Identify the toxic agent
  • Perform active elimination when indicated, for example by gastric emptying and gastric lavage
  • Give activated charcoal or dialysis treatment when indicated
  • Antidote treatment when a clear indication is present and the benefit contemplates the risks
  • Refer the patient into a department with the correct level of care and avoid low levels of care when consciousness is reduced or breathing is impaired
  • Arrange a follow-up service through psychiatry and social services

Establish Free Airway

  • Recovery position
  • Nasal tube, oropharyngeal airway device or, in exceptional cases, laryngeal mask
  • Endotracheal intubation if necessary, in case of emergency laryngeal mask
  • Assisted ventilation if required
  • Oxygen is given liberally
  • Pulse oxymetry
  • Prevent aspiration, emptying the stomach by a nasogastric tube

Establish Venous Access 

  • Peripheral venous catheter (PVC), with unconsciousness, preferably two
  • Arterial line if unconsciousness, metabolic acidosis or circulatory impairment
  • CVC, unconsciousness or circulatory failure 

Gastric Emptying – see also below during treatment

  • Manually, only on toddlers at the initial stage
  • Emetic syrup is no longer recommended in the treatment
  • Gastric lavage through a coarse tube by the mouth

Activated Charcoal see also below during treatment

  • Manually in mug or pediatric closed cup
  • Dissolved in water and disposed (instilled) into the stomach via a nasogastric tube

Laboratory Tests

  • Blood and urine samples according to local routines for cases of acute intoxication (ethanol, methanol, paracetamol, etc.)
  • Biological alcohol markers in suspicion of alcohol abuse (PEth, CDT)
  • Drug screening of urine samples (in patients with urinary catheter)
  • Targeted toxicological samples (urine, serum, possibly hair or nails)
  • Serial electrolyte status checks (routine status, Na, K, Mg, Ca)
  • Arterial blood gases with acid base status (including lactate and CO-Hb)
  • SvO2 and lactate in case of suspicion of cyanide poisoning or severe heart failure
  • B-glucose
  • Myoglobin in serum (rhabdomyolysis)
  • Heart failure enzyme markers (TNT, Pro-BNP) in carbon monoxide poisoning or ECG changes or cardiac ischemic indicators plus CO-Hb
  • Save and freeze blood serum from time of admittance of supplementary diagnostics in unclear or very serious cases

Differential Diagnosis

Any patient under the age of 50 with unclear unconsciousness should be regarded as poisoning or intoxication until the opposite is proven!  The diagnosis intoxication or poisoning should always be considered in case of unclear unconsciousness, and rarely is the correct diagnosis when stroke has been the preliminary diagnosis! Conversely, the diagnosis of intoxication has been erroneously set when the correct diagnosis has been, for example, hypoglycemic coma! Drug test strips may quickly give an indication if poisoning is present.

Always consider a differential diagnosis in case of unclear unconsciousness! Consider alcohol and drugs when patients are messy and worried. Smell the breath! Among patients with unclear unconsciousness below 40 years of age, more than 80 percent have been reported to be poisoned or intoxicated, whereas more than 90 percent of patients over 60 years of age are caused by other causes than acute poisoning. In case of unclear unconsciousness, a CT brain scan should be performed on relatively wide indications. Trauma and poisoning are common parallel diagnoses.


Circulatory and respiratory monitoring

  • ECG with arrhythmia monitoring, continuous and stored in the patient’s electronic records at the time of admittance. Determine cardiac rhythm, QT-time and QRS-time.
  • Invasive monitoring, continuous arterial pressure and central venous pressure (CVP) in severe cases.
  • Ultrasound of the heart (UCG) in cardiac failure or pronounced hypotension.
  • Pulse oximetry and respiratory rate.
  • Spirometry on ventilator-treated patients as well as after exposure to irritant gas
  • Urinary catheter with urinary output and body core temperature measurement.

Prolonged QT time is relatively common in drug poisoning. In repeated episodes of ventricular tachycardia or ventricular fibrillation, consider drug-induced prolonged QT time.


Continuous grading of the patient’s alertness and consciousness must be performed and recorded. Consciousness grading should be done continuously (1-2 times/hour) and several different scales are available for this purpose. A common scale in the Nordic region is the so-called RLS scale (Reaction Level Scale, 0-8 p) , but internationally, Glascow Coma Scale (GCS) is more commonly used. What scale you use is less important. The important thing is that the level of consciousness is graded and recorded regularly. Neurological deficit symptoms must be reported and investigated promptly.

A grading instrument that can be used clinically to assess the severity of poisoning is the Poisoning Severity Score (PSS). A negative change in the patient’s degree of consciousness must be observed and adequate countermeasures taken. Serious poisoning symptoms such as respiratory distress or cardiac arrhythmias often occur suddenly after a decrease in vigilance.

An anxious patient may have a clinical picture compatible with a so-called “toxicodrome”. Various “toxicodromes” (clinical syndromes due to poisoning) have been described in connection with poisons, namely

  • Anticholinergic syndrome
  • Serotonergic syndrome
  • Malignant neuroleptic syndrome
  • Agitated delirium

Patients with a toxicodromes have a characteristic clinical picture and may require specific treatment. Common to these syndromes is that they are often associated with hyperthermia and anxiety that can be life threatening. Basic treatment for these syndromes therefore becomes sedation and cooling. Most important is to detect hyperthermia and control the temperature in the care of an anxious or drug-affected patient. Note that patients taking amphetamine usually have hyperthermia but may also come across with hypothermia.

Blood Sampling

Quantitative concentration determination should be followed when poisoning with any of the following substances:

  • Paracetamol (4, 8, 12 and 24 hours after ingestion)
  • Carbamazepine
  • Salicylic acid
  • Digoxin
  • Ethanol
  • Ethylene glycol
  • Iron
  • Isopropyl alcohol
  • Lithium
  • Methanol
  • Theophylline

Measure serum concentrations of relevant drugs 1-4 times on the first day. The following day or when concentrations have fallen below toxic values, controls can be taken once a day. Note that when a given elimination treatment such as hemodialysis is interrupted, the serum concentrations may rise (rebound), for example, by lithium poisoning. In refined diagnostics, both arterial and venous samples can be taken to provide information about continued uptake of drug from the intestine or redistribution in the different compartments of the body. In most cases, it is sufficient to follow venous blood concentrations. Note that alcohol can be measured in both blood, exhaled air and urine.

Drug Screening

Drug screening is taken on the patient’s urine to detect psychoactive substances, which can often explain unconsciousness in acute poisoning cases. This applies in particular to the occurrence of psychomotoric anxiety and psychotic symptoms or seizures. Drug screening test strips usually measure the presence of cocaine, cannabis, morphine, amphetamine and benzodiazepines. New drug test strips can measure more substances, usually between 8 and 14 different drugs. This screening should be performed liberally in the case of unclear unconsciousness in younger patients with known addiction.

A screening test usually provides responses within 5-10 minutes, facilitating the emergency diagnosis of a poisoned patient. Also send urine samples to laboratory chemistry for analysis with GC-MS (gas chromatography mass spectrometry) for verification or suspicion of GHB poisoning. Note that GHB and LSD are usually not available on regular drug screening test strips. Newer test strips can provide answers to as many as 14 different substances. Selected strips are now also available for “Spice” (synthetic cannabinoids), buprenorphine, methadone, ecstasy and GHB.

Indications for Admittance to an Intensive Care Unit (ICU)

  • Life-threatening poisoning
  • Ingestion of very toxic substances
  • Large quantities of drugs or other poisons have been taken
  • Significant respiratory irritation when exposed to irritant gas
  • Significant alertness reduction
  • RLS 3 or higher
  • GCS lower than 10
  • Significantly worried or confused patient
  • Sudden consciousness reduction
  • Inability to keep the airway free in the supine position
  • Cardiac arrhythmias
  • Hypoxia with SaO2 <90% on air breathing or SaO2 < 95% with oxygen
  • Respiratory rate less than 10 or greater than 30 breaths per minute
  • Pulse below 40 or above 130 beats per minute
  • Systolic blood pressure below 90 mm Hg despite fluid administration
  • Myoclonic seizures
  • Metabolic acidosis or marked lactatemia (> 5 mmol/L)
  • Hypothermia or hyperthermia
  • Pronounced electrolyte disturbances
  • Other significant worrying states!


The treatment of acute poisoning is essentially symptomatic and antidotes are available only in a limited number of cases. Conscioussness, breathing and hemodynamics can change suddenly during the first six hours. Seizures, psychomotor dysfunction, unconscioussness, nausea and vomiting are common. Insufficient breathing is supported as needed by endotracheal intubation and respiratory treatment in an intensive care unit. Uncomplicated poisoning cases often require no more than four hours of close monitoring; in complicated cases, longer time is required as the condition varies. 

Activated Charcoal

Activated charcoal is valuable if administered early in treatment, preferably within one hour after ingestion of toxic agents. Activated charcoal administration should be the standard treatment of acute drug poisoning. Charcoal is of limited value if it is given late in treatment, more than six hours after the poisoning offer. The usual dose is 50 g of activated charcoal for adults and 1 g/kg for children up to 12 years of age. Charcoal adsorbs most drugs; but not iron, lithium, ethanol, methanol or cyanide. Activated charcoal can be given later than one hour in life-threatening poisoning and should supplement gastric lavage when carried out. See special guidelines for gastric lavage and activated charcoal.

Gastric Lavage

Gastric lavage is of limited value and should only be performed if the patient arrives early in hospital after the poisoning, usually within one hour after ingestion (e.g. less than 25 % of all cases). In case of very serious poisoning (life-threatening poisoning), after intake of very large doses or in anticholinergic drugs, gastric lavage may be advantageous and performed at a later stage or repeatedly, in each case up to 24 hours after ingestion.

See special guidelines for gastric lavage. Examples of particularly toxic agents are chloroquine, potassium and various heavy metals.

Sodium bicarbonate is an important part of the treatment of many toxins, especially in pronounced metabolic acidosis as in poisoning with methanol, ethylene glycol and other toxic alcohols. Sodium bicarbonate is also an important part of overdose of tricyclic antidepressant drugs and some other cardiovascular preparations. Alkalinization means that a smaller proportion of overdose drug is free in the bloodstream, with a small amount being able to pass to the cells of the myocardium. The toxicity decreases by tricyclic antidepressants when treated with sodium bicarbonate. In case of serious poisoning give an initial dose of about 200 ml sodium bicarbonate (120 mmol). Then titrate after blood gas analysis. Strive for a pH above 7.45 and a positive Base Excess.

Sleeping or Comatose Patient

If the patient is sleeping deeply and cannot be awakened, he or she should be monitored in an intensive care unit with intubation preparedness.

If vital parameters are stable and the patient breathes calmly and regularly it is usually enough with careful supervision and the patient is allowed to sleep until he or she wakes up. Comatose patients are placed stable on the side and turned every other hour. Any other reason for deep unconsciousness than poisoning should of course be ruled out. Check electrolytes, intoxication blood samples and an arterial blood gas as well as the blood alcohol level (BAL). Perform a CT scan with x-ray of the brain (and sometimes stomach as well) in unclear cases of unconsciousness or in the presence of focal neurological symptoms.

In drug poisoning, the patient usually sleeps for 3-12 hours. Longer unconsciousness than 12 hours often depends on other causes, but may be compatible with certain poisons, such as antidepressant drugs, barbiturates or long-life depot preparations (Voxra®, Propavan®, Lithium®). The awakening is usually calm and if the patient appears to be extremely worried during awakening, the patient should be sedated to provide further sleep and a quieter awakening, for example, with midazolam (Dormicum®) 1-2 mg iv.

Serious incidents with poisoned patients usually occur within six hours of arrival in hospitals such as seizures, blood pressure fall or cardiac arrhythmias.

Confused or Agitated Patient

If the patient is agitated and mentally unstable, you can give sedative drugs, for example benzodiazepines. Although sedative neuroleptics have been used they should possibly be avoided in poisoning with other neuroleptics or at unstable blood pressure; Clomethiazole (Heminevrin®) should be avoided completely.

The following medications may conveniently be used for sedation:

  • Midazolam (Dormicum®) 1-5 mg i.v., i.m. or in continuous infusion 1-5 mg/h (1 mg/ml). Can also be given orally (10-15 mg).
  • Diazepam (Stesolid®) 2.5-5 mg i.v.
  • Propofol 20-40 mg i.v. or in continuous infusion, 20 mg/ml with 3-10 ml/h.
  • Olanzapine (Zyprexa®) 5-20 mg i.m. x 2.
  • Droperidol (Dridol®) 5-10 mg i.m. (SIC)

Note that the vigilance fluctuates and that the patient can quickly become unconscious with insufficient breathing after administration of sedative drugs.

If the patient is heavily agitated and/or violent, it may be necessary to completely sedate or anesthetize the patient, secure the airway by intubation and connect him or her to a ventilator. This may only be done when it benefits the patient. One can then use midazolam (Dormicum®) 5 mg i.v. plus propofol (Propofol) 50-200 mg i.v. until the patient is sleeping lightly. Patients usually require continuous infusion of propofol for 3 to 8 hours. Infusion rate is controlled by the degree of alertness, approximately 200-400 mg of propofol is given per hour (5-10-20 ml/hour).

The patient should be monitored in an intensive care unit and the respiratory tract must be secured by endotracheal intubation and respiratory treatment. After that, you can usually wean off sedation and the patient usually wakes up calmly and peacefully.

Sedation of the patient with propofol intravenously should only be done by an anesthesiologist when the situation is unsustainable with immediate danger to the patient’s life. This usually requires intubation and respiratory treatment for at least 4-6 hours.

Agitated patients should not be discharged from emergency care when they are still drug-affected, worried with lack of self-control. They can still be violent against themselves, relatives and staff. Patients with anxiety and agitation and a so-called “Anticholinergic Syndrome” may be significantly improved by administration of physostigmine intravenously, for example after poisoning with antidepressants, phenothiazines or neuroleptics. However, there is a risk that the seizure threshold will be lowered; Physostigmine has been described to induce seizures and bradycardia why one should be careful in the initial phase of a poisoning.

In case of severe poisoning, such as methanol poisoning or severe hepatic failure due to paracetamol poisoning, you should refer the patient to a regional hospital.

Antidote Treatment

Antidotes are given when the patient’s condition so requires and there is an opportunity to significantly improve outcome. Some common and important antidotes are:

  • N-Acetylcysteine ​​when poisoning with paracetamol or fly fungus. Note that overdose with paracetamol in modified release form (MR) 665 mg requires a particular acetylcysteine ​​schedule with prolonged phase II dosage.
  • 4-methylpyrazole (Fomepizol®) in poisoning with methanol or ethylene glycol
  • Hydroxocobolamine (Cyanokit®) when poisoned with cyanide (hydrogen cyanide by inhalation) or other cyanide compounds
  • Beclometasone (Becotide®) in the case of poisoning with irritant gases (corticosteroids by inhalation)
  • Desferoxamine (Desferal®) in poisoning with iron
  • Digoxin antibodies (DigiFab TM®) in poisoning with digoxin
  • Flumazenil (Lanexat®) when poisoned with benzodiazepines
  • Naloxone (Naloxon®, Nexodal®) in case of poisoning with opioids
  • Obidoxime (Toxogonin) in nerve gas poisoning (unregistered)
  • Immune serum (Vipera TAB®) in European viper bites, other exotic snakes require specific serum according to species.

Treatment with Vasoactive Drugs

In case of difficulty in maintaining blood pressure after delivery of crystalloid and colloid fluid, vasoactive drugs can be used to raise blood pressure and cardiac output and increase oxygen delivery to vital organs and peripheral tissues. Essentially, you use the same drugs as in pronounced cardiac failure of other origin. The most commonly used drugs are dopamine, dobutamine, norepinephrine and adrenaline in continuous infusion. In addition, isoprenaline is used for severe heart failure with bradycardia, for example after poisoning with calcium channel inhibitors, beta blockers or tricyclic antidepressants. Even inotropic drugs that act as cardiac enhancers independent of beta-receptors in the heart can be used, such as glucagon. Glucagon may be tested by poisoning with beta blockers or calcium channel inhibitors. Also high-dose glucose-insulin can be tested. In case of pronounced bradycardia and heart failure, treatment with transvenous pacemaker may also be positive. Calcium administration may improve blood pressure and circulation but often only temporarily.

Intravenous Lipid Emulsion Therapy (ILE)

Intravenous Lipid Emulsion therapy (ILE) treatment may be lifesaving in cardiovascular collapse following overdose with local anesthetics, especially bupivacaine (Marcain®) and several other drugs. In case of overdose of other fat-soluble drugs, eg verapamil (Isoptin®), intravenous lipid emulsion (Intralipid®) treatment has been effective in several cases. One theory is that intravenous lipid therapy creates a depot in the bloodstream that extracts toxic agents from the cardiac cells so that cardiac toxicity is reduced (“sink theory by redistribution”).

Initially, 100-200 ml of Intralipid® is administered intravenously at the same time as cardiopulmonary resuscitation is initiated (CPR). See treatment of overdose with local anesthetic agents. The treatment is still controversial and is only recommended as a last resort for cardiovascular collapse after ingestion of fat-soluble drugs.

Treatment with ExtraCorporeal Circulation Support (ECCS, ECMO, Aortic Balloon Pump)

In cardiovascular collapse due to poisoning, mechanical circulation support can be lifesaving. In case of poisoning, pronounced heart failure is usually transient, for a few hours or up to 2-3 days. Initially, a mechanical cardiac compression device can be lifesaving, like a Lucas® pump. Thereafter, the patient can be transported to a thoracic surgery or intensive care department where you can insert an aortic balloon pump or other mechanical circulation support (ECMO/ECCS). If this procedure can be initiated quickly without injuring the brain, life will usually be saved. ECMO may be required for 2-3 days after which the cardiac function usually is restored. The method is invasive and resourceful but very effective. Consideration should be given to this treatment in the presence of heavily widespread QRS complexes (> 160 msec) and pronounced hypotension, severe bradycardia or very low SvO2 (< 45 %). Examples of drug overdoses where ECMO may be relevant is poisoning with:

  • Tricyclic antidepressant drugs (TCA)
  • Antipsychotic drugs
  • Antiepileptic drugs
  • Chloroquine
  • Beta-blocking drugs
  • Rhythm-regulating cardiac medications (flecainide)
  • Calcium-channel inhibitors (calcium antagonists)

Several of these drugs are described as membrane-stabilizing drugs with negative inotropic effects due to blockade of fast sodium ion channels. In the case of overdose, a gradual broadening of the QRS complex on ECG is usually seen while decreasing blood pressure and bradycardia transfers into circulatory shock.


Psychiatric and social follow-up of the patient is important as the poisoning occurs in connection with suicide attempts or when the patient has an active substance abuse with pharmaceutical drugs, alcohol or illicit drugs. Referral to psychiatric treatment, dependence care or social services is desirable. In case of life-threatening addiction (GHB, opioids, amphetamine), social services should always be contacted, by writing a referral or orally.

Abuse of central stimulants (amphetamines, cocaine, ecstasy, party drugs) and cannabis is common among younger patients with drug poisoning as well as general social problems in these cases. Cases with adolescents under the age of 18 must be reported to social authorities and adolescent psychiatric consultants (child and adolescent psychiatric clinic). Even school healthcare may need to be connected.

In case of repeated acute overdose, notification to the social service should be made and care under the Youth Care Act (<20 years) or Law on Care of Abusers should be considered. The application for social services may be oral or written.

Long-term Side Effects

A drug overdose usually does not cause long lasting side effects unless severe complications occur such as apnea, aspiration pneumonia, acute liver failure, acute renal failure or pronounced general hypoxia. The risk of developing withdrawal after abuse of alcohol, or drugs must always be taken into account at discharge. A transient sleep disorder with severe sleep difficulties for 3-4 weeks is not uncommon. Other side effects described are abdominal pain, difficulty concentrating, numbness, anxiety and impotence. Many patients experience low quality of life for a long time after being treated for acute poisoning. The risk of a new lethal poisoning within a week after the current care is though very low.

 ICD-10 Codes

  • Poisoning of drugs, drugs and biological substances T36-T50
  • Toxic effect of substances with substantially non-medical use T51-T65
  • Toxic effect of alcohol T51
  • Toxic effect of other and unspecified substances T65
  • Poisoning accidents and exposure to harmful substances by accident X40-X49
  • Intentional self-destructive action through poisoning X60-X69
  • Abuse by poisoning X85-X90
  • Poisoning with obscure intention Y10-Y19
  • Mental disorders and behavioral disorders caused by sedatives and hypnotics, acute infections F13.0


  1. Jones AL, Volans G. Management of self poisoning. BMJ 1999;319:1414–1417.
  2. Bateman DN, Bain M, Gorman D, Murphy D. Changes in paracetamol, antidepressants and opioid poisoning in Scotland during the 1990s. QJM 2003; 96:125–132.
  3. Burillo-Putze G, Munne P, Duenas A, Pinillos MA, Naveiro JM, Cobo J, Alonso J. National multicentre study of acute intoxication in emergency departments of Spain. Eur J Emerg Med 2003; 10:101–104.
  4. Hovda KE, Bjornaas MA, Skog K, Opdahl A, Drottning P, Ekeberg O, Jacobsen D. Acute poisonings treated in hospital in Oslo: A one-year prospective study (I): Pattern of poisoning. Clin Toxicol 2007.
  5. Dargan PI, Jones AL. Management of paracetamol poisoning. Trends Pharmacol Sci 2003; 24:154–157.
  6. Newton RW. Physostigmine salicylate in the treatment of tricyclic antidepressant overdosage. JAMA 1975; 231:941–943.
  7. Vale JA. Position statement: Gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711–719.
  8. Nice A, Leikin JB, Maturen A, Madsen-Konczyk LJ, Zell M, Hryhorczuk DO. Toxidrome recognition to improve efficiency of emergency urine drug screens. Ann Emerg Med 1988; 17:676–680.
  9. Merigian KS, Woodward M, Hedges JR, et al. Prospective evaluation of gastric emptying in the self-poisoned patient. Am J Emerg Med 1990;8:479483.
  10. Neuvonen PJ, Olkkola KT. Oral activated charcoal in the treatment of intoxication. Role of single and repeated doses. Med Toxicol 1988;3:3358.

Published with permission from Internetmedicin AB

Gastric Emptying and Activated Charcoal

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Gastric emptying and gastric lavage have long been standard procedures in the treatment of acute poisoning patients who have toxic substances left in the gastrointestinal tract. Today, there are significantly fewer poisoned patients undergoing gastric emptying compared with 10-20 years ago. This since several studies has shown doubts about the usefulness of the procedure. However, it is still a method that can be lifesaving in some cases and how to do this practically in a safe and easy way should be known to everyone serving a medical emergency department.

Gastric emptying has been previously done by gastric lavage with water via a tube or by vomiting (manually or by emetic medication). There is no longer considered to be scientific support for gastric emptying using emetic drugs. Manual vomiting provocation is only performed on toddlers immediately after ingestion of toxic agents, e.g. at home or in preschool. Adult gastric emptying can be performed at the correct indication by using a orogastric tube performing gastric lavage with normal tap water.

The benefit of gastric lavage is evidence-based in scientific animal experiments and experimental human studies. However, in controlled randomized clinical trials, the benefit of gastric lavage has been demonstrated only when performed very early in the poisoning course, usually within one hour after ingestion of toxic substances. The same applies to the supply of medical charcoal (activated charcoal). Gastric emptying later than one hour after ingestion of toxic drugs has not been shown to improve the clinical course in controlled randomized scientific studies.

However, in clinical studies it is difficult to select those patients who may benefit from the procedure. Experience has shown that some patients may still benefit from gastric lavage even in late stages of severe poisoning (> 1 hour) or in the case of poisoning with slow release preparations (depot preparations). Each case of poisoning must therefore be evaluated and tested individually with regard to what has been ingested, what amount and the condition in which the patient is.

The following advice should act as General Guidelines

The guidelines concern both gastric emptying and gastric lavage. The supply of activated charcoal to reduce the adsorption of toxic substances is a routine procedure following gastric emptying. Charcoal can also be supplied without gastric lavage through a nasogastric tube or by mouth (oral suspension – suspension of charcoal). The supply of medical charcoal is considered the first-hand measure in the treatment of acute poisoning and should be far more common than gastric lavage. All patients entering the hospital with serious poisoning should be evaluated for gastric emptying and treatment with medical charcoal.

Guidelines for Gastric Emptying in Acute Poisonings 

Gastric Lavage

Gastric emptying in adults should be performed by means of gastric lavage through a coarse tube (28-32 Ch) ​​in the stomach by the mouth. The procedure is subject to gastric emptying plus a gastric lavage, usually with tap water.

After performing gastric lavage, in most cases activated charcoal should be supplied to the patient through the same tube, usually 50 g of charcoal, in some cases more. Gastric emptying should be carried out within a reasonable time (<1 h) if very serious poisoning is estimated based on data on the toxicity, intake and timing of ingestion. Gastric emptying should be conducted liberally in complex and severe cases.

Complicated and serious poisoning cases often occur after overdose with any of the following drugs:

  • Beta blockers
  • Calcium channel inhibitors
  • Digoxin
  • Tricyclic antidepressant drugs
  • Antiepileptic drugs
  • Barbiturates
  • Chloroquine
  • Oral antidiabetics
  • Potassium tablets
  • Slow release-formulations

Gastric Emptying should be Performed in Case of Acute Poisoning


  • Within 1 hour after overdose of tablets or liquid preparations (drug mixes, suspensions).

Gastric lavage can be considered:

  • Within 12 hours after overdose of tablets in a very large amount, or after ingestion of strong toxic agents or slow release preparations. For example, paracetamol in modified release form 665 mg or antidepressive agents in depot form.
  • Within 24 hours if toxic plants or mushrooms have been taken (amatoxin-containing fungi).


If the medicines taken are not highly toxic and more than one hour elapsed after ingestion, most of the cases can be prevented from gastric lavage. In many of these cases one can just supply medical charcoal or refrain from the whole procedure. However, gastric lavage can be performed later than one hour after ingestion of hard-smelting material such as sponges and parts of plants, antidepressant drugs (TCA) or in the formation of conglomerate in the intestine (iron, lead, potassium) or otherwise impaired intestinal peristalsis. Deeply unconscious patients usually have no or severely impaired intestinal peristalsis. The presence of conglomerate can and should be detected by X-rays (abdominal overview by x-ray or CT scan). Note that paracetamol in the preparation 665 mg contains a double layer drug with sustained release, therefore gastric lavage and activated charcoal may be considered even later than 1 hour. There is a risk that this preparation may form conglomerate in the intestine. If the circulation and respiration is stable, the patient’s alertness is adequate (the patient is responding to verbal information) and the ingested drug is unknown as well as the time of intake, one can usually refrain from gastric emptying.

Note that patients after ingestion of some highly toxic drugs may be relatively unaffected initially. This includes intake of, for example, chloroquine (Chloroquine Phosphate Recip®), paracetamol (Alvedon®, Reliv®, Panodil®, etc.), venlafaxine (Efexor Depot®) or digoxin (Digoxin®). Therefore, careful documentation of intake preparation, intake amount, timing of intake, and observation of alertness, respiration and circulation is necessary. Note if paracetamol taken is in immediate release or modified release form.

The patient’s clinical picture must be weighed in each case so that the benefit of the gastric lavage is set against the risk of the procedure. The amount of drug or toxin eliminated by gastric lavage must have a beneficial effect on the clinical course for the patient to be given the procedure. This aspect is, of course, difficult to evaluate in advance and some overwork becomes necessary.

Gastric lavage should not be performed if there is suspicion of corrosive acids, alkali, lye, petroleum products such as ignition and lamp oil, or alcohol intake. In exceptional cases, it may be warranted to perform gastric lavage even after ingestion of alcohols in cases where the patient has taken very large amounts recently (for example at the hospital!). However, in most cases it is meaningless in poisoning with ethanol, methanol, ethylene glycol, isopropyl alcohol or GHB. The measure only means an extra risk moment for the patient. In case of ingestion of isopropyl alcohol (2-propanol, hand disinfectant, lavage fluid) it may be warranted with gastric lavage for up to one hour after ingestion. 

Gastric Lavage – Procedure

A routinely performed gastric lavage in habit is a relatively simple and safe procedure. In case of insufficient or insufficient airway, the patient should be intubated before gastric lavage. The assessment of the airway is free and the in vivo reflexes are clinical and may be difficult. If you are very doubtful, the patient should be intubated first to ensure the airway and to avoid complications. Anesthetist should then assist during the procedure.

  • In gastric lavage use a coarse tube (28-32 Ch) ​​which allows aspiration of tablets from the stomach.
  • The patient is stably left in the left side position during the procedure and the tube is put into the stomach through the mouth. One can sometimes be helped by a tongue pad to insert the tube through the mouth. The tube should be gelled. The tube is inserted when the patient swallows. The position of the tube may need to be changed a few times in the stomach during the procedure. A normal distance down to the stomach is 35-50 cm. If the tube has not been inserted properly in the stomach, there is an increased risk of respiratory distress (beyond cardia). There is also a risk of leakage of gastric contents beside the tube.
  • Oxygen is supplied to the patient via catheter or nasal cannula throughout the procedure (2-4 L/min O2).
  • When the orogastric tube is placed in the stomach, empty the stomach by aspiration (gastric aspiration) before lavage with water or saline through the tube. Simply use tap water to lavage the stomach. You should use no more than 200 ml at a time to not flush the contents of the stomach into the intestine. You lavage and aspirate the instilled water. You lavage with tap water until you get a clear exchange, but the procedure should not take more than 10 minutes.
  • One can use a closed coil system (similar to urinary bladder system) with two bags and coarse hose clips to the hoses that allow for flushing and flushing without air mixing. You must then check that there is no net fluid left in the patient.
  • One should assume that a certain part (about 25%) of the contents of the stomach is flushed into the small intestine during the procedure. There is some risk that the conglomerate of tablets will be dissolved. An increased risk of toxic reactions may therefore occur 20-30 minutes after the lavage has ended. During this period, the patient should not be in transit between departments or at an X-ray department!
  • After gastric lavage, administration (instill) 50 g of medical charcoal is dissolved in a suspension through the oral tube.
  • When you then pull out the tube it is advisable to turn it off proximally with a pinch (clamping the tube). The tube is closed so that the tip of the tube does not drain into the pharynx at the level of the laryngeal introitus and into the trachea.
  • It’s not uncommon for the patient to choke just the moment you retract the orogastric tube out of the mouth, you have to be prepared with a suction catheter. Soak cleanly in the pharynx.
  • Careful observation of the patient is necessary immediately after gastric lavage.
  • Intubated patients should not be extubated directly after completion of gastric lavage without being monitored in the respirator for at least four hours following the procedure.

Bowel Irrigation, “Whole Bowel Irrigation”

Bowel irrigation may be indicated in heavy metal poisoning, e.g. poisoning with lead or arsenic, but has also been used in potassium poisoning. One method of accelerating the elimination of toxic agents from the gastrointestinal tract is to try to flush tablets through the intestine with as fast intestinal passage as possible, thus a type of bowel lavage. This method is used more in some countries than others and is common in, for example, Canada and Australia. Liquids are given by drink or tube with laxative effect, such as Laxabon®. A regular dose is 4 liters in adults and 25 ml/kg in children. 1-1.25 liter is initially transmitted via tube. The first bowel emptying occurs approximately one hour after the intake of Laxabon has begun, so the method is considered to be somewhat slow. The active ingredient is mainly macrogol but note that Laxabon also contains potassium, why this preparation should be avoided in potassium poisoning! An alternative to Laxabon is to lavage with a polyethylene glycol solution.

Activated Charcoal

All patients who enter the hospital as an incidence case of acute poisoning should be valued if they are to receive medical charcoal (activated charcoal). The benefit of activated charcoal is greatest within the first hour after ingestion of toxic agent. The effect then decreases rapidly over time.

Activated charcoal should be given routinely in the case of overdose of a toxin that is adsorbed to charcoal when a toxic reaction can be avoided within the hour. Almost all drugs bind to activated charcoal except iron and lithium, but potassium is also poorly adsorbed to charcoal. Neither ethanol, methanol nor cyanides bind to activated charcoal. Activated charcoal slurried in water can also be given prehospital if the patient is cooperative. However, it should not be given if there is a significant risk of vomiting and pulmonary aspiration of charcoal.

Supply of medical charcoal without gastric lavage can be applied when poisoning is judged to be mild to moderate (unaffected vital parameters) or when the patient arrives relatively late after the poisoning, for example later than one hour after drug intake or in case of mushroom poisoning, even late.

In such cases, activated charcoal can be given to the patient as a suspension via a beverage cup where the patient drinks himself or via a gastric tube. In these cases, a thinner tube (18 Ch) than the one used for gastric lavage can be used as then inserted through the nose. Provision of activated charcoal through a tube passed through the nose is suggested with the patient half-seated in the back condition. The nasal opening, like the nasogastric tube, is properly gelled and the procedure is usually done quickly and painlessly when performed by skilled staff.

The amount of medical charcoal supplied to the patient should exceed the intake of poisoning amount ten times by weight. Routinely, a single dose of 50 g of charcoal in suspension is added. Thus, if the intake of toxin exceeds 5000 mg, more than 50 grams of charcoal must be added.

Children up to one year of age are given 1 g/kg body weight. Children between 1 and 12 years of age are given 25-50 grams. Adolescents and adults are given 25-100 grams of charcoal in a single dose.

In case of serious poisoning, the supply of activated charcoal should be repeated four to six times the first day. This procedure is simply referred to as “repeated activated charcoal”. In this procedure, gastric lavage has also been performed. A gastric tube can be left in the stomach after it is rinsed with saline and fixed with tape. Adults are given 25 g of medical charcoal via the tube every four hours the first day (25 g x 6), children are given 5-10 g of charcoal every four hours (5-10 g x 6).

Repeated Activated Charcoal should be given in case of serious poisoning with:

  • Barbiturates (Fenemal®)
  • Phenytoin (Epanutin®, Fenantoin®, Lehydan®)
  • Carbamazepine (Hermolepsin®, Tegretol®, Trimonil retard®)
  • Kinin (Kinin Recip®)
  • Chloroquin (Chloroquine Phosphate Recip®)
  • Salicylates (Albyl minor®, Aspirin®, Alka-Seltzer®, Asasantin Retard®, Bamyl®, Magnecyl®, Treo®, Trombyl®)
  • Theophylline (Theo-Dur®)
  • Poisonous mushroom (white and lame fly fungus)


Diagnostic Code according to ICD-10

  • V9227 Insertion of gastric tube
  • V9229 Gastric lavage


1. National Institute for Public Health and Environment. The Dutch Public Health Status and Forecast Report 2006.

2. Jones A. L., Volans G. Clinical review; Recent advances Management of self poisoning. National Poisons Information Service (London), Medical Toxicology Unit, Guy’s and St. Thomas’s NHS Trust, London SE BMJ 1999; 319: 1414-1417.

3. American Academy of Clinical Toxicology and European Association of Poisons Centers and Clinical Toxicologists. Position paper: Single dose of activated charcoal. Clinical Toxicology 2005: 43; 61-87.

4. Jurgens G., Graudal N.A. Position paper: The effect of single dose activated charcoal on drug absorption during the first 6 hours after drug ingestion- A metanalysis. Clin Toxicol 2005: 43: 61-87.

5. Alaspaa A.O., Kuisma M.J., Hoppu K. Out-of-hospital administration or activated charcoal by emergency medical services. Annals of Emergency Medicine 2005: 45; 2.

6. Person M. Use of activated charcoal in the pre-hospital situation. Journal of Toxicology 2004: 42; 4; 395-564.

7. Lamminpaa A., Vilska J., Hoppu K. Medical Charcoal for a child’s poisoning at home: Availability and success of administration in Finland. Human and Experimental Toxicology 1993: 12 29-32.

8. Vale JA: Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poison Centers and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35: 711-719

9. Position paper: gastric lavage. American Academy of Clinical Toxicology; European Association of Poison Centers and Clinical Toxicologists. J Toxicol Clin Toxicol 2004; 42,933-943.

10. Arnold FJ, Hodges JB, Barta RA. Evaluation of the efficacy of lavage and induced emesis in treatment of salicylate poisoning. Pediatrics 1959 23: 286-301.

11. Corby DG, Lisciandro RC, Lehman RH, Decker WJ. De efficiëntie van de methoden die gebruikt worden om te evacueren de stomach na acute ingesties. Pediatrics 1967; 40: 871-874.

12. Abdallah AH, Tye A. A comparison of the efficacy of emetic drugs and stomach lavage. Am J’s Child 1967; 113: 571-575.

13. Auerbach PS, Osterloh J, Braun O, et al. Efficacy of gastric emptying: gastric lavage versus emesis induced with ipecac. Ann Emerg With 1986; 15: 692-698.

14. Tandberg D, Diven BG, McLeod JW. Ipecacinduced emesis versus gastric lavage : a controlled study in normal adults. Am J Emerg With 1986; 4: 205-209.

15. Young WF, Bivins HG. Evaluation of gastric emptying using radionuclides: gastric lavage versus ipecac-induced emesis. Ann Emerg With 1993; 22: 1423-1427.

16. Tenenbein M, Cohen S, Sitar DS. Efficacy of ipecac-induced emesis, orogastric lavage , and activated charcoal for acute drug overdose. Ann Emerg With 1987; 16: 838-841.

17. Danel V, Henry JA, Glucksman E. Activated charcoal, emesis, and gastric lavage in aspirin overdose. BMJ 1988;296:1507.

18. Lapatto-Reiniluoto O, Kivisto KT, Neuvonen PJ. Gastric decontamination performed 5 min. after the ingestion of temazepam, verapamil and moclobemide: charcoal is superior to lavage. Br J Clin Pharmacol 2000; 49:274–278.

19. Lapatto-Reiniluoto O, Kivisto KT, Neuvonen PJ. Efficacy of activated charcoal versus gastric lavage half an hour after ingestion of moclobemide, temazepam, and verapamil. Eur J Clin Pharmacol 2000;56:285–288.

20. Lapatto-Reiniluoto O, Kivisto KT, Neuvonen PJ. Effect of activated charcoal alone or given after gastric lavage in reducing the absorption of diazepam, ibuprofen and citalopram. Br J Clin Pharmacol 1999;48:148–153.

21. Grierson R, Green R, Sitar DS, Tennenbein M. Gastric lavage for liquid poisons. Ann Emerg Med 2000;35:435–439.

22. Position paper update: Gastric lavage for gastrointestinal decontamination. Benson B E et al. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Clinical Toxicology 2013;51,140–146.

23. Position paper: Whole Bowel Irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 2004;42,843–854.

24. Position paper update: ipecac syrup for gastrointestinal decontamination. Höjer J et al. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Clinical Toxicology 2013;51,134–139.


Kai Knudsen

Dep of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.

Published with permission from Internetmedicin AB

Alcohol Intoxication

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Acute alcohol intoxication is the most common of all intoxications in many countries and occurs in thousands every month. Common alcohol abuse gradually changes into alcohol intoxication without any specific boundary. About 5% of all adult men and 2% of all women in Sweden have alcohol dependence. Approximately 300,000 people in Sweden are expected to have risky alcohol consumption, but in some estimates, a significantly higher number is indicated.

About 20% of the population has more or less temporary alcohol problems. These figures are estimated and therefore relatively uncertain, as large variations occur in different estimates and scientific studies from, inter alia, the Federal Association for Alcohol and Drug Information (CAN), which publishes annual reports. Total alcohol consumption in Sweden has decreased slightly in recent years from a peak 2004 when the average consumption was 10.5 liters of pure alcohol per person per year and 9 liters of pure alcohol per person and 2016. Alcohol consumption is distributed in 42% of wine, 37% of beer, 21% spirits, 5% almonds and 1% cider.

Risky alcohol consumption refers to an intake of alcohol which eventually causes medical and social complications. Risky alcohol consumption usually refers to intake of more than 14 standard glasses of alcohol per week for men and 9 standard glasses per week for women. This corresponds to men 56 cl liquor or 2.2 bottles of wine and for women 36 cl liquor or 1.4 bottles of wine per week. A standard glass (or standard unit) corresponds to 12 g of alcohol or a jar of medium strong beer of 50 cl, a bottle of strong beer of 33 cl, 12 cl of table wine or 4 cl of alcohol.

Binge Drinking

Binge drinking usually means that men drink 5 standard glasses and women 4 standard glasses or more at one and the same time. A bottle of wine is counted as 6 standard units.

Mild and moderate alcohol intoxication is usually not subject to hospital care. Most patients who come to hospital with alcohol intoxication also have physical injuries they need medical treatment for, for example, scrubbing, stabbing, contusions, fractures or cuts. Other serious incidents such as drowning, drug intoxication, smoke inhalation injury, abuse or hypothermia are common in acute alcohol intoxication. Hypothermia with intake of drugs mixed with alcohol can lead to prolonged uptake of the drugs, which causes a drunk person to become increasingly drug-poisoned when he or she is warmed up. Vomiting and diarrhea are common in alcohol intoxication, sometimes with pulmonary aspiration. Fluid balancing and electrolyte disturbances are common in prolonged drinking. Hypokalemia, hyponatremia and hypomagnesaemia are relatively common in alcohol abuse. In acute care, these electrolyte disturbances should be checked.

Pure alcohol intoxication can cause hospitalization if it is pronounced, is part of a mixed drug or affects young, retarded, sick or particularly sensitive individuals. Expression of alcohol intoxication usually occurs with an alcohol content of blood alcohol level (BAL) > 2.0 per mille but with large individual differences depending on the degree of tolerance. Usually you can stand up stable up to about 2 per mille. The most common cause of death due to alcohol intoxication is respiratory depression with hypoxia, pulmonary aspiration of gastric contents. Hypothermia is also common in fatal alcohol intoxication.

Approximately 150-200 people die every year due to acute alcohol intoxication in Sweden, of which only 2-3 are under 30 years of age. Approximately 2000 people die annually due to adverse effects. The dose of alcohol can be about 30-40 cl pure alcohol (100%), which corresponds to 1-1.5 full bottles of alcohol (75 cl, 40%) or 3.3-4,4 bottles of wine or 11-14 cans of strong beer intake for a short period of time. At very high levels alcohol (> 3 per mille) in the blood, it is usually spirits that is consumed. Wine and beer usually take longer to drink, so the maximum concentration is rarely as high as after drinking spirits.

Moderate alcohol consumption has been described in several studies with positive health effects. These positions are controversial and may be regarded as scientifically unsafe. Observational studies are limited by methodological problems, mainly confusion factors and error classification. It is always difficult to prove causality as opposed to cohabitation among groups with low alcohol consumption and stable social conditions.

Amount of alcohol in regular drinks

DrinkVolume (cl)Concentration (%)Amount of alcohol (g)
Beer 3.5%503.512
Beer 5.0%50520

Translation of amount of alcohol in beer, cider, wine to corresponding amount spirit

SortAlkohol Conc (%)Volume (cl)Corresponding
amount of
40% spirit (cl)
Light Beer2.25331.9
Intermediate Beer3.5504.4
Strong Beer5.6507
Strong Wine187533.8
Strong Wine227541.5

Technical alcohol solutions

Various chemical alcohol solutions are used as fuel, detergents and solvents in technical spirits. Common solutions with technical spirits are T-Red, T-Blue, T-Yellow, K-Spirits and M-Spirits. Intoxication with these agents is not uncommon.

Alcohol content in technical spirits varies between 70 and 95%. Technical spirits generally contain denaturing additives that will make the solution undrinkable, but some people, usually battered alcoholics or experimental young people, still drink denatured spirits.

In addition to ethanol, technical spirits contain methyl ethyl ketone, acetone, ethyl acetate, propanol, paraffin and, in some cases, Bitrex. Denatured spirits are also found in many hand cleaning products, disinfectants, after shaving solution, perfumes and in some drug solutions. In Sweden, methanol is not used as denaturant, but it occurs in some other countries.

Pharmacokinetics of Alcohol

Consumed alcoholic beverages are quickly absorbed into the bloodstream from the mucous membrane of the duodenum and small intestine but not as much in the stomach. Alcohol has no protein binding but is distributed into the body’s different tissues. Apparent volume of alcohol distribution (Vd) is 0.7 L/kg. The effect in the brain (“target site”) occurs within a few minutes after ingestion (about 60-90 sec), which is familiar to most normal consumers. Alcohol levels in blood may increase for about one hour after ingestion.

A normal adult who drinks 3-4 cans of strong beer or 4-6 glasses of wine (12 cl, 12%) achieves an approximately BAL at 1 g/L blood concentration equivalent to 1 per mille. An adult woman achieves the same BAL after ingestion of about 3 cans of strong beer or 3-5 glasses of wine (12 cl).

1 per mille corresponds to 27 mmol/L ethanol in blood. Conversion factor from mmol to per mille: mmol/L x 0.0376.

Achieved per mille content varies with body size, how fast you drink alcohol while taking food.

Ninety percent of alcohol is broken down by oxidation if the majority occurs in the liver. Ethanol degrades at relatively constant velocity in the human body using the enzyme alcohol dehydrogenase. Ethanol is converted into acetaldehyde which is then rapidly decomposed into acetic acid and then into carbon dioxide and water. The degradation of acetaldehyde is already started in the stomach but occurs mainly in the liver. Acetaldehyde (etanal) is an intermediate in the decomposition of alcohol. There is some evidence that acetaldehyde causes some of the classic symptoms of hangover, such as nausea, dizziness, headache, nausea and tiredness. Acetaldehyde, in turn, is broken down to acetic acid by the enzyme acetaldehyde dehydrogenase in the peripheral cell respiration. The acetic acid is then broken down to carbon dioxide and water in several steps.

The enzyme alcohol dehydrogenase, which breaks down alcohol, is already saturated at a BAL above 0.1, above this limit, the degradation is constant with an elimination according to the 0:th order pharmacokinetics. About 90% of alcohol is eliminated by hepatic decomposition and 10% eliminated via exhalation, sweating and urine. The distribution between blood and exhalation air is approximately 2100: 1. Normal degradation of alcohol is about 0.1 g/kg body weight per hour, i.e. 5-10 g alcohol per hour for most people. This corresponds to 2-3 cl of spirits, 6-12 cl of wine or 12-25 cl of beer per hour, i.e. about 1 “unit of alcoholic drink” per hour. In an adult, it is estimated that the amount of per mille usually decreases by about 0.15 per hour. The alcohol in a light beer is degraded in about 15-30 minutes while a strong beer usually takes 60-90 minutes. Relatively large individual variations occur.

Normal Degradation of Alcoholic Beverages

Beverage and AmountDegradation Time (approximately)
Bottle of light beer, 33 cl (2.2%)1 hour
Can of intermediate beer, 50 cl (2.8%)1,5 - 2 hours
Bottle of intermediate beer, 33 cl (3,5 %)1,5 - 2 hours
Can of intermediate beer, 50 cl (3,5 %)2 - 2,5 hours
Bottle of strong beer, 33 cl (5.0%)2 - 2,5 hours
Glass of wine, 15 cl (12%)2 - 2,5 hours
Glass of wine, 12 cl (13 %)2 - 2,5 hours
Bottle of wine,, 75 cl (13 %)11 - 12 hours
Spirit, 4 cl (40 %)2 - 2,5 hours
Half bottle of spirits, 35 cl (40 %)16 - 17 hours


The tolerance for alcohol is heavily varied depending on age and experience. The more often you get intoxicated, the higher the degree of tolerance will develop over time. Most people without alcohol problems have difficulty drinking to levels above 2 per mille of ethanol in the blood.

Life-threatening intoxication is usually found at an alcohol content of 4.5 per mille in women and over 5 per mille in men but even lower concentrations can be life-threatening and have resulted in death. It is difficult to get into these levels by simply drinking beer or wine, usually consuming spirits in large quantities. It is not entirely unusual for alcoholics who are taken care of in hospital for acute alcohol intake have a per mille content of 5, sometimes up to 7-8 per mille, in some cases even higher. Serious alcohol intoxication among adolescents already occurs at a level of more than 2.5 per mille. Serious alcohol intoxication is usually associated with memory loss, hangover and anxiety symptoms in the aftermath.

Symptoms of Intoxication

Degree of alcohol poisoningBlood Alcohol Level (g/L)Symptoms
Mild alcohol poisoning0,5-1,0 per milleVerbosity, intoxication, euphoria, slowered speech, slowered reaction time
Moderate alcohol poisoning1,0-2,0 per milleCoordination difficulties, severe intoxication, alcohol drowsiness, nausea, mood swings, aggressiveness, balance difficulties, hanging eyelids, moist glance, slurred speech
Pronounced alcohol poisoning2,0-4,0 per milleNausea, vomiting, very severe intoxication, abdominal pain, diarrhea, difficulty walking, unstable temperament, violent or messy behavior, detoriation of consciousness, somnolence, cohesion in speech and thought
Life-threatening alcohol poisoningMore than 4-5 per milleComa, seizures, deep sleep with snoring, slow breathing, circulatory instability, respiratory depression, hypoxia (blue-scintillating skin, cyanotic lips/face), hypercapnea (reddish/bluish face color), hypothermia

Light (social) intoxication is considered to be present at an alcohol content of 0.5-1 per mille (see table above). At levels in the blood of 1-1.5 per cent, most adults feel as moderately drunk (some units of strong beer or a bottle of wine) and over 1.5 per mille most people feels heavily drunk (one to two bottles of wine). Young girls in lower teens may feel drunk only with one single strong beer and show clear symptoms of intoxication after two strong units of beer.

Mixed intoxication

Concomitant intake of drugs, such as sleepers or analgesics (opioids) potentiates the toxic effect of alcohol. Particularly risky is the use of opioids, benzodiazepines, neuroleptics, barbiturates or some antidepressants while taking alcohol. Over 2 per mille alcohol in combination with flunitrazepam, opioids or other respiratory deprivatory drugs are considered to be life threatening. Moderate alcohol intoxication can turn into life-threatening intoxication in combination with moderate or high levels of sleepers or analgesics. The combination of alcohol and energy drinks makes you get excited and many do not know the drunkenness as clearly why you drink more and achieve a higher degree of intoxication, not seldom associated with memory loss.

Technical alcohol

The symptoms of intoxication with denatured spirits are similar to those with “common” ethanolic beverages; different degrees of intoxication, loss of consciousness, impaired balance, hyperventilation, nausea and vomiting. Often a characteristic acetone-like odour occurs from the exhaled air. The risk of metabolic acidosis, nausea and vomiting is high.

Clinical and Laboratory Investigation

  • S-ethanol
  • S-methanol
  • S-acetone
  • Pulse and blood pressure
  • Oxygen saturation with pulse oximetry (SaO2)
  • Drug screening for illegal drugs (drug test strips)
  • Arterial acid base status (blood gas measurement)
  • Measure the anion gap
  • Infection Parameters (CRP, SR, Pro-Calcitonin)
  • Hb, glucose, Na, K, Mg
  • Ev alcohol markers such as B-PEth (phosphatidyl ethanol), S-CDT (low-fat transferrin)
  • Ev U-Ethylglucuronide (EtG), U-Etylsulfate (EtS) (demonstrates alcohol consumption last 3 days)
  • Liver enzyme parameters
  • ECG
  • Body Temperature
  • Check neurologic status, palpate the skull, exclude trauma. CT brain on unconsciousness and on suspicion of trauma to exclude epi- or subdural hematoma, as well as other intracranial haemorrhage or stroke
  • In case of suspicion of respiratory distress, X-ray of the lungs
  • In case of intoxication with illegal liquor or home burn products, control of methanol and ethylene glycol levels
  • In serum as well as anion gap and osmolal gap.

Electrolyte disturbances

Observe the risk of electrolyte disturbances. It is common with hyponatraemia, hypokalaemia and hypomagnesaemia in alcohol intoxication and alcohol abuse.

  • Pronounced hyponatraemia causes a risk of brain edema and consciousness reduction. Acute hyponatraemia usually results in a significant reduction in alertness. Pronounced hyponatraemia (<120 mmol/L) with low degree of consciousness indicates chronic hyponatraemia. Chronic hyponatraemia must be corrected slowly over several days. All too fast correction of hyponatraemia can lead to membrane damage in brain cells (myelin lesions), so called “pontin myelysis”, with severe neurological damage as a consequence. Hyponatremia is most commonly seen in beer alcoholists, but increased risk is also present when co-administered with SSRIs (antidepressant drugs).
  • Hypocalcaemia causes fatigue and risk of cardiac arrhythmias.
  • Hypomagnesaemia increases the risk of cardiac arrhythmias (common, especially atrial fibrillation) and seizures.

Other deviations in routine samples 

Note the occurrence of anemia and hypoglycaemia.

Biological alcohol markers

  • U-Etylglucuronide (EtG) and U-Etylsulfate (EtS) indicate alcohol consumption for the last 3 days.
  • CDT (months) (low-fat transferrin) rises after a couple of weeks of high alcohol consumption and can show chronic high alcohol consumption. CDT has high specificity for determining high consumption of alcohol.
  • B-PEth (phosphatidyl ethanol) is a collective name for a group of phospholipids formed from phosphatidylcholine in the presence of alcohol. PEth reflects the last few weeks of alcohol consumption.
  • S-GT (gamma-glutamyltransferase) is a membrane protein that is predominantly in the liver and is increased in chronic alcohol consumption. Some drugs may induce increased GT levels in plasma. The GT can also be elevated in diabetes, brain tumors, obesity and biliary disease. A good control of high alcohol consumption can consist of EtG, CDT and PEth. One can say that EtG reflects high alcohol consumption in recent days, PEth in recent weeks and CDT in recent months.

It is likely that one week of high consumption of alcohol is required for PEth to rise, but a high value clearly speaks for high alcohol consumption, because the value has high specificity.


In particular, note the risk of acute vitamin B deficiency. K and B vitamins often need to be substituted with intramuscular injections for three days. 

Substitute B vitamins and K vitamins in alcoholics as needed:

  • Neurobion (B-vitamine complex) 3 ml x 1 i.m. in 3 days
  • Phytomenadion (Konakion) 1 ml x 1 i.v. (10 mg/ml)


Observe the risk of severe withdrawal symptoms during the recovery with risk of delirium and general myoclonal seizures.


Metabolic acidosis is common in the case of intoxication with both ordinary alcoholic beverages and technical spirits. If pH measured in the arterial blood gas is below 7.1, intoxication is considered to be life threatening. Base excess less than -10 mmol/L indicates a different cause than ingestion of common ethyl alcohol.


All patients, including those who are alcoholic, have the right to good general care and to be treated with respect. Stay calm and safe in contact with the patient. General supervision to prevent traumatic injury and moody behavior is the primary. The treatment of acute alcohol intoxication is essentially symptomatic and no antidote is present. Determine the appropriate level of care, but keep in mind that waking and breathing can change suddenly. In case of uncomplicated alcohol intoxication, food canister, liquid, sleep under supervision and antacids may be sufficient. Avoid high-rise bed or bunk to reduce the risk of fall injuries. Resting on the mattress on the floor can be an option. For example, in the case of anxiety and restlessness, give diazepam (Stesolid) 2.5-5 mg intravenously with caution or orally.

In case of more severe intoxication or when complicating factors exist, the situation is different:

  • Monitor alertness and breathing carefully.
  • Give oxygen liberally
  • Suck cleanly in the mouth and throat when there is an increased incidence of mucus or any gastric contents
  • Support breathing and circulation if necessary (ensure free airway, treat hypoxia)
  • Fluid and possibly inotropic drugs at circulation failure. See below for details.
  • In the presence of paradoxical breathing patterns, improve airway conditions (orolaryngeal airway device) and usually intubation are needed.
  • Check body temperature. In hypothermia, heating.
  • Treat acute confusion and motor anxiety.
  • Fluid, per os or intravenously. Poisoned patients usually need rehydration with intravenous fluid. Give isotonic solutions or buffered glucose solutions. If necessary, adjust any electrolyte disturbances.
  • In case of suspicion of respiratory distress, X-ray of the lungs and antibiotics against respiratory infection (cefotaxim (Zinacef) 1.5 g x 3 i.v.). With pulmonary aspiration: intubation, ventilation and respiratory treatment with PEEP. Bronchoscopy.
  • Possible prophylaxis against delirium and general seizures (ex carbamazepine (Hermolepsin, Tegretol) 200 mg 1 × 3 p.o. or levetiracetam). Exclude status epilepticus.
  • Gastric lavage and activated charcoal are only administered when the intoxication is mixed with drugs when the patient is received within 1 hour after ingestion.

Free airway

The respiratory tract may be more or less blocked in alcohol intoxication. Free airway creation has the highest priority. Suck cleanly in the mouth and throat when there is an increased incidence of mucus. Nose tube or oropharyngeal airway device is the first aid. Note that the nasal tube may cause severe nasal bleeding and that the risk of nasal bleeding is increased during alcohol intoxication (due to the vasodilatory effect of alcohol). Therefore, use plenty of gel when introducing into the nose. The position of the patient under vigilance should be in a lateral position, the tongue drawn through a solid jaw lift. Patients who fail to keep the airway in the supine position or not wakeful should be monitored in the intensive care department. Endotracheal intubation is made if necessary in case of insufficient airway, hypoxia or carbon dioxide retention (hypercapnia).


Avoid hypoxia and hypercapnia, liberate treatment with oxygen. If breathing is insufficient, endotracheal intubation and respiratory treatment on a ventilator in the intensive care unit must be considered. Clean the airways from mucus.


Treat blood pressure drops with intravenous fluid and, if necessary, sympathomimetic drugs (inotropic drugs), e.g. ephedrine, phenylephrine, dopamine or norepinephrine. 

Confusion and Aggressiveness

Stubborn and aggressive patients may need to be tranquilized with drugs to prevent the patient from injuring himself or others. Such sedation is difficult and difficult to handle properly. The treatment itself involves risks in the form of a drop in blood pressure or sudden onset of somnolence with difficulty in maintaining free airway and respiratory depression. Therefore, sedative drugs must be used with caution and under supervision. The treatment requires the ability to take over the patient’s respiration with controlled ventilation and respiratory treatment. Suitable agents for sedation are haloperidol (Haldol) 1-5 mg iv, droperidol (Dridol), midazolam (Dormicum) 1-5 mg iv or propofol (Propofol) 20-100 mg iv. Propofol should only be used by an experienced anesthetist who can handle respiratory problems, as there is a significant risk of hypotension and apnea. Haloperidol (Haldol) should not be used in patients with convulsions or previously known convulsions.


The hangover is characterized by nausea, dizziness, fatigue, feeling uneasiness, anxiety and headache. The hangover occurs when the blood alcohol level is close to zero. The hangover is primarily explained by the amount of alcohol consumed, but also at the rate of drinking and on the type of alcoholic beverages consumed. Colored beverages such as whiskey are considered to give more hangovers compared to unleavened spirits. Red wine often gives more hangover than white wine. When taking alcohol at the same time, the risk of hangover and headache increases. Alcoholic beverages should therefore not be used as thirst extinguishers. The hangover is explained, among other things, by acetaldehyde but not entirely. New theories suggest an inflammatory component as a cause of the hangover. The susceptibility to hangover is individual but affects most people who have reached an alcohol level of over 1.5 per mille. About 25% of the population gets little or no hangover. The symptoms are also due to relative dehydration and the intake of so called congeners. Congeners are by-products formed in the fermentation of alcohol and consist of furfural, tannins and fusel oil. Whether drinking water after alcohol can prevent hangover is scientifically unclear, although many people have good personal experience of it. The main cause of the nausea experienced and the general discomfort is due to acetaldehyde that is formed during the breakdown of alcohol. The treatment of the hangover is symptomatic of primarily rehydration, rest, sleep, simple analgesics and antacids.


In case of pronounced alcohol abuse, the patient is monitored through psychiatry, dependence medicine and social services. Possible mental cohabitation (comorbidity) is investigated and treated accordingly.

Diagnostic codes according to ICD-10

  • F10 Mental disorders and behavioral disorders caused by alcohol
  • T51.0 Ethanol
  • Y91.0 Alcoholic toxicity
  • Y91.1 Moderate alcohol toxicity
  • Y91.2 Difficult alcohol intoxication
  • Y91.3 Very severe alcohol toxicity  


  1. Alcohol tests in hospitals not quite easy to use for legal use. Conversion of ethanol to plasma or serum to blood level. Jones AW, Medical Journal No. 6 2008 Volume 105 Link to the article
  2. Norwegian Public Health Institute, Statistics Sweden (2011). National Public Health Review – Health on equal terms. More about the survey
  3. Andersson P, Moller L & Galea G (2012). Alcohol in the European Union: Consumption, harm and policy approaches. WHO Regional Office for Europe. Link
  4. Anderson P & Baumberg B (2006). Alcohol in Europe – A public health perspective. A report for the European Commission. London: Institute of Alcohol Studies. Link
  5. CAN (2012). Drug development in Sweden 2011. Report no. 130. Stockholm: Central Association for Alcohol and Drug Information. Link to the report
  6. Hibell B and others (2012). The ESPAD report 2011. Alcohol and Other Drug Use Among Students in 36 European Countries. Stockholm: Swedish Council for Information on Alcohol and Other Drugs (CAN), the European Monitoring Center for Drugs and Drug Addiction (EMCDDA), and the Pompidou Group at the Council of Europe. Link
  7. Ramstedt M, Lindell A & Raninen J (2013a). Talk about alcohol – a statistical annual report from the Monitor project. SoRAD. University of Stockholm.
  8. Kühlhorn E, Ramstedt M, Hibell B, Larsson S & Zetterberg H (1999). Alcohol consumption in Sweden in the 1990s. Stockholm: Ministry of Social Affairs.
  9. Stockwell T, Zhao J, Panwar S, et al. Do “moderate” drinkers have reduced mortality risk? A systematic review and meta-analysis of alcohol consumption and all-cause mortality. J Stud Alcohol Drugs. 2016; 77 (2): 185-198. Link to the article

Published with permission from Internetmedicin AB

Bensodiazepines – Intoxication and Abuse

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Benzodiazepines are a group of anxiolytics that began to be used in Sweden and other countries in the 1960s as sedatives and hypnotics. Benzodiazepines are internationally accepted standard remedies for treatment of anxiety disorders and temporary sleep disorders. They have also to varying degrees been used in the treatment of milder forms of anxiety and restlessness. Women are more commonly prescribed benzodiazepines, which may be related to that anxiety disorders are more common in women than in men. The use of benzodiazepines is also related to age. People over the age of 65 accounts for more than half of the consumption.

Benzodiazepines are commonly associated with drug-induced overdose and acute toxicity, often associated with alcohol. Diazepam is converted in the body into various active metabolites, mainly nordiazepam and temazepam, but also oxazepam which is excreted in the urine. Maximal blood concentrations of diazepam occur after 30-90 minutes with a half-life that can vary between 20-40 hours for diazepam and 50-99 hours for nordiazepam (long half-life!).

All benzodiazepines have a certain risk of addiction development. Dependence means when an individual persists in use of the drug despite problems related to use of the substance. Compulsive and repetitive use may result in tolerance to the effect of the drug and withdrawal symptoms when use is reduced or stopped. In Sweden it is estimated that 65,000 people have a drug addiction and that 315,000 have a risk use. Being addicted means feeling in need of the drug, difficulty in controlling the use, difficulty in discontinuing the drug, and developing withdrawal without it. The different preparations do not have the same risk of addiction but have a substantially similar pharmacological profile with comparable risks in overdose and abuse. Diazepam is classified as a drug according to LVFS 2011: 10, list IV.

The benzodiazepines with the greatest risk of addiction are those who have rapid onset and high potency. These are flunitrazepam, alprazolam, oxazepam and lorazepam. The greatest risk of addiction appears today with alprazolam (Xanor®, Alprazolam®, Xanor Depot®). Regular intake of some of these benzodiazepines implies a risk of tolerance increase and the occurrence of withdrawal symptoms in discontinuation trials.

Flunitrazepam (Flunitrazepam Mylan® 0.5 mg/1 mg) is primarily a sedative hypnotic, but due to a significant abuse risk, it is also illegal in Sweden. Previously, flunitrazepam was present in several preparations such as Rohypnol®, Flupam® and Fluscand®, all of which are now unregistered preparations.

Benzodiazepines are predominantly prescribed as sleep inducer for elderly patients, but they are also used as premedication for surgical operations. In premedication, benzodiazepines have had a minor role in recent years and have been replaced by other pharmacological preparations, e.g. clonidine.

As a sleeping tablet, flunitrazepam has been extensively replaced by the so-called Z-formulations zopiklon (Imovane®), zolpidem (Stilnoct®) and zaleplon (Sonata®). Zopiklon is recommended as a first aid in treating sleep disorders. As an additive, flunitrazepam has to a certain extent been replaced by these agents, as well as diazepam (Stesolid®), oxazepam (Sobril®), lorazepam (Temesta®) and alprazolam (Xanor®).

Bensodiazepines and similar drugs

BensodiazepineBrand nameFormula
DiazepamStesolid, Diazepam, (Valium Apozepam - unreg)Tablet, rectal solution
KlonazepamIktorivil, RivotrilTablet, injektionslösning, oral solution
LorazepamTemesta, LorazepamTablet
MidazolamDormicum, Midazolam, BuccolamInjection solution, blend
NitrazepamNitrazepam, Mogadon, ApodormTablet
FlunitrazepamFlunitrazepam, (Fluscand, Rohypnol - unreg)Tablet
OxazepamSobril, OxascandTablet
AlprazolamXanor, Xanor depot, Alprazolam, XanacTablet, Tablet extended release
ZolpidemStilnoct, Zolpidem, EdluarTablet
ZopiklonImovane, Zopiklon, Zopiclon, ZopicloneTablet
ZaleplonSonata (unreg. 2015)Tablet

Approximate equipotent doses and clearance times of different benzodiazepines

BensodiazepineEquivalent dose (mg)Terminal half-life (h)


Benzodiazepines can be used as intoxicants since they have a relaxing and euphoric effect with some risk of abuse, often in combination with alcohol. The relaxing and restraining effect is enhanced by alcohol. Often, development goes from regular use via overuse to risk use and abuse. This development is seen as in chronic pain conditions and in long-term anxiety and nervous disorders.

In case of drug abuse, the recommended daily dose is usually exceeded by more than twice (from one to two tablets to four five tablets or more per day). Misuse of benzodiazepines occurs as a mere drug addiction or as a substance abuse with alcohol, analgesics or other illicit drugs. One can see a sliding transition from normal consumption, to risk use and abuse. Flunitrazepam, alprazolam (Xanor®) and oxazepam (Sobril®) are those with the greatest potential for addiction development, but there is a risk of dependence in all benzodiazepines without exception. At the same time, there are many patients who work well with unchanged dosage without tolerance development or dose increase, especially older ones.

Alprazolam (Xanor®) has a significant risk of addiction and abuse. The effect of higher doses than 1 mg of alprazolam or more than 10 mg of diazepam usually causes, but not always, drowsiness and sleepiness that passes into sleep, deeper sleep or coma. A person who has taken such a dose may be drunk and have symptoms such as widened pupils, flushing, pride, slow reflexes, relaxed muscles, numbness, drowsiness, sleepiness, and finally coma.

In some individuals, a paradoxical effect may occur with increased intake, with “increased vigilance” (“excitation state of mind”) in combination with an inhibition effect. The risk of an excitation state increases with the concurrent intake of amphetamine or other central stimulants. It is not uncommon with psychomotor disorders, such as difficulty in being still, hyperactivity, as well as increased aggressiveness and increased impulsivity. This paradoxical effect has occurred in connection with surgical premedication, both among children and adults. The effect on children is sometimes described as the child “climbs on the walls”.

The excitatory stage involves a change of vigilance that can pass into sleep or coma. However, people with regular abuse may maintain the “increased alertness” and avoid sleep by choosing the right dose range or by combining benzodiazepines with central stimulants such as amphetamine, methamphetamine, cocaine, synthetic cannabinoids or ecstasy. This is seen primarily among people with a substance abuse and an increased tolerance for the drug. The excitation stage can be transformed into acute confusion with agitation, rarely with aggressiveness, numbness and hallucinations. Several illegal benzodiazepine preparations are present in European countries or purchased online. These include adinazolam, bromazepam, flubromazepam, diclazepam, flubromazolam, flunitrazolam, N-desmethylflunitrazepam, norfludiazepam, phenazepam, clonazolam, cloniprazepam, zapizolam, meclonazolam, pyrazolam and etizolam.


In the case of developed dependence on benzodiazepines, withdrawal symptoms occur during abrupt drug withdrawal. Symptoms such as feeling complacent, increased nervousness, unspecified discomfort, intrusive anxiety and nervousness. Seizures may develop. Somatic symptoms such as palpitations, tremors, stomach pain, cold sweating and abstinence seizures are also present. In case of prolonged abuse, a slow and gradual drug discontinuation usually requires, for example, tablet diazepam (Stesolid®), which may take several months and up to one year. The withdrawal symptoms start to occur a few days after the end of the drug. Not so often, such a discontinuation begins far above recommended daily doses. Initial doses may be as high as 60-100 mg diazepam per day, which is then given in a decreasing dose. Alternative medicines in the treatment of withdrawal symptoms have not yet shown better results than treatment with benzodiazepines in declining doses. Among the drugs tested are beta blockers and buspirone (Buspiron®). 

Special risks of Substance Abuse 

There are particular risks of abuse where benzodiazepines and analgesics (opioids) are combined. The enhancement of depressant effects on the brain’s respiratory and circulatory centers can lead to overdoses and death, especially in combination with opioids or alcohol. When the use of different drugs is discontinued at the same time, different withdrawal symptoms occur. Benzodiazepines enhance the anti-inflammatory effect of analgesics. Benzodiazepines reinforce the rush of other drugs such as cannabis, amphetamines and opiates.

Cross Tolerance

When tolerance of a drug within a specific group of drugs occurs, tolerance also increases for other preparations within the same category. For example, anesthesia personnel who is to be anesthetizing a patient prior to an operation finds that the patient does not fall asleep on a normal dose of anesthetic drugs. It is usually because the patient is a major consumer of a similar preparation. 

Cross Sensitization

Certain drug effects are instead reinforced for prolonged use, such as the “drug affection”, but also the psychosuppressive effects. Sensitization to a drug can lead to cross-sensitization to another drug. In practice, it means that the person dependent on a drug becomes more dependent on another.



Twentyfive to fifty (25-50) mg alprazolam in combination with alcohol at a blood level of 2 per mille has given lethal toxicity. 0.3 mg/kg to 8-year-old gave moderate – severe intoxication. 10 mg to 13 years gave moderate toxicity. 15 mg (and alcohol) in adults gave severe toxicity, while 20-40 mg to adults only caused moderate inhibition.

Symptoms of Acute Overdose

  • Somnolence, drowsiness
  • Dizziness
  • Hypotension
  • Bradycardia
  • Hypothermia
  • Apnea episodes
  • Mydriasis, large pupils (even small miotic pupils occur especially in unconsciousness)
  • Ataxia
  • Dysartria, slow slurred speech
  • Nausea
  • Muscle weakness
  • Respiratory depression
  • Anxiety
  • Excitation
  • Tachycardia
  • Hallucinations
  • Coma


Treatment of Acute Overdose

  • General supervision to prevent injuries and disability
  • Establish free airway. The patient should be placed in advanced side position. The so-called “orofacial airway device” or equivalent can be used.
  • Oxygen liberally
  • If a significant amount of drug has been taken, gastric lavage should be performed within 1 hour after ingestion
  • Active charcoal is given only within 1 hour after ingestion
  • Monitoring of respiration, circulation and alertness
  • Intravenous fluid supply of isotonic crystalloid solutions, e.g., Ringer Acetate
  • Intubation and controlled ventilation at deep unconsciousness or respiratory depression
  • Antidote treatment with flumazenil (Lanexat®), as appropriate


Specific antidote flumazenil (Lanexate® 0.1 mg/ml, 5 ml in an ampoule = 0.5 mg) can be given slowly intravenously to wake a comatose or semicomatous patient at doses of 0.3-0.5 mg.The dose should be repeated after one minute in case of no effect. Usually 2 to 3 doses are sufficient. The maximum dose for adults is 2 – 5 mg flumazenil. Note the number of ampoules. New injection is sometimes necessary after 1 – 4 hours. In some cases, flumazenil may be administered in continuous infusion. Flumazenil can be combined with naloxone in case of unclear unconsciousness in suspicion of drug-induced unconsciousness. Flumazenil (Lanexat®) is unsuitable for co-administration with drugs that can induce general seizures, such as antidepressant drugs, as the antidote lowers the seizure threshold.

In case of doubt, the patient may instead be monitored for respiratory and respiratory tract care in an intensive care unit. Treatment should be guided by what is best for the patient and not after the ICU availability situation. Gastric lavage should be performed only if a large amount of benzodiazepines have been taken or if the drug has been taken in combination with other dangerous preparations up to one hour after ingestion. If there is doubt as to whether the patient can protect his respiratory tract, experienced anesthetist should participate in the procedure.

Patients who are deeply unconscious or who have insufficient breathing should be intubated and monitored in an intensive care unit. Patients usually wake up after overdosage of benzodiazepines after 4-12 hours depending on intake and type of preparation. Note that several benzodiazepines have active metabolites with a long half-life, which means that even longer-term unconsciousness more than 12 hours occurs.

The half-life is further prolonged in case of reduced hepatic function. With guaranteed vital features where breathing and airway is ensured, the prognosis is usually very good with only symptomatic treatment.


It is important to control the patient during the emergency phase at the correct level of care so that vital functions can be ensured in a medical emergency department or an intensive care unit.

In the aftermath, the drug abuse must be treated; assessment of psychiatrists and referral to dependence clinic and contact with social services are some measures that are almost always needed. Discontinued withdrawal treatment should be planned as expected with severe withdrawal.

The application for social services must always be performed in life-threatening addiction, in the treatment of children under the age of 18 or when adults have children at risk of neglect.

Psychosocial support efforts are necessary to give parallel to drug treatment of existing withdrawal symptoms. It is important to get a picture of the patient’s personality, emotional state and cognitive ability to give the patient the correct treatment. The investigation needs to assess whether psychotic symptoms, increased suicidality or addiction are present. Provided depression and psychotic symptoms, the risk is great for suicide.

Outpatient treatment is individualized and based on frequent contacts with psychiatrists or psychologists who have experience of drug dependence, as well as regular urine tests with benzodiazepine, THC (tetrahydrocannabinol) and other drugs. Initially after a period of abuse, it is common with a disturbance of attention and poor motivation for drug-freeness.

Social aspects must also be evaluated in the patient’s treatment and the curator (social services) is connected. In addition, it should be understood that the risk factors and the safety factors (relatives) the patient has in his/her immediate environment in order to be able to provide the correct support measures. An important issue to investigate is the type of living the patient has. A personal interaction between dependent clinics and social services is often necessary in these cases. A referral to a psychologist or curator with special skills regarding dependence diseases and the use of benzodiazepines is essential for the continued care of the patient. In the treatment of schoolchildren, school health care should also be announced. An assessment of the patient’s addiction development and suicidality should be done with established psychological instruments such as ASI interview, AUDIT and measuring instruments to assess suicide risk.

Diagnostic code according to ICD-10

  • T42.4 Benzodiazepines
  • X60-X69 Intentional self-destructive action through poisoning
  • Y10-Y19 Poison with obscure intention
  • F13.0 Mental disorders and behavioral disorders caused by sedatives and hypnosis, acute intoxication

Call as required your local Poisons Information Center.


  1. Rohypnol – not just a sleep piller. A mapping of drug abuse. Gunnar Hermansson. Polish Academy of Law 1998.
  2. Abuse liability of flunitrazepam among methadone-maintained patients. Magi Farré et al. Psychopharmacology 1998: 140: 486-495
  3. Benzodiazepines – side effects, abuse risk and alternatives. Lance P. Longo et al. American Family Physician April 1, 2000, Vol 61, No. 7, 2121-2128
  4. Abuse of Flunitrazepam (Rohypnol) and other benzodiazepines in Austin and South Texas. Sarah R. Calhoun et al. Journal of Psychoactive Drugs. Vol. 28 (2), April-June 1996.
  5. Benzodiazepines and other psychotropic drugs abused by patients in a Methadone maintenance program: familiarity and preference. Christian Barnas et al. Journal of Clinical Psychopharmacology Vol. 12 No. 6 1992.
  6. Dépendence aux psychotropes et traitements de substitution: tendances récentes. X. Thirion et al. Therapy 1999; 54: 243-249.
  7. Consommation abusive de flunitrazepam par les toxicomanes aux opiacés. J. Salvaggio et al. Ann. With. Internal 151, Suppl. A, pp. A6-A9, 2000 France
  8. The role of benzodiazepines in elderly suicides. Anders Carlsten et al. Scand J Public Health 2003; 31: 224-228.
  9. Sudden Death and Benzodiazepines. The American Journal of Forensic Medicine and Pathology 17 (4): 336-342, 1996. O. H. Drummer and David L. Ranson
  10. Flunitrazepam: an evaluation of use, abuse and toxicity. Henrik Druid et al. Forensic Science International 3123 (2001) 1-6
  11. Club Drugs: methylenedioxymethamphetamine, flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate. Kelly M.Smith et al. Am J Health-Syst Pharm vol 59 jun 1, 2002.
  12. Adverse effects of prolonged benzodiazepine use. Heather Ashton. Adverse Drug Reaction Bulletin june 1986 no 118 440-443
  13. Comment: use and abuse of flunitrazepam. Marta Mas et al. The Annals of Pharmacotherapy 1998 September, vol 32, 980-981
  14. Flunitrazepam consumption among heroin addicts admitted for in-patient detoxification. Luis San et al. Drug and Alcohol Dependence, 32 (1993) 281-286.
  15. Benzodiazepine misuse in poly-drug users L. Ferreira et al.
  16. Date rape among adolescents andyoung adults. V.I. Rickert and C.M. Wiemann. J Pediatr Adolesc Gynecol 1998:11:167-175
  17. Flunitrazepam (Rohypnol) abuse in combination with alcohol causes premditated grievous violence in male juvenile offenders. Anna M Dåderman and Lars Lidberg. J Am Acad Psychiatry Law vol 27, no 1, 1999.
  18. Flunitrazepam abuse and personality characteristics in male forensic psychiatric patients. Anna M. Dåderman and Gunnar Edman. Psychiatry Research 103 (2001) 27-42
  19. Violent behaviour, impulsive decision-making, and anterograde amnesia while intoxicated with flunitrazepam and alcohol or other drugs: a case study in forensic psychiatric patients. Anna M. Dåderman et al. The Journal of the American Academy of Psychiatry and the Law 30:238-51, 2002



Kai Knudsen

Dep of Anesthesia and Intensive Care,

Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB

Tricyclic Antidepressant Agents

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Tricyclic antidepressant drugs (TCAs) constitute second-generation antidepressants that became common in the treatment of depression in most countries in the 1970s. These drugs are predominantly prescribed against endogenous mental depression but also against several other conditions such as severe pain states, OCD, panic syndrome, PTSD, narcolepsy and nocturia. Several nearby pharmacological variants occur as bicyclic and tetracyclic antidepressant drugs.

Poisoning with tricyclic antidepressant drugs (TCAs) is still common and deaths occur regularly, although serious poisoning was significantly more common in the 1980s and 90s than today. Antidepressants are common in self-inflicted deliberate poisoning and have significant morbidity and mortality. Poisoning with TCA has higher mortality compared with other antidepressant drugs. The suicide risk of depressed patients remains during treatment until remission has occurred and may even increase initially, as in some cases the inhibition may decrease before mood is improved. Amitriptyline is one of the most common drugs in fatal suicide poisoning worldwide. TCA poisoning is usually diagnosed according to ICD with the code T43.0. In 2014, 47 deaths of these poisons were caused in Sweden, 24 women and 23 men (about 250 deaths per year in England).

Drug poisoning with TCA usually requires intensive care. In total, approximately 12 million daily doses (DDD) of TCA are sold per year in Sweden, compared to the SSRIs sold in approximately 170 million DDD. A number of tricyclic antidepressants have been deregistered in Sweden in recent years, due to the fact that they have been replaced by more modern drugs with fewer side effects. Classical TCAs have relatively strong side effects that may be felt in early treatment such as orthostatism with dizziness and feeling unwell, as well as palpitations, dry mouth and constipation.

Acute poisoning with TCA may give rise to an anticholinergic syndrome with large pupils, palpitation, big pupils, excitement and mental confusion. The anticholinergic syndrome should be distinguished from the serotonergic syndrome that may occur after overdose with SSRIs. Serious poisoning is characterized by coma, seizures and cardiac arrhythmias. In ECG, widened QRS complexes and irregular rhythm are commonly seen. Really wide-necked QRS complexes indicate serious poisoning, the wider the more dangerous. QRS width over 140 msec indicates serious poisoning, and over 160 msec very serious poisoning.


The toxic effect of overdose is mainly due to:

  • An inhibition of noradrenaline uptake presynaptically in nerve terminals
  • A direct alpha receptor blockade
  • A membrane stabilizing effect in myocardium (quinidine-like)
  • An anticholinergic effect

Highest toxicity has amitriptyline and dosulepin.

Degree of poisoning

Intake of less than 10 mg/kg gives easier poisoning. Intake of 15-20 mg/kg is likely to cause serious poisoning. Ingestion of 1 to 2 g usually causes moderate poisoning; over 2.5 g causes serious poisoning. Intake over 5 g produces very serious poisoning.

Common cyclic antidepressants 

  • Amitriptylin
  • Clomipramine
  • Nortriptyline
  • Maprotilin
  • Mianserin

Other antidepressant drugs

These have previously been prescribed in Sweden but have been deregistered in recent years of which some may be available in other countries:

  • Desipramine
  • Imipramine
  • Lofepramin
  • Protriptylin
  • Trimipramine
  • Opipramol
  • Trimipramine
  • Dothiepin
  • Dibenzepin
  • Protriptyline
  • Doxepin
  • Iprindole
  • Melitracen
  • Butriptyline
  • Dosulepin
  • Amoxapine
  • Dimetakrin

Symptoms of acute poisoning

  • Somnolence and coma

Reduced alertness to unconsciousness, ranging from little influence to deep unconsciousness for several days. The length of the comatous period depends on the preparation taken, the amount taken and the plasma half-life. In case of serious poisoning, it is common for at least one day of unconsciousness.

  • Confusion

Confusion and agitation are common

  • Large pupils

Depend on an anticholinergic effect.

  • Hypotension

Blood pressure may initially be increased but is more often slightly lowered with a systolic blood pressure around 80-90 mm Hg. Blood pressure may become even lower in case of severe poisoning.

  • Cardiac arrhythmias

Tachycardia is common, as is ventricular arrhythmias. In severe cases, multiple VES with complete irregularity and “Torsade de Pointes” arrhythmias. Arrhythmias often coincide with heart failure.

  • Respiratory depression

Slow, regular but insufficient breathing with risk of hypoventilation and carbon dioxide retention (hypercapnia).

  • Seizures

Increased “excitement”, with tingling in the extremities is common as well as convulsive seizures.

Anticholinergic Syndrome

  • Big pupils
  • Dry hot skin
  • Tachycardia
  • Confusion
  • Hallucinations

The English Anti-Cholinergic Syndrome Memory Frame is nice to keep in mind

  • Mad as a hatter
  • Dry as a bone
  • Red as a beet
  • Blind as a bat
  • Hot as a desert

Serious poisoning (intake over 2500 mg) 

  • Severe hypotension
  • ECG changes
  • Broadened QRS complex, AV block, extended QT time, ST-T changes.
  • Heart failure

Cardiogenic shock is associated with bradycardia and pronounced broadening of QRS on ECG and ventricular arrhythmias. In the end, bradycardia and asystoli and a sinusoidal curve on ECG develops. At a QRS over 100 ms, the risk of seizures increases. At a QRS over 160 ms, the risk of ventricular arrhythmias increases significantly.


Medical history

  • What preparation? Amount? Time of intake? Mixed poisoning with other substances? Signs of deliberate suicide action?


  • Clinical diagnostics
  • Intox samples, including blood alcohol level (BAL)
  • ECG
  • Pulse oximetry
  • Blood pressure
  • Check blood samples including myoglobin for signs of prolonged unconsciousness
  • Drug screening

The treatment is predominantly symtomatic and one should avoid hypotension, hypoxia and metabolic acidosis. Most TCAs have high fat solubility and a large volume of distribution, which means that elimination methods like hemodialysis become ineffective in treatment. Tricyclic antidepressants have anticholinergic effects that are dose dependent and decrease during treatment. Antidotal treatment with physostigmine may be considered after the initial phase when circulation and respiration is stable.

Preparedness must be prepared for the treatment of respiratory depression, convulsions, cardiac arrhythmias and blood pressure drop, which means that the patient should always be treated within the ICU (> 2.5 g) in severe cases. In case of pronounced hypotension, isotonic fluids is given crystalloid fluid, hypertonic salt (RescueFlow) and sodium bicarbonate.

It should also be avoided to provide membrane-stabilizing drugs such as quinidine, beta blockers, calcium antagonists and flecainide (Tambocor). Amiodarone (Cordarone) should probably be avoided in the treatment of arrhythmias as it may prolong QT interval, and cause hypotension, bradycardia and possibly arrhythmias.


  • Gastric lavage

Within an hour of intake – until clear exchange. Upon later arrival, gastric lavage may be considered for life-threatening poisoning up to 24 hours after the incidence.

  • Medical charcoal

The dose should be at least 50 g. Give at least 10 times the dose taken of TCA.

  • Alkalinization

Sodium bicarbonate is given on wide indications – correct acidosis until Base Excess (BE) becomes positive in the blood gas analysis. The pH should be above 7.45. Alkalinization can reverse parts of the conduction barrier in the heart and improve depolarization. Even hypotension can be improved. Sodium bicarbonate reduces the free fraction of the drug in the bloodstream, which allows smaller amounts of TCA to bind into the heart, plasma protein binding increases. You can often start immediately with two bottles of 100 ml Sodium Bicarbonate (60 mmol/unit).

  • Hypertonic saline

For wide-spread QRS complexes on ECG (> 160 ms). Immediately give 200 mmol sodium intravenously.

  • Oxygen

Intubation and controlled ventilation in respiratory insufficiency

  • Adequate fluid supply, sodium chloride and optionally. dextran (macrodex)
  • Physostigmine

In the case of anticholinergic symptoms, symptoms of confusion, psychomotor disturbance and agitation physostigmine can be given intravenously, but not if circulatory instability or bradycardia occurs. There is a small risk that physostigmine induces convulsions.

  • Inotropic treatment with vasopressor substances

Noradrenaline or adrenaline may be given continuously. Dopamine sometimes has insufficient effect. Adrenaline has given rise to less arrhythmias than noradrenaline in experimental studies and may be preferred. In case of pronounced bradycardia, isoprenaline may be given.

  • Arrhythmia therapy

Magnesium sulphate (20-40 mmol intravenously) may be given, in ventricular tachyarrhythmias, or in rare cases lidocaine. In the treatment of arrhythmias, polypharmacy should be avoided.

  • Diazepam  In case of seizures or anxiety, 5 mg iv.
  • In case of circulatory collapse, extracorporeal support such as arteriovenous ECMO may be life-saving.
  • ILE (Intravenous Lipid Emulsion Therapy)

ILE can be considered during circulatory collapse. ILE has been shown to be efficient primarily with overdose with local anesthetic agents, mainly bupivacaine. In case of overdose with TCA, a large number of positive case reports are published. However, a thorough review of the topic published in 2016 has left a major question mark for the effectiveness of this treatment in TCA poisoning. In controlled animal studies, a small entrapment has been demonstrated by amitriptyline, but no beneficial hemodynamic effect or improved survival. The evidence for this treatment is therefore considered to be only low when poisoned with TCA. In some animal studies, even increased mortality has been detected with ILE and theoretically there is a risk of ARDS and pancreatitis as a result of treatment.


  • Tricyclic and tetracyclic antidepressant drugs T43.0
  • Observation of suspected toxic effect of intake substance Z03.6


  1. Kerr GW, McGuffie AC, Wilkie S. Tricyclic antidepressant overdose: a review. Emerg Med J 2001;18:236–41. Länk
  2. Hawton K, Bergen H, Simkin S, Cooper J, Waters K, Gunnell D et al. Toxicity of antidepressants: rates of suicide relative to prescribing and non-fatal overdose. Br J Psychiatry 2010;196:354–8. Länk
  3. Body R, Bartram T, Azam F, Mackway-Jones K. Guidelines in Emergency Medicine Network (GEMNet): guideline for the management of tricyclic antidepressant overdose. Emerg Med J 2011;28:347–68. Länk
  4. Levine M, Hoffman RS, Lavergne V, Stork CM, Graudins A, Chuang R, et al. Systematic review of the effect of intravenous lipid emulsion therapy for non-local anesthetics toxicity. Clin Toxicol (Phila) 2016;epubl ahead of print. Länk
  5. Engels PT, Davidow JS. Intravenous fat emulsion to reverse haemodynamic instability from intentional amitriptyline overdose. Resuscitation 2010;81:1037–9. Länk
  6. Harvey MG, Cave G. Case report: successful lipid resuscitation in multi-drug overdose with predominant tricyclic antidepressant toxidrome. Int J Emerg Med 2012;5:8. Länk
  7. Kiberd MB, Minor SF. Lipid therapy for the treatment of a refractory amitriptyline overdose. CJEM 2012;14:193–7. Länk
  8. Litonius ES, Niiya T, Neuvonen PJ, Rosenberg PH. No antidotal effect of intravenous lipid emulsion in experimental amitriptyline intoxication despite significant entrapment of amitriptyline. Basic Clin Pharmacol Toxicol 2012;110:378–83. Länk
  9. Heinonen JA, Litonius E, Backman JT, Neuvonen PJ, Rosenberg PH. Intravenous lipid emulsion entraps amitriptyline into plasma and can lower its brain concentration – an experimental intoxication study in pigs. Basic Clin Pharmacol Toxicol 2013;113:193-200. Länk
  10. Forsberg M, Forsberg S, Höjer J. Inget stöd för att lipidterapi är en effektiv antidot vid akut förgiftning. Lakartidningen 2015;112:1723-6. Länk
  11. Knudsen K, Abrahamsson J. Effects of magnesium sulfate and lidocaine in the treatment of ventricular arrhythmias in experimental amitriptyline poisoning in the rat. Crit Care Med 1994;22:494–8. Länk
  12. Knudsen K, Abrahamsson J. Magnesium sulphate in the treatment of ventricular fibrillation in amitriptyline. Eur Heart J;18:881–2. Länk
  13. Knudsen K, Heath A. Effects of self poisoning with maprotiline. BMJ 1984;288:601–3. Länk
  14. Knudsen K, Abrahamsson J. Effects of epinephrine and norepinephrine on haemodynamic parameters and arrhythmias during a continuous infusion of amitriptyline in rats. Clin Toxicol 1993;31:461–71. Länk
  15. Knudsen K, Abrahamsson J. Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning. Crit Care Med 1997;25:669–74. Länk

Author Kai Knudsen

Anesthesia department, Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB


By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

The prescription of other antidepressants than classical tricyclic antidepressive agents (TCA) has increased significantly over the past 20 years in Sweden. By 2015, it is estimated that approximately 600,000 patients were treated with antidepressants. The drugs can be divided into three groups; SSRIs – Selective Serotonin Reuptake Inhibitors, SNRI preparations – Selective Norepinephrine Reuptake Inhibitors and NaSSA Preparations – Noradrenergic and Specific Serotonergic Antidepressants. Generally, the SSRIs have taken over most of the antidepressant drug market. SSRIs were sold in 2015 at 82 doses per 1000 inhabitants per day (DDD). SSRIs accounted for 413,000 of a population of 600,000 patients (68%) treated with antidepressant drugs.

Clinical cases of poisoning of SSRIs or other antidepressants have therefore become common in the emergency department. SSRIs have significantly lower acute toxicity compared to classical TCAs, while SNRIs have an intermediate status for toxicity. About 7% of all poisonings with these agents are reported as serious cases. Cardiac toxicity is lower for SSRIs but pronounced heart failure may occur after intake of high doses, usually more than 5 g. General seizures occur relatively often and may be difficult to treat. In addition, SSRI preparations may cause a so-called “Serotonin syndrome”. This syndrome may occur after taking several drugs that inhibit reuptake of serotonin in the CNS – such as an SSRI preparation and an analgesic (tramadol, fentanyl) – or various illicit drugs such as amphetamine and ecstasy which give an increased risk of seizures. Some special SSRIs require special attention in case of acute poisoning and are described below. In 2013, 49 people died in Sweden as a result of poisoning with classical antidepressants, while 69 people died of other and unspecified antidepressants (Death Register Data – Code T43.2).

Some common Antidepressive Agents




Venlafaxine (Efexor®) is an antidepressant drug that acts by inhibiting the reuptake of both noradrenaline and serotonin in the brain and is classified as so-called SNRI. Even dopamine uptake is inhibited to some extent. Efexor is sold as tablets in the strength of 37.5 and 75 mg, respectively, and in the depot form at the strength of 75 or 150 mg. The high strength of the tablets causes the risk of excessive overdose to be high. This medicine deserves some extra attention in case of acute overdose. Intake of up to 1 g venlafaxine in adults is a mild poisoning and intake of 1-1.5 g is moderate poisoning.

Intake of 1.5-2.5 g is considered to be serious poisoning and over 2.5 g as very serious poisoning. Note that patients taking Efexor Depot® may deteriorate up to 24 hours after ingestion. A mild symptomatology upon arrival at a hospital does not therefore rule out a stormy poisoning process. There are several poisoning cases reported in Sweden in recent years with fatal outcome. In one case, the intake amount was approximately 4.8 g Efexor Depot and in another case 7.5 g Efexor and an unknown amount of oxazepam (Sobril®) for suicide intention.

Similar preparations

There are several antidepressants such as mianserin (Mianserin®), mirtazapine (Remeron®, Mirtazapin®), bupropion (Zyban®), reboxetine (Edronax®), atomoxetine (Strattera®) and duloxetine (Cymbalta®, Yentreve®) that not classified under tricyclic preparations or as SSRIs, but as SNRIs or NaSSAs. Edronax® and Strattera® are selective noradrenaline reuptake inhibitors. Strattera is a relatively new preparation used for concentration difficulties in the indication of ADHD in children and adults. Bupropion (Zyban®, Voxra®, Bupropion®) has a special indication of smoking cessation. Bupropion has been present as an addictive substance and may in this context have some central stimulant effect. In the case of overdose, bupropion has two long-term metabolites (> 30 h) that allow patients to be comatose for a very long time, in some cases for several days.

Clinically these drugs have similar effects to overdose of the SSRIs, but the pharmacological effect varies. In particular, note the risk of prolonged QT-time and the risk of seizures in acute poisoning. Myoclonus or convulsions may start without other warning signs, for example, following venlafaxine intake (Efexor®) or bupropion (Zyban®, Voxra®). In case of moderate or severe poisoning, extra attention should be paid to the occurrence of muscle spasms or general seizures. These may appear suddenly in a condition with only mild symptomatology. The seizures may be prolonged and persistent and recur after the addition of diazepam (Stesolid®). ST-T changes in ECG and prolonged QT time have also been observed in younger heart-healthy patients. Unexpected ECG changes do not exclude serious poisoning as opposed to poisoning with classical antidepressants. Patients with moderate or high intake of these drugs and initially mild symptomatology should therefore be monitored in an intensive care unit with careful monitoring for at least 12 hours in severe poisoning and for at least 24 hours in severe poisoning with depot preparations (Efexor depot®). Pay attention to QT time on ECG as prolonged QT time increases the risk of severe cardiac arrhythmias. Check with prolonged QT time especially when venlafaxine poisoning (Efexor®), citalopram (Cipramil®) and mirtazapine (Remeron®) are poisoned.

In the case of unconsciousness in the elderly, the clinical picture may be relatively unspecific and other clinical signs are missing. Diagnosis can easily be missed; a careful history is extremely important as well as checking empty cartons. Sampling of urine can be performed in unclear cases.

Symptoms and Clinical Picture

CNS symptoms in Overdose

  • Excitation with anxiety, agitation, confusion, dizziness, hallucinations
  • Tremor, chills
  • Ocular oscillations
  • Dizziness
  • CNS depression with coma or decreased consciousness.
  • Seizures may occur suddenly, even in relatively unaffected patients
  • Extrapyramidal side effects; rigidity, rupture, tremor, acatasia (inability to remain still)
  • Easily resolved late reflexes, clonus
  • Hyperthermia

Circulatory symptoms

  • Blood pressure drops, but blood pressure may also be elevated (autonomic instability)
  • Tachycardia or bradycardia. AV blocks, prolonged QT time, ST-T changes, broad-range QRS complexes
  • Ventricular arrhythmias and extrasystoles
  • Circulatory collapse and ventricular fibrillation in pronounced cases. Ventricular fibrillation can occur suddenly without significant previous ECG changes. Ventricular fibrillation is often preceded by convulsions.

Other symptoms

  • Rigidity, tremor, hyperthermia, rhabdomyolysis, serotonin syndrome
  • Respiratory failure
  • Myoclonus (muscle twitching)
  • Mydriasis
  • Sweating
  • Gastrointestinal symptoms; diarrhea, nausea and vomiting
  • Liver and kidney injury in rare cases
  • Electrolyte disorders – hyponatraemia, hypokalaemia, hypomagnesaemia

Serotonin Syndrome

Overdose with SSRIs, SNRIs and atypical antidepressants may all cause a serotonergic syndrome. The syndrome may occur after acute overdose but also after ingestion of therapeutic doses. Serotonin syndrome refers to a major overactivity in the serotonergic neurotransmission of the CNS and the symptomatology that this causes. Symptomatology is dominated by CNS symptoms with acathasia, tremor, sweating, anxiety, agitation, confusion, diarrhea, hyperreflexia, clonus, tachycardia, rigidity and hyperthermia. It is a serious condition that in the worst case leads to death. The risk is especially great if an antidepressant drug is combined with other agents that also release serotonin. Examples of other agents are different analgesics and central stimulant drugs such as amphetamine, cocaine and ecstasy. Also, sumatriptan (Imigran®), valproate (Absenor®, Ergenyl®, Orfiril®), levodopa (Madopark®, Sinemet®), bromocriptine (Pravidel®), lamotrigine (Lamictal®), lithium (Lithionit®) and certain health food preparations may induce a serotonin syndrome. Among the analgesics are tramadol (Dolatramyl®, Gemadol®, Nobligan®, Tiparol®, Tradolan®, Tramadol®), petidin (Petidin®) and fentanyl (Leptanal®, Fentanyl®). Symptoms may be rapid ingestion of fever, muscle rigidity and excitation as a rule.

Usually, the syndrome is relatively modest and transient. In severe cases rhabdomyolysis, general seizures, renal failure, respiratory insufficiency, liver failure and multiple organ failure occur. The most important thing in the treatment of the syndrome is sedation and suffocation. If necessary, specific drugs may be given with some “antidote effect” such as cyproheptadin (Periactin® license preparation) and haloperidol (Haldol®). Beta-blockers (metoprolol, atenolol), bromocriptine (Pravidel®) or dantrol (Dantrium® license preparation) have no place in the treatment.

In the case of serotonin syndrome, treatment with any of the following medicines may be considered:

Treatment and Medical Care

The treatment of acute poisoning with SSRIs and SNRIs is essentially symptomatic and similar to the treatment of poisoning with classical antidepressants. Awareness, breathing and hemodynamics can suddenly deteriorate without warning. Seizures, psychomotor disorders, nausea and vomiting are common. Insufficient breathing is supported as needed by endotracheal intubation and respiratory treatment in an intensive care unit. If vital parameters are stable and the patient breathes calmly and regularly it is usually enough for supervision and the patient is allowed to sleep until he or she wakes up. Comatose patients are placed stable in side mode and turn every other hour. Another reason for deep unconsciousness than poisoning should of course be ruled out.

Check electrolytes, toxicology samples and an arterial blood gas as well as the blood alcohol level. Perform a CT scan with x-ray in unclear cases of unconsciousness or in the presence of focal neurological symptoms. 

Activated charcoal is valuable if administered early in treatment, especially within one hour after ingestion of toxic agents. Medical charcoal administration should be standard treatment in case of serious poisoning. Coal is of limited value if it is given later than one hour after the poisoning ingestion. Early-administered charcoal is very effective and adsorbs most antidepressants. Medical charcoal can also be given later than one hour in life-threatening poisoning and should supplement gastric lavage when carried out. See special guidelines for gastric lavage and medical charcoal.

Gastric lavage is of value but should only be performed if the patient arrives early in hospital after the poisoning occurs, preferably within one hour. In case of very serious poisoning (life-threatening poisoning), after intake of very large doses or after ingestion of depot preparations, gastric lavage may need to be performed at a later stage. See special guidelines for gastric lavage.

See Overview Gastric Lavage

  • Gastric lavage if warranted.
  • Activated charcoal (Carbomix, Charcoal suspension 150 mg/ml) 50 g orally, or more if poisoned with more than 5 g of any drug. Insert a nasogastric tube if repeated activated carbon is to be given.
  • Appropriate fluid substitution with crystalloid infusion solutions; for example 2000-3000 ml Ringer’s Acetate, or dextran (Macrodex®) 500 ml.
  • Monitoring of circulation, respiration and diuresis. Follow lactate.
  • Diazepam 5-10 mg i.v. in case of anxiety, hyperthermia, rigidity or seizures. Treatment with diazepam has resulted in prolonged unconsciousness.
  • Sodium Bicarbonate in acidosis, arrhythmias or broad-scale QRS complexes. Initially give 100-300 ml of sodium bicarbonate i v.
  • Be liberal with intubation and controlled ventilation.
  • Inotropic treatment, dopamine, norepinephrine or adrenaline in refractory hypotension.
  • In case of pronounced circulatory failure consider treatment with extracorporeal circulation (ECMO system).
  • In case of circulatory arrest, cardiopulmonary resuscitation should be performed immediately and intravenous lipid therapy (ILE) may be tested.
    • The bolus of a 20% lipid emulsion (Intralipid®) 1.5 ml/kg i.v. or 100 ml quickly intravenously.
    • Start an infusion with a lipid emulsion of 0.25 ml/kg/min for 10 minutes, while cardiovascular resuscitation is performed, give 100 ml intravenously – which can be repeated.
    • Bolus doses can be repeated every 5 minutes, two or three times if necessary, 1 ml/kg Intralipid. More than 8 ml/kg lipid emulsion should not be given.
  • Hypertonic saline (Rescue-flow®) can be tested in broad-scale QRS complexes (200 mmol over 20 minutes).
  • Possible arrhythmia treatment with magnesium sulphate. Twenty (20) mmol of magnesium in 100 ml of sodium chloride is administered intravenously for 20 minutes.
  • In Serotonin syndrome: sedation and cooling. Muscle relaxation.
  • Specific treatment for serotonin syndrome may be given with: Cyproheptadin (Periactin®) 8 mg x 3 orally  – license preparation.
  • Other symptomatic treatment, such as treating acidosis, hypovolemia, hypotension, arrhythmias and electrolyte disturbances.
  • In hyperthermia:
    • Undress the patient.
    • Cool the patient with cold bags in the axils, groins and over the forehead.
    • Give 1000 ml cold sodium chloride intravenously into the peripheral catheter over 30 minutes. NOTE! Never give cold solutions in a central venous catheter!
    • In pronounced conditions with hyperthermia: sedation, respiratory care and muscle relaxation.
  • Register in the medical journal time for tablet intake, type of drug, amount (total in mg), possibly empty drug packages and from whom the data comes.
  • Control of any signs of external trauma, needle marks etc.
  • Call as required your local Poisons Information Center


Psychiatric and social follow-up of the patient is important as the toxicity occurs in connection with suicide attempts or when the patient has an active substance abuse with drugs, alcohol or drugs. A visit to psychiatry or social services is desirable. Referral should always be written. Evaluate the patient’s degree of depression and the presence of psychotic symptoms. In case of increased suicidality with an active death wish, treatment under restricted conditions (LPT) must be considered.

Persistent symptoms

A drug overdose usually does not last but unless serious complications are given as apnea, aspiration pneumonia, acute liver failure, acute renal failure or pronounced general hypoxia. The risk of developing withdrawal after abuse of alcohol, pharmaceutical drugs or illicit drugs must always be taken into account. Transient sleep disturbance with severe sleep difficulties for 3-4 weeks is not uncommon as well as fatigue and muscle aches. Other side effects described are stomach pain, difficulty concentrating, numbness, anxiety and impotence.


T43 Poisoning with psychotropic drugs not classified elsewhere

T43.2 Other and non-specified antidepressant drugs

X60-X69 Intentional self-destructive action through poisoning

Z03.6 Observation of suspected toxic effect of intake substance


  1. Howell C, Wilson AD, Waring WS. Cardiovascular toxicity due to venlafaxine poisoning in adults: a review of 235 consecutive cases. Br J Clin Pharmacol. 2007;64(2):192-7.
  2. Kelly CA, Dhaun N, Laing WJ, Strachan FE, Good AM, Bateman DN. Comparative toxicity of citalopram and the newer antidepressants after overdose. J Toxicol Clin Toxicol. 2004;42(1):67-71.
  3. Colbridge MG, Volans GN. Venlafaxine in overdose – experience of the National Poisons Information Service (London centre) [abstract]. J Toxicol Clin Toxicol. 1999;37:383.
  4. Blythe D, Hackett LP. Cardiovascular and neurological toxicity of venlafaxine. Hum Exp Toxicol. 1999;18(5):309-13.
  5. Cumpston S, Chao M, Pallasch E. Massive venlafaxine overdose resulting in arrythmogenic death [abstract]. J Toxicol Clin Toxicol. 2003;41:659.
  6. Mazur JE, Doty J, Krygiel A. Fatality related to a 30-g venlafaxine overdose. Pharmacotherapy. 2003;23(12):1668-72.
  7. Pascale P, Oddo M, Pacher P, Augsburger NM, Liaudet L. Severe rabdomyolysis following venlafaxine overdose. Ther Drug Monit. 2005;27(5):562-4.
  8. Daniels RJ. Serotonin syndrome due to venlafaxine overdose. J Accid Emerg Med. 1998; 15:333-4.
  9. Whyte I, Dawson A, Buckley N. Relative toxicity of venlafaxine and selective serotonin reuptake inhibitors in overdose compared to tricyclic antidepressants. QJM. 2003;96:369-74.
  10. Hernández JL, Ramos F, Infante J, Rebello M, Gonzales-Macias J. Severe serotonin syndrome induced by mirtazapine monotherapy. Ann Pharmacother. 2002;36:641-3.
  11. Personne M, Sjöberg G. Toxicitet vid överdosering av nya antidepressiva. Läkartidningen 2008; 105 (3):125-7.
  12. Hanekamp, et al. Serotonin syndrome and rabdomyolysis in venlafaxine poisoning. The Netherlands Journal of Medicine. 2005;63(8):316-318
  13. Danescu I L, Macovei R Al, Caragea G, Ionica M and Cioca G. Rabdomyolysis in a venlafaxine poisoning case [abstract]. Toxicology Letters. 2008;180:S1, Page S129

Author Kai Knudsen

Anesthesia department, Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB

Local Anaesthetics – Toxic Reactions (LAST)

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Local anesthetics are used to give patients pain relief in a range of surgical procedures and medical examinations. They are also used in dental practice, veterinary surgery and in the treatment of acute or chronic severe pain.

Local anesthesia is usually administered as an injection fluid but may also be given in ointment, gel or in sprays. Injections are performed by infiltration locally with syringe and injection needle or through peripheral nerve blocks, e.g. epidural, spinal or plexus blockade. Blocks are either administered as a single dose (bolus dose) or via repeated doses or in continuous infusion of a local anesthetic via catheter. It is common for epidural blocks to be given as a combination of local anesthetics and opioids.

A toxic reaction may occur unexpectedly and suddenly after an injection of local anesthetic agents with a dramatic influence on the patient’s condition, in pronounced cases the reaction can be life threatening. In modern English-language literature, toxic reactions triggered by local anesthetic systemic toxicity are called LAST. Dominant symptoms in a toxic reaction are CNS symptoms and cardiovascular symptoms, in particular cases of cardiovascular collapse with a risk of sudden death. Prior to major blocks (regional anesthesia), an intravenous peripheral venous catheter (PVC) must always be inserted on the patient for intravenous treatment. Access to anesthesia equipment and possibilities for artificial respiration and life-saving efforts must also be available. The same applies always when more than 20 ml of local anesthetic is administered.

Toxic reactions are distinguished from allergic reactions, vasovagal reactions with fainting and side effects of adrenaline supplements. Vasovagal reactions with pulse and blood pressure drop occur easily in painful injections – especially in young, nervous, irritated, distressed or obese individuals. Genuine allergic reaction to local anesthetic agents is extremely rare and is often confused with other unpleasant reactions, such as fainting, but allergic reaction to additives (carriers) in local anesthetic agents occurs. Referral to allergologists should be written in the event of a suspected true allergic reaction and a skin test should be carried out under supervision, preferably in an operating department. Carefulness with the term “Cave” shall apply to medical records.

In addition to system toxic reactions, it should be noted that in high doses, prilocaine (Prilocaine, EMLA) may cause methemoglobinemia with impaired oxygen transport capacity in the blood. In methemoglobinemia, the patient becomes cyanotic or grayish and the blood gets a chocolate brown color. Methemoglobinemia over 25% is considered to be life threatening and should be treated with the antidote methylene blue (methylthionine) given i.v. (1-2 mg/kg). Even when using Prilocaine in cream form, EMLA, the reaction may occur. Excessive lubrication with EMLA cream, for example in case of skin burns, especially on toddlers, should be avoided. Methemoglobinemia has also occurred after overdose with local anesthesia in the bladder (tampon).


Local anesthetics are divided into two groups; amino amides and amino esters. Esters generally have higher toxicity than amino amides and all preparations have been deregistered in Sweden but are found in many other countries. The present preparations in Sweden, all of which are of amide type, are Mepivacaine, Lidocaine, Prilocaine, Ropivacaine, Levobupivacaine and Bupivacaine. The preparations are present in different concentrations, usually half (5 mg/ml) or one-percent solution (10 mg/ml) with or without adrenaline additive. Nesacain (chloroprocaine) occurs in single clinics as licensing agent (rapid action).

Local anesthetic agents are relatively fat soluble, absorbed in the tissues are related to local blood flow. The agents readily cross the blood brain barrier, and central nervous effects and system toxic effects usually occur within a few minutes after an intravenous injection. Metabolism occurs mainly in the liver. Some drugs metabolized in the liver delay the degradation of local anesthetics, such as antidepressant drugs. Drug interactions can affect system toxicity.

Different local anesthetic agents have different properties of system toxicity. Mepivacaine, lidocaine and prilocaine can be categorized as low toxicity drugs, ropivacaine and levobupivacaine as medium-toxic drugs and bupivacaine as a high toxicity agent.

The circulation effect caused by bupivacaine is more pronounced and more difficult to treat compared to other local anesthetics. When CNS symptoms occur, the cardiac effect of toxic reaction of bupivacaine is more potent than those of ropivacaine.

The risk of a toxic reaction becomes particularly high if bolus doses are given on top of a continuous infusion that goes into an infusion pump. Particularly sensitive is the continuous infusion of bupivacaine, which has a relatively long half-life. Extra bolus doses for a patient who is continuously injecting bupivacaine must be administered with extreme caution and preferably with other drugs with lower toxicity, such as lidocaine or mepivacaine. The toxicity of different local anesthetics given simultaneously is additive.

The absorption of local anesthetic agents (i.v.) in the nerve blockade varies with the type of blockade. At most, it is at intercostal blockade followed by caudal block, epidural block, plexus block and femoral block. Therefore, great caution should be observed when placing an intercostal block or caudal block. Infraclavicular block is more dangerous than axillary plexus block.

Maximum Doses of Local Anesthetic Agents

 Mepivacaine (Carbocaine®)Lidocaine (Xylocaine®)Prilocaine (Citanest®)Ropivacaine (Naropin®)Levobupivacaine (Chirocaine®)Bupivacaine (Marcaine®)
Maximum dose singel blockade (4 hours)400 mg400 mg400 mg300 mg150 mg150 mg
Maximum dose mg/kg5 mg4 mg5 mg3 mg2 mg2 mg
Maximum daily dose1000 mg1200 mg1200 mg800 mg400 mg400 mg

Maximum dose of local anesthetics to children

Dose in ml according to body weight
Body weight (kg)Bupivacaine 2,5 mg/mlBupivacaine 2,5 mg/ml + adrenalinBupivacaine 5 mg/mlBupivacaine 5 mg/ml + adrenalinLidocaine 10 mg/mlLidocaine 10 mg/ml + adrenalinMepivacaine 5 mg/mlMepivacaine 5 mg/ml + adrenalinVikt (kg)
108,0 ml12,0 ml--5 ml7,0 ml10 ml14,0 ml10
129,6 ml14,4 ml--6 ml8,4 ml12 ml16,8 ml12
14--5,6 ml8,4 ml7 ml9,8 ml14 ml19,6 ml14
16--6,4 ml9,6 ml8 ml11,2 ml16 ml22,4 ml16
18--7,2 ml10,8 ml9 ml12,6 ml18 ml25,2 ml18
20--8,0 ml12,0 ml10 ml14,0 ml20 ml28,0 ml20
22--8,8 ml13,2 ml11 ml15,4 ml22 ml30,8 ml22
24--9,6 ml14,4 ml12 ml16,8 ml24 ml33,6 ml24
26--10,4 ml15,6 ml13 ml18,2 ml26 ml36,4 ml26
28--11,2 ml16,8 ml14 ml19,6 ml28 ml39,2 ml28
30--12,0 ml18,0 ml15 ml21,0 ml30 ml42,0 ml30
32--12,8 ml19,2 ml16 ml22,4 ml32 ml44,8 ml32
34--13,6 ml20,4 ml17 ml23,8 ml34 ml47,6 ml34
36--14,4 ml21,6 ml18 ml25,2 ml36 ml50,4 ml36
38--15,2 ml22,8 ml19 ml26,6 ml38 ml53,2 ml38
40--16,0 ml24,0 ml20 ml28,0 ml40 ml56,0 ml40

Administration of Local Anaesthetics

High concentrations of local anesthetic agents in the bloodstream may occur due to involuntary intravascular injection, overdose or unusually rapid absorption from rich vascularized tissue. Rapid absorption occurs during infiltration anesthesia, especially if the injection occurs in the face around the oral cavity, nose or throat. Absorption increases with peripheral vasodilatation and high cardiac output with fast pulse.

Central blocks (face, throat, scalp, above and below the clavicle) cause greater risk of toxic reaction than peripheral blocks.

In epidural blocks, a toxic reaction occurs more easily if the injection occurs in a vein (epidural vein). The epidural space is richly vascularized and an epidural catheter may accidentally penetrate or perforate a vein. If local anesthetic is given in an epidural vein, it circulates into the heart within one minute, which can cause a serious toxic reaction with sudden circulatory arrest. In the case of bloody aspiration in an epidural catheter, the catheter should be replaced. Injection of a bolus dose of local anesthetic epidurally should therefore always be preceded by an aspiration test for blood and administration of a test dose, which may detect excessive uptake in system circulation. Addition of adrenaline in the test dose may facilitate the detection of an intravenous injection by responding to the patient with rapid heart rate (tachycardia). Adrenaline is usually not used in the majority of epidurally administered local anesthetics (8-14 ml) but only in the test dose (4 ml).

Toxic reactions are due to high plasma concentrations, usually short term. Adrenaline administration in local anesthetic agents causes local vasoconstriction, which inhibits absorption and reduces the risk of system toxic reaction in properly established epidurals. As a rule, therefore, higher doses of local anesthetic agents with adrenaline are tolerated better than local anesthetics without adrenaline.

SYMPTOMS of Toxicity

At high concentrations of local anesthetic agents in the blood, mainly CNS and cardiovascular systems are affected by system toxicity. All amide-type local anesthetic agents cause high-dose similar CNS symptoms, while the cardiovascular effects differ between different drugs, both quantitatively and qualitatively.

When administering local anesthetics in high doses, patients must always be monitored carefully. A common conversation can often reveal a systemic toxic reaction by suddenly getting the patient unclear, somnolent, slow talking or obnoxious speech. Patients who have just received a blockade, such as an axillary plexus anesthesia, should therefore never be left alone in anticipation of the blockade’s effects.

CNS toxicity occurs gradually with symptoms and reactions of increasing severity. Common initial symptoms are stiffness in mouth and tongue, making it harder to speak (perioral anesthesia and stiffness, slurred speech). Tinnitus and acute hypersensitivity (hyperacusia) may also occur early. Symptoms usually occur in the order of drowsiness, paresthesia in the tongue and mouth, tinnitus, muscle seizures, seizures, coma, respiratory distress and eventually cardiac arrest. Observe the difficulty of detecting the initial symptoms of an anesthetized patient!

CNS symptoms indicate that a cardiovascular reaction is imminent, so the immediate release of local anesthetic agents must be discontinued immediately.

Common CNS symptoms of toxic reaction of local anesthetic agents

  • Feeling drunk
  • Perioral paresthesia
  • Drowsiness in the tongue
  • Hyperacusia, hearing hallucinations
  • Tinnitus
  • Visual disturbances
  • Difficulty to articulate
  • Slow, slurred speech
  • Twitching
  • Difficulties to fix your eyes
  • Tremor
  • Generalized seizures
  • Unconsciousness

Cardiovascular Symptoms

If the patient is sedated with drugs or anesthetized, it may be difficult to detect early signs of CNS toxicity due to local anesthetics. In these patients, cardiovascular symptoms may be the first alarming signs of a toxic reaction.

A cardiovascular reaction often results in tachycardia. Thereafter, blood pressure drops, cardiac arrhythmias of various kinds, broad-range QRS complexes, bradycardia, repeated short-term asystoles and finally cardiac arrest follow. The course of a toxic reaction with cardiovascular symptoms may be rapid.

In an anesthetized patient, bradycardia and irregular rhythm (skipped strokes – sinus arrest) may be the first symptom of a toxic reaction followed by blood pressure drop and asystole.

Metabolic symptoms of a toxic reaction are oxygen deficiency, hypercapnea, metabolic acidosis and hypercalcaemia. Metabolic acidosis in itself increases the risk of a toxic reaction because a larger fraction of the drug circulates freely in plasma and affects the heart.

Acute Care

In case of a toxic reaction, action must be taken immediately. Weakness, breathing and hemodynamics can change rapidly. Seizures, psychomotor disorders, vomiting and nausea are relatively common. The treatment is essentially symptomatic. Usually, the toxic symptoms are rapidly transient within a few minutes. Initial measures mean that vital functions regarding breathing and circulation are ensured. Often it is enough to give oxygen and possibly some anticonvulsants like diazepam.

Emergency measures (see headings below for details)

  • Cancel the supply of local anesthetic agents immediately
  • Put the patient down in the supine position with a slightly raised head end
  • Give oxygen (always!) via breathing mask (Ruben blow)
  • Careful monitoring of alertness and breathing
  • Support breathing and circulation, avoid hypoxia and hypercapnia
  • If required: assisted ventilation, mask ventilation or intubation
  • If seizures do not stop spontaneously within 15-20 seconds, thiopentone (Pentothal Sodium) is given 1-3 mg/kg i.v. (50-100 mg) or diazepam 0.1 mg/kg i.v. (5-10 mg, slightly slower)
  • Alternatively to thiopentone, small doses of propofol are given 10-60 mg slowly intravenously. Risk of blood pressure drop.
  • Injection of muscle relaxants, e.g. suxametonium 0.5 mg/kg should be given in case of difficulty in ventilating the patient.
  • In the case of hypotension/bradycardia, a vasopressor is given, e.g. ephedrine 5-10 mg i.v. (may be repeated after 2-3 minutes) or adrenaline 0.05-0.1 mg i.v. (repeated doses 0.1 mg/ml). Even phenylephrine 0.1-0.2 mg IV can be tested.
  • Atropine (atropine) 0.5-1 mg i.v. given in bradycardia.
  • Sodium bicarbonate (50-100 ml, 60-120 mmol) is given at acidosis on liberal indication. Seek for positive Base Excess (BE).
  • Insert an artery needle and control blood gases
  • Hypertonic saline should be given in broad-scale QRS complexes (200 mmol Sodium fast i.v.)
  • In case of circulatory arrest, cardiac pulmonary resuscitation should be performed immediately and intravenous lipid therapy (ILE) should be tested.
  • Give a bolus of a 20% lipid emulsion (Intralipid), 1.5 ml/kg i.v. all 100 ml fast intravenously.
    • Start an infusion with a lipid emulsion of 0.25 ml/kg/min for 10 minutes, while cardiovascular rescue is performed, all. 100 ml intravenously.
    • Bolus doses can be repeated every 5 minutes, two or three times if necessary, 1.5 ml/kg Intralipid.
    • More than 12 ml/kg lipid emulsion should not be given in total (840 ml to 70 kg patient). Stop the infusion after stabilized circulation.
  • Blood sampling: arterial blood gas analysis with acid-base status, frequent electrolyte controls (routine status), B-glucose
  • Continued treatment is managed according to the patient’s condition
  • In severe arrhythmias, amiodarone (Cordarone) may be used
  • Avoid calcium blockers and beta blockers in treatment
  • Long-term cardiopulmonary resuscitation may be required in the toxic reaction of bupivacaine
  • If the patient is not responding to lipids and vasopressor treatment, treatment with an extracorporeal system (arteriovenous ECMO) should be initiated if possible. Since such treatment is usually started with delay, it may be wise to contact the nearest unit with resources for extracorporeal treatment. Geographical reasons can make this treatment impossible.

Free airway

  • Supine position with heightened head end for optimal intubation and ventilation position
  • Assisted ventilation
  • Jaw lift, nasal tube or oropharyngeal airway advice for mechanical ventilation
  • Endotracheal intubation, in case of emergency a laryngeal mask
  • Oxygen
  • Pulse Oximeter
  • Prevent and avoid aspiration

Venous access

  • Peripheral venous catheter (PVC), at unconsciousness at least two
  • Arterial catheter, unconsciousness or circulatory effects
  • Central venous catheter (CVC), unconsciousness or circulatory effect

Circulatory monitoring

  • ECG with arrhythmia monitoring, continuously and on paper
  • Invasive monitoring, continuous arterial pressure and central venous pressure (CVP) in case of severe circulatory failure
  • Pulse Oximeter
  • Urinary bladder catherization with urinary output

Lipid treatment (ILE)

Several animal experimental studies and case studies in humans have shown that rapid delivery of lipids intravenously (ILE) in circulatory collapse following overdose with bupivacaine increases survival. The mechanism is not yet fully understood, it is believed that the lipids bind a part of the free fraction of the drug in plasma, whereby local anesthetic agents diffuse out of the myocardium and the toxicity is reduced (“sink theory”). You get a diffusion gradient from cardiac cells into the bloodstream, which reduces cardiac toxicity. Another theory is that the fat constitutes a nutrient substrate for the heart with positive effects. What was previously called the “sink theory” has now been replaced by “shuttle theory”. Lipids are thought to change the distribution of local anesthetic agents in various compartments in a favorable manner. ILE also causes a vasoconstriction that causes blood pressure to rise even when common vasopressors such as adrenaline do not work.

Further studies on humans are needed to confirm these data, but studies are so convincing that several national specialist associations in anesthesia recommend this treatment in the event of cardiovascular collapse, especially in the case of overdose with bupivacaine. The concept is supported by several case reports on humans. However, data on the use of ILE on other poisons with circulation collapse are more contradictory.

Treatment of general seizures

Despite a certain respiratory depression effect, diazepam is a well-proven preparation for general seizures in the treatment of a toxic reaction. Appropriate starting dose is 5-10 mg i.v. Diazepam is then given in the dose of 5 mg x 3, plus if necessary.

Check ECG and ST depression! If diazepam is not sufficient, one can use thiopental (Pentothal Sodium) or propofol (Diprivan). Tiopental is given intravenously in small doses, 50-100 mg. Propofol should also be given in small doses, 20 mg i.v. or in continuous infusion (20 mg/ml 5-10 ml/hour). Observe the risk of blood pressure drop.


Local anesthetics T41.3


  1. Albright GA. Cardiac arrest following regional anesthesia with etidocaine or bupivacaine. Anesthesiology. 1979; 51: 285-287.
  2. Di Gregorio G, Neal JM, Rosenquist RW, Weinberg GL. Clinical presentation of local anesthetic systemic toxicity: a review of published cases, 1979-2009. Reg Anesth Pain Med. 2010: 35: 179-185.
  3. Scott DB, Lee A, Fagan D, Bowler GM, Bloomfield P, Lundh R. Acute Toxicity or Ropivacaine Compared to That of Bupivacaine Anesth Analg. 1989 Nov; 69 (5): 563-9.
  4. Knudsen K, Beckman Suurküla M, Blomberg S, Sjövall J, & Edvardsson N. Central nervous and cardiovascular effects of i.v. infusions of ropivacaine, bupivacaine and placebo in volunteers. British Journal of Anaesthesia, 1997; 5: 507-514.
  5. Corcoran W, Butterworth J, Weller RS, et al. Local anesthetic-induced cardiac toxicity: a survey of contemporary practice strategies among academic anesthesiology departments. Anesth Analg. 2006; 103: 1322-1326.
  6. Mayer E. The toxic effects following the use of local anesthetics. JAMA. 1924; 82: 876-885.
  7. Moore DC, Bridenbaugh LD. Oxygen: the antidote for systemic toxic reactions from local anesthetic drugs. JAMA., 1960; 174: 102-107.
  8. Prentice JE. Cardiac arrest following caudal anesthesia. Anesthesiology. 1979; 50: 51-53.


Kai Knudsen

Department of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB

Publicerat med tillstånd av Internetmedicin AB

Cannabis – Marijuana

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

It is estimated that 147 million people worldwide use cannabis. Most commonly, use appears in New Zealand, Australia and the United States. Cannabis is also widely used in Europe where 14.6 million, or 11.2 percent of all young adults (15-34 years), have used cannabis sometime in recent years.

Cannabis is the most widely used drug among young people around the world. Essentially, cannabis is a juvenile drug in the age group 15-25 years, but addiction also occurs higher in the ages. In Sweden, 50 percent of those who seek help for cannabis abuse are under 20 years of age. Eighty percent (80%) of all seizures of drugs in the EU are cannabis. Two thirds of these seizures are captured in Spain and England.

Cannabis is usually consumed by smoking, either as hashis (cannabisharts) or marijuana. In recent years, supply has increased significantly on marijuana in the EU and in Sweden.

Acute cannabis poisoning does not usually require care in an emergency medicine department but can be administered in a psychiatric clinic or in dependence medicine, as well as withdrawal symptoms and other negative symptoms associated with addiction. Cannabis is commonly used in combination with other drugs. Cannabis use is also common among heavy drug addicts of heroin or amphetamine. Use of cannabis is categorized as heavy abuse when used daily or virtually daily (20 days or more per month).

The treatment of acute cannabis poisoning is directed by other drugs that have been taken simultaneously, but is mainly symptomatic. The most important issue about acute cannabis poisoning is careful monitoring of alertness, breathing, mental functions and circulation, as well as conducting the patient to the correct level of care. Many patients with cannabis abuse first need medical treatment and then assessment of psychiatric health, referral to dependence clinic and further to social services.

The prognosis for acute cannabis poisoning is usually good except for severe mixed drug toxicity.


Cannabis harvested from the plant Cannabis Sativa (Indian hemp) or from the plant Cannabis Indica or a blend of these two. Cannabis plants are grown mainly in North Africa (Morocco, Algeria), but can be grown in many other countries, even in scandinavian countries (indoors and outdoors). Market share for domestically produced, powerful marijuana has increased in recent years, and data now indicates that imported cannabis products has also become more powerful. Cannabis is included in hashish, marijuana and hash oil, all of which are used as intoxicants. Hashish has been the most common cannabis preparation in Sweden for a long time, accounting for about 85% of the market in 2011, but marijuana has become more prevalent in recent years. Since 2013, marijuana is more common than hashish in Europe. Among Swedish schoolars, the use of marijuana is more common than hashish. Marijuana is produced from cultivated dried flowers and top shoots while cannabis resin consists of the stem parts of the cannabis plant (female plant), compressed with plant harts. Hashish is usually mixed with regular tobacco while marijuana is mostly smoked without tobacco. Cannabis is usually smoked in joints, or in a pipe (hollow), but can also be eaten in cakes, candies or consumed in beverages, for example in tea. All cannabis consumption is illegal in most European countries. Common nickname of cannabis is “Brown, Green, Grass, Weed, Ganja, Braja, Smoke, Joint, Goose, Spliff” etc. One gram of marijuana on the street costs about 10 USD, 2.5 g costs about 30 USD. In a roll cigarette (joint), 200-400 mg cannabis is usually mixed with tobacco when you smoke alone or together with others. In a pipe (hollow), usually 700 mg is mixed at a cost of about 10 USD. The price for marijuana is about the same as for hash. Intense cannabis users usually consume more than 2 g per day.

The most psychoactive substance in cannabis is delta-9-tetrahydrocannabinol (THC) that provides a relaxing and euphoric substance. Other active cannabinoids are delta-9-tetrahydrocannabivarin, delta-8-tetrahydrocannabinol, cannabigerol, cannabinol, cannabichromium and cannabidiol. THC is considered to be psychotomimetic whereas cannabidiol is considered antipsychotic. There are a variety of cannabinoids (at least 60-80) and it is not entirely clear who are psychologically active. The level of THC in marijuana is usually lower than in cannabis, about 5-10% in marijuana against 7-14% active substance in hashish. A variant of cannabis called skunk is stronger and contains 6-15% THC. Skunk is considered to be extremely strong and has been shown to cause damage to the white substance in the brain near the corpus callosum. The concentration of THC has increased in recent years, preparations with levels of THC up to 30% have been seized, but usually it is not more than 14%. One variant of the cannabis plant called “sensimilla” contains no seeds and therefore contains extra high levels of THC. Cannabis, like opium, is a drug that has been used for a long time in some cultures as tranquilizing drug, for anxiety disorder, as an analgesic and mood enhancing agent. The use of cannabis has increased worldwide over recent years. Cannabis is considered to be moderately addictive. Dependence is present when the user continues to use the drug regularly despite behavioral, cognitive, perceptual and emotionally negative symptoms. Of all who use cannabis, approximately 9% develop an addiction. Of those who start using cannabis regularly during high school, approximately every sixth (16.7%) develops an addiction. Of those who are daily users (20 days per month or more) before age 17, 50-60% develops an addiction. There is robust scientific evidence that cannabis increases the risk of mental illness but to what extent is it controversial. Usually, the risk is estimated as “twice as big” as without cannabis use.

SYMPTOMS of Cannabis abuse

Smoking of cannabis gives the user a comfortable feeling of relaxation, calm, pain relief, peace of mind and joyful excitement. In high doses, perception may be enhanced and altered; experiencing increased and changed perception, above all, of sound and light. Cannabis is also a pain reliever and to some extent convulsive. In some parts of the world, cannabinols are used for medical purposes (“medical cannabis”) under regulated forms as analgesics, including multiple sclerosis (MS) and chronic disabilities with muscular contractures and spasticity. Medical studies have shown that cannabis does not help to improve MS disease. Research is ongoing in the field, also regarding effects on diabetes. What is meant by medical cannabis varies between countries and between different states in the United States, several preparations have been defined as medical cannabis.

Symptoms of cannabis abuse:

  • Drunkenness, excitement
  • Freakiness, cheerfulness, “hazy and giggly”, smiling
  • Talkative, more socially active
  • Ixoid (adhering) in speech and thoughts
  • Grandiose in thoughts
  • Red-eyed sclerae, shiny eyes
  • Wide pupils, hanging eyelids
  • Dry mouth and throat
  • Candy craving
  • Slow reflexes, relaxed muscles, (low tone)
  • Fumblingness, sloppy, floppy
  • Slurred speech
  • Heart palpitation, palpitations (tachycardia)
  • Sleepiness, fatigue, drowsiness
  • Inconsistent in speech and thoughts
  • Passivity, introversy, withdrawn
  • Anxiety attacks, panic attacks
  • Paranoid thoughts
  • Delusions, hallucinations

Abstinence – Withdrawal

Cannabis may cause withdrawal symptoms, such as:

  • Irritability
  • Blackouts
  • Concentration difficulties
  • Insomnia
  • Nightmares
  • Derealisation
  • Anxiety
  • Depression

Hallucinations and psychotic symptoms occur in more severe cases, even genuine psychosis occur especially after intensive use or use of very strong preparations. Cannabis is usually calming but aggressive breakthroughs with psychotic symptoms occur.


Mental effects

People with cannabis abuse have a higher degree of psychiatric comorbidity compared with the normal population (higher degree of mental ill health). There is a higher incidence of depression, dysthymia, mania, hypomania, panic disorder, agoraphobia, social phobias, other specific phobias and general anxiety disorder. Contemporary abuse of other substances is common. Abuse of cannabis can lead to withdrawal symptoms like anxiety, confusion, delusions and hallucinations. In high doses and especially after long-term abuse, other mental symptoms may develop as:

  • Depressions
  • Apathy, weakness
  • Memory problems
  • Mood swings, numbness, anxiety
  • Amotivation syndrome, insomnia, shiftlessness
  • Personality change, increased inwardness (introversy), boundness, silence
  • Changed reality perception
  • Cognitive failure
  • Paranoid ideas
  • Psychotic symptoms

The personality change may persist if the user continues to smoke cannabis after developing the primary psychosis. Psychotic symptoms may occur in sensitive individuals soon after a few weeks of intensive abuse or use of stronger preparations commonly called acute cannabis psychosis. If there is a connection to cannabis at first-rate disease in psychiatric disease, this worse forecast predicts more days in hospitals and more entries. Some users risk over time, after months of intensive use to develop impaired cognitive function with poor learning ability, short-term memory, executive functions and simultaneous capacity. Personality change, as well as changed reality, with “schizophreniform symptoms” may occur. These symptoms usually do not occur until after several years of regular use. An Australian study has reported poor intellectual development among those who used cannabis before age 17. A Swedish study has shown 40% increased mortality among those using cannabis in teens compared with the normal population (OR 1.4).

The risk of developing schizophreniform symptoms is significantly higher for those who use the drug daily (double risk) compared to those who smoke only a few times. The risk is higher for those who started smoking in young years compared with those who started later (after 18 years of age). The risks of developing acute psychosis, personality change and depression follow the same pattern. Girls appear to be more sensitive than boys, but the use is much more common among boys.

Differential diagnosis between Cannabis Induced Psychosis (CIP) and Primary Psychosis (PP)

The following factors are more common in cannabis-induced psychosis (CIP) compared to psychosis caused by schizophrenia (primary psychosis – PP): male sex, expansiveness in emotions and ideas, derealisation or depersonalisation, visual hallucinations and altered sensory. Time of last drug intake can indicate if the patient’s psychotic symptoms are due to cannabis poisoning or withdrawal symptoms. Premorbid personality disorder is more common in underlying schizophrenia disease. Note that 25% prevalence of positive cannabis urinary toxicology has been reported in schizophrenia. It is important to have meticulous history. Carefully understand the difference between CIP and cannabis intoxication.

Characteristics of cannabis-induced psychosis (CIP):

  • Symptoms occur during or after heavy substance abuse or after increasing the strength of cannabis
  • A positive toxicology screening can provide a clear time relationship
  • Antipsychotic drugs do not always improve the symptoms
  • Often associated with visual illusions and paranoid ideas
  • The patient is more aware of symptomatology, has more insight into the disease
  • Thoughts are more organized and sequential compared to PP
  • It is common for heavy use of cannabis in the last month
  • Symptoms decrease with reduced drug use
  • Sudden onset of mood and paranoid symptoms within 1 week after use but as early as 24 hours after use.
  • More mood-related symptoms compared to primary psychosis (more anxiety)

Characteristics of primary psychiatric psychosis (PP):

  • The symptoms usually occur before or without heavy substance abuse
  • Antipsychotic drugs significantly improve the symptoms
  • Combined with delusions, hallucinations and thought errors
  • The symptom persists despite drug failure
  • Less insight into the psychotic state
  • Disorganized thoughts (eg loose associations, loose or even numbers)
  • More mood stable compared to CIP

Abuse of Cannabis can lead to:

  • Impulsive acts of violence
  • Suicide acts
  • Changed perception of time
  • Impaired ability to “understand the world”
  • Loneliness, social isolation, introversy
  • Personality change, schizophreniform symptoms

Teenagers may have delayed identity development and late personal maturity due to cannabis abuse. The typical character of teenage uprising can last for many years. Psychomotor features that require simultaneous capacity can also deteriorate. The ability to drive a car or to perform complicated tasks is deteriorating.

Physical effects

Abuse of cannabis has a lower degree of glucose metabolism in the brain, especially in the cerebellum. Cannabis smoking means an increased exposure to tar (50 percent more than in cigarettes), which increases the risk of cough and bronchitis, both acute and chronic, as well as for chronic lung disease. There is an increased risk of lung cancer and a number of other cancers and increased risk of cardiovascular disease. Fertility impairment may occur in cannabis abuse. In pregnancy there is an increased risk of growth inhibition in the fetus. Nor can it be excluded that there is an increased risk of malformations on the fetus, for damage to its mental functions and the risk of acute non-lymphatic leukemia. Cannabis is often detected in various acute drug poisoning. In drug-related deaths, cannabis affects are common, but rarely cause death due to overdose.


  • Drug Screening (urine sample, U-tox)
  • Several urine samples for tetrahydrocannabinol (THC)
  • Control of electrolytes
  • Temperature Control
  • Lung X-ray on broad indications
  • Routine tests in blood
  • Haemoglobin
  • Na, K, Calcium
  • Liver enzyme parameters
  • CRP, SR
  • WBC, thrombocyte count
  • Creatinine
  • PK, APT
  • Psychological Assessment
  • Counselor contact
  • Possible referral to dependency clinic
  • Assess what type of cannabis has been used
  • Assess how many grams are consumed per week
  • Estimate how much money is spent on cannabis consumption per week


There is no specific pharmacological treatment for cannabis addiction. Rimonabant is a type of antagonist, a competitive cannabinoid receptor agonist (CB-1 receptor) that blocks the effects of THC and has shown positive results in some studies to reduce acute physiological problems associated with cannabis smoking. Rimonabant, however, is unregistered in Sweden and has no place in treatment.

Therefore, treatment is mainly symptomatic in combination with psychosocial support therapy. Treatment can usually be done in outpatient care, but end-care is required in case of acute cannabis poisoning and acute psychosis. The primary treatment is total abstinence from continued cannabis consumption. Cannabis may cause severe withdrawal symptoms after intensive use, usually abstinence for about a week. Pharmacological treatment because of anxiety, withdrawal and anxiety status usually needs to continue for a long time after cannabis abuse. Contact with psychiatrist or psychologist with special knowledge about the effects of cannabis is important.

The treatment focuses on the negative effects of abuse on thought function, motivation and cognitive functions. Disease insight is usually low with poor motivation for treatment and abstinence. Psychiatric comorbidity is common. The investigation needs to assess whether psychotic symptoms or increased suicidality are present. Providing depression and psychotic symptoms is the risk of suicide acts. The outpatient treatment is individualized and based on frequent contacts with psychiatrists or psychologists, as well as regular checks of urine samples with analysis of THC. Cannabis can induce depressive reactions and psychoses. The risk of deep depression is increased threefold among cannabis users compared to non-cannabis users. Initially, it is common with a memory disorder, low disease insight and poor motivation for drug-freeness. Social aspects must also be evaluated in the patient’s treatment and the curator is connected. Psychosocial treatment for those with less problems focuses on short-term treatment (3-6 visits in outpatient care) while patients with more severe problems receive a longer treatment program, at least 14 visits to a psychologist or curator for a four-month period. In some cases, support for family and related parties may also be justified. Cannabis users have higher levels of social dependence, higher unemployment and poorer education than the normal population.

Pharmacological Treatment

The treatment of acute cannabis intoxication focuses on immediate abstinence from cannabis. If necessary, parenteral fluid is given, severe dehydration occurs. Also substitute electrolytes. Give the patient a quiet, dark room and rest, food and sleep. In the initial stage, pharmacological treatment of withdrawal symptoms is often necessary. The pharmacological treatment is gradually stepped out for 3-6 months while support therapy is in place. Abstinence treatment can be performed with, for example, an oxazepam schedule (oxazepam in gradual escalating dose for 4-7 days. The heavy oxazepam schedule involves 30 mg x 4 the first day, followed by gradual escalation. The abbreviated symptoms should be followed, but if the withdrawal symptoms are pronounced as after a long period of intensive abuse, the heavy schedule can be followed. Studies have been done with lithium against withdrawal symptoms, as well as acetylcysteine, buspirone, lofexidin (clonidine-like) and cannabinol.

  • Insert at least one PVC. Take HgB, WBC, platelets and screening of the urine.
  • If necessary, drop, for example, Ringer acetate or 1000 ml buffered glucose 5% per day.
  • Neuroleptics of the type olanzapine (Zyprexa) 5-10 mg x 1-2 (sedating) may be used, such as risperidone (Risperdal) 1 mg x 2 or haloperidol (Haldol) 4 mg x 1.
  • Antihistamines as an alternative: hydroxizin (Atarax) 25-50 mg by night.
  • Oxazepam (Oxascand) 15 mg, according to schedule, “light” or “heavy oxascand schedule”.
  • Nitrazepam (Nitrazepam) 5-10 mg to the night for 3 days.
  • Mirtazapine (Remeron) 30 mg to the night.
  • Acetylcysteine ​​may be considered. N-acetylcysteine ​​is an antioxidant that is a prodrug to the naturally occurring amino acid cysteine. It is used as anti-mucous drug and is sold prescription free in many countries, including in Sweden. The mechanism of action for cannabis addiction is not known.

Supportive Measures

Identify possible cognitive impairment, psychotic symptoms, the occurrence of schizophreniform symptoms and depression, and assess suicidality. Offer different types of support:

  • Psychosocial supportive efforts
  • Motivational improving therapy (MI) or Contingency management (CM)
  • Supportive social assistance for drug-related shortcomings
  • Clinical investigation and supportive measures for drug-related memory losses
  • Motivate total abstinence (MI)

Note that the deterioration of cognitive functions may initially be subtle and must be valued by structured methods. In case of cannabis abuse or addiction, Contingency Management (CoM), a behavioral therapeutic method in addition to Cognitive Behavioral Therapy (CBT) or relapse prevention (OPP) and motivational treatment (MET), provides better results.

  • A small effect on cannabis use compared to CBT or OPP only with MET during treatment or at end of treatment (moderately strong scientific basis).
  • A small effect on cannabis use compared to CBT or OPP with MET 6-12 months follow-up (moderately strong scientific basis).


  • Cannabis and its derivatives T40.7
  • Mental disorders and behavioral disorders caused by cannabis, harmful use F12.1
  • Mental disorders and behavioral disorders caused by cannabis, psychotic disorder F12.5


  1. WHO statistics Internet
  2. Drogutvecklingen i Sverige 2017, Rapport nr 164, Centralförbundet för alkohol- och narkotikautveckling, Stockholm 2017.
  3. Skolelevers drogvanor 2016, Rapport nr 161, Anna Englund CAN 2016.
  4. Narkotikan i Sverige: Metoder för förebyggande arbete en kunskapsöversikt Sven Andréasson (red.) Statens folkhälsoinstitut, Östersund, R 2008:23 ISSN 1651-8624 ISBN 978-91-7257-573-8
  5. Moore T et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet 2007; 370: 319-28
  6. D’Elia G, Perris C, Persson G. Psykoser i anslutning till cannabismissbruk. Läkartidningen 67;32:1970.
  7. Areseneault L et al. Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. BMJ 2002;325:1212-3. Länk
  8. Patton GC. Cannabis use and mental health in young people: cohort study. BMJ 2002;325:1195-8. Länk
  9. Editorial. Cannabis and mental health. BMJ 2002;325:1183-4
  10. Zammit S. et al. Self reported cannabis use as a risk factor for schizofrenia in Swedish conscripts of 1969: historical cohort study. BMJ 2002;325:1199-201
  11. Mass R et al. Relationship between Cannabis use, schizotypal traits, and cognitive function in healthy subjects. Psychopathology 2001;34:209-214. Länk
  12. Fletcher JM et al. Cognitive correlates of long-term cannabis use in Costa Rican men. Arch Gen Psychiatry 1996;53:1051-7. Länk
  13. Ashton CH. Adverse effects of cannabis and cannabinoids. Br J Anaesth 1999;83:637-49. Länk
  14. Volkow, ND et al. Psychiatry research: Neuroimaging, 67, pp 29-38, 1996.
  15. Fergusson and Boden, Cannabis use and later life outcomes are dose dependent. Addiction, 103: 969-976, 2008. Länk
  16. Gray, KM, Carpenter, MJ, Baker, NL, DeSantis, SM, Kryway, E, Hartwell, KJ, et al. A double-blind randomized controlled trial of N-acetylcysteine in cannabis-dependent adolescents. The American journal of psychiatry. 2012; 169(8):805-12. Länk
  17. Manrique-Garcia E, et al. Cannabis, Psychosis, and Mortality: A Cohort Study of 50,373 Swedish Men. Am J Psychiatry 2016; 00:1–9; doi: 10.1176/appi.ajp.2016.14050637. Länk


Kai Knudsen

Department of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB

Heroin and other Opioids

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21


Among 185 million drug users worldwide about 26-36 million are using opioids as the main drug. In Europe, 1.3 million people are estimated to abuse opioids (0.4% of the population). Of all drug users, 13-26 million are estimated to use heroin as the main drug. Opioids include opiates naturally extracted from opium and synthetic analogues. Abuse has increased in Asia and Africa, while it has been stable or decreased slightly in Europe in recent years. In Europe, abuse has been highest in Scotland, England and France, which is usually associated with metropolitan regions. The relationship between men and women who regularly uses opioids is around 4:1.

About 44% of opioid users are intravenous addicts. Nearly half of all who receive treatment for drug addiction have heroin as the main drug. Heroin abuse in the EU is stable and slightly downward in recent years. The number of deaths related to heroin generally decreases, but deaths related to synthetic opioids increase. Heroin constitutes 4% of all seizures of illegal drugs while cannabis accounts for 80%. Heroin abuse in the EU is stable and slightly downward in recent years.

The number of deaths related to heroin is generally reduced, but deaths related to synthetic opioids increase and in Sweden these have increased markedly in recent years. In the National Board of Death’s register, 765 drug-related deaths were registered in 2014. An increase of 30 percent compared with the previous year. The registry records deaths where both legal drugs and illegal drugs such as heroin, cocaine and amphetamine were the cause of death or contributory cause of death. The so-called Toxicology Registry at the Karolinska Institute records only deaths where one or more drug-based preparations, legally or illegally, are judged to be the dominant or contributory cause of forensic autopsy.

Opioids were considered to cause death or being contributory cause of death according to the Toxicology register in the following number of cases in 2014; morphine 53 (28), Methadone 104 (10), buprenorphine 84 (14), fentanyl 47 (5) and oxycodone 42 (4). By comparison, it can be mentioned that deaths related to heroin are generally at the same level in 2014 as 1994. The most common illegal drug among opioid users is heroin. It is estimated that in Sweden there are between 8000 and 13,000 heroin abusers among 29,000 heavy addicts. The number of new addicts in Europe is approximately 41,000 per year. Opioids are administered mainly intravenously but may also be taken orally, transdermally in patches or by inhalation (smoke heroin). The drugs that are inhaled are opium and smoke heroin but also fentanyl. Smoke heroin is a brownish heroin base, also known as “Brown Sugar” (free base). Opioids are used as potent analgesics in the health care industry, especially for the treatment of severe acute pain but also chronic pain in severe conditions. Among drug-related deaths, opioids are present in 90% of cases. The medical use of opioids has increased significantly over the past ten years.Opioids are considered to be the drugs that have the strongest addictive effect. Among those receiving treatment for drug dependence worldwide, opiate addiction is the most common cause (50-85% of patients).

Common opiates are:

  • Heroin
  • Morphine
  • Hydromorphone
  • Raw opium
  • Codeine
  • Ethyl morphine
  • Buprenorphine

Common opioids are:

  • Ketobemidone
  • Oxycodone
  • Fentanyl
  • Petidin (meperidine)
  • Methadone
  • Tramadol
  • Dextropropoxyphene

Acute overdose is usually caused by heroin, fentanyl, buprenorphine or methadone. Serious cases and deaths in the overdose of dextropropoxifen were common in the past, but have decreased significantly after most preparations have been deregistered. A significant abuse of oxycodone has been reported, especially from the United States, from 2000 onward. In 2010, approximately 16,000 deaths were reported with oxycodone involved! In Sweden there is a significant abuse of Tramadol and buprenorphine. Still, more than 100 people die annually in Sweden due to acute heroin overdose. Of the deaths 90 percent are older than 25 years. About 80 percent of deaths are among men.


Heroin (diacetylmorphine) is the opioid that is primarily associated with drug addiction and illegal drug abuse. The most common is the brown form of heroin, which usually originates in Afghanistan, less common is the white form (hydrochloride salt), which usually originates in Southeast Asia. Brown heroin costs on the street usually between 30 and 70 USD/g. Purity is between 10-20%.

Heroin has pain relieving, sedative and anxiety-inducing properties. It is metabolized to morphine in the liver and is excreted mainly via the urine. The drug can be smoked, sniffed or injected; injections are the most common (44%).


A normal dose heroin in addiction is around 15-50 mg intravenously. An overdose is seen when taken over 100 mg, severe ingestion at intake above 300 mg or more. The effects and tolerances vary considerably between different individuals. Note that heroin has a relatively short half-life of 2-3 hours versus 16-60 hours for methadone.

Methadone is usually taken in oral solution or as tablets but is also used in injection. In the treatment of heroin addiction, a normal dose methadone is 60-130 mg, which is dosed in oral solution once a day.

A capsule or bag of heroin usually contains 250 mg of 30-percent heroin when purchased on the street (a so-called “cab”). Heroin is produced from opium, mainly cultivated in Far East Asia, especially in Afghanistan. Even raw opium is abused and imported into several European countries. Raw opium is mostly abused by smoking. An increasing proportion of addicts smoke heroin (diacetylmorphine, freebase) instead of injecting it, but many smokers eventually pass into injection abuse.

Heroin is well known to provide rapid and powerful addiction development with increased tolerance and moderate or severe withdrawal symptoms upon discontinuation.

An overdose of opioids is characterized by:

  • Decreased consciousness, somnolence
  • Small pupils
  • Tiredness, tranquility
  • Slurred speech
  • Feeling cold, freezing
  • Anesthesia
  • Coma
  • Muscular rigidity (stiffness)
  • Urinary retention
  • Respiratory depression, respiratory failure
  • Hypoxia, cyanosis, gray-colored skin color
  • Bradycardia
  • Hypotension
  • Cardiovascular collapse

Life-threatening overdose may occur after injection as well as after smoking but is much more common after injections. Respiratory depression is the most serious symptom of overdose which can quickly become life-threatening. Alert patients usually have no respiratory depression but the vigilance can change rapidly.

Withdrawal symptoms

  • Chills
  • Faint tremor
  • Sweating
  • Palpitation
  • Shakes
  • Uneasiness
  • Concern
  • Agitation
  • Aggressiveness
  • Unstable temperament
  • Messiness
  • Violence

Sometimes the withdrawal symptoms are described as flu-like. These symptoms may occur as soon as 4-6 hours after the last intake.

Health risks

An intravenous drug abuse of heroin is characterized by high risk of contagious diseases (HIV, hepatitis B and C) and acute overdose. Abuse is associated with significant criminality and asocial life style. It has been reported that 66% of all heroin abusers at one time had a life-threatening overdose, 34% had attempted suicide.

White heroin (diacetylmorphine hydrochloride) has become more pure in the last ten years, i.e. an all-new “better” product worldwide. This speaks for a more controlled and refined production. The addict himself never really knows what concentration of heroin is injected during use. Concentration and dose can vary significantly between different heroin preparations, which explains many overdoses and deaths.

Another reason for overdose is reduced tolerance. Decreased tolerance develops within a few weeks after heroin abstinence. The craving after the drug can still be strong, but the tolerated amount significantly less than before. Many overdoses are therefore taking place among people who have recently been released from a detention center with forced abstinence.

Heroin addiction is a common cause of drug-related deaths, estimated between 100 and 200 cases occur annually in Sweden (Death registry). Of these, 40-60 cases are estimated to be due to acute overdose. In the case of overdose and abuse of heroin, there is a common occurrence of other potentially fatal diseases such as hepatitis B and C, acute hepatic failure, pneumonia, acute fasciitis, abscesses, cardiac failure, sepsis, myocarditis, DIC, ARDS, etc. New studies suggest that the most common cause of death in this group of addicts are trauma, usually drug-related trauma. In total, the number of drug-related deaths has fallen in the EU from about 7700 in 2009 to 6500 in 2011.


Methadone is a pure opioid with soothing, analgesic, anxiolytic and sedative properties. Methadone has been used for the detoxification of heroin addiction since the 1960s, but has its strong opioid properties due to its own opioid potential. About 2,500 patients in Sweden with opioid dependence are included in different substitution programs and medicate with either methadone or buprenorphine.

Methadone is considered to have a better effect as substitution medicine on heavier and more recent heroin addicts compared to buprenorphine (Subutex). The effect sought by methadone is to block the craving of heroin as well as to prevent new heroin intake. Methadone treatment has helped more patients to work, more goes back to studies, and more maintain social structures within family and cohabitation.

Methadone is usually taken as tablets or in oral solution but is also available in the form of injection. In the treatment of heroin abuse, a normal dose of methadone is 60-130 mg, which is dosed in oral solution once a day. A normal dose for treatment of pain states is 5-10 mg 4-6 times daily in tablet form, the daily dose should not exceed 100 mg. Methadone in overdose may cause nausea and vomiting, severe respiratory depression and severe cardiac symptoms with dangerous arrhythmias (Torsade de Pointes arrhythmias, prolonged QT interval).

Methadone has significantly longer half-life compared with heroin, 16-60 hours, versus 2-3 hours for heroin, which means that the effect lasts significantly longer and covers all hours of the day. Side effects associated with methadone treatment include weight gain and impotence, and decreased libido. When treated with antidote naloxone hydrochloride (Naloxone) after overdose of methadone, the risk is significant that the effect becomes short-lived and transient. The sedative and respiratory depression effects of methadone may therefore come back after a period of awakening and cause serious symptoms. The number of deaths after overdose with methadone has increased in recent years in the 21st century.


Oxycodone shows affinity to kappa, my- and delta-opioid receptors in the brain and spinal cord. It acts to these receptors as an opioid agonist without antagonistic effect. The therapeutic effect is predominantly analgesic and sedative. The absolute bioavailability of oxycodone is 60-87% after oral administration, and peak plasma concentrations are reached after approximately 1 to 1.5 hours. At steady state, the plasma elimination half-life is approximately 3 hours. Oxycodone and its metabolites are excreted via urine.

The prescription and consumption of oxycodone has increased markedly in recent years as well as the addiction problem. In 2014, approximately 250,000 prescriptions were prescribed for less than 50,000 in 2006. Oxycodone has been assessed as the cause or contributory cause of 42 deaths in 2014 in Sweden against only 4 cases in 2006. Oxycodone is sold as a fast-acting drug (OxyNorm) or as a depot preparation (OxyContin, Targinic). OxyNorm is available as capsules or injection solutions. Targinic is a combination preparation containing both oxycodone and naloxone in a ratio of 2:1. Oxicodone is also available in injection with approximately the same potential as morphine. Oral preparation of oxycodone is approximately twice as potent as oral morphine (higher bioavailability).

Fentanyl (Fentanyl, Durogesic, Matrifen)

Fentanyl is a potent opioid routinely used in conjunction with surgery and anesthesia. Fentanyl is approximately 100 times as potent as morphine, but the oral bioavailability is significantly lower (<2%). Fentanyl may be abused; it can be inhaled, swallowed, insufflated or injected. An increasing problem in recent years has been the abuse of fentanyl from various patches commonly used for transdermal pain management. These patches usually secrete 25, 50, 75 or 100 μg fentanyl per hour. When the patches are used for abuse, the fentanyl is scrapped to extract it from the patch for inhalation. Most common is smoking it, for example, in a sliced ​​light bulb used as a kind of container. Seizures have also been made of fentanyl in spray form. Fentanyl is easy to overdose and a number of deaths have occurred in Sweden in recent years. In Estonia and several other countries, fentanyl-related deaths are greater than the number of heroin-related. Fentanyl is available in many different chemical varieties with different potency. Some potent variants are carfentanil, alfentanil, remifentanil, furanylfentanyl, 4-fluorobutyrentanyl, 4-methoxybutyrentanyl (4-MeO-BF) and acetylfentanyl. Most are significantly more powerful than morphine, 100-1000 times stronger, because fentanyl is usually dosed in micrograms and morphine in milligrams.

Desomorphine (“Crocodile”)

A simple variant of opioid is desomorphine manufactured by addicts in Russia under the name “Crocodile”. Desomorphine is manufactured from codeine that can be purchased without prescription in pharmacies. Desomorphine has sedative and analgesic properties and is more potent than morphine. In the manufacture, codeine, iodine and phosphorus are used which have given a compound that is heavily contaminated and very unclean. Injections of desomorphine have given severe skin infections, wounds, dermatitis, fasciitis and necrosis. Abuse has led to extensive scarring and amputations of extremities. Several deaths have occurred and abusers of desomorphine usually have short survival (<1 year). The hose name Crocodile has also been used for the synthetic opioid 3-methylphentanyl which is also used most in Russia.


Mental effects

Opioid effects cause drowsiness, relaxation, pain relief, anxiety disorder and mental depression. Regular use may lead to concentration difficulties and increased risk of traumatic injury due to decreased attention. Movements and reflexes become sluggish and slow as well as speech, even breathing can be slow. The voice may be low and dull under the opioid effect. There is a risk of chronic misery due to abuse and the personality becomes flattened.

Physiological effects

  • Mios (small pupils)
  • Impaired intestinal function (constipation, paralytic ileus)
  • Renal impairment, urinary retention
  • Nausea, vomiting
  • Itching (with tearing ulcer)
  • Neurological damage, numbness and numbness
  • Complications in pregnancy

Heroin addiction can lead to impaired immune system and opportunistic infections. Abusers have an increased incidence of infectious diseases, including hepatitis B and C, HIV, wound infections (S. aureus), skin infections, tetanus, botulism, endocarditis and sepsis. The risk increases for bronchitis, pneumonia and other lung diseases. Note that renal impairment (creatinine clearance <60 ml/min) increases the plasma concentration of oxycodone by 50%. Stick marks on the arms and legs as well as thrombophlebitis are seen in intravenous abuse. Poor dental status with severe caries, impaired hygiene, loss of appetite and cachexia are common.


  • Drug screening and intoxication samples
  • Pupil controls
  • Severe urine tests for opioids (U-tox)
  • Check electrolyte status
  • Check infection parameters
    • Hepatitis serology
    • HIV test
  • X-ray chest and lungs
  • Cultivation of blood, sputum and urine
  • Routine tests, blood samples
    • Hgb
    • CRP, SR, Temperature
    • Liver enzyme parameters
    • WBC, TPC
    • Creatinine
    • PK, APT
    • Ethanol in serum (BAL)
    • Myoglobin in serum

Patients in poor condition should be examined with the ultrasound of the heart (UCG) with the question: heart failure (cardiomyopathy), heart valve vitium. In poor dental status, the patient should receive a referral for dental care. The clinical investigation includes psychological assessment and contact with the curator and social services. The application for social services must always be issued in case of life-threatening overdose or life-threatening addiction.


Treatment in case of acute overdose Start life-saving measures according to CPR principles for life-threatening overdose and provide antidote naloxone in case of respiratory depression. Acute poisoning with heroin is often part of a mixed drug overdose with other drugs, alcohol, especially benzodiazepines. Make a drug screening on urine samples. 65% of heroin users in a Norwegian study had ever overdosed heroin. Respiratory rate below 10 per minute or saturation below 90% indicates overdose and need for naloxone.

The treatment is controlled according to the means taken, but is mainly symptomatic.


Naloxone (naloxone hydrochloride) has a central place in treatment and should be given intravenously (0.4 mg) as well as intramuscularly (0.8 mg). Higher doses may need to be given. Note that the antidote has a shorter half-life than the intake of heroin. After treatment with antidote, the patient should be monitored for 2 hours due to the risk of new severe respiratory depression. The necessity of this monitoring is scientifically controversial. Several recent studies from Norway (F Heyerdal et al) have shown that patients who are discharged directly from the ambulance after life-saving measures do not have increased mortality compared with hospital-treated cases. Currently, nasal administration of naloxone is being investigated as life-saving treatment given by related persons in connection with life-threatening overdose.

The most important treatment is careful monitoring of vigilance, breathing (oxygen saturation/respiratory rate) and circulation, as well as transferring the patient to a department where vital life functions can be ensured.

  • Secure free airway, provide assisted breathing and oxygen if necessary
  • Monitor patient in hospital for at least 2 hours
  • Insert at least one venous cannula. Check Hgb, WBC, CRP, platelets, liver status and drug marks.
  • Intravenous fluid supply of isotonic crystalloid solutions, for example Ringer-Acetate. Note the risk of pulmonary edema.
  • Check ECG
  • In case of unconsciousness, intubation and controlled ventilation.
  • X-ray of the lungs with the issue of edema (heroin lung) or pulmonary infection should be performed on liberal indications.

Pharmacological treatment:

  • Naloxone hydrochloride (Naloxone) 0.4 mg intravenously as antidote, possibly more. The dose may be repeated every 3-4 minutes until normal breathing occurs and the patient wakes up. Thereafter, the double intravenous dose is given intramuscularly, usually 0.8 mg. The effect of naloxone may be delayed in mixed oral toxicity, mainly with benzodiazepines or if anoxic brain injury has occurred. The intravenous dose has effect after 30-60 seconds and lasts for 45-60 minutes. The intramuscular dose has effect after approximately 10 minutes and lasts for 2-3 hours.
  • Flumazenil (Lanexat) 0.1-0.3 mg/min intravenously may be tested in combination with opiates and benzodiazepines. Adults are usually given 0.3 mg intravenously, and then repeat the dose at one minute intervals until effect is obtained. Often, 2-3 doses and a total dose of 2 mg are sufficient. The maximum dose for adults is 2-5 mg. Flumazenil is not a first aid in suspected opioid poisoning.
  • Inotropic treatment at circulation failure; Dopamine (Abbodop) in continuous infusion 2-10 μg/kg/min or noradrenaline (Noradrenaline) 0.05-0.15 μg/kg/min.

During treatment with naloxone sudden awakening occurs with anxiety, pain and aggressiveness. The patient may then run out and deviate from the hospital. Lung edema also occurs after administration of naloxone due to sympathetic activation and blood pressure increase, but may also be a consequence of overdose with heroin itself.

Many patients need a psychiatric assessment after acute treatment, as well as referral to dependent medical clinic and social services. The prognosis for acute heroin poisoning is usually good if the patient has not already received anoxic brain damage due to oxygen deficiency.


Weaning addiction usually requires outpatient treatment in a dependency medicine clinic. Studies on withdrawal treatment indicate that more patients complete treatment (retention) if this occurs in primary care rather than in outpatient care. Such treatment is usually elective with scheduled insertion of substitution therapy according to specific treatment protocols. A dedicated care and treatment plan for each patient must be established. The patient first receives a medical withdrawal treatment and then a medical substitution treatment. In parallel, psychosocial supportive therapy is given (CBT; MI; Contingency Therapy). Patients are normally called to an assessment interview before withdrawal treatment. After a period of hospital care (3-6 months), some patients may continue the withdrawal treatment with maintenance treatment in outpatient care, but the risk of recurrence is significant.

Substitution Therapy

Some addiction clinics substitute the heroin with lighter opiates such as codeine, but not without difficulty. More clinics instead use pure opiates such as methadone (Methadone) in the substitution treatment or partial agonists such as buprenorphine (Subutex) or buprenorphine in combination with naloxone (Suboxone). Methadone is not significantly better than buprenorphine. The introduction of buprenorphine has made it possible for more patients to be drug-free compared to Methadone, but both Methadone and buprenorphine give a significant risk of opioid dependence. Many patients receive prolonged substitution treatment under controlled forms, initially available and after a few weeks (months) outpatients with daily subcutaneous injection.

New and younger addicts are getting Subutex more often, while older and heavier addicts are often given methadone. A new drug, Suboxone (buprenorphine plus naloxone), has been introduced in treatment with a lower risk of side effects and intravenous abuse compared to Subutex. Substitution treatment has enabled more patients to work socially with marital relationships and studies or work compared with untreated controls. Anti-sympathetic stimulant agents have also been used in the treatment of opioid abstinence such as clonidine (Catapresan) and dexmedetomidine (Dexdor).

Needle exchange programs

At some clinics, intravenous addicts allow replacement of syringes to new sterile in a so-called needle replacement program. This program is an attempt to reduce the risk of criminal activities and infectious diseases as well as being able to follow the patients carefully (“Harm reduction program”). Attempts are also made with hepatitis vaccinations and treatment. These addicts should be introduced to the use of nasal naloxone in case of overdose. The risk of premature death is significant among intravenous addicts (20-50 times normal). Intravenous heroin abusers have often gone a long time in their addiction; most are between 30 and 40 years old and have extremely low quality of life with significant social and marginalized life. A certain spontaneous healing occurs after 10 years of abuse or more.

Psychosocial treatment

  • Psychosocial treatment for opioid abuse and addiction has some effect on the extent of abuse.
  • The psychosocial treatment should have a clear structure, focus on the abuse and be long enough to give effect.
  • A dedicated care and treatment plan must be established.
  • Psychosocial treatment is usually given in parallel with abstinence treatment.
  • No single psychosocial treatment method seems superior to anyone else.
  • Psychotherapy such as family therapy, dynamic and cognitive therapy appears to be effective in maintaining patients in treatment programs.


  • Mental disorders and behavioral disorders caused by opiates, acute infections F11.0
  • Mental disorders and behavioral disorders caused by opiates, harmful use F11.1
  • Mental disorders and behavioral disorders caused by opiates, depression syndrome F11.2
  • Mental disorders and behavioral disorders caused by opiates, abstinence F11.3
  • Heroin T40.1
  • Other opiates T40.2
  • Methadone T40.3
  • Other synthetic drugs T40.4
  • F11 Mental disorders and behavioral disorders caused by opiates


1.      Drug development in Sweden 2011, Report No. 130, Central Federation for Alcohol and Drug Development, Stockholm 2012.

2.      Annual report EMCDDA The situation in the field of drugs in Europe 2011.

3.      Pre-Hospital Treatment of Acute Poisonings in Oslo: A One-Year Observational Study. F Heyerdahl, KE Hovda, MA Bjornaas, AK Nore, JC Figueiredo, O Ekeberg, D Jacobsen BMC Emergency Medicine 2008, 8:15.

4.      Steentoft A, Teige B, Ceder G, Vuori E, Kristinsson J, Simonsen KW, Holmgren P, Wethe G, Kaa E: Fatal poisoning in drug addicts in the Nordic countries. Forensic Sci Int 2001, 123: 63-69.

5.      Traces KA: Acute heroin overdose. Ann Intern With 1999,130: 584-590.

6.      Boyd JJ, Kuisma MJ, Alaspaa AO, Vuori E, Repo JV, Randell TT: Recurrent opioid toxicity after pre-hospital care of presumed heroin overdose patients. Acta Anaesthesiol Scand 2006,50: 1266-1270.

7.      Buajordet I, Naess AC, Jacobsen D, Brors O: Adverse events after naloxone treatment of episodes of suspected acute opioid overdose. Eur J Emerg With 2004, 11: 19-23.

8.      Spores KA, Dorn E: Heroin-related noncardiogenic pulmonary edema: a case series. Chest 2001, 120: 1628-1632.

9.      Warner-Smith, M, Darke S, Lynskey M, Hall W. Heroin overdose. Addiction 2001; 96 (8) 1113-1125

10.  Bach, Peter B .; Lantos, John. “Methadone dosage, heroin affordability, and the severity of addiction.” American Journal of Public Health. 1999, May. 89 (5): 662-665.

11.  Cook, Stephane; Moeschler, Olivier; Michaud, Katarzyna; Yersin, Bertrand. “Acute opiate overdose: Characteristics of 190 consecutive cases.” Addiction. 1998, 93 (10): 1559-1565.

12.  Darke, Shane; Hall, Wayne; Weatherburn, Don; Lind, Bronwyn. “Fluctuations in heroin purity and the incidence of fatal heroin overdose.” Drug and Alcohol Dependence. 1999, 54: 155-161.

13.  Fugelstad A; Ågren G; Romelsjö A. “Changes in mortality, arrests, and hospitalizations in nonvoluntarily treated heroin addicts in relation to methadone treatment.” Substance Use and Misuse. 1998. 33 (14): 2803-2817.


Kai Knudsen

Anesthesia Clinic, Sahlgrenska Hospital, Gothenburg Published with permission from Internetmedicin AB


By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Increased interest in hallucinogenic drugs can be seen among young people in recent decades, all over Europe. Ecstasy (MDMA) is an addictive drug that became popular in the 1990s as dance and party drug. Ecstasy is classified as an illegal drug and every use is illegal.

New psychoactive substances (NPS) include drugs such as ecstasy (MDMA), phenethylamines, katinones, synthetic cannabinoids (Spice), tryptamines and several other new hallucinogens. The drugs are also called “Designer Drugs, Legal Highs, and Smart Drugs.” Ecstasy has long been the most common and can be compared to as a reference substance. Most of these substances can be classified as substituted amphetamine derivatives. These agents have all pharmacological effects similar to amphetamine. The majority have been classified as illegal drugs according to The Controlled Substances Act (CSA), category I, but some are classified as hazardous products.

Benzylpiperazine (BZP), dextromethorphane (DXM), mephedrone, methedrone, nafyron, etc. may also be included under the term “New Psychoactive Substances (NPS)”. These drugs are all related to amphetamine with varying degrees of euphoric and hallucinogenic effects.

Acute poisoning with NPS and alcohol and various drugs, especially benzodiazepines, is not uncommon among mixed-use adolescents. Poisoning with hallucinogenic fungi and different gases, eg nitrous oxide, occurs among the same group of users.

This overview mainly deals with poisoning with ecstasy. Multiple variants of ecstasy (MDMA, MMDA, MDE, MDA, PFMPP) are sold over the internet as well as on the black market.


Ecstasy (3,4-methylenedioxymethamphetamine – MDMA) is a central stimulant amphetamine-like agent that has become a common party drug in Europe in the 1990s. Ecstasy is classified as a drug according to The Controlled Substances Act (CSA), category I. Ecstasy was already synthesized by Merck in Germany in 1912. MDMA was first used as a psychotherapeutic aid in the 60’s in the United States through its “entactogenic” (empathy-seeking “trustworthy”) characteristics and later developed into a so-called party drug around Europe, such as England and Germany. Music events with mainly electronic dance music (“techno, psychtrance”).

In Sweden, Ecstasy was first found in 1986 and became drug-classified during the following year. The use of young people in Sweden increased sharply in the late 1990s, but has decreased significantly in recent years. The drug is used sporadically by adolescents between the ages of 15 and 25 in connection with parties and intensive dancing. Ecstasy is used more often by boys than by girls. In the drug survey in 2014 among Swedish schoolchildren, two percent reported that they tested ecstasy in upper secondary school’s grade 2 against 3 percent in 2006. Of those who tested drugs in grade 2, 12 percent reported that they tested ecstasy in 2013. Only a few abusers demand treatment for ecstasy-related problems. Ecstasy is more common in metropolitan areas and major cities.

Content and appearance

Ecstasy is a central stimulant with slightly weaker physiological, but more euphoric, hallucinogenic (psychotropic) and entactogenic effects compared with amphetamine. You get an increased sensory perception. There are several different substituted amphetamines with similar effects to ecstasy, for example:

  • MDEA/MDE (methylenedioxyethylamphetamine) “Eve”
  • MDA (methylenedioxyamphetamine) “Sally, SASS, Sassafras”
  • TFMPP (trifluoromethylphenylpiperazine) “Legal X”
  • MBDB (methyl-benzodoxol-butanamine) “Eden, Methyl-J”
  • PMA (para-methoxyamphetamine) “Dr Death”
  • PMMA (para-methoxy-methamphetamine) “Superman”

The drugs have many different popular names among the users, such as “XTC, Love and Kissing Pills, Adam, Eve, Eden, E, Mandy, Molly, Superman and X”.

Ecstasy is usually sold as colorful tablets taken orally with different appearance in the strength of 50-100 mg. Content and strength may vary between different tablets and are rarely known to the user. The effect is therefore hard to predict. The tablets are often stamped with a logo, such as a Smiley, Mitsubishi brand, Superman logo, Mercedes star or similar. In the illegal market, a tablet costs about 10 USD. Ecstasy in powder form can also be snorted, inhaled or dissolved and injected which is unusual. One tablet costs between 6-20 USD/pc.

Analyzes of the contents of various ecstasy tablets have shown the presence of a variety of chemical substances such as MDMA, MDEA, MDA, MDB etc. This allows the user to experience varying effects between different tablets of the same appearance. Party drugs are imported from Russia, Poland, Germany and Holland, among others.

The majority of party drugs can be analyzed in blood and urine in suspicion of drug impact in extended analysis. Rapid tests of urine samples are available for drug screening, but these only take the most common preparations such as ecstasy. MDMA can usually be detected in the urine up to 2-4 days after ingestion.

Molecular structure

Symptoms of Abuse

The effects of ecstasy and similar substances are characterized by euphoria, social empathy, openness and increased mental and physical energy. Well-being increases and a positive sense of lust occurs within 1 to 3 hours after ingestion. Self-confidence is increasing and you get an experience that all problems disappear. The drugs give an increased sense of communication, understanding and empathy. You experience increased trust and intimacy to other people in the environment. Odor, vision and hearing and perception are amplified. The pupils widen (mydriasis).

The central nervous effect is mainly caused by serotonin infiltration in the central parts of the brain, primarily the limbic system and hippocampus, but after prolonged use, serotonergic depots are depleted and patients may develop negative mental symptoms, depression and sometimes psychosis.

Examples of negative effects

  • Uncontrollable thoughts
  • Unstable temperament
  • Hyperactivity and hypomania
  • Anxiety, restlessness, anxiety, irritability
  • Decreased self-control, unstable behavior
  • Unlimited sexual activity
  • Increased appetite, sweating (but also loss of appetite and anorexia)
  • Headache
  • Psychosis-like reactions, hallucinations

The drug user eventually becomes exhausted, irritated and depressed after repeated intake. The patient’s drowsiness can be difficult and long-lasting. Experimental animal data indicate that damage to dopamine pathways and, above all, serotonin pathways is morphological and partly irreversible. Even general seizures occur.

Symptoms that may occur after a few months of abuse are:

  • Fatigue, numbness, depression
  • Insomnia
  • Stereotype behavior, tics
  • Visual tinnitus
  • Depression
  • Paranoia
  • Anxiety
  • Mutism
  • Catatonic behaviour

Treatment with antidepressant drugs (SSRIs) for depression is less effective than normal after abuse of ecstasy. The user is affected by a renewed intake of ecstasy. In the case of long-term abuse, many patients develop a cognitive dysfunction – memory and learning ability are significantly impaired.

Symptoms of acute overdose

A normal addiction dose is estimated at 100 mg orally, common variations are 50-250 mg. Mild overdose is 250-500 mg, moderate overdose 500-1000 mg and excessive overdose over 1000 mg.

In acute overdose of ecstasy and other central stimulant party drugs, widened pupils, hyperactivity, excitation, excitement, increased sweating, restlessness and agitation are noted. The patient can behave unnaturally and have a psychomotor disorder with involuntary movements. Tachycardia, palpitations and tremors may occur, as well as hypertension and chest pain. Aggressiveness occurs, as well as confusion and hallucinations. In a study of acute poisoning with NPS, psychosis was reported in 6% of patients. There is a risk that the patient may suffer from muscle rigidity, muscle twitching, spasms and seizures, and hyperthermia. The risk of hyperthermia is significant and can be very serious and life threatening. Ecstasy is metabolized in the liver via CYP2D6.

In case of acute overdose, the patient is at risk of:

  • Water intoxication with hyponatremia
  • Acute Confusion
  • Cardiac arrhythmias
  • Myoclonal seizures
  • Hyperthermia (fever)
  • Serotonin syndrome
  • Hepatic failure
  • Acute kidney injury

Water intoxication

May occur after ingestion of a couple of ecstasy tablets and excessive intake of water; Girls are more sensitive than boys. Water intoxication with pronounced hyponatremia (S-Na <120 mmol/l) may lead to brain edema, headache, blurred vision, seizures and coma. Individual deaths have been reported in Sweden and several cases in England and Europe.

Heat Stroke

May occur after intake of ecstasy and prolonged dance or stay in a warm environment (night club environment). The patient is at risk of developing hyperthermia with muscular rigidity, seizures and rhabdomyolysis. Poor intake of drink increases the risk of hyperthermia. Hyperthermia is often one of the symptoms of a “Serotonergic Syndrome” (see below) and can lead to hyperkalemia, cardiac arrhythmias, coma and multiple organ failure. Hyperthermia is probably due to a dominance of serotonin in hypothalamus and striatum with a down-regulation of dopamine.Body temperature above 41 degrees of Celsius is dangerous and over 42 degrees C is directly life threatening, such a strong hyperthermia requires immediate disposal with active sedation and cooling. Hyperthermia can be pronounced and prolonged, especially after ingestion of PMA or PMMA. Isolated cases with hepatic failure and renal failure are also described. Probably renal failure occurs secondary to rhabdomyolysis and myoglobin precipitation in the kidneys. Always check myoglobin in serum. CT brain scan or MRI scan should be performed if pronounced hyponatremia occurs (S-Na <120 mmol/L), to exclude brain edema, or in focal neurological symptoms. Morphological damage to serotonergic pathways can be detected by a PET camera (f-MRI). Other serious symptoms that may develop are impaired coagulation, DIC (disseminated intravascular coagulation) and respiratory failure with risk of pulmonary edema. Seizures and coma may occur. There is also a risk of cerebral hemorrhage, pulmonary embolism and cardiovascular collapse.

Serotonin syndrome

Serotonin syndrome refers to an over activity in the serotonergic system of the brain. It is a serious condition that may occur in the overdose of different NPS, often in combination with antidepressant drugs or analgesics. At worst, it leads to multiple organ failure and death. Serotonin syndrome usually occurs with fever (hypertension) and these cases should be treated in an intensive care unit.

Symptoms of serotonin syndrome include:

  • Involuntary movements (“Psychomotor restlessness”)
  • Tremor
  • Sweating
  • Enlarged pupils
  • Concern
  • Agitation
  • Confusion
  • Diarrhea
  • Clonus (easily resolved extremity reflexes), mainly lower extremities
  • Tachycardia
  • Rigidity
  • Hyperthermia


The clinical treatment of acute overdose with central stimulant amphetamine analogues is essentially symptomatic and similar to most substances.

Specific antidotes are missing.

Most importantly, careful monitoring of:

  • Alertness
  • Breath
  • Circulation
  • Temperature
  • Mental functions

It is important to direct the patient to the right medical department so that vital life functions can be secured urgently. In the aftermath, drug abuse should be treated; assessment of psychiatrists and referral to dependence clinic and social services is often relevant. The application for social services must always be done in case of life-threatening addiction.

The prognosis for poisoning with party drugs is usually good unless serious complications are already granted before arrival at the hospital. Screening with drug stitches can sometimes, but not always, provide information about which drugs have been taken. Negative screening does not exclude poisoning with party drugs.

Treatment of acute overdose

Check heart rate, blood pressure, temperature and mental functions regularly. Invasive blood pressure measurement should be performed in case of severe blood pressure increase in moderate or severe intoxication. Place the patient in a quiet and dark room at mild to moderate poisoning and let him or her eat, sleep and rest (sleep morning). Treat anxiety and agitation as needed. Observe the risk of hyperthermia. Rehydrate with crystalloid liquids and check electrolytes in serum. Do drug screening of urine samples or plasma.

Suggestion of pharmacological treatment in case of anxiety or agitation:

  • Diazepam 5-20 mg 3 times daily or oxazepam 15-50 mg 3 times daily
  • Nitrazepam 5-10 mg to the night of sleep
  • Droperidol 10 mg im x 1.
  • Olanzapine 10 mg x 2 alt risperidone 1 mg x 2
  • Midazolam 2-5 mg i.v. in the event of anxiety and restlessness
  • Propofol i.v. for sedation in an intensive care department
  • Dexmedetomidine in severe restlessness in an intensive care unit
  • Symptomatic treatment in general
  • Caution with beta blockers

CT scan of brain in profound hypertension or neurological symptoms, such as cerebral edema or stroke. Check myoglobin in serum to see if rhabdomyolysis is present. Forced alkaline diuresis may be needed with crystalloid solutions, sodium bicarbonate and furosemide (10-40 mg/h).

In hyperthermia, active cooling and sedation may be required:

  • 1-2 liters cold saline intravenously
  • Diazepam 5-20 mg i.v. for sedation
  • External cooling with cooling sheet or similar
  • In extreme hyperthermia, cooling can be instituted extracorporeally through ECMO

In case of serotonin syndrome, treatment with any of the following medicines may be given:

  • Cyproheptadin – 8 mg x 3 orally (license preparation, antihistamine) alt.
  • Chloroprotixene 25 mg x 3
  • Risperidone 2 mg x 3

In case of severe hypertension (> 200 mm Hg) is it important with invasive blood pressure monitoring with arterial catheters:

  • Infusion of glyceryl nitrate (Nitroglycerin®) 0.2-0.5 μg/kg/min
  • Infusion of magnesium sulfate, 20 mmol in 100 ml NaCl for 20 minutes followed by 20 mmol for 20 hours
  • Beta-blockers with caution, eg metoprolol (2-5 mg iv) or labetalol (10-20 mg iv)
  • Alfa-blocker with caution, such as doxazosin (Alfadil®), labetalol (Trandate®)


  • F16.0 Mental disorders and behavioral disorders caused by hallucinogens, acute intoxication
  • F16.1 Mental disorders and behavioral disorders caused by hallucinogens, harmful use
  • F14.2 Mental disorders and behavioral disorders caused by cocaine, depression syndrome
  • T43.6 Psychostimulants with substance abuse
  • T40.6 Other and non-specified narcotic drugs
  • F15.1 Mental disorders and behavioral disorders caused by other stimulants, including caffeine, harmful use
  • F15.0 Mental disorders and behavioral disorders caused by other stimulants, including caffeine, acute intoxication


  1. Gouzoulis-Mayfrank E. & Daumann J. Neurotoxicity of methylenedioxyamphetamines (MDMA; ecstasy) in humans: how strong is the evidence for persistent brain damage? Addiction 2006; 101:3: 348-361
  2. Ecstasy, the serotonin syndrome, and neuroleptic malignant syndrome – a possible link? JAMA feb 17, 1993, Vol 269, no 7.
  3. Skolelevers drogvanor 2013. Kunskapskällaren 2013, rapport 2013:1. Göteborgs Stad, Social resursförvaltning.
  4. Årsrapport EMCDDA Situationen på narkotikaområdet i Europa 2006. ISSN:1609-6207.
  5. Piper BJ. A developmental comparison of the neurobehavioral effects of ecstasy (MDMA). Neurotoxicol Teratol. 2007 Mar-Apr;29(2):288-300.
  6. Bankson MG, Cunningham KA. 3,4-Methylenedioxymethamphetamine (MDMA) as a unique model of serotonin receptor function and serotonin-dopamine interactions.J Pharmacol Exp Ther. 2001 Jun;297(3):846-52.
  7. Montoya AG et al. Long-term neuropsychiatric consequences of “ecstasy” (MDMA): a review. Harv Rev Psychiatry 2002 10(4):212-20.
  8. Karlsen SN, Spigset O, Slördal L. The dark side of ecstasy: neuropsychiatric symptoms after exposure to 3,4-methylenedioxymethamphetamine. Basic Clin Pharmacol Toxicol. 2008;102(1):15-24.
  9. Dar KJ, McBrien ME. MDMA induced hyperthermia: report of a fatality and review of current therapy. Intensive Care Med 1996;22(9):995-6.
  10. Bråbäck L, Humble M. [Young woman dies of water intoxication after taking one tablet of ecstasy. Today’s drug panorama calls for increased vigilance in health care] Läkartidningen 2001;98(8):817-9.
  11. Parrott AC. Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic neurotoxicity. Pharmacol Biochem Behav. 2002;71(4):837-44.
  12. Stolaroff MJ, Wells CW. Preliminary results with new psychoactive agents 2C-T-2 and 2C-T-7. Yearbook for Ethnomedicine 1993:99-117.
  13. Balíková M. Nonfatal and fatal DOB (2,5-dimethoxy-4-bromoamphetamine) overdose. Forensic Sci Int. (2005) 153, 85–91.
  14. Bowen JS, Davis GB, Kearney TE, Bardin J. Diffuse vascular spasm associated with 4-bromo-2,5-dimethoxyamphetamine ingestion. JAMA. 1983;249(11):1477-9.
  15. Rammer L, Holmgren P, Sandler H. Fatal intoxication by dextromethorphan: A report on two cases. Forensic Sci Int. 1988;37(4):233-6.


Kai Knudsen

Dep of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg

Published with permission from Internetmedicin AB


By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Globally, there are about 185 million drug users. Of these, approximately 34 million use amphetamines as primary drug. Amphetamine abuse is relatively common in Sweden and other Scandinavian countries compared to other countries in Europe. It is estimated that between 10,000 and 25,000 people use amphetamine in Sweden. Of these, approximately 8,000 users have amphetamines as their primary drug, about 32% of those with severe addiction. Of the intravenous drug users in Sweden, it is estimated that the majority, about 60-70 percent, use amphetamines and the remainder uses heroin.

Injecting drugs in itself significantly increases the risk of medical complications such as infectious diseases and thrombosis. The mortality rate among amphetamine users is approximately 2% annually.

Amphetamine users have increased mortality compared to normal population, but lower compared to opiate drug users. Amphetamine is the drug in Sweden, which usually causes most frequent police interventions in society, about 7,000 seizures are made annually. In other words, the use of central stimulants is an extensive medical and social problem. Among the central stimulants, amphetamine, dexamphetamine, methamphetamine and methylphenidate are primarily used.

Many so-called new psychoactive substances (NPS) are derivatives of amphetamine and have similar central stimulatory effects. Several closely related agents are classified as phenethylamines or synthetic catinones. Even cocaine and ecstasy are central stimulants but are usually classified in a separate category of addictive drugs. Damage due to amphetamine is a relatively common problem in our medical and surgical emergency services and in drug addiction while isolated amphetamine intoxication is relatively unusual. Amphetamines are usually classified as illicit drugs or in some cases as hazardous to health.

Different central stimulants

  • Lisdexamphetamine (Elvanse®, Elvanse Adult®)
  • Methylphenidate (Concerta®, Ritalin®, Methylphenidate Sandoz®)
  • Dexamphetamine sulfate (Metamina®, Attentin®) (licensing agent)
  • Modafinil (Modiodal®)
  • Amphetamine (Amphetamine Recip®, Adderal XR®)

In other countries, a wide range of other amphetamine preparations are available, for example amphetamine sulphate (Amphetamine), dextroamphetamine (Dexedrine®), fenmetralin (Fenmetrazine®) and fentermine (Mirapront®). Of all patients treated for addiction in Sweden, approximately half use amphetamines regularly. Most people with amphetamine abuse have a mixed drug use with other illicit drugs, not seldom cannabis and benzodiazepines. Legal use of central stimulant drugs has increased significantly in recent years, mainly methylphenidate (Concerta® and Ritalin®), but lisdexamfetamine (Elvanse®) has also been significantly increased, both in children, adolescents and adults. Only Ritalin® and Elvanse® are approved for primary use in adults.


Amphetamine is a central stimulant that, after ingestion, provides increased energy, increased activity, increased stamina and elevated vigilance, the appetite decreases. It is the oldest, most well known and most abusive drug of all different central stimulants. Among all drug users in Sweden, about 4% have reported that they once tried amphetamine.

Amphetamine is chemically produced and is a white powder, sometimes with a slight shift to yellow, brown or gray. As a rule, amphetamine is injected, but it can also be swallowed or dissolved in a beverage (“bombing”). Between 40 and 80% of users indicate that they inject amphetamine. A dose of amphetamine usually has clinical effect for one to two hours, sometimes longer. Some common username on amphetamine is “Jack”, “Up Jacket,” “Watched”, “White”, “Dose” and “Speed”. Bags containing powder, capsules or tablets are sold illegally.

Normal dose at nasal, oral or intravenous intake is usually about 100-200 mg.


Metamphetamine is an amphetamine variant that has become popular in recent years. Some common names are “Meth”, “Speed” and “Yaba”. In Sweden, it is often called “Metatjack”, for example. The drug is smuggled to Sweden from, among other countries, Thailand and is described as providing more intensive euphoria with stronger perception than amphetamine (more psychotropic). Methamphetamine has become more common in in recent years and now accounts for about 20 percent of amphetamine use.

Methamphetamine is usually sold as a white powder in capsules, but it also occurs in crystalline form, commonly called “Ice” because the crystals resemble small ice cubes or coarse salts. Ice is usually transparent. Some other nicknames are “Los Angeles Glass”, “Glass” and “Crystal”.

Ice gives a stronger intoxication than usual amphetamine with a sense of intense excitement and energy. Methamphetamine has a longer half-life compared to usual amphetamine. The effect lasts longer than 24 hours. With repeated intake, the effect may last for several days. Abuse of methamphetamine is relatively extensive in the United States, Japan, South Africa, Southeast Asia (Thailand) and Australia. Metamphetamine is also used intravenously. Normal dosage is 10-30 mg, strong dose is 30-60 mg and very strong dose is 40-150 mg.


The classic effect of amphetamine consists of a short-term euphoric effect with increased vigilance, self-confidence, increased energy, hyperactivity and heightened mood followed by a prolonged dysphoric period. During euphoria, wisdom and self-esteem increase, an increase in self-esteem appears and one becomes expansive in speech and thought, which can be perceived as hyperactivity and hypomania. Increased mental and physical energy, thought retention, increased impulsivity, increased appetite, increased sexual desire, increased mood, increased concentration and hypomania. Clinical symptoms of the effect of amphetamine may be large pupils, stare glance, hyperactivity, strange behavior, tics, flushing, dyspnea, itching, monotonous movements, tactile hallucinations, chewing, difficulty in stagnation and intense behavior; one gets “speeded”. Euphoria occurs as a result of increased release of several central nervous system (CNS) catecholamines, mainly dopamine and norepinephrine. Amphetamine gives up to 1000% increase in dopamine level in the nucleus accumbens compared to 150% for cannabis in animal studies. Subsequently, tolerance increases, with the risk of hallucinations and delusions. Amphetamine is therefore usually abused with a few hours interval for a few days or up to a week. After this, the addict needs to recover – sleep and rest. The abuse is often periodic and often includes other drugs.

Common symptoms after a long time of abuse are:

  • Concern
  • Anxiety
  • Irritability, aggressiveness
  • Hallucinations
  • Depression
  • Paranoid delusions

Paranoia usually disappears after a time of withdrawal.

Effects of addiction

Symptoms of abuse of amphetamine include hyperactivity with excitation and psycho motor anxiety. The affected person may over time have a characteristic springy, bouncing walk and suffer from involuntary, strange and dull movements (choreo athetosis). Additional symptoms/clinical signs of intoxication:

  • Big pupils
  • Tactile hallucinations, tingling
  • Itching
  • Monotonous movements
  • Chewing
  • Tics

Physiological effects

Pulse and blood pressure increase – the increase is dose dependent and can cause high blood pressure and tachycardia at high doses. It is not uncommon for amphetamine users to get intracerebral hemorrhage (ICH) – systolic blood pressure over 250 mm Hg has been measured. The bleeding (ICH) that occurs in the CNS is often punctured, making it difficult to evacuate the blood surgically. In the case of CT scan with angiography it may be difficult to detect a bleeding source. Instead, treatment is often conservative with invasive blood pressure control. An increased risk exists for the development of cerebral aneurysm that can burst and cause severe subarachnoid bleeding.

Hematoma is eventually resorbed, but neurological damage of varying degrees can persist.

Amphetamine abuse may eventually lead to thromboembolic complications with cardiovascular and vessel damage with increased risk of aortic aneurysm and vascular dissection, and heart failure (dilated cardiomyopathy).

Other physiological effects are reduced convulsion threshold, weight loss, impaired dental status with strong caries and dry mucous membranes, vitamin deficiency, and impaired immune system. Amphetamine abuse can also lead to increased risk of:

  • Miscarriage during pregnancy
  • Fetal injury with increased perinatal mortality
  • Hepatitis B and C, HIV
  • Liver cirrhosis
  • Stroke
  • Damaged heart valves (endocarditis)

Mental effects

Abuse of central stimulants can give psychological health issue in the form of hyperactivity, hypomania, distantness, anxiety, restlessness, anxiety, unstable temper and increased aggressiveness, both outward and inward.

Other mental symptoms and effects that abuse can lead to are:

  • Racing
  • Increased impulsivity
  • Manic episodes
  • Decreased self-control, disinhibited behavior
  • Increased appetite, sweating (but also loss of appetite)
  • Panic attacks, phobias
  • Compulsive behavior (forced and compulsive)
  • Psychosis-like reactions
  • Tics
  • Skin rash, tactile hallucinations (“Meth Bugs”)
  • Increased suicidality
  • Depression, malaise and suicide attempts

Acute overdose

In case of overdose, the addict receives a strong sympathetic boost with hypertension, tachycardia, sweating, rigidity and hyperthermia. Psychic symptoms listed below are commonplace.


Moderate overdose occurs at intake above 200 mg amphetamine, high overdose over 500 mg and life threatening overdose over 1000 mg (lower doses of methamphetamine). Normal intake is 100-200 mg per time. Intake of 500 mg may lead to:

  • Confusion
  • Anxiety attacks
  • Psychomotor anxiety
  • Aggressiveness
  • Acute psychosis
  • Kidney failure
  • Liver failure
  • Hyperthermia
  • Cardiovascular collapse

Hyperthermia can cause rhabdomyolysis and metabolic acidosis with potassium release and risk of cardiac arrhythmias. General seizures, hypotension and metabolic acidosis may occur suddenly.


Amphetamine has a moderately addictive effect. In a study in adolescents 11% developed dependence of those who tried amphetamine. Tolerance development is described as well as strong psychological dependence. Dependence’s pathophysiology appears to involve the brain’s dopamine system. In both animal models and human PET studies, decreased mesolimbic dopamine levels have been demonstrated following amphetamine intake, changes that have also been associated with severity of withdrawal symptoms. The treatment of abuse is mainly symptomatic and therapeutically focused with the aim of absolute withdrawal. Attempts have been made with medical substitution treatment.

As far as drug treatment of dependence is concerned, there is insufficient scientific evidence to draw some safe conclusions on effective treatment. The proportion of intravenous addicts has decreased during substitution treatment. There is only limited evidence that substitution treatment in amphetamine dependence has positive effects with regard to addiction, withdrawal symptoms and drug withdrawal.

  • There are newer studies suggesting that treatment with dextroamphetamine (Dexedrine®), methylphenidate (Concerta®) and disulfiram (Antabus®) has an effect on central stimulants, especially in cocaine abuse. Lisdexamfetamine appears to reduce the risk of addiction compared to dexamfetamine but possibly this is only a dose question. Other studies are taking place with opioid antagonists.
  • There is ongoing studies of treatment with baclofen (Lioresal®) and naltrexone (Naltrexon Vitaflo®).
  • Treatment with benzodiazepines is the first choice in treating sleep disorders, and anxiety disorder.
  • Psychosis can be treated with neuroleptic drugs, for example, olanzapine (Zyprexa®), risperidone (Risperdal®) or zuclopentixol (Cisordinol®).
  • Caution is advised with high dose neuroleptics (levomepromazin) due to the risk of hemodynamic instability and reduced convulsion threshold.

Psychosocial treatment

Treatment in the form of learning and behavioral therapeutic methods has shown positive effects in the use of amphetamine, especially during the first six months of treatment. Only psychotherapy as a treatment method has resulted in increased retention in structured treatment programs compared with other interventions (higher retention rate).

Acute treatment

The treatment of acute overdose of central stimulants is controlled by the substances taken, but is mainly symptomatic. It is important to direct the patient to the correct level of care so that vital life support can be ensured. After acute treatment, many patients require assessment of psychiatry and referral to dependence clinic and social services.

In acute care of confusion abusers, regular monitoring of mental status and vital functions such as heart rate, blood pressure and temperature is important. Place the patient in a quiet and dark room and let him/her eat, sleep and rest (sleep morning). In case of severe hypertension (systolic blood pressure above 200 mmHg), invasive blood pressure measurement via an arterial line should be used. Rehydrate with crystalloid fluids and check electrolytes in serum.

Benzodiazepines should be given to control anxiety and to prevent or treat general seizures. In the case of oral overdose of amphetamine, activated charcoal and gastric emptying should be considered in the same way as in other poisoning conditions, i.e. it is generally recommended for serious poisoning only up to one hour after ingestion.

Increased blood acidity enhances the elimination of amphetamine, but is not generally recommended as it is unfavorable in rhabdomyolysis at the same time. Be liberal with echocardiography (UCG) to diagnose possible valve problems and cardiomyopathy. In neurological symptoms, a CT brain scan should be made and in the case of intracranial bleeding, cerebral angiography should be performed.

Pharmacological treatment:

  • Diazepam (Stesolid®) 5-20 mg 3-4 times daily against anxiety/irritability or oxazepam (Sobril®) 15-50 mg 4-6 times daily.
  • Nitrazepam (Apodorm®) 5-10 mg to the night of sleep.
  • Risperidone (Risperdal®) 1 mg 2 times daily, alternatively:
  • Olanzapine (Zyprexa®) 10-20 mg x 2, alternatively:
  • Haloperidol (Haldol®) 5 mg 1-2 times daily (avoid high dose neuroleptics) alternatively oral solution 1-2 mg, no more than 4 hours against psychotic symptoms. If oral treatment is not possible, Haldol can be given i.m. 2.5-5 mg x 4 alternatively zuclopentixol (Cisordinol-Acutard®) 100-150 mg i.m.
  • Midazolam (Dormicum®) 2-5 mg intravenously in the event of anxiety and restlessness.
  • Dexmedetomidine (Dexdor®) by continous infusion if treatment is given in an intensive care unit.
  • At heart palpitations and moderate hypertonia beta-blocker may be used – propranolol (Inderal®) 40 mg x 3 or metoprolol (Seloken®) 50 mg x 3.
  • Symptomatic treatment in general.

Severe hypertension

In case of pronounced hypertension (> 200 mm Hg), blood pressure should be monitored invasively.

Treatment of high blood pressure must be done with caution. Beta-blockers given intravenously have been described to give paradoxical effects on the toxic effects of cocaine and amphetamine. High blood pressure should therefore be treated primarily with vasodilators such as nitroglycerin. Magnesium sulphate is a mild vasodilator that works well in the treatment of sympathomimetic states and can be tested in amphetamine toxicity.

  • Infusion of glyceryl nitrate (Nitroglycerin®) 0.2-0.5 μg/kg/min.
  • Infusion of magnesium sulfate: 20 mmoles in 100 ml Sodium Chloride for 20 minutes followed by another 20 mmol for 20 hours.
  • Clonidine (Catapress®) can be tested in continuous infusion, 0.25-0.5 μg/kg/h alternatively dexmedetomidine (Dexdor®). Clonidine can also be given orally 75-150 microg x 3.
  • Caution with beta blocker intravenously
  • CT brain in hypertonic crisis or neurological symptoms


Sedation and cooling in hyperthermia is important. Active treatment may be required.

Sedation is achieved primarily with benzodiazepines, such as midazolam (Dormicum® 1 mg/ml) or diazepam (Stesolid® 5 mg/ml) intravenously, second choice may be propofol (Diprivan® 20 mg/ml).

Active cooling may be accomplished by intravenous delivery of 1-2 liters of cold saline (from the refrigerator).


The prognosis for acute poisoning with central stimulants is usually good if the patient has not already experienced complications in the form of cerebral hemorrhage, serotonin syndrome or cardiovascular collapse. A “sympathetic or serotonin syndrome” may develop in the event of overdose with amphetamine with multiple organ failure as a consequence in severe cases. Every year about 100 people in Sweden die in drug-related deaths due to amphetamine.

About half of all deaths due to amphetamine abuse depend on cardiovascular collapse, the rest dies differently; through accidents, trauma, suicide, severe infections, dilated cardiomyopathy, pulmonary embolism, myocardial infarction, other injuries, etc.


  • F 15.1 Mental disorders and behavioral disorders caused by other stimulants, including caffeine, harmful use
  • T43.6 Psychostimulants with substance abuse
  • X60-X69 Intentional self-destructive action through poisoning
  • Y10-Y19 Poison with obscure intention


  1. WHO Statistics Internet, 2018
  2. Drug development in Sweden 2007, Report No. 107, Central Federation for Alcohol and Drug Development, Stockholm 2007.
  3. Lan KC, Lin YF, Yu FC, Lin CS, Chu P. Clinical manifestations and prognostic features of acute methamphetamine intoxication. J Formos Med Assoc 1998; 97 (8): 528-33
  4. Robertsen A, Kowalczyk M, Gabrielsen AM, Jacobsen D. Amphetamine Poisoning. Tidsskr Nor Laegeforen. , 1998; 20; 118 (28): 4340-3
  5. Brown JM, Hanson GR, Fleckenstein AE. Methamphetamine rapidly decreases vesicular dopamine uptake. J Neurochem 2000; 74 (5): 2221-3
  6. Anglin MD, Burke C, Perrochet B, Stamper E, Dawud-Noursi S. History of the methamphetamine problem. J Psychoactive Drugs 2000; 32 (2): 137-41
  7. Yui K, Goto K, Ikemoto S, Ishiguro T, Kamata Y. Increased sensitivity to stress in spontaneous recurrence or methamphetamine psychosis: noradrenergic hyperactivity with contribution from dopaminergic hyperactivity. J Clin Psychopharmacol 2000; 20 (2): 165-74
  8. Abraham HD, Fava M. Order of onset of drug abuse and depression in a sample of depressed outpatients. Compr Psychiatry 1999; 40 (1): 44-50
  9. Xu JH, Shen H, Zhang YP. Amphetamine-induced rage response in mice and its mechanism. Yao Xue Xue Bao 1992; 27 (8): 566-71
  10. Silverstone T. Appetite suppressants. A review. Drugs 1992; 43 (6): 820-36
  11. Baucum AJ 2nd, Rau KS, Riddle EL, Hanson GR, Fleckenstein AE. Methamphetamine increases dopamine transporter higher molecular weight complex formation via a dopamine and hyperthermia-associated mechanism. Neurosci. , 2004; 24 (13): 3436-43
  12. Volkow ND, et al. Effects of dopamine and serotonin releasing agents on methamphetamine discrimination and self-administration in rats. Psychopharmacology (Berl). , 1999; 141 (3): 287-96
  13. Horrigan JP, Barnhill LJ. Low-dose amphetamine salts and adult attention deficit/hyperactivity disorder. J Clin Psychiatry 2000; 61 (6): 414-7
  14. Pelham WE, et al. Once-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings. Pediatrics 2001; 107 (6): E105
  15. Roffman JL, Raskin LA. Stereotyped behavior: effects of d-amphetamine and methylphenidate in the young rat. Pharmacol Biochem Behav 1997; 58 (4): 1095-102
  16. Ellinwood, E.H. Amphetamine Psychosis. I. Description of the individuals and processes. Journal of Nervous and Mental Disease. 1967; 144, 273-283
  17. Shoptaw SJ, Kao U, Ling WW. Treatment for amphetamine psychosis. Cochrane Database Syst Rev 2008; (4): CD003026
  18. N Buxton and N S McConachie. Amphetamine abuse and intracranial haemorrhage. J R Soc Med. 2000; 93 (9): 472-477
  19. Goodman, SJ; Becker, DP. Intracranial hemorrhage associated with amphetamine abuse. JAMA. 1970; 212 (3): 480-480
  20. Borbély A A, Baumann I R and Waser P G. Amphetamine and Thermoregulation: Studies in the unrestrained and curarized rat. 1974; 281 (4): 327-40
  21. Callaway CW, Clark RF. Hyperthermia in psychostimulant overdose. Ann Emerg With 1994; 24 (1): 68-76
  22. Bloniecki Kallio V, Guterstam J, Franck J. Substitution therapy is being tested against amphetamine dependence. Pharmacy 2016; 113: DSU6.


Kai Knudsen

Department of Anesthesia and Intensive Care,

Sahlgrenska University Hospital, Gothenburg, Sweden

Published with permission from Internetmedicin AB

Cocaine – Abuse and Overdose

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Cocaine is a myth-induced central stimulant drug with a strong euphoric effect that is considered to be rapidly addictive. Cocaine is extracted from Coca leaves from the bush plant Erythroxylum coca. Cocaine preparations are classified as a central stimulant drug in a separate pharmacological entity different from the amphetamine group. Cocaine is an alkaloid with the chemical name benzoyl methyl ecgonine. The drug gives a strong euphoric intoxication and is considered to be strongly addictive.

The cocaine preparations can be divided into cocaine powder (a hydrochloride salt) which most often is sniffed or injected and crack (free base) which is normally inhaled. Ecgonine is a type of local anesthetic agent with strong vasoconstrictor effects, therefore cocaine has similar effects and is sometimes used as a local anesthetic in some medical settings such as eyes and nasal surgery.

The production, distribution, and sale of cocaine products is restricted (and illegal in most contexts) in most countries as regulated by the Single Convention on Narcotic Drugs, and the United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances.

In 2014, about 78,000 seizures of cocaine were reported in the EU, which meant that 62.6 tonnes of cocaine were confiscated. The number of seizures has fallen slightly from 2008 to 2013. Cocaine is most common in southern and western Europe.

Today, cocaine is primarily known as a widespread party drug, and is therefore relatively common in the club and nightclub environment in the big cities, especially in the United States, Great Britain and southern Europe. 2.4 million people, or 1.9 percent of all young adults (15-34 years), have used cocaine in the last year in the EU. Cocaine accounts for 10% of all seizures of drugs where cannabis accounts for more than 80%. Nineteen EU countries reported cocaine-related deaths in 2013 with more than 800 cases in total. Seventy percent of all who receive treatment for cocaine dependence come from Spain, Great Britain and Italy. Cocaine takes second place among seized drugs after cannabis. One gram of cocaine usually costs between 52 and 72 Euro. The purity varies between 36% and 50%.

About twice as many men as women use cocaine, which is most common in the age group 18-25 years. At the age of 20, it is more common for women than men, young women are often invited by male acquaintances. Today, cocaine is likely to be more common among young people in Sweden than in the 1990s, but it is still significantly more uncommon than cannabis and amphetamine. Among adults, less than 0.5% say they have tested cocaine sometime in the past year.

In the United States, cocaine is much more common than in Sweden. It is estimated that about 50 million Americans used cocaine at some point and that 6 million use it regularly. Cocaine is the second most common drug after marijuana in the United States and the drug that causes the most visits to hospital emergency services after alcohol and tobacco. Of the patients who made emergency visits, 40% complained of chest pain caused by cardiovascular symptoms.

Cocaine Hydrochloride

Cocaine extracted from Coca leaves (Erythroxylum coca). The cocoa plant grows in South America and is produced almost exclusively in Colombia, Peru and Bolivia. Coca leaves are crushed and pressed together with solvents. This stewed primary product is called coca paste. Cocaine hydrochloride is prepared from coca paste by the addition of hydrochloric acid while heating.

Chewing of coca leaves is a relatively common habit in the Andes, which gives a moderate central stimulant effect. When chewing it takes about half an hour before the effect is noticeable and after two hours, maximum uplifting and hunger dampening effects are reached. Coca leaflet contains about 0.5% cocaine and by chewing the leaves with basic ashes, the cocaine is dissolved in low doses.

Cocaine is usually produced in primitive plants in the jungle and is then smuggled through Mexico, mainly to the United States, Canada and Europe. It is sold as a white powder in the form of cocaine hydrochloride which is sniffed, smoked or injected. Mexico has been exposed to significant crime in the context of smuggling and trafficking in cocaine – the so-called cocaine war. Cocaine was widely used in the United States in the late 1800s, and was completely banned in 1915.

In the first place, cocaine is consumed by snorting through a tube or a rolled note, but cocaine can also be injected intravenously. Cocaine is rapidly absorbed in the veins of the nasal mucosa and provides a rapid onset and a relatively short-term intoxication. Cocaine hydrochloride is rapidly metabolized to two inactive metabolites called benzoylecgonine and ecgonine methyl ester. Benzoylecgonine metabolite  has a longer half-life (3-10 h) compared to cocaine (1-2 h). Benzoylecgonine is the substance that is usually detected when sampling for cocaine intake.

Some common street names on cocaine among users include Snow Flake, Girl, Lady, Pimps Drug, Speed ​​Ball (with heroin), Blow, Nose Candy, Liquid Lady, and more.


By boiling cocaine hydrochloride with bicarbonate, cocaine base is extracted into crystallized free form, known as “Crack”. Crack is fat-soluble and rapidly absorbed into lung capillaries when smoke. It appears in grayish or yellowish lumps with a porous surface and greasy texture that can be smoked after heating. Crack is mostly used by marginalized addicts.

Crack is considered to give a very intensive but short-term intoxication. Cocaine base is absorbed by smoking in the lung capillaries endothelium and gives a high within 6-8 seconds

Synthetic Cocaine

Different variants of synthetic drug drugs similar to cocaine have begun to appear on the market in recent years. Some of these are dimethocaine and camfetamine. The drugs have different usernames or serial names, such as “syntecaine”. The drugs have also been called “legal cocaine”. Several of these drugs called cocaine have been found to contain other synthetic psychoactive substances than cocaine, for example, synthetic cannabinoids have been detected.


Effects of addiction

The effect of cocaine is short-lived (20-40 min) after “snorting” and the drug needs to be taken repeatedly to keep the high. The euphoric state occurs 3-5 minutes after sniffing and the maximum concentration in the brain occurs after about 4 minutes. Euphoria is as strongest during the initial phase of the rush. The effect occurs most rapidly upon inhalation, then intravenous administration, nasal and last oral administration. You usually become spicy, happy, energetic and “upward” (euphoric) of the intoxication.

Cocaine primarily stimulates dopamine receptors, as well as noradrenaline and serotonin receptors with increased release of catecholamines as a consequence.

Cocaine rush is described as leading to increased:

  • Vitality
  • Euphoria
  • Mind sharpness
  • Energy and endurance

Acute cocaine poisoning is a rarity in Sweden and the direct effects of cocaine rush rarely cause hospital visits. Emergency hospital visits are more often the result of complications of abuse, overdose or joint poisoning.

Mental effects

In addition to the above effects, hyperactivity and hypomania also occur. Appetites may increase, leading to overeating, but also loss of appetite and anorexia. Insomnia, anxiety, restlessness, anxiety, irritability are other adverse effects that the drug may cause, as well as:

  • Thought escape, unstable temperament
  • Decreased self-control, uncontrolled behavior
  • Increased unrestrained sexual activity
  • Psychosis-like reactions
  • Self-centered thinking, paranoid ideas
  • Pseudo hallucinations (Magan’s sign), auditory hallucinations
  • Depression, depressed mood
  • Acts of suicide

Physiological effects

Sympathetic overdrive in cocaine intake may lead to hypertension, tachycardia and palpitations (tachycardia). The drug blocks the rapid sodium channels in the myocytes of the heart, resulting in increased calcium concentration and decreased magnesium concentration intracellularly and increased cardiac stress. Brugadas syndrome can be seen on ECG in the form of a J-wave with elevated early ST waves.

Cocaine has a strong vasoconstrictor effect that can cause serious cardiovascular complications due to ischemia in the the esophagus, brain and heart. Heart and vascular damage may eventually lead to heart failure, cardiomyopathy and myocarditis. Insufficient oxygen supply for a long time in the brain can cause memory disorder, occasionally severe memory disorder leading to an Alzheimer-like condition. Cocaine affects the components of the blood and induces platelet aggregation. Thrombocytopenia and increased atherogenesis may also be at risk of severe thromboembolic complications. There is a risk of renal failure due to rhabdomyolysis and in rare cases severe liver failure. Most deaths due to cocaine abuse is due to cardiovascular collapse.

Cocaine can also cause rupture of the blood vessels in the brain due to vasospasm, hypertension and micro-infarction with cerebral hemorrhage or stroke. In the United States, stroke due to cocaine abuse is not uncommon, even aortic dissection has been described. Sudden death is not completely uncommon among cocaine addicts, it is often preceded by Brugada’s syndrome.

Other physiological signs:

  • Tremor
  • Seizures
  • Hyperemia and wounds in the nasal mucosa
  • Inhibited immune system
  • Multiple skin ulcers

Acute overdose

A normal dose of cocaine is around 25-100 mg. Moderate overdose occurs at intake above 500 mg, excessive overdose at intake above 1000 mg and life-threatening overdose at intake above 3 000 mg. No real antidote exists. The most common symptoms after overdose are palpitations, intense sweating and seizures.

Life-threatening overdose is seen primarily among those who smuggle cocaine through bodily packers, or among those who swallow drugs to avoid being stunned by the body stuffers.

In case of acute overdose, the patient may develop severe sympathy boosts with hypertension, tachycardia, cold sweating, rigidity and hyperthermia (heat stroke). It is not uncommon with excitation, psychomotor disturbance, agitation and psychotic symptoms.

Intake of 500 mg may lead to:

  • Confusion
  • Psychomotor disorder
  • Aggressiveness
  • Psychosis
  • Mania
  • Cardiovascular collapse
  • Rhabdomyolysis
  • Kidney failure
  • Liver failure

Hyperthermia can cause rhabdomyolysis and metabolic acidosis with potassium release and risk of cardiac arrhythmias (broad-range QRS complexes on ECG). General cramps, hypotension and acid deficiency may occur suddenly.

Other symptoms of cocaine intake:

  • Big pupils (mydriasis)
  • Hyperactivity, excitation
  • Tremor
  • Breast pain, ECG changes

Neurological withdrawal symptoms may occur. There is a risk that the patient may suffer from brain edema and pulmonary edema with respiratory distress, as well as cardiovascular collapse and coma.

Clinical investigation

In acute care of abusers, cocaine screening is necessary as well as control of pulse, blood pressure, ECG and body temperature. Cocaine is included in most screening tests for drugs. Cocaine has a number of active metabolites: norcocaine, benzoylecgonine and ecgonine methyl ester. In addition, when consuming alcohol, cocaethylene can be formed. In the analysis of the incidence of cocaine abuse, it is primarily the metabolite benzoylecgonin which is measured.

Cocaine toxicity can be verified by HCMS following a simple drug screening of urine samples.

In case of acute toxicity, adequate patient monitoring is important, especially of:

  • Alertness
  • Breathing
  • Circulation
  • Mental functions
  • Body temperature
  • Renal function

See also “Treatment” below.

CT brain is performed at very high blood pressure or neurological symptoms.

Treatment of addiction

Cocaine has a significant addictive effect, physical tolerance development is described as well as a strong psychological dependency. The treatment of abuse is mainly symptomatic and therapeutically oriented. Regarding pharmacological treatment, there is insufficient scientific evidence to draw some safe conclusions on the effectiveness of different preparations.

  • Treatment with benzodiazepines is the first choice in treating sleep disorders, anxiety and anxiety.
  • Treatment with antidepressant drugs appears to have a positive effect on restoration in therapeutically oriented treatment compared to placebo
  • Some recent studies suggest that treatment with dextroamphetamine (Dexedrin) and disulfiram (Antabus) has an inhibitory effect on cocaine abuse. Studies are underway with modafinil treatment (Modafinil) which is a central stimulant of non-amphetamine type.
  • Treatment with baclofen (Lioresal) and naltrexone (Naltrexon) is doubtful but have been suggested
  • Psychotic symptoms can be treated with haloperidol (Haldol), risperidone (Risperdal) or olanzapine (Zyprexa).
  • Caution is advised with high dose neuroleptics (levomepromazine) due to the risk of hemodynamic instability and reduced convulsion threshold.

In the field of psychosocial treatment, learning and behavioral therapeutic methods have shown positive effects, especially during the first six months. It has been shown that psychotherapy as a treatment method has resulted in increased retention in psychiatric treatment programs compared with other psychosocial interventions.

General care of poisoning

Mixed poisoning with cocaine, alcohol and drugs (especially benzodiazepines and opioids) are common. The treatment is controlled by the different substances taken but is mainly symptomatic. There is no real antidote to cocaine. Concomitant intake of alcohol, which is common, can increase toxicity by forming ethylbenzoylcgonin, commonly called cocaethylene and delay the intoxication.

Most importantly, careful monitoring of alertness, breathing, circulation, mental functions and controlling the patient is at the correct level of care so that vital life functions can be safeguarded in the acute phase.

When taken over 3 g of cocaine, the risk is associated with life-threatening cardiac arrhythmias, and the patient must then be cared for in a department with adequate cardiac monitoring and the ability to quickly respond to ventricular fibrillation. Check ECG and carefully observe the presence of increased QRS complexes or prolonged QT time that increases the risk of ventricular arrhythmias.

Many cases result from the emergency phase assessment of psychiatry and referral to dependence clinic and social services.

The prognosis for acute cocaine poisoning is usually good if the patient has not received ventricular cardiac arrhythmias before arrival at the hospital or other severe complications.

Treatment in case of acute overdose

In case of oral cocaine ingestion, activated charcoal and gastric emptying should be considered in the same way as with other poisoning conditions, ie it is generally recommended for serious poisoning up to one hour after ingestion.

Rehydrate the patient with crystalloid fluids. Check heart rate, blood pressure and temperature regularly. Institute invasive blood pressure measurement in severe hypertension via an arterial line. Check electrolytes in serum.

Treat metabolic acidosis with sodium bicarbonate until base excess is positive in blood gas analysis. In the presence of ventricular arrhythmias, try lidocaine (Xylocard). Even magnesium sulphate intravenously can be tested.

In case of mild to moderate poisoning, place the patient in a quiet and dark room. Ordinate sleep, food and rest (sleep morning). Benzodiazepines are used as a first-aid kit in anxiety states, and to prevent or treat general seizures.

  • Inset at least one peripheral venous catheter. Take hemoglobin, white blood cell count, platelets and drug screening.
  • If necessary, give an intravenous drip, for example, Ringer’s Acetate. Rehydrate the patient until satisfactory urinary output.
  • Check regularly alertness, heart rate, blood pressure and body temperature.
  • Diazepam (Stesolid) 5-20 mg may be given 3 times daily
  • Alternatively, oxazepam 15-50 mg 3 times daily
  • Zopiclone (Imovane) 7.5 mg by night or nitrazepam 5-10 mg by night of sleep
  • Haloperidol (Haldol) 5 mg 1-2 times daily (avoid high dose neuroleptics) or as an oral solution 1-2 mg. If oral treatment is not possible, haloperidol may be administered intramuscularly 2.5-5 mg x 4.
  • Alternatively, zuklopentixol (Cisordinol-Acutard) 100-150 mg may be given intramuscularly (50 mg/ml, 2-3 ml).
  • Droperidol 10 mg i m.
  • Midazolam (Dormicum) 2-5 mg intravenously or orally in motor anxiety and restlessness (1 mg/ml).

Hypertension and hyperthermia

Treatment of high blood pressure and tachycardia in cocaine toxicity must be given with caution. High blood pressure should primarily be treated with vasodilators such as glyceryl nitrate or magnesium. Magnesium sulphate is a mild vasodilator that can be tried in coca toxicity.

  • In severe hypertension (> 200 mm Hg) intravenous blood pressure control
  • Infusion of glyceryl nitrate (Nitroglycerin) 0.2-0.5 μg/kg/min
  • Infusion of magnesium sulfate 20 mmol in 100 ml Sodium Chloride for 20 minutes followed by 20 mmol for 20 hours
  • Avoid beta blockers intravenously – it has been described to give paradoxical and irreversible effects

In case of hyperthermia, sedation and cooling are important:

  • 1-2 liters of cold saline intravenously
  • Inj. diazepam (Stesolid) 5-20 mg i.v., alternatively midazolam (Dormicum) 2-5 mg i.v.


  • Mental disorders and behavioral disorders caused by cocaine, acute infections F14.0
  • Mental disorders and behavioral disorders caused by cocaine, harmful use F14.1
  • Mental disorders and behavioral disorders caused by cocaine, depression syndrome F14.2
  • Cocaine T40.5


  1. Drug development in Sweden 2007, Report no. 107, Central Association for Alcohol and Drug Development, Stockholm 2007.
  2. Annual report EMCDDA The situation in the drugs area in Europe 2016. ISSN: 1609-6207
  3. Kelly BC, Parsons JT. Predictors and comparisons of polydrug and non-polydrug use in club subcultures. Am J Drug Alcohol Abuse. 2008: 34 (6): 774-81.
  4. Wood DM, Dargan PI, Hoffman RS. Management of cocaine-induced cardiac arrhythmias due to cardiac ion channel dysfunction. Clin Toxicology. 2008, Sep 24: 1-10.
  5. Characteristics of primary amphetamine users in Sweden: a criminal justice population examined with the Addiction Severity Index. Håkansson A, Schlyter F, Berglund M. Eur Addict Res. 2009: 15 (1): 10-8.
  6. Maurer, HH .; Sauer, C; Theobald, DS. Toxicokinetics of Drugs of Abuse: Current Knowledge of the Isoenzymes Involved in the Human Metabolism or Tetrahydrocannabinol, Cocaine, Heroin, Morphine, and Codeine. Therapeutic Drug Monitoring. 28 (3): 447-453, June 2006.
  7. Death of a female cocaine user due to the serotonin syndrome following moclobemide-venlafaxine overdose. Kłys M, Kowalski P, Rojek S, Gross A. Forensic Sci Int. 2009 Jan 6. (Epub).
  8. Wu S, Pearl-Davis MS, Manini AF, Hoffman RS. Use of antipsychotics to treat cocaine toxicity? Acad Emerg Med. 2008 Jan; 15 (1): 105.
  9. Fareed FN, Chan G, Hoffman RS. Death temporally related to the use of a Beta adrenergic receptor antagonist in cocaine associated myocardial infarction. J With Toxicol. 2007 Dec; 3 (4): 169-72.
  10. Billman GE. Cocaine: a review of its toxic action on cardiac function. Crit Rev Toxicol. 1995; 25 (2): 113-32.
  11. Robledo-Carmona J, Ortega-Jimenez M, Garcia-Pinilla J, Cabra B, the Teresa E. Severe Cardiomyopathy Associated to Cocaine Abuse. Int J Cardiol. 2006; 112: 130-131.
  12. Serper M R; Bergman A; Copersino M L; Chou J C; Richarm D; Cancro R. Learning and memory impairment in cocaine-dependent and comorbid schizophrenic patients. Psychiatry research 2000; 93 (1): 21-32.
  13. Pani, PP, Trogu, E, Vecchi, S, Amato, L. Antidepressants for cocaine dependence and problematic cocaine use. The Cochrane database of systematic reviews. in 2011; (12): CD002950.

Published with permission by Internetmedicin AB

Spice – Synthetic Cannabinoids

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Interest among young people for the consumption of cannabis and cannabis-like substances has increased significantly in recent years. Some of the cannabis-like drugs are semisynthetic herbal preparations, known as “Spice”. Spice consists of Indian spices mixed with different synthetic cannabinoids. Spice is usually smoked in a similar way to marijuana, usually in roll cigarettes, but you can also take synthetic cannabinoids in other ways, for example by swallowing or by injections.

The effects of synthetic cannabinoids are similar to cannabis effects, but these substances often give more hyperactivity and have more central stimulant effects than natural cannabis. Most synthetic cannabinoids are manufactured in China and then shipped to Europe with legitimate transport and distribution networks. During the first half of 2013, eighteen countries reported more than 1800 seizures of synthetic cannabinoids. The largest herds were reported from Spain (20 kg) and Finland (7 kg). In an English study from 179 cases of that sought an emergency care due to drug effects, synthetic cannabinoids were detected in 10% of cases. Of these, only 50% admitted taking these substances.

The use of Spice has become more common in recent years among young people in Sweden until 2015. In 2012 and 2013, questioning about Spice to the Swedish Poison Information Center in Stockholm were the most common case of different types of drugs purchased on the internet. Among illegal seizures made by Customs and Police in 2012, Spice was 4%. During the latter part of 2014, a number of young people collapsed after smoking Spice and demanded intensive care around Sweden. The number of seizures by police and the customs system has increased dramatically by the end of 2014 but has fallen significantly after 2015. Abuse therefore appears to have decreased significantly since 2015, although it has not completely disappeared. Several varieties of Spice have been narcotics in recent years.

The purchase of Spice is usually via the internet via various websites or abroad in the so-called “Head Shops”. Delivery comes by mail, often in small “zip bags”.

Spice has caused many serious incidences that have required intensive care and some cases of fatalities are described. A number of cases with fatal outcome have been under forensic investigation, most of which have been mixed poisoning, but single pure fatal spice intoxications are rare but have occurred. Reports on acute renal failure and reports of acute myocardial infarction have been published. The risk of emergency medical care after ingestion of synthetic cannabinoids appears to be significantly higher than natural cannabis, one study reported 30 times higher risk.

This overview deals with poisoning with Spice. At present, approximately 15 new substances are classified in Sweden each year and approximately 100 different substances are identified throughout Europe every year. The drugs are subsequently classified as either narcotic drugs or health hazardous drugs. Until such classification, the drugs can still be sold legally. Of the 81 new psychoactive substances reported in 2013 there were 29 synthetic cannabinoids.


Spice consists of a mixture of about ten Indian indigenous herbs and spices with effects after intake similar to cannabis. These herbs are known as “Blue Lotus”, “Lions Tail” and “Indian Warrior”. The herbs themselves have weak psychotropic properties. The spice herbs are mixed with additives of synthetic psychoactive substances that have activity on the cannabinoid receptors of the brain. Spice tends to be addictive and in recent years several serious overdoses including a few deaths have been reported.

Some common variants of Spice are called:

  • Spice Silver, Spice Gold, Spice Diamond, Black Ice, Spice Arctic Synergy, Spice Tropical Synergy, Spice Egypt, Spice Yukatan Four, Boom, Double Dutch, Remix, Vegas, Earth Impact, etc.

By oral intake or injection, it is usually the raw material, that is, the synthetic cannabinols used in powder form. Effects and side effects after ingestion are cannabis-like with an euphoric, relaxing, comfortable rest. The psychoactive supplements in Spice are commonly called cannabinoids but are not genuine cannabinols, so the correct term instead would be “cannabinoid receptor agonists” or synthetic cannabinoids. In the preparation of dry matter of cannabinoids, acetone is often used because patients sometimes also smell acetone.

Because the substances bind to the same types of brain receptors (CB1 and CB2) as THC, they primarily give a cannabis-like substance that is perceived as euphoric and relaxing. The various cannabinoids usually refer to the chemical structural formula which is a difficult mixture of letters and numbers, for example CP 47,497. This term may also contain the initials after the chemist who developed the synthesis of the substance, such as in various variants of JWH.

Most cannabinoids are fat-soluble, small nonpolar molecules with 20-26 carbon atoms. Many are more potent on the CB1 receptor than THC and the active dose becomes relatively small, usually below 1 mg. Daily dose for an addict varies between 1-15 mg of active substance. Several cannabinoids have been drug-classified, for example, HU-210, JWH-018, JWH-073, and CP 47,497-C7 substances and several others are on their way. Most cannabinoids are weaker than THC, but some are stronger and some even much stronger, such as JWH-004, JWH-180, JWH-250, and CP 47,497-C6. Chemically, most of the cannabinoids in Spice belong to five different main groups, of which naphthoyl indoles are the most common, see Table.

NaftoylindolesCyclohexylphenoles – CPIndol-derivatives (bensoyl-indoles)DibensopuranesIndazol-derivativesOthers
JWH-007CP 47,497-C6AM-694,HU-2105F-AKB-48 (5F-APINACA)UR-144
JWH-015CP 47,497-C7AM-2233,HU-243AKB-48 (APINACA)5F-UR-144 (XLR-11)
JWH-018CP 47,497-C8STS-135HU-308SDB-001 (APICA)WIN 55,212-2
JWH-018 N-(5-kloro-pentyl) derivat)CP 47,497-C95F-PB-22CUMYL-5F-P7AICA,MAM-2201
JWH-073 (metylderivat)M-CHMICSDB-0055F-ADB
JWH-081BB-22 (QUCHIC)SDB-006
JWH-203AM-22015C-AKB48 (5C-APINACA)
AB-001 (JWH-018 adamantoyl derivat)CUMYL-5FPICAMDMB-CHMICA
JWH-018 adamantyl karboxamid (SDB-001, 2NE1, APICA)APP-CHMINACA

Most of the cannabinoids are classified as narcotics and the list will be longer for each year. Among these substances may be mentioned:

  • CP 47,497 in several different subtypes (different cyclohexylphenols – CP)
  • JWH-015, -018, -019, -073, -081, -122, -203, -250 (different naphthoylindoles)
  • HU-210
  • 5F-AKB-48, 5F-PB-22, 5F-UR-144 and some variants of JWH-018 are classified as hazardous goods.
  • Some other recently reported substances are SDB-006, 5F-SDB-006 and FUB-PB-22 (2014).

Spice is difficult to find in routine blood sampling but can be detected in blood and urine through extended and targeted analysis. Special specific drug sticks are available for Spice. Spice and other synthetic cannabinoids can be difficult to detect through drug analyzes. Blood samples can detect more variants of Spice than urine samples. The right-wing laboratory in Linköping and the Department of Clinical Pharmacology, Karolinska University Hospital in Solna, can detect several different variants of Spice.

Immediately after the pleasant rush, negative symptoms may occur after consuming Spice. The negative symptoms after intake of Spice are characterized by:

  • Dry mouth
  • Panic feelings
  • Hunger feelings
  • Anxiety
  • Nausea, vomiting
  • Tiredness
  • Somnolence
  • Big pupils, red blood-stained eyelashes
  • Memory disorders
  • Elevated pulse, irregular pulse, even slow pulse
  • Increased blood pressure

In a clinical study conducted in the United States in 2012, tachycardia was presented in 37.5%, agitation in 21.8%, drowsiness in 17.9%, vomiting in 15.4%, 9.9% hallucinations, nausea in 9.8% , 9% confusion and high blood pressure in 8.5% of cases. Reports have come in recent years about more serious side effects such as acute renal failure, acute myocardial infarction (ischemic signs of ECG) and liver affect. Even single deaths and cases of grave neurological deficit have been reported, for example after ingestion of MDMB-CHMICA and ADB-CHIMINACA. In the case of renal failure, the substance 5F-UR-144 (XLR-11) has been common. In a German study (abstract EAPCCT congress, 2016) of 45 patients received after intake of AB-CHMINACA or MDMB-CHMICA, 29% showed general seizures, 25% aggressive behavior, 13% psychosis (including self-injury) and 13% syncope. As many as 16% (7 of 45) were assessed as life-threatening poisoning, which underlines the severity of Spice intoxications.


In case of acute overdose of Spice, you will notice

  • Big, wide-eyed pupils
  • Red eye witness
  • Hyperactivity
  • Excitation
  • Excitement, restlessness and agitation.
  • Aggressive behavior
  • The patient can tease himself unnaturally and be psychologically worried.
  • He or she may suffer from tachycardia, palpitations and shaking, as well as high blood pressure and chest pain.
  • Confusion and hallucinations occur.
  • Syncope
  • There is a risk that the patient may suffer from muscle tension, muscle twitching, cramps and eventually collapse.

Overdose also involves a risk of:

  • Somnolence
  • Tachycardia
  • Disorientation
  • Acute Confusion – Acute Psychosis
  • Hyperglycemia
  • Hypokalemia
  • Hypertension
  • Nausea, vomiting
  • Amnesia can be long-term
  • Metabolic acidosis
  • Myoclonic general seizures, rhabdomyolysis
  • Kidney failure
  • Liver failure
  • Intermittent apneas
  • Cardiac arrhythmias, ECG changes

There is also a small risk of acute myocardial infarction and cardiovascular collapse.


The treatment of acute overdose with Spice is mainly symptomatic. Specific antidotes are missing. It is important to direct the patient to hospital if the caretaker is so unclear that he or she cannot account for or have difficulty standing or walking so that vital life functions can be secured urgently. In the aftermath, drug abuse should be treated; assessment of psychiatrists and referral to dependence clinic and social services is often relevant. The application for social services (notification of concern ) must always be done in case of life-threatening addiction. One can also consider urgent notification. Most importantly, careful monitoring of:

  • Alertness
  • Breathing
  • Circulation
  • Temperature (risk of hyperthermia)
  • Mental functions

The prognosis for poisoning with Spice is usually good unless serious complications are already granted before arrival at the hospital. Screening with drug stitches can sometimes, but not always, provide useful information about which drugs have been taken. Negative screening does not exclude poisoning with Spice. It is important to work with updated urine stitches during drug screening.

In case of acute overdose, symptomatic treatment and supervision of vital parameters are important.

Therefore, make sure that:

  • Checks are regularly done for:
    • Pulse
    • Blood pressure
    • Temperature
    • Mental functions
  • Place the patient in a quiet place in case of mild to moderate poisoning and let him or her eat, sleep and rest (sleeping morning).
  • Treat anxiety and agitation (see below).
  • Observe the risk of hypokalaemia, rhabdomyolysis and hyperglycaemia.
  • Rehydrate with crystalloid fluids and check electrolytes in serum.
  • Do drug screening of urine samples or plasma.
  • Request a targeted analysis of urine samples with regard to Spice.

Pharmacological treatment in case of anxiety or agitation

  • Oxazepam (Sobril) 15-50 mg 3 times daily, alternatively diazepam (Stesolid) 5-20 mg 3 times daily
  • Nitrazepam (Nitrazepam) 5-10 mg to the night of sleep
  • Olanzapine (Zyprexa) 10 mg x 2 in psychotic symptoms
  • Dridol (Droperidol) 10 mg im. Provides good effect after about 20 minutes.
  • Haloperidol (Haldol) 5 mg 1-2 times daily (avoid high dose neuroleptics) alternatively oral solution 1-2 mg, no more than every 4 hours. If oral treatment is not possible, haloperidol can be administered i.m. 2.5-5 mg x 4. Alternatively to haldol, zuclopentixol (Cisordinol-Acutard) is 100-150 mg i.m.
  • Midazolam (Dormicum) 2-5 mg i.v. (1 mg/ml) in motor anxiety and anxiety. Can also be given perorally (10-15 mg) or intramuscularly 2-5 mg.
  • Propofol (Propofol) i.v. in severe anxiety in an intensive care department
  • Symptomatic treatment in general


The prognosis is usually good after taking Spice unless serious complications occur with rhabdomyolysis, hyperthermia or seizures. Particular attention should be paid to liver or kidney and rhabdomyolysis.


  • Mental disorders and behavioral disorders caused by hallucinogens, acute infections F16.0
  • Mental disorders and behavioral disorders caused by hallucinogens, harmful use F16.1
  • Psychostimulants with addiction risk T43.6
  • Mental disorders and behavioral disorders caused by multiple drugs in combination and other psychoactive substances F19


  1. Drug development in Sweden 2011, Report no. 130, Central Association for Alcohol and Drug Development, Stockholm 2012. Link
  2. School leader’s drug habits 2013. Kunskapskällaren 2013, report 2013: 1. Gothenburg City, Social resource management.
  3. Annual report EMCDDA The situation in the drug field in Europe 2012.
  4. EMCDDA; Action on new drugs briefing paper: Understanding the “Spice” phenomenon. 2009. Lisbon. Link
  5. EMCDDA; Perspectives on drugs: Synthetic cannabinoids in Europe, Lisbon. Link
  6. Centers for Disease Control and Prevention (2013), Acute kidney injury associated with synthetic cannabinoid use – Multiple States, Morbidity and mortality weekly report 62, pp. 93-8. Link
  7. Hurst, D., Loeffler, G., and McLay, R. (2011), Psychosis associated with synthetic cannabinoid agonists: a case series, American Journal of Psychiatry, 168, pp. 1119. Link
  8. Hermanns-Clausen, M., Kneisel, S., Szabo, B., and Auwärter, V. (), Acute toxicity due to confirmed consumption of synthetic cannabinoids: Addiction, 2013, 108, pp. 534-44. Link
  9. Uchiyama, N. et al. Chemical analysis of synthetic cannabinoids as designer drugs in herbal products, Forensic Science International, 2010, 198, pp. 31-8. Link
    Mixmag “The Mixmag / Guardian drug survey”, Mixmag (2012). Link
  10. Harris CR, Brown A. Synthetic cannabinoid intoxication: A case series and review. J Emerg Med. 2012; [Epub ahead of print] Link
  11. Hermanns-Clausen M, Kneisel S, Szabo B, et al. Acute toxicity due to confirmed consumption of synthetic cannabinoids: Clinical and laboratory findings. Addiction. 2012; [Epub ahead of print]
    Grotenhermen F. Pharmacokinetics and pharmacodynamics or cannabinoids. Clin Pharmacokinet. 2003; 42: 327-60. Link
  12. Drogutvecklingen i Sverige 2011, Rapport nr 130, Centralförbundet för alkohol- och narkotikautvecklingen, Stockholm 2012. Länk
  13. Skolelevers drogvanor 2013. Kunskapskällaren 2013, rapport 2013:1. Göteborgs Stad, Social resursförvaltning.
  14. Årsrapport EMCDDA Situationen på narkotikaområdet i Europa 2012.
  15. EMCDDA; Action on new drugs briefing paper: Understanding the “Spice” phenomenon. 2009. Lissabon. Länk
  16. EMCDDA; Perspectives on drugs: Synthetic cannabinoids in Europe, Lissabon. Länk
  17. Centers for Disease Control and Prevention (2013), Acute kidney injury associated with synthetic cannabinoid use — multiple States, Morbidity and mortality weekly report 62, pp. 93–8. Länk
  18. Hurst, D., Loeffler, G., and McLay, R. (2011), Psychosis associated with synthetic cannabinoid agonists: a case series, American Journal of Psychiatry, 168, pp. 1119. Länk
  19. Hermanns-Clausen, M., Kneisel, S., Szabo, B., and Auwärter, V. (), Acute toxicity due to the confirmed consumption of synthetic cannabinoids: clinical and laboratory findings Addiction, 2013, 108, pp. 534–44. Länk
  20. Uchiyama, N. et al. , Chemical analysis of synthetic cannabinoids as designer drugs in herbal products, Forensic Science International, 2010, 198, pp. 31–8. Länk
  21. Mixmag ‘The Mixmag/Guardian drug survey’, Mixmag (2012). Länk
  22. Harris CR, Brown A. Synthetic cannabinoid intoxication: A case series and review. J Emerg Med. 2012;[Epub ahead of print] Länk
  23. Hermanns-Clausen M, Kneisel S, Szabo B, et al. Acute toxicity due to the confirmed consumption of synthetic cannabinoids: Clinical and laboratory findings. Addiction. 2012;[Epub ahead of print]
  24. Grotenhermen F. Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet. 2003;42:327–60. Länk

Publicerat med tillstånd av Internetmedicin AB

New Psychoactive Substances (NPS)

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

The interest of young people for drugs purchased online has increased in recent years. These new drugs are commonly called new psychoactive substances (NPS) which are psychotropic drugs that can be purchased over the net. The drugs are similar to several established illicit drugs, usually they are central stimulants (amphetamine-like), opioid-like or cannabis-like. Several benzodiazepines that are not registered in Sweden can also be purchased online. Among NPS are different groups labeled as:

  • Synthetic cathinones (eg mefedron, metedron, nafyron)
  • Phenethylamines
  • Tryptamines
  • Piperazines
  • Opioids
  • Benzodiazepines
  • Several new hallucinogens
  • Synthetic cannabinoids (cannabis-like “spice”)

The NPS are also called “Research Chemicals (RC Drugs), Designer Drugs, Legal Highs or Smart Drugs.”

Most internet drugs have mainly amphetamine or cannabis-like effects but opiate-like and benzodiazepine-like drugs are also available. Many of the substances can be classified as substituted amphetamine derivatives or synthetic cannabinoids (SC). Most drugs are chemically related to phenethylamine, where alpha-methylphenethylamine is best known as amphetamine. Amphetamine analogues give the user increased energy and reduced appetite; Usually, the user feels good and upward and more focused. Excessive intake, on the other hand, provides a number of negative consequences with increased risk of psychosis. Some of the cannabis-like drugs are synthetic or herbal preparations, such as synthetic cannabinoids (“Spice”). The effects of these substances are similar to cannabis but produce relatively more hyperactivity due to some central stimulant effect.

The purchase of NPS is done different national or international websites. Delivery comes by regular mail or via a local pusher. NPS have given rise to many serious cases demanding intensive care and cases of fatal outcome are described.

Most new psychoactive substances are difficult to find in routine blood sampling but can be detected in blood and urine through extended and targeted chemical analysis. Rapid tests of urine samples are available for drug screening, but these often only detect the most common drugs, such as ecstasy, cocaine, cannabis and amphetamines, and risk losing the presence of NPS. Spice and other synthetic cannabinoids are more difficult to detect, but there are several new urine sticks available for detecting Spice and other illicit drugs.

This overview deals with poisoning with various new psychoactive substances. Currently, about 100 new substances are identified throughout Europe every year. A peak was noted in 2014 and 2015, after which the number of newly discovered substances has decreased slightly in number, both in Sweden and in Europe. The drugs are subsequently classified as either narcotic drugs or health hazard substances. Until such classification, the drugs can be sold legally. In total, more than 700 new substances have been reported and more than 400 have been discovered in the last 5 years.


Spice is a mixture of several herbs and spices with additives of synthetic cannabinoids that produce psychotropic effects similar to cannabis. Spice is mixed with tobacco and smoked by pipes or cigarettes. The synthetic cannabinoids are often dissolved in acetone before spraying over a spice mixture that is then smoked. Substances have psychotropic properties and are called synthetic cannabinoids or, more correctly, cannabinoid receptor agonists. The effect in the CNS is mainly performed via CB1 receptors. Effects and side effects after ingestion are cannabis-like with an euphoric and stimulant effect.

The most common side effects are:

  • Dry mouth
  • Nausea, vomiting
  • Red eye whistle, eye sore
  • Memory disorders
  • Elevated heart rate
  • Increased blood pressure
  • Panic
  • Hunger
  • Anxiety
  • Hyperactivity
  • Psychomotor disorder
  • Confusion
  • Seizures (especially PB-22)
  • Kidney failure (especially XLR-11)

The synthetic cannabinoids have a complex chemical nomenclature (abbreviation plus order number) and in most cases the usernames are completely different. Most of the cannabinoids are drug-class and the list will be longer for each year. Among these substances may be mentioned:

  • CP 47,497 in several different subtypes (different cyclohexylphenols – CP)
  • JWH-015, -018, -019, -073, -081, -122, -203, -250 (different naphthoyl indoles)
  • HU-210
  • 5F-AKB-48, 5F-PB-22, 5F-UR-144 and some variants of JWH-018 are classified as hazardous goods.
  • Some other recently reported substances are SDB-006, 5F-SDB-006 and FUB-PB-22 (2014).


The cathinones are a group of synthetic agents with weak central stimulant effects similar to the phenethylamines. Among the cathinones are some newer preparations like Mephedrone, MDPV, Methylone, Metedrone and Naphylone. The substances are present in powder, tablet and capsule form. Mephedrone has user names like “Crab” and “Subcoca”.

Cathinones are synthesized chemically from norephedrine and norpseudoephedrine. The effects are similar to the phenethylamines, i.e., central stimulation with a strong euphoric effect and increased socialization rate. Side effects may, for example, consist of:

  • Headache
  • Nausea
  • Dizziness
  • Abdominal cramps
  • Tachycardia, palpitations
  • Anxiety
  • Concern
  • Slurred speech
  • Confusion

Acute poisoning with confusion, cold sweating, fever, shaking, abrasive speech and psychotic symptoms have occurred. Individual cases of unconsciousness and death have been reported.


Mephedrone (4-methyl methatinone) was rapidly spread among adolescents in Sweden 2009 and 2010. Mephedrone is highly euphoric and a fast-acting craving of the drug has been described.

Symptoms of overdose may be:

  • Hyperactivity
  • Racing
  • Increased energy
  • Mydriasis (dilated pupils)
  • Tachycardia
  • Hypertension
  • Increased risk of seizures
  • General seizures, respiratory arrest and single deaths have occurred.

Seizures of mephedrone in Sweden have come from China and Austria. The substance has a light scent of seafood, hence the hose name “Crab fish”. Mephedrone has been classified as a narcotic drug since 2009.


MDPV is an abbreviation of 3,4-methylenedioxypyrovalerone. MDPV provides central stimulatory effects similar to amphetamine but with significantly more hallucinogenic effects. Like pyrovalerone, MDPV is likely to significantly increase the amount of several neurotransmitters in the brain, such as dopamine, norepinephrine and serotonin.

Some common usernames are “MDPV, MDPK, Sonic, Magic, Monkey Dust, Skutz”.

MDPV belongs to the group of cathinones and resembles pyrovalerone (4-methyl-α-pyrrolidino-valerophenone) listed in the 1971 Psychotropic Convention (Group IV). The presence of MDPV has increased dramatically in Sweden in recent years and seems to be one of the most common illicit drugs. MDPV has caused several deaths, mainly through drug-related trauma.

MDPV appears as powder, ampoules and tablets. For a normal to strong dose, the reported effects may last between 5 and 12 hours and the effects are described by users as strong euphoric effect. MDPV provides a strong stimulating sensation with unstable temperament, the experience varies greatly and switches quickly between pleasure and discomfort. Regular use of MDPV may be addictive and provide tolerance development (i.e. increasing dosage is required for continued efficacy). A so-called serotonin syndrome can occur that can last for up to a week. Serotonin syndrome refers to an overdrive of serotonin in the brain which affects vital functions throughout the organism. This condition usually requires intensive care.

A normal dose of MDPV is between five and ten milligrams. Among the negative effects is the high risk of acute psychosis with agitation and confusion. Patients can become violent and aggressive with powerful hallucinations and delusions. Other side effects listed are nausea, vomiting, anxiety, dizziness, dizziness, sweating, temperature increase, high heart rate, high blood pressure, visual hallucinations, cardiac arrhythmias and paranoia. Neurological symptoms such as involuntary tricky spastic movements may occur, e.g. dystonia and acatiasis. Several cases of acute poisoning with a messy and violent disposal have been described in emergency care and from the police force. High doses have been reported to cause severe anxiety attacks in inexperienced users and repeated intake can lead to addiction. Side effects are anxiety, panic attacks, self-destructive actions, depression, paranoid delusions and aggressiveness. Several cases of sudden impulsive suicide attempts and complete suicide have been observed. Impacted persons have been reported to be able to throw themselves through glass doors and into traffic in front of cars and buses. Repeated intake for a prolonged period has also been reported to give withdrawal symptoms similar to those of methamphetamine.


5-IT (5-(2-Aminopropyl) Indole or 2-(1H-indol-5-yl)-1-methylethylamine) is an indole and an isomer of alpha-methyltryptamine (AMT). The compound is chemically related to phenethylamine derivatives such as 5-APB, 6-APB.

5-IT mainly has central stimulatory rather than psychedelic effects. It is noted that “at 20 mg orally, the substance causes increased heart rate, anorexia, urine excretion and some heat stroke for about twelve hours.” In different discussion forums, the effective dose is described around 100-250 mg.

Acute overdose with 5-IT has been described to give rise to symptoms similar to those associated with other central stimulants; anxiety, agitation, and hyperthermia.


Phenethylamines (PEA) are chemical derivatives of amphetamine with closely related properties. Phenethylamine is actually the basic chemical structure of amphetamine. There are at least one-fifty different phenethylamines; everyone is not classified as narcotics. Some are instead classified as hazardous goods, which prohibits possession unless professional handling can be substantiated.

The effect on intake is an increased release in varying degrees of dopamine, serotonin and norepinephrine. The drugs generally have psychotropic, i.e. hallucinogenic and energy-generating effects. The effect when using it resembles LSD and meskalin. Several of the phenethylamines affect the autonomic nervous system with the risk of blood pressure increase and peripheral vasoconstriction (amphetamine was originally used for its vasoconstrictive effects such as cold medicine, eg benzedrine).

Some examples of phenethylamines are:

  • BDB (benzodioxolylbutanamine)
  • 2C-B (bromodimethoxyphenethylamine)
  • 2C-T-2 (dimethoxyethylthiophenethylamine)
  • 2C-T-7 (dimethoxypropylthiophenethylamine)
  • DOC (4-chloro-2,5-dimethoxycloramphetamine)
  • MBDB (methylbenzodoxolbutanamine)
  • TMA-6 (2,4,6-trimethoxyamphetamine)
  • PMA (Para-Methoxy Amphetamine)
  • PMMA (Para-methoxy-methamphetamine)

2C-B is usually sold in the form of pink tablets. Some common snake names are Bromo, Venus and Eve. 2C-T-2 is similar to 2C-T-7, but does not have the same toxicity.

DOB (Dimethoxibromomethetamine)

DOB is a substituted amphetamine with stronger psychotropic activity than other phenethylamines. Usually, DOB appears as a white synthetic powder sold in capsules or tablets. The substance has also been found in soft tissues, so called “blotters”. DOB can also be “snorted”, that’s pulled through the nose. DOB has slow onset (about an hour) and gives a long lasting high. DOB has a strong vasoconstrictor effect. A common user name is “Golden Eagle”.


Bromo-Dragonfly (bromo-benzodifuranyl-isopropylamine) is a synthetic phenethylamine similar to DOB, LSD and amphetamine. The drug has a pronounced affinity for serotonin receptors. Bromo-Dragonfly occurs as a powder, “blotters”, fluid or tablets. Common user doses are 50-800 μg.

Bromo-Dragonfly is hallucinogenic, but also has effects similar to amphetamine. The drug is strongly vasoconstrictive and has caused pronounced vasoconstriction (pseudoergotism) leading to ischemia and amputation of the fingers and toes. Pseudoergotism has also occurred after taking DOI. Deaths after intake have occurred in Sweden. Common symptoms of overdose are psychomotor disorders and confusion.


This substance is actually a piperazine but has effects similar to opioids with sedation, analgesia and respiratory depression. In 2013 and 2014, MT-45 was detected in twelve hospitalized poisoning cases. All cases were men aged 17-35 years. In eight of twelve cases, other drugs were also detected, most of which were new synthetic substances. In three cases, cannabis was also detected. In nine cases of twelve patients were unconscious at the encounter, a person died. In many cases, ototoxicity with impaired hearing developed. MT-45 has also caused depigmentation of hair and eyebrows and other body hair. It has also given rise to large flaming eczema skin changes as well as cataracts.


Methylenedioxyethylamine is a derivative of phenethylamine which is ecstasyl-like with euphoric and empathogenic (“entactogenic”) properties. The drug increases the levels of serotonin, norepinephrine and dopamine. MDEA is often called “Eve”. Common doses are slightly higher compared to ecstasy, 100-200 mg for a high.


Methylenedioxyamphetamine is a derivative of amphetamine which is ecstasy-like with euphoric, empathogenic and hallucinogenic properties. MDA is also known as tenamphetamine. MDA is often called “Sally, SASS, or Sassafras”.


Methyl benzodoxole-butanamine is a derivative of amphetamine which is ecstasy-like with mild euphoric and hallucinogenic properties. MBDB is often called “Eden or Methyl-J”. The drug appears to be slightly less potent compared with ecstasy (MDMA).


Para-methoxy-amphetamine is a derivative of amphetamine which is ecstasy-like with euphoric and hallucinogenic properties. PMA is also known as 4-methoxyamphetamine and has predominantly serotonergic effects. PMA has caused a number of deaths and is often called “Death or Dr. Death”. The drug can induce severe cardiac arrhythmias and is also a potent MAO inhibitor which can cause a pronounced serotonin syndrome with severe hypertension and severe hyperthermia.


Para-methoxy-methamphetamine is a derivative of methamphetamine which is ecstasy-like with euphoric and hallucinogenic properties. PMMA is also called methyl-MA or 4-methoxy-methylamphetamine. In 2011, PMMA was detected in 12 deaths in Norway. The drug is often called “Superman or Superman-ecstasy“.


Tryptamines are a group of synthetic drugs with LSD and measles-like effects. Tryptamins are more hallucinogenic than phenethylamines. Tryptamins are similar to structural serotonin. Among these are noted:

  • DiPT (diisopropyltryptamine)
  • 5-MeO-DiPT (5-methoxy-diisopropyltryptamine)
  • AMT (alpha-methyltryptamine)
  • DMT (n, n-dimethyltryptamine)
  • 5-MeO-AMT (5-methoxy-alpha-methyltryptamine)
  • 5-MeO-DMT (5-methoxy-DMT)
  • dimethyl-5-methoxytryptamine
  • DPT (dipropyltryptamine)

Typically, tryptamines are sold in the form of capsules or tablets and are taken orally. The substances can also be powdered or smoked. Psilocin and psilocybin, found in hallucinogenic fungi, can be classified as tryptamins.

Intake of tryptamins reinforces the senses, mainly hearing. An overdose causes, like other party drugs, symptoms such as:

  • Hyperactivity
  • Agitation
  • Confusion
  • Visual hallucinations

There is a risk of psychotic symptoms and general seizures. Tryptamines may cause severe blood pressure increase in case of overdose. They can also cause serious drug interactions.

Benzylpiperazin (BZP)

Benzylpiperazine is related to amphetamine and has similar effects to other party drugs. Piperazines were medically used in the 1970s as antidepressant drugs due to their serotonin enhancing effects. However, they did not have any positive long-term effects and were therefore removed from the pharmaceutical market. BZP has instead established itself as a party drug and a drug addiction among young people, especially in New Zealand and Australia. It is not drug-class and can be ordered home via the internet or purchased abroad.

BZP usually occurs in capsule form which is taken orally. Ruset lasts for six to eight hours. Overdose shows the same type of symptoms as when taking other amphetamine analogues, such as high blood pressure, tachycardia and psychomotor disorders.

TFMPP (trifluoromethylphenylpiperazine), has effects which, according to users, are instead entirely ecstacylic. TFMPP is often called “Legal X”.

Dextrometorphane (DXM)

Dextromethorphane (DXM) is a cough suppressant NMDA antagonist sold as non prescription drugs in some countries, including Denmark, Finland and the United States. DXM has opiate-like effects with sedative and dissociative properties. An increased use of DXM for intoxication has been reported among younger teens in Sweden. DXM at high doses has hallucinogenic effects. Acute poisoning with DXM and benzylpiperazine has until recently been relatively unusual in Sweden. However, in 1988, two DXM-related deaths were reported. In 2008, new deaths have been reported in Sweden.

Dextromethorphan is now drug-classified but can be ordered home via the internet or purchased abroad. DXM is sold abroad under drug names like Dexofan, Dexalon, Coricidin, Wick’s formula, Neo-Tussan, Resilience and Robitussin.

Some user names on the dextrometorphan are “DXM”, “Dex”, “Robo”, “Skittles”, “Syrup”, “Triple-C” and “Tussin”.

Symptoms of poisoning with DXM include:

  • Fever (hyperthermia)
  • Gastrointestinal symptoms
  • Itching
  • Somnolence
  • Respiratory failure
  • Dreamlike experiences
  • Feelings of isolation
  • Dissociation
  • Disorientation
  • Hyperesthesia
  • Ataxia

Increased suicidality occurs.


Several different unregistered benzodiazepine preparations appear on the black market and are sold online. Flunitrazepam registered in Sweden (Flunitrazepam Mylan) is also illegally sold online. In the past, Rohypnol (flunitrazepam) was a commonly used drug in the illegal market. A relatively new benzodiazepine is phenazepam. It is a substance with a very long half-life, up to three days, which in case of overdose can produce very long-lasting effects. Memory disorder, coordination difficulties and disorientation have been described for up to one week after the intake of phenazepam. Fenazepam is imported into Sweden from mainly Russia.

Various unregistered benzodiazepine preparations available online:

  • Adinazolam
  • Bromazepam
  • Diklazepam
  • Desmetylflunitrazepam
  • Flubromazepam
  • Flubromazolam
  • Fludiazepam
  • Flurazepam
  • Flunitrazolam
  • Etizolam
  • Phenazepam
  • Camazepam
  • Clonazolam
  • Cloniprazepam
  • Loprazolam
  • Lorazepam
  • Lormetazepam
  • Meklonazolam
  • Meklonazolam
  • Norfludiazepam
  • Pyrazolam
  • Zapizolam


Impact of NPS

The effect of most NPS such as cathinones, phenethylamines and various amphetamine analogues is euphoria, social empathy, openness and increased mental and physical energy. Well-being increases and a positive sense of lust occurs within 1-3 hours of intake. Self-confidence is increasing and you get an experience that all problems disappear. The drugs give an increased sense of communication, understanding and empathy with empathogenic or entactogenic effects. Odor, perception of hearing and perception is enhanced. The pupils widen (mydriasis). The central nervous effect is mainly caused by serotonin release in the central parts of the brain, primarily the limbic system, striatum and hippocampus. After prolonged use, the serotonergic depots are depleted and patients are at risk of developing negative mental symptoms, depression and psychosis.

Examples of negative effects:

  • Hyperactivity and hypomania
  • Thought escape, unstable temperament
  • Anxiety, restlessness, anxiety, irritability
  • Decreased self-control, distancelessness, unstable behavior
  • Boundless sexual activity
  • Increased appetite, sweating (but also loss of appetite and anorexia)
  • Headache
  • Psychosis-like reactions, hallucinations

The drug user eventually becomes exhausted, irritated and depressed after repeated intake. The humility can be difficult and long-lasting. Animal data suggest that damage to dopamine pathways and, above all, serotonin pathways is morphological and partly irreversible. Even general seizures occur.

Symptoms that may occur after a few months of abuse are:

  • Fatigue, irritability
  • Insomnia
  • Stereotypic behavior
  • Depression, suicidal thoughts, increased suicidality
  • Paranoia
  • Anxiety
  • Mutism
  • Catatonia

Acute Overdose

In acute overdose of NPS, large-scale pupils, hyperactivity, excitation, excitement, restlessness and agitation are noted. The patient can behave unnaturally and be psychologically worried. He or she may suffer from tachycardia, palpitations and tremors, as well as hypertension and chest pain. Confusion and hallucinations occur. There is a risk that the patient may suffer from muscle tension, rigidity, muscle twitching and seizures; Cramp in the jaw crotch (trismus) is common.

Overdose poses a risk of:

  • Water intoxication (acute hyponatraemia)
  • Cerebral edema
  • Acute confusion
  • Acute psychosis
  • Cardiac arrhythmias
  • Myoclonal seizures
  • Hyperthermia (fever)
  • Serotonin syndrome
  • Hepatic failure
  • Kidney failure

Heat stroke, rhabdomyolysis and serotonin syndrome may occur especially after ingestion of various synthetic cathinones or phenethylamines and long lasting dance or stay in a warm environment, as well as poor hydration. Hyperthermia may be accompanied by muscular rigidity, seizures and rhabdomyolysis. Hyperthermia is often one of the symptoms of a “serotonin syndrome” (see below) and can lead to hypercalcaemia, cardiac arrhythmias with heart failure, acidosis, coma and multiple organ failure. Other serious symptoms that may develop are impaired coagulation ability – DIC (disseminated intravasal coagulation) and respiratory failure with risk of pulmonary edema. There is also a risk of intracerebral bleeding and cardiovascular collapse.

Body temperature above 41 degrees is dangerous and above 42 degrees is directly life threatening – liver failure and renal failure have been described. Probably renal failure occurs secondary to rhabdomyolysis and deposition of myoglobin in kidneys. Kidney failure has also been reported after ingestion of some Spice varieties. CT or MRI brain should be performed to exclude brain edema if pronounced hyponatraemia occurs (S-Na <120 mmol/L), as well as in focal neurological symptoms. Morphological damage to serotonergic pathways can be detected by PET camera or functional MRI.


General Care

The care of acute overdose with central stimulant drugs is generally symptomatic. Specific antidotes are missing.

Most importantly, careful monitoring of

  • Alertness
  • Breathing
  • Circulation
  • Temperature
  • Mental functions

It is important to steer the patient to the right medical department so that vital life functions can be secured urgently. In the aftermath, drug abuse should be treated; assessment of psychiatrists and referral to dependence clinic and social services is often relevant. The application for social services must always be done in case of life-threatening addiction.

The prognosis of poisoning with NPS is usually good unless serious complications are already granted before arrival at the hospital. Screening with drug stitches can sometimes, but not always, provide information about which drugs have been taken. Negative screening test does not exclude poisoning with any party drugs.

Treatment in case of acute overdose

Check heart rate, blood pressure, temperature and mental functions regularly. Invasive blood pressure measurement should be performed in case of severe blood pressure increase in moderate or severe intoxication. Place the patient in a quiet and dark room at mild to moderate poisoning and let him or her eat, sleep and rest (sleep morning). Treat anxiety and agitation (see below). Observe the risk of hyperthermia.

Rehydrate with crystalloid fluids and check electrolytes in serum. Do drug screening of urine samples or plasma. Request a targeted analysis of urine samples with regard to mesh drugs.

Pharmacological treatment in case of anxiety or agitation

  • Diazepam 5-20 mg 3 times daily, alternatively oxazepam (Sobril®) 15-50 mg 3-4 times daily
  • Midazolam 2-5 mg i.v. (1 mg/ml) in motor anxiety and anxiety
  • Olanzapine 10 mg x 2 alternatively Risperidone 1 mg x 2.
  • Droperidol 10 mg in x 1.
  • Haloperidol 5 mg 1-2 times daily or oral solution 1-2 mg, no more than 4 hours. If oral treatment is not possible, haloperidol can be administered i.m. 2.5-5 mg x 4. Propofol  i.v. in severe intimacy in an intensive care department
  • Dexmedetomidine in continuous infusion with severe concern in an intensive care unit
  • Symptomatic treatment in general
  • Caution with beta blockers

CT brain is performed at blood pressure or neurological symptoms, such as brain oedema or stroke. Check myoglobin in serum to see if rhabdomyolysis is present. Consider forced alkaline diures if so.

In hyperthermia, active cooling and sedation may be required:

  • 1-2 liters of cold saline i.v.
  • Diazepam 5-20 mg i.v.
  • External cooling with cooling blanquet or the like
  • In extreme hyperthermia, consider extracorporeal cooling through ECMO systems or the like

In case of serotonin syndrome, treatment with any of the following medicines may be given:

  • Cyproheptadin – 8 mg x 3 per os (license preparation, antihistamine)
  • Risperidone 2 mg x 3

In case of severe hypertension (> 200 mmHg) – invasive blood pressure control with arterial catheters:

  • Infusion of glyceryl trinitrate (Nitroglycerin®) 0.2-0.5 μg/kg/min
  • Infusion of magnesium sulfate (Addex-Magnesium) 20 mmol in 100 ml NaCl for 20 minutes followed by 20 mmol for 20 hours
  • Beta-blockers with caution, eg metoprolol, labetalol
  • Alfablocker with caution, such as doxazosin, labetalol


  • Mental disorders and behavioral disorders caused by hallucinogens, acute infections F16.0
  • Mental disorders and behavioral disorders caused by hallucinogens, harmful use F16.1
  • Mental disorders and behavioral disorders caused by cocaine, depression syndrome F14.2
  • Psychostimulants with addiction risk T43.6
  • T40.6 Other and non-specified narcotic drugs
  • F15.1 Mental disorders and behavioral disorders caused by other stimulants, including caffeine, harmful use
  • F15.0 Mental disorders and behavioral disorders caused by other stimulants, including caffeine, acute intoxication


  1. Drug Development in Sweden 2014, Report No. 144, Central Federation for Alcohol and Drug Development, Stockholm 2014.
  2. Gouzoulis-Mayfrank E. & Daumann J. Neurotoxicity of methylenedioxyamphetamines (MDMA; ecstasy) in humans: how strong is the evidence for persistent brain damage? Addiction 2006; 101: 3: 348-361
  3. Ecstasy, the serotonin syndrome, and neuroleptic malignant syndrome – a possible link? JAMA Feb 17, 1993, Vol 269, No. 7.
  4. Skolelevers drug habits 2013. Knowledge Source 2013, Report 2013: 1. Gothenburg City, Social Resource Management.
  5. Annual report EMCDDA The situation in the field of drugs in Europe 2012.
  6. EMCDDA; Action on new drugs briefing paper: Understanding the “Spice” phenomenon. 2009. Lisbon.
  7. Borek HA, Holstege CP. Hyperthermia and multiorgan failure after abuse of “bath salts” containing 3,4-methylenedioxypyrovalerone. Ann Emerg Med. 2012 Christmas; 60 (1): 103-5.
  8. 8Jerry J, Collins G, Streem D. Synthetic legal intoxicating drugs: the emerging ‘incense’ and ‘bath salt’ phenomenon. Cleve Clin J Med. 2012 Apr; 79 (4): 258-64.
  9. Lindeman E, Hultén P, Ström S, Enlund M, Al-Saffar Y, Helander A. Increased abuse of the drug drug MDPV in Västmanland. Severe cases of poisoning have given healthcare major problems.
  10. Läkartidningen. 2012 Oct 24-Nov 6; 109 (43-44): 1954-7.
  11. Murray BL, Murphy CM, Beuhler MC. Death following recreational use of designer drug “bath salts” containing 3,4-Methylenedioxypyrovalerone (MDPV). J With Toxicol. 2012 Mar; 8 (1): 69-75.
  12. Penders TM, Gestring RE, Vilensky DA. Intoxication Delirium following Use of Synthetic Cathinone Derivatives. The American Journal of Drug and Alcohol Abuse. 2012: 38 (6) 616-617.
  13. Ross EA, Reisfield GM, Watson MC. Psychoactive “bath salts” intoxication with methylenedioxypyrovalerone. The American Journal of Medicine. September 2012, 125: (9) 854-858.
  14. Schneir AB, Cullen J. Ly, BT. “Spice” Girls: Synthetic Cannabinoid Intoxication. The Journal of Emergency Medicine 2011; 40 (3) 296-299.
  15. Wood DM, Davies S, Puchnarewicz M, et al. Recreational use of 4-methylmethcathinone (4-MMC) with associated sympathomimetic toxicity. J With Toxicol 2010; 6: 327-330.
  16. Wood DM, Greene SL, Dargan PI. Clinical pattern of toxicity associated with the novel synthetic cathinone mephedrone. Emerg Med J 2011; 28: 280-282.
  17. Piper BJ. A developmental comparison of the neurobehavioral effects of ecstasy (MDMA). Neurotoxicol Teratol. 2007 Mar-Apr; 29 (2): 288-300.
  18. Bankson MG, Cunningham KA. 3,4-Methylenedioxymethamphetamine (MDMA) as a unique model or serotonin receptor function and serotonin-dopamine interactions. J Pharmacol Exp Ther. 2001 Jun; 297 (3): 846-52.
  19. Montoya AG et al. Long-term neuropsychiatric consequences of “ecstasy” (MDMA): a review. Harv Rev Psychiatry 2002 10 (4): 212-20.
  20. Karlsen SN, Spigset O, Slördal L. The dark side of ecstasy: neuropsychiatric symptoms after exposure to 3,4-methylenedioxymethamphetamine. Basic Clin Pharmacol Toxicol. 2008: 102 (1): 15-24.
  21. Dar KJ, McBrien ME. MDMA-induced hyperthermia: report of a fatality and review of current therapy. Intensive Care With 1996; 22 (9): 995-6.
  22. Bråbäck L, Humble M. [Young woman dies of water intoxication after taking one tablet of ecstasy. Today’s drug panorama calls for increased vigilance in health care] Medical Journal 2001; 98 (8): 817-9.
  23. Parrott AC. Recreational Ecstasy / MDMA, the serotonin syndrome, and serotonergic neurotoxicity. Pharmacol Biochem Behav. 2002; 71 (4): 837-44.
  24. Stolaroff MJ, Wells CW. Preliminary results with new psychoactive agents 2C-T-2 and 2C-T-7. Yearbook for Ethnomedicine 1993: 99-117.
  25. Balíková M. Nonfatal and fatal DOB (2,5-dimethoxy-4-bromoamphetamine) overdose. Forensic Sci Int. (2005) 153, 85-91.
  26. Bowen JS, Davis GB, Kearney TE, Bardin J. Diffuse vascular spasm associated with 4-bromo-2,5-dimethoxyamphetamine ingestion. JAMA. 1983; 249 (11): 1477-9.
  27. Rammer L, Holmgren P, Sandler H. Fatal intoxication by dextromethorphan: A report on two cases. Forensic Sci Int. 1988; 37 (4): 233-6.

Published with permission from Internetmedicin AB


By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

GHB är en flytande kemikalie som används som berusningsmedel bland många ungdomar, framför allt för att få ett alkoholliknande starkt rus. Missbruket av GHB har global omfattning sedan 1990-talet med spridda endemiska utbrott i olika länder däribland USA, Schweiz, Spanien, Norge och Sverige. Under 2014 rapporterades GHB- eller GBL-beslag av 18 länder i Europa. De 1 243 beslagen uppgick till 176 kg och 544 liter av drogen, där Belgien (40 procent) och Norge (34 procent) var och en för sig stod för mer än en tredjedel av beslagen.

GHB är narkotikaklassat i Sverige och förbjudet att använda fritt sedan år 2000. GHB-missbruket har varit intensivt i vissa regioner mellan åren 2000-2010 men har minskat betydligt sedan dess. Visst missbruk förekommer fortfarande fast i mindre omfattning. Några närliggande kemikalier som också missbrukas som berusningsmedel är GBL och butandiol.

GHB som missbruksmedel intas vanligen i en genomskinlig oral lösning och brukas mest av män i åldern 20-30 år, främst i Västsverige kring Göteborg.

GHB (gamma-hydroxybutyrat) är en organisk syra och ett derivat av karboxylsyran smörsyra. I medicinskt bruk används GHB som läkemedel mot narkolepsi och i vissa länder även mot alkoholabstinens framför allt för sina starkt sömngivande egenskaper. GHB finns registrerat som läkemedel i Sverige på indikationen narkolepsi, preparatnamnet är Xyrem (natriumoxibat) 500 mg/ml. Som läkemedel benämns GHB ofta som ”Oxybate” eller ”Sodium oxybate”. Vanliga preparat är Xyrem, Alcover, Anetamin, Gamanest, Gioron, Somsanit.

GHB konsumeras vanligen i en genomskinlig lösning, lite simmig eller oljig till konsistensen. Lösningen är klar eller halmgul till färgen. GHB luktar lite som lösningsmedel, ungefär som linoleummatta och smakar vanligen lite salt.

Intag av 0,5-2 centiliter GHB (20-30-% lösning) ger ett rus med en euforiserande och avslappnande effekt, liknande en blandning av bensodiazepiner och alkohol. Drogen intas mest i flytande form men säljs även i kristallin form i kapslar. Ruset förstärks av alkohol och sömnmedel, och det är vanligt att man intar andra illegala droger samtidigt med GHB. GHB i brukarkretsar har många smeknamn, bl a ”Gobbe”, ”Liquid Ecstasy” och ”Tvål”.

Recept för hur man tillverkar GHB finns på internet och drogen kan enkelt framställas av kemikalier i ett vanligt kök. GHB kan kokas ihop av GBL (gammabutyrolakton) och natriumhydroxid (kaustiksoda, lut). Färdigblandat GHB i lösning konsumeras vanligen från en tömd Sprite- eller Coca-colaflaska (PET-flaska). Den färdiga lösningen intas kapsylvis (”korkas”), en vanlig missbruksdos är en till två kapsyler (0,5-2 centiliter motsvarar ungefär 2-4 g [200 mg/ml]) GHB. En rusgivande dos kan variera mellan några gram upp till 18 gram.

I Göteborgs drogvaneundersökning bland skolelever 2013 så har andelen ungdomar som prövat GHB minskat under senare år. Den uppgick år 2013 till 2% av dem som provat narkotika. År 2014 uppgav 0,4% av pojkarna och 0,1% av flickorna i årskurs 2 att de någon gång provat GHB. GHB-missbruket i Sverige har varit fokuserat kring Göteborg, Västra Götaland och Sundsvallsregionen. Missbruket har minskat markant under senare år. Många fall har presenterat sig som dramatiska och stökiga akutfall med antingen djup medvetslöshet, kramper och andningsstillestånd eller med påtaglig aggressivitet, allmän stökighet och psykomotorisk oro (”raptus”).


GHB förekommer naturligt (endogent) i kroppen som substrat (prekursor) för GABA i mycket små mängder och påverkar bl. a vakenhet och kramptröskeln. GHB passerar snabbt blodhjärnbarriären och ger en centralnervös påverkan på framför allt monoaminerga synapser med påverkan på dopamin och specifika GHB-receptorer. GABA utgör en kemisk transmittorsubstans för ungefär 30 % av alla celler i CNS. GABA är i huvudsak en lugnande signalsubstans i sina funktioner och påverkar flera andra signalsubstanser, bl a dopamin. GHB binder huvudsakligen till specifika GHB-receptorer som är excitatoriska samt till GABAB-receptorer. GHB frisätter både dopamin och glutamat. Teurapeutiska serumkoncentrationer av GHB är inte helt kända men man tror att runt 100 mg/L ger ett euforiskt rus och över 500 mg/L ger ett livshotande tillstånd. Stora interindividuella skillnader förekommer.


Intag av GHB ger kliniska effekter liknande en blandning av alkohol och bensodiazepiner. Berusningskänslan inträder 10-20 minuter efter intag med maximal effekt efter 30-60 minuter, vilket ger ett betydligt långsammare tillslag än alkohol. GHB ger upphov till berusning, dåsighet och eufori. I för hög dos förekommer medvetslöshet och ibland kramper och muskelryckningar, såväl av typen ”muscular jerks”, “petit mal” som “grand mal”. Det är vanligt med oro, muskelryckningar, ofrivilliga rörelser, stökighet och aggressivitet. Märkliga koreoatetotiska rörelser har observerats och dokumenterats.

  • GHB ger i små doser eufori och ett ökat välbefinnande men också ökad självkänsla, sexuell stimulans och styrkt manlig identitet (”machoeffekt”, “reinforcement”).
  • Intag av en måttlig dos GHB ger ett alkoholliknande rus som först är uppiggande, avslappnande och sedan kraftigt sömngivande.
  • GHB kan ge en känsla av avspänning, lugn, fridfullhet, ökad sensualitet, mild upprymdhet, positiva kickar, “ökad verbalitet” och muskelslapphet.
  • Upprepat intag av GHB över tiden kan snabbt ge upphov till toleransutveckling med intag av allt större doser.
  • Risken för beroende och missbruk är betydande.
  • GHB kan relativt snabbt orsaka ett fysiskt och psykiskt beroende (inom 3-6 månader).
  • Drogen ger vanligen inget bakrus (snarare mår man bra dagen efter) och har låg organtoxicitet.

Biverkningar av GHB-missbruk kan vara sömnsvårigheter, slöhet, yrsel, minnesförlust, ataxier, magsmärtor, choreoatetoser, mental avflackning, illamående, kräkningar, magont, impotens, blodtrycksfall och huvudvärk. Missbruk ger betydande abstinensbesvär.

Koncentration och dosering:

  • Normaldos är 0,5-4 centiliter (20-30 % lösning) med stora individuella skillnader och variationer i lösningens styrka.
  • En kapsyl GHB ger ett rus motsvarande ungefär 2 starköl och sitter i ca en timma.
  • Två kapsyler kan leda till sömn inom 20-30 minuter.
  • Tre till fyra kapsyler kan orsaka koma i 3-5 timmar.
  • Fem till sex kapsyler hos den ovane kan leda till djupt koma (RLS 8), andningsdepression, långsam hjärtrytm med risk för kramper och plötslig död.
  • Pojkar/män förefaller tolerera högre doser jämfört med flickor/kvinnor.
  • GHB inducerar en betydande toleransutveckling efter 1-6 månaders användning.

Koncentrationen av drickbart GHB varierar påtagligt mellan olika lösningar. En vanlig styrka är 20-30 % GHB i flytande form (källa SKL/NFC). GHB har ett snävt dosintervall (smalt terapeutiskt fönster), ger varierande berusningseffekter från gång till gång, och är mycket lätt att överdosera. Stora skillnader i individuell tolerans förekommer och ovan angivna effekter avser en ovan användare. En missbrukare med toleransutveckling tål betydligt större mängd för motsvarande symptom.

Symtom vid överdosering

  • dåsighet
  • berusning
  • snabbt insättande sömnighet
  • fluktuerande vakenhet (vaknar/somnar periodiskt är ett relativt typiskt fenomen)
  • frånvaroperioder (absenser)
  • illamående
  • kräkningar
  • skakningar
  • yrsel
  • muskelkramper
  • ataxier
  • choreoatetoser
  • kortvarig medvetslöshet
  • långsam puls
  • motorisk oro
  • avflackning
  • affektlabilitet, aggressivitet

En stor överdos ger

  • snabbt insättande sömnighet
  • fluktuerande vakenhet
  • medvetslöshet, koma
  • små pupiller, oftalmoplegi (skelning)
  • blodtrycksfall
  • långsam hjärtrytm. bradykardi
  • EKG-påverkan, ev AV-block I-III eller höga QRS-amplituder
  • oregelbunden puls
  • långsam och oregelbunden andning, andningsdepression
  • generella kramper
  • kräkning
  • risk för aspiration av maginnehåll i lungorna
  • hypotermi


Behandlingen vid akut överdosering är i huvudsak symtomatisk och något motgift (antidot) finns inte. Vakenhet och andning kan fluktuera. GHB-förgiftning har normalt ett påtagligt dynamiskt förlopp med snabba fluktuationer i vakenhet. Kramper, illamående och kräkningar är relativt vanligt. Otillräcklig andning understöds med hjälp av endotrakeal intubation och respiratorbehandling på en intensivvårdsavdelning.

Det viktigaste i behandlingen är:

  • noggrann övervakning av vakenhet, syremättnad och andning
  • understödja andning och cirkulation vid behov
  • behandla hypoxi med syrgas
  • säkerställa fri luftväg (nästub, svalgtub, intubation)
  • behandla blodtrycksfall med tillförsel av intravenös vätska samt vid behov blodtryckshöjande mediciner (efedrin, noradrenalin)
  • ge en rimlig grad av sedering vid behov
  • behandla akut förvirring och motorisk oro på ett lugnt och säkert sätt
  • lägga in patienten på rätt vårdnivå
  • göra en uppföljande utredning och behandling av beroendeproblematiken genom psykiatrin, beroendemedicinsk klinik och socialtjänsten

Magsköljning (ventrikelsköljning) och installation av aktivt kol är av begränsat värde och bör undvikas.

Sovande patient

Om patienten sover djupt och inte kan väckas bör han eller hon övervakas på en intensivvårdsavdelning (IVA) med beredskap för intubation. Är vitala parametrar stabila och patienten andas lugnt och regelbundet räcker det i regel med övervakning och patienten får sova ruset av sig. Håller patienten fri luftväg i ryggläge och syresätter sig väl behövs vanligtvis inte inläggning på IVA men observera att vakenheten kan försämras plötsligt och dramatiskt.

Annan orsak till djup medvetslöshet bör uteslutas. Kontrollera elektrolyter och en arteriell blodgas. Utför röntgen med CT-hjärna i osäkra fall eller vid fokalneurologiska symptom.

Vid GHB-förgiftning sover patienten djupt i 1-5 timmar. Längre tids medvetslöshet än 6 timmar beror i regel på andra orsaker, t ex blandförgiftning med andra läkemedel. Uppvaknandet sker i regel lugnt och patienten känner sig snabbt återställd. Patienten kan vanligen utskrivas till hemmet.

Förefaller patienten orolig under uppvaknandefasen bör man sedera patienten något för att förlänga sömnen och ge ett lugnare uppvaknande. Man kan sedera patienten med diazepam eller midazolam (Dormicum) 1-2 mg intravenöst (1 mg/ml) eller propofol (20 mg/ml, 1-10 ml). I vissa fall övergår tillståndet i en akut abstinensfas som kan vara uttalad och kräva akut abstinensbehandling.

Indikationer för inläggning på IVA

  • Påtaglig vakenhetssänkning
    • RLS 3 eller högre värde
    • GCS lägre än 10
  • Påtagligt orolig eller förvirrad patient
  • Plötslig medvetandesänkning
  • Oförmåga att hålla fri luftväg
  • Hjärtarytmier
  • Hypoxi (< 90 %)
  • Andningsfrekvens mindre än 10 eller högre än 30 andetag per minut
  • Puls under 50 eller över 130 slag per minut
  • Systoliskt blodtryck under 90 mmHg trots vätska
  • Generella krampanfall
  • Uttalad metabolisk acidos

Drogscreening och provtagning

Gör en drogscreening på urinen för att upptäcka blandförgiftningar och andra möjliga orsaker till medvetslöshet. Skicka urinprov till kliniskt kemiskt-laboratorium för analys av GHB med GC-MS (gaskromatografi-masspektrometri). GHB kan även analyseras med en ny immunohistokemisk analys som kan fastställa GHB-förgiftning samma dag som provet tas. GHB finns på vissa snabbstickor för drogscreening.

Orolig patient

Om patienten är agiterad och orolig kan patienten sederas med midazolam (Dormicum 2-5 mg i.v.) eller propofol i.v., vilket kan upprepas. Även sederande psykofarmaka har använts framgångsrikt i den akuta fasen, exempelvis droperidol (Dridol) 10 mg i.m. eller haloperidol (Haldol) 2,5-5 mg i.v. eller i.m. Heminevrin (klometiazol) bör undvikas helt.

Observera att vakenheten fluktuerar och att patienten snabbt kan bli medvetslös med otillräcklig andning.

Är patienten kraftigt agiterad och/eller våldsam kan man tvingas söva patienten fullt ut och lägga honom eller henne i respirator. Man kan då starta med midazolam (Dormicum) 5 mg i.v. och därefter ge propofol (Diprivan) 50-300 mg i.v. efter behov tills patienten sover lätt. Dessa patienter kräver i regel kontinuerlig infusion av propofol i 5 till 8 timmar på en intensivvårdsavdelning. Man ger då 100-400 mg i timmen och styr infusionshastigheten efter vakenheten. Patienten bör övervakas på IVA och luftvägen måste vara säkrad genom endotrakeal intubation och respiratorbehandling. Därefter kan man lätta på sederingen och extubera när patienten vaknar lugnt och fridfullt.

Sövning av patienten med propofol intravenöst bör endast ske om situationen är ohållbar med omedelbar fara för patientens liv (nödvärn). Detta kräver i regel aktiv medverkan av anestesiläkare och intubation med respiratorbehandling under minst 4-6 timmar. Överväg LPT.

Om patientens vakenhetsförändring, “typiskt för GHB-överdosering” inte förändras efter 3-5 timmar, bör annan diagnos övervägas. Kontrollera övriga intoxikationsprover, liksom elektrolyter (hyponatremi), b-glukos, och en arteriell blodgas. Överväg röntgen med CT-hjärna.

Agiterade och oroliga patienter bör inte släppas ut från akutmottagningen medan de fortfarande är drogpåverkade eftersom de kan vara våldsamma och okontrollerade både mot sig själva, anhöriga och personal.


Om patienten uppvisar abstinens med oro, hallucinationer, skakningar, illamående, huvudvärk eller psykotiska symtom, kan akut avgiftning behöva genomföras. Patienten bör då vårdas inneliggande, företrädesvis på en psykiatrisk avdelning eller vid en beroendeenhet. Akut svår abstinens kan följa direkt på en akut överdosering.

Första dygnet kan kräva sedering med inj. midazolam (Dormicum) eller propofol (Diprivan). Därefter kan man använda tablett diazepam (Stesolid) eller tablett lorazepam (Temesta). Patienten behöver i regel höga doser Stesolid första dygnen. Lämplig startdos är 60 mg/dygn eller mer (Sic). Vid behandling med Propofol bör patienten vårdas på en intensivvårdsavdelning.

Zuklopentixol (Cisordinol) kan ges i form av Cisordinol-Acutard 50 mg/ml 1 ml i.m., alternativt ges olanzapin (Zyprexa) 10 mg x 2 eller mer, alternativt risperidon (Risperdal) 1 mg x 2 om patienten har inslag av hallucinationer eller kraftig oro trots Stesolid.

Behöver man omedelbar effekt kan man i stället ge Haldol (5 mg/ml) en halv till en milliliter (2,5-5 mg) i.v. eller i.m.

I en senare fas kan man behöva lägga till ett antidepressivum, t ex mirtazapin (Remeron) 30 mg x 1 eller sertralin (Zoloft) 50 mg x 1. Remeron har en relativt kraftigt sederande effekt. Även sertralin har sederande effekt, särskilt i inledningen av en behandling eller i höga doser. Behandling med ett antidepressivt läkemedel gör det möjligt att komma till rätta med den sömnstörning som är vanlig vid långvarigt GHB-missbruk. Besvär med sömnen är det som ofta oroar patienterna mest. Många patienter med GHB-missbruk utvecklar en depression som kan vara farmakologiskt behandlingskrävande.

Observera att man bör vara försiktig med poliklinisk förskrivning av stora doser bensodiazepiner till GHB-missbrukare då samtidigt intag av GHB och bensodiazepiner kan vara kraftigt andningsdeprimerande. Flunitrazepam bör undvikas helt.


Det är viktigt med en psykiatrisk och social uppföljning av patienter med etablerat GHB-missbruk då ett blandmissbruk med läkemedel, alkohol och narkotika är vanligt. En vård- och behandlingsplan bör upprättas. Återbesök till psykiatrin inom beroendesjukvården eller till socialtjänsten är önskvärt, remiss bör alltid skrivas till socialtjänsten. Nedstämdhet med självmordstankar och ökad suicidalitet förekommer.

Missbruk av centralstimulantia (amfetamin, kokain, ecstasy) är vanligt bland patienter med GHB-missbruk liksom allmän social oreda. Fall med ungdomar under 18 år bör anmälas till sociala myndigheter och BUP (barn- och ungdomspsykiatrisk klinik). Även skolhälsovården kan behöva kopplas in.

Vid upprepade akuta överdoseringar bör anmälan till socialtjänsten göras akut och omhändertagande enligt LVU eller LVM tas under omedelbart övervägande.

Bestående men

En GHB-överdosering ger i regel inga bestående men, såvida inte allvarliga komplikationer tillstöter som luftvägsaspiration, kramper, apnéer eller hypoxi. Däremot om andningsuppehåll med hypoxi förekommit kan allvarliga bestående men bli bestående.

En övergående sömnstörning med kraftiga sömnsvårigheter under 3-4 veckor är vanligt. En efterföljande depression är också vanligt.

Andra biverkningar som beskrivits är magont samt impotens. Beroendet kan kräva behandling under flera månader.


  • Psykiska störningar och beteendestörningar orsakade av sedativa och hypnotika, akut intoxikation F13.0 
  • Andra psykotropa medel som ej klassificeras annorstädes T43.8 


Länkar till försäkringsmedicinskt beslutsstöd från Socialstyrelsen:

F13 Psykiska störningar och beteendestörningar orsakade av sedativa och hypnotika


  1. Persson S-Å, Eriksson A, Hallgren N, Eklund A, Berkowicz A och Druid H. GHB – farlig, beroendeframkallande och svårkontrollerad ”partydrog”. Läkartidningen Nr 38 2001 Vol 98 4026-34.
  2. Engelsen J & Rolighed Christensen H; Gammahydroxybutyrat en endogen substans og et nyt rusmiddel. Ugeskr Laeger 199;161:6903-7.
  3. Liechti ME, Kupferschmidt H. Gamma-hydroxybutyrate (GHB) and gamma-butyrolactone (GBL): analysis of overdose cases reported to the Swiss Toxicological Information Centre. Swiss Med Weekly. 2004 Sep 4;134 (35-36):534-7.
  4. Caldicott DG, Chow FY, Burns BJ, Felgate PD, Byard RW. Fatalities associated with the use of gamma-hydroxybutyrate and its analogues in Australasia. Med J Aust. 2004 Sep 20;181(6):310-3.
  5. Couper FJ, Thatcher JE, Logan BK. Suspected GHB overdoses in the emergency department. J Anal Toxicol. 2004 Sep;28(6):481-4
  6. Dyer, J.E., Roth, B., Hyma, B.A. Gamma-hydroxybutyrate withdrawal syndrome. Ann Emerg Med 2001;37:147-153.
  7. Knudsen, K., Greter, J., Verdicchio, M. High mortality rates among GHB abusers in Western Sweden. Clinical Toxicology 2008;46:187-192.
  8. Knudsen, K., Greter, J., Verdicchio, M., Cederquist, T. [GHB, GBL and butanediol poisonings–a serious problem in Western Sweden]. Lakartidningen 2005;102:3294-3296.
  9. Liechti, M.E., Kunz, I., Greminger, P., Speich, R., Kupferschmidt, H. Clinical features of gamma-hydroxybutyrate and gamma-butyrolactone toxicity and concomitant drug and alcohol use. Drug Alcohol Depend 2006;81:323-326.
  10. Skolelevers drogvanor, CAN rapport nr 146, Centralförbundet för alkohol- och narkotikautvecklingen, Stockholm 2014.
  11. Skolelevers drogvanor 2013. Kunskapskällaren 2013, rapport 2013:1. Göteborgs Stad, Social resursförvaltning.


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Snake Bites – Envenomation

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Bett av giftorm i Sverige sker i huvudsak av huggorm (Vipera berus) som är den enda giftiga art som förekommer naturligt i landet. Ormbett inträffar vanligast längs med kusterna, framför allt sommartid. Cirka 70 patienter per år läggs in på sjukhus i Sverige för vård efter ormbett. Vuxna huggormar blir runt 60 cm långa, är grå eller ljusbruna med ett karaktäristisk svart sicksackformat mönster över ryggen men ormen kan även vara helt svart eller grå. Yngre exemplar kan även vara rödbruna. Huggorm kan ibland förväxlas med hasselsnok som dock har en rund pupill till skillnad från huggormen som har en vertikal slitsformad pupill. Snoken är oftast större än huggormen och kan bli över en meter i längd. Snoken har oftast två gula, vita eller brandgula fläckar i nacken.

Huggormsgiftet innehåller en rad proteolytiska enzymer (proteaser, peptidhydrolaser, hyaluronidas, fosfolipider, fosfodiesteraser samt L-aminosyraoxidas) som i huvudsak ger lokala symptom som svullnad, smärta och blödningar men kan också ge generella symptom med svimning, yrsel, illamående, kräkningar, andningsbesvär och chock. Giftet är hemorragiskt och nekrotiserande men inte neurotoxiskt. Huggormsgift kan orsaka uttalade fokala nekroser med blåsbildningar, särskilt i fingrar och tår men reaktionen inskränker sig oftast till måttlig rodnad och svullnad och ett karaktäristiskt bettmärke. Huggormens tänder är ca 4 m m långa och orsakar ett ganska typiskt bettmärke med 2 stickmärken (”fang marks”) på ett avstånd av 6-9 mm. Giftet kan även leda till blödningar, tromboser och en dissiminerad intravaskulär koagulation (DIC-bild).

Ormar indelas vanligen i viperidae (huggormar) och elapidae (giftsnokar). Bland viperidaearterna märks europeiska huggormar inklusive den svenska, skallerormar och Russels huggorm (eng. Russels viper). Bland elapidaearter märks kobror, mambor, korallormar, taipaner och krait (Sydostasien). Flertalet elapidaearter ger neurotoxiska effekter medan viperidaearter i huvudsak ger muskelsönderfall och koagulationspåverkan inklusive dissiminerad intravaskulär koagulation (DIC). I Sverige inträffar cirka 200 bett per år vilket renderar något enstaka dödsfall varje årtionde, senast kända dödsfallet var år 2000. I hela Europa anges dödligheten till 30-50 personer per år. Mortaliteten av huggormsbett är så låg som 1-2 promille och sjunker stadigt.

En rad exotiska ormar finns i både privata och offentliga terrarier. Behandling av bett av tropiska giftormar är därför inte helt ovanligt i Sverige. Regler för tillstånd att hålla en giftorm i privat ägo varierar runt om i landet och bestäms av den regionala hälsovårdsmyndigheten. Man räknar med att inte mindre än 120 olika arter av giftormar finns runtom i Sverige.

Flertalet av de tropiska giftormarna kan ge livshotande symptom som kan kräva behandling med motgift i form av ormserum. Det finns ett tjugotal specifika ormsera tillgängliga i Sverige. Dessa tjugo olika ormsera täcker in flertalet av de olika ormarter som finns i landet. Flera ormsera är polyvalenta, dvs täcker in mer än en sorts ormgift. Å andra sidan kan ormar av samma art men olika typer, t ex skallerormar kräva behandling med olika sorters ormserum. Specifika monovalenta sera med fraktionerade antikroppar har bäst effekt. Serum med fraktionerade antikroppar ger upphov till betydligt färre allergiska reaktioner jämfört med ofraktionerat serum (t ex Zagrebserum). Det är därför viktigt vid ormbett att identifiera ormen så att rätt sorts ormserum används. Experter som kan identifiera ormen finns exempelvis vid Skansenakvariet i Stockholm och Universeum i Göteborg.

Ormserum mot huggormsbett (Vipera Tab) finns tillgängligt runt om i landet på de större sjukhusen men tillgängligheten kan variera stort och det är viktigt att varje sjukhus har en aktuell förteckning över vilka ormsera som finns tillgängliga. Observera bäst-före datum. Apoteket Scheele i Stockholm har ett centralt lager av ormsera och härifrån kan man rekvirera serum vid behov. Ormserum från apoteket Scheele kan nå fram till alla sjukvårdsinrättningar runt om i Sverige inom 4-6 timmar vid akutrekvisition.

Dödligheten av tropiska ormar varierar mellan olika länder och med olika ormarter. I Afrika, Sydostasien och i Indien är dödligheten betydligt högre än i Europa vilket bl a beror på längre avstånd till medicinsk behandling och sämre tillgänglighet till relevanta sera.

Det sker betydligt fler dödsfall i Asien jämfört med Australien där endast 2-3 dödsfall per år äger rum.

Bland världens allra mest giftiga ormar kan nämnas kungskobra, svart mamba och australiensisk (brun) taipan. Giftigheten mellan olika varianter inom samma art kan variera betydligt, t ex olika kobraarter. Generella symptom blir mer uttalade när bettstället är mer centralt beläget på kroppen, t ex på bålen och runt huvudet. Äldre och små barn är generellt känsligare liksom personer med astma och allergi. Lokalsymptom blir mer uttalade på extremiteterna. Vanligaste bettställena är på fötterna och händerna. Risken för compartmentsyndrom ökar vid perifera bett, t ex i en hand eller en fot. Det är vanligare att män blir bitna än kvinnor. I olika studier har ormbett varit mer än dubbelt så vanligt bland män som bland kvinnor. Ormbett är vanligast i åldern 20-50 år.


Symptomen är i regel lokala och/eller generella. Generella symptom indikerar allvarlig förgiftning. Cirka 25 % av huggormsbetten ger allmänsymptom och 75 % endast lokalsymptom i form av rodnad, svullnad och smärta runt bettstället. Bett av svensk huggorm liknar bett av många exotiska giftormar men merparten av huggormsbetten ger endast lokala symptom. I en svensk studie på 231 fall utgjorde de allvarliga betten 13 % av alla fall och 29 % hade moderata symptom (Karlsson-Stiber, 2006).

Vanliga symptom på ormbett är smärta följt av svullnad och missfärgning. Smärtan är ofta intensiv och analgetikakrävande. Vissa tropiska ormar som “flerbandad krajt” som injicerar ett neurotoxiskt gift kan orsaka allvarliga förlamningar inklusive andningsförlamning utan påtagliga lokalsymptom eller smärta.

Ormgift är i huvudsak hemorragiskt, nekrotiskt eller neurotoxiskt. Detta varierar med ormens art men dominerande symptom är ofta en lokal svullnad, smärta, missfärgning och i uttalade fall en nekrotisering av vävnaden. Hemorragiskt toxin ger mer omfattande vävnadsskada med svullnad, blödning och nekrotisering jämfört med neurotoxin. Risken för utveckling av ett kompartmentsyndrom är betydande vid ormbett i armar och underben. Neurotoxiskt gift (kobra, flerbandad krait) kan i värst fall ge upphov till komplett paralys med andningsinsufficiens och behov för assisterad ventilation och respiratorvård.

Ormgift sprids i huvudsak i vävnaden via lymfan. Hemorragiskt ormgift påverkar blodets koagulationsförmåga och kan inducera ökad blödningsbenägenhet och en dissiminerad intravaskulär koagulation (DIC) (särskilt Russels viper). Vissa ormgifter kan dock ge blödningsrubbning med trombocytopeni utan DIC. Det är viktigt att kontrollera patientens status avseende blödning såväl kliniskt som i laboratorieparametrar. Vid bett av mycket giftiga tropiska ormar kan såväl initialstatus som initiala prover avseende koagulationen vara helt normala för att inom 24 timmar derangeras fullständigt med kraftig trombocytopeni och ökad blödningsbenägenhet. Kontrollera blödningspåverkan i munslemhinnan, ögonvitan och i retroperitoneum, där stora spontana blödningar kan uppkomma, vid kliniska tecken på blödning (CT).

Svullnaden efter ett ormbett kan variera påtagligt och progrediera under flera dagar. Svullnad som sprider sig över en större led, som armbågen vid bett i handen eller knäet vid bett i foten är tecken på allvarligt bett och utgör en indikation för serumbehandling. Svullnaden i sig kan skapa ett kompartmentsyndrom i t ex en hand eller ett ben. Kompartmentsyndromet kan kräva kirurgisk intervention med fasciotomi (helst inte) men bettstället skall primärt lämnas i fred och ej skäras i eller diatermeras. Däremot bör trycket i vävnaden mätas vid compartmentsyndrom.

Missfärgningen blir ofta hemorragisk, rödblåfärgad eller mörklila övergående till svart vid nekrotisering av vävnaden. Nekrotiseringen omfattar hud, mjukdelar och djupare delar. Fingrar kan behöva amputeras partiellt eller helt. Missfärgningen och svullnaden kan vara omfattande även utan nekrotisering, ibland över ett helt ben och upp över bålen.

På bettstället finns oftast men inte alltid spår efter två huggtänder med 0,5 till 2 c m avstånd. Avståndet mellan tänderna kan ge en vägledning om vilken orm som bitit och storleken på ormen. Det kan förekomma både ett, två eller tre punktformiga eller strimformiga bettmärken (”fang marks”).

Lokala symptom

  • Smärta
  • Svullnad
  • Missfärgning (hemorragier, ekymoser)
  • Domningar
  • Förlamningar, paralys
  • Parestesier
  • Nekroser
  • Blödningar
  • Compartmentsyndrom

Generella symptom

  • Illamående
  • Kräkningar
  • Oro, stark rädsla
  • Ångest, hyperventilation
  • Smärta
  • Svimning
  • Hjärtklappning, takykardi
  • Hypotension (blodtrycksfall)
  • Cirkulatorisk chock
  • Andnöd, bronkkonstriktion, obstruktivitet
  • Allergisk reaktion
  • Koagulationspåverkan, generell DIC-bild


När en skadad person kommer in med ett bett av en giftorm skall detta handläggas skyndsamt.

Vid allvarlig skada underrätta genast följande personer:

  • Ansvarig jourläkare på akuten
  • Aktuell bakjour på akutmottagningen
  • Anestesijour eller intensivvårdsjour

Kontakta om möjligt, även följande:

  • Giftinformationscentralen i Stockholm, telefonnummer: 08-331 231
  • Apotekare som tillhandahåller sjukhusets antidotförråd
  • Polisen eller Räddningstjänsten för att infånga orm som kommit lös
  • Ormexpert för att identifiera ormen om detta okänt


  • Tillse att alla patienter med ormbett kommer in till sjukhus och inte avvaktar i hemmet, även vid lindriga bett.
  • Patienten skall omhändertas omedelbart och får inte läggas att vänta utan tillsyn. Även hos en relativt opåverkad person kan allvarliga symptom uppträda plötsligt.
  • Ansvarig läkare beslutar i samråd med IVA-jouren om inläggning på IVA. Vid behov av serumbehandling rekommenderas inläggning och behandling på en intensivvårdsavdelning.
  • Ormserum kan anskaffas akut från Apoteket Scheele i Stockholm (tel. 0771-450450) med brådskande flyg- eller taxitransport. Scheele klarar oftast en leverans inom 3 timmar. Skansenakvariet i Stockholm (tel. 08-442 80 39) och enstaka andra privata terrarier tillhandahåller vissa ormsera som är verksamt vid bett av exotiska ormar. Ormserum är i regel polyvalent, d v s är verksamt mot mer än en sorts ormgift. Kontrollera utgångsdatum och hållbarhet. Vissa sera anses hållbara viss tid även efter utgånget datum.


Allmänna råd

  • Skapa lugn och ro för patienten. Patienten skall sitta eller ligga, även under transporter. Försök att förebygga att patienten får panik. Ge sedativa eller analgetika vid behov. Exempelvis injektion diazepam (Stesolid) (5-10 mg i.v.) vid ångest och oro eller morfin/ketobemidon (Morfin/Ketogan) (5-10 mg i.v.) vid smärta och oro. Patienten får inte springa på väg till sjukhus.
  • Ev kompressionsförband. I vissa länder, t ex Australien, lägger man rutinmässigt en fast elastisk binda över biten extremitet för att förlångsamma resorptionen av toxinet och motverka ödembildningen. Bindan läggs utifrån och in, man börjar distalt och lindar i proximal riktning. Den motverkar spridningen av ormgiftet samt minskar ödembildningen. Bindan får inte vara avsnörande. Bindan avlägsnas vanligen inte förrän patienten fått ormserum. Tanken är att antikroppar skall finnas i blodet när antigenet (ormgiftet) kommer ut i systemcirkulationen. Kompressionsförband fungerar bättre efter bett av neurotoxiska ormar än nekrotiserande hemorragiska ormgifter. Som regel är det därför mer tillämpbart efter bett av australiska eller asiatiska ormar än europeiska, afrikanska eller amerikanska ormarter. Bättre vid bett av elapidaearter än viperidaearter.
  • Immobilisera biten kroppsdel, i högläge efter lindningen. Vid bett i handen, kan handen läggas ovanpå en kudde eller hängas upp i en mitella.
  • Lämna bettstället ifred.
  • Skaffa fram specifikt ormserum vid allvarlig förgiftning. Behandling bör påbörjas inom 12 timmar efter ormbettet, helst inom 4 timmar. Vid uttalad allmänpåverkan bör serumbehandling påbörjas snarast. Chock kan utvecklas inom 30 minuter efter ormbett men är vanligare efter 2-3 timmar.
  • Tetanusskydd rekommenderas men vetenskapliga belägg är mycket svaga.
  • Antibiotikabehandling endast vid symptom på infektion. Rutinmässig behandling med antibiotika behövs inte.
  • Undfallande kommentarer från den bitne som “det är inte så farligt”, “jag mår bara bra” är vanliga och bör ignoreras!

Undvik följande

  • Epiduralanestesi. Vid smärtor i benet bör EDA undvikas då ökad risk för generella trombos/blödningskomplikationer föreligger.
  • Att patienten själv kör bil till sjukhus
  • Inte suga, skära, kyla, värma eller diatermera bettstället.
  • Att patienten springer eller anstränger sig på vägen till sjukhus
  • Avsnörande förband, undvik att linda uppifrån och ner.
  • Hysteri och panik
  • Behandling med osäkert eller utgånget ormserum vid bett av icke identifierad orm.
  • Behandling med ormserum då endast måttliga lokalsymptom föreligger.

Behandling av lindriga bett

När endast lokal rodnad och svullnad föreligger.

Patienten handläggs på akutmottagningen och medicinsk akutvårdsavdelning (MAVA) eller motsvarande. Patienter som tillhör riskgruppen, dvs gamla, svaga, små barn, och astmatiker bör observeras i minst 8 timmar före hemgång.

  • Patienten handläggs av medicinjouren.
  • Sätt minst en PVK. Ta Hb, LPK, trombocyter och urinsticka. Vid behov sätt dropp, t ex Ringer-acetat.
  • Lägg in alla barn samt allmänpåverkade patienter på sjukhus i minst ett dygn.
  • Opåverkade patienter bör observeras i minst 6-8 timmar.
  • Kortison (Solu-Cortef, 100 mg x 1 i.v. eller i.m.). Vetenskapliga belägg är bristfälliga för behandling med steroider vid huggormsbett men utgör en väl beprövad rutin och rekommenderas främst vid allergiska symptom, bronkospasm eller efter behandling med serum framställt på häst. Är sannolikt även av nytta vid påtaglig inflammatorisk reaktion.
  • Antihistamin, t ex Klemastin (Tavegyl, 1 mg i.v). Observera att behandlingen kan vara sederande. Vetenskapliga belägg för effekt är svaga.
  • Morfin/ketobemidon (Morfin/Ketogan) (5-10 mg i.v.) vid smärtor.
  • Kontrollera och följ blodprover, observera förekomst av:
    – Metabolisk acidos (arteriell blodgas)
    – Hemolys (S-haptoglobin, LD), leukocytos, trombocytopeni
    – Rabdomyolys (myoglobin i serum, CK)
    – Hb, LPK, TPK, CRP, PK/APTT

Behandling av allvarliga bett

Kraftig lokalreaktion eller tydlig systempåverkan föreligger (grumlat medvetande, lågt blodtryck (systoliskt blodtryck < 90 mm Hg), hög hjärtfrekvens, hög andningsfrekvens).

Patienter med prechock/chock handläggs på en intensivvårdsavdelning (IVA). Kontrollera noggrant blödningsparametrar efter ankomst och efter 12 och 24 timmar.

  • Kortison (Solu-Cortef 100-200 mg i.v.).
  • Ge antihistaminpreparat (Tavegyl 1 mg i.v. x 2). Observera att behandlingen kan vara sederande. Vetenskapliga belägg för effekt är svaga.
  • Ge serumbehandling, v g se instruktioner nedan.
  • Immobilisering av biten kroppsdel, helst i högläge. Vid bett i handen häng upp armen högt i en mitella till en sängstolpe eller liknande.
  • Morfin/ketobemidon (5-10 mg i.v.) vid smärtor. Observera att behandlingen i sig kan vara sederande.
  • Vid allergiska/anafylaktiska reaktioner eller bronkospasm, ge adrenalin (1 mg/ml, 0,3-0,5 ml i.m. i lårets utsida).
  • Vid bronkospasm ge behandling med betastimulerare i inhalation, t ex salbutamol eller terbutalin (Ventoline/Bricanyl).
  • Vid cirkulatorisk chock kan adrenalin ges intravenöst, 0,1-0,5 mg (0,1 mg/ml) i.v. som titreras efter blodtrycket.
  • Ge adekvat vätskesubstitution, t ex Ringeracetat, Voluven eller Macrodex. Ge volymsubstitution med balanserad elektrolytlösning samt kolloider, gärna i form av dextran. Ge dock inte stora mängder dextran, då detta kan påverka blodets koagulationsförmåga.
  • Om dextran inte ges bör annan trombosprofylax övervägas, t ex dalteparinnatrium (Fragmin) i lågdos (2500-5000 enheter s.c.) alt enoxaparinnatrium (Klexane) 40 mg s.c. oavsett vikt.
  • Inotropt stöd och övrig chockbehandling ges på sedvanliga indikationer vid cirkulatorisk svikt t ex infusion noradrenalin.
  • Syrgas på grimma eller via näskateter.
  • Kontrollera Hb, LPK, TPK, CRP, myoglobin, PTK/APTT, FDP, S-haptoglobin, LD.
  • Ev trombelastogram eller ACT.


Behandling bör påbörjas inom 12 timmar efter ormbettet, helst inom 4 timmar. Vid uttalad allmänpåverkan bör serumbehandling påbörjas snarast. Serumbehandling är den behandling som fungerar bäst vid allvarliga ormbett.

Serumbehandling bör ges då allvarliga allmänsymptom föreligger eller då markant progress av svullnad och missfärgning sker, t ex över en större led (knäled, armbågsled).

Indikation för att starta serumbehandling är:

  • Cirkulationspåverkan som inte svarar på initial vätskebehandling
  • Medvetslöshet eller sänkt vakenhet
  • Långdragna eller återkommande gastrointestinala symptom
  • Bronkospasm eller stridor
  • Progress av lokalreaktion i den bitna extremiteten, svullnaden går över en led, t ex knäet eller armbågen inom 6 timmar.
  • Tydlig allmänpåverkan

Vid tveksamhet stöder följande faktorer indikationen för serumbehandling:

  • Leukocytos > 15-20 x 109
  • Metabolisk acidos
  • Bett av mycket giftiga ormar såsom vissa kobror, svart mamba eller australisk taipan.
  • Hemolys (högt LD, lågt haptoglobin)
  • Nytillkomna EKG-förändringar:
    – Arytmier
    – ST-T-förändringar
    – Andra ischemitecken
  • Koagulationsrubbningar (trombocytopeni, högt PK/INR eller högt APTT)

Huggormsbett behandlas vanligen med antidoten Vipera Tab. 2 ampuller = 200 mg löses i 10 ml sterilt vatten och spädes i 100 ml NaCl (9 mg/ml) och ges som en intravenös infusion under 30 minuter. Samma dos ges till barn som till vuxna. En andra, lika stor dos (200 mg), kan vara indicerat vid recidiv av cirkulationspåverkan eller vid ihållande gastrointestinala symptom, vid allvarlig koagulopati eller hemolys samt vid fortsatt kraftig progress av lokalreaktionen med risk för engagemang av bålen.

Vid serumbehandling efter bett av tropiska ormar, följ bipacksedelns anvisningar noggrant.

Vid tveksamhet, rådgör med giftinformationscentralen i Stockholm.

Uppföljning efter ormbett

En till två veckor efter serumbehandling kan en allergisk reaktion uppstå, s k serumsjuka. Uppmana patienten att höra av sig om symptom som feber, ledvärk eller trötthet uppträder. Serumsjuka bör behandlas med kortison.

Efter allvarliga bett eller när serum getts mot tropiska ormar rekommenderas ett polikliniskt återbesök 1-2 veckor efter utskrivningen. Kontrollera då SR, CRP, Hb, TPK, Kreatinin och LPK. Uttalad trötthet och nedsatt allmäntillstånd kan förekomma lång tid efter ormbett liksom kvarstående lokalsymtom som svullnad och domningar med parestesier. Återbesök bör planeras.


Toxisk effekt av ormgift T63.0


  1. Russell FE, Carlson RW, Wainschel J, Osborne AH. Snake venom poisoning in the United States. JAMA 1975; 233(4): 341.
  2. Karlson-Stiber C, Salomonsson H., Persson H. A nationwide study of Vipera Berus bites during one year – epidemiology and morbidity of 231 cases. Clinical Toxicology 44:25-30, 2006.
  3. Forks TP. Evaluation and treatment of poisonous snakebites. American Family Physician. 1994;50(1):126.
  4. Karlsson-Stiber C. Exotiska ormar på hugget även här! Läkartidningen 1996;93(48):4393-4399
  5. Holmen C. Tropiska ormar olycksrisk även i Sverige. Läkartidningen 1996;93(48):4409-4411
  6. Karlson-Stiber C, Persson H. Antivenom treatment in Vipera berus envenoming–report of 30 cases. J Intern Med. 1994;235(1):57-61.
  7. Persson H, Karlson-Stiber C. Huggormsbett – klinik och behandling. Läkartidningen 1995;92:2906-10.
  8. Karlson-Stiber C, Persson H, Heath A, Smith D, Al-Abdulla IH, Sjöström L. First clinical experiences with specific sheep Fab fragments in snake bite. Report of a multicentre study of Vibera berus envenoming. J Intern Med 1997;241:53-8.
  9. Cederholm I., Lennmarken C. Vipera berus Bites in Children—Experience of Early Antivenom Treatment. Acta Pædiatrica 1987;76(4):682 – 684
  10. Persson H. Envenoming by European vipers antivenom treatment–influence on morbidity. Przegl Lek. 2001;58(4):223-5.
  11. Harborne DJ. Emergency treatment of adder bites: case reports and literature review. Arch Emerg Med. 1993 Sep;10(3):239-43.
  12. Tanos PP, Isbister GK, Lalloo DG, Kirkpatrick CM, Duffull SB. A model for venom-induced consumptive coagulopathy in snake bite. Toxicon. 2008 Dec 1;52(7):769-80.
  13. Currie BJ, Canale E, Isbister GK. Effectiveness of pressure-immobilization first aid for snakebite requires further study. Emerg Med Australas. 2008 Jun;20(3):267-70.
  14. Kuruppu S, Smith AI, Isbister GK, Hodgson WC. Neurotoxins from Australo-Papuan elapids: a biochemical and pharmacological perspective. Crit Rev Toxicol. 2008;38(1):73-86.
  15. Whitehall JS, Yarlini, Arunthathy, Varan, Kaanthan, Isaivanan, Vanprasath. Snake bites in north east Sri Lanka. Rural Remote Health. 2007 Oct-Dec;7(4):751.
  16. Sutherland SK, Coulter AR, Harris RD. Rationalisation of first-aid measures for elapid snakebite Lancet 1979 Jan 27;1(8109):183-5.
  17. Currie BJ. Treatment of snakebite in Australia: the current evidence base and questions requiring collaborative multicentre prospective studies. Toxicon. 2006 Dec 1;48(7):941-56.


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Mushroom Poisoning

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

I Norden växer cirka 10 000 olika svampar ute i naturen, varav endast ett hundratal är ätliga. Svampar växer inte bara i jorden utan även på stubbar och träd, på växter och andra biologiska organismer och många andra ställen. Totala antalet arter på jorden uppskattas till över en miljon. Svampar består av rottrådar, ett mycel och en fruktkropp. Det är vanligen fruktkroppen som vi benämner för svamp och är den del som äts.

Svampförgiftning inträffar vanligen efter förtäring av giftig svamp som förväxlats med ätlig svamp. I sällsynta fall förekommer förgiftning på annat sätt, t ex genom rökning av hallucinogena svampar eller efter inandning av ångor vid förvällning av murklor. Några vanliga ätliga svampar är kantarell, tryffelsvamp, stensopp (Karl-Johansvamp), champinjon, skiitake (ekmussling) och ostronmussling.
Uppskattningsvis uppsöker 50-200 personer sjukvården i Sverige för misstänkt svampförgiftning varje år. Allvarliga förgiftningar är ovanliga, men enstaka allvarliga fall förekommer årligen. Dödsfall är mycket sällsynt och inträffar sporadiskt.

Svampförgiftning är vanligast under svampsäsongen, d v s under hösten. Förgiftningar kan dock dyka upp året runt, exempelvis är stenmurklan en vårsvamp. Trattkantareller som ibland förväxlas med toppig giftspindling (giftspindelskivling) växer i huvudsak sent om hösten. Vid förgiftningstillbud kontakta gärna Giftinformationscentralen för rådgivning. Spara aktuell svamp för identifiering av svampexpert. På senare år har ett antal fall av allvarlig svampförgiftning inträffat bland nyanlända invandrare, både i Sverige och andra länder som Tyskland och USA. Oätliga svenska svampar har ofta förväxlats med ätliga svampar från hemlandet.


I Sverige växer ett flertal giftiga svampar, bland de mest giftiga noteras:

  • Vit flugsvamp (växer i barrskogar, ffa granskog. Kan förväxlas med skogschampinjoner)
  • Lömsk flugsvamp (växer i ek- och bokskog. Kan förväxlas med grönkremla)
  • Gifthätting (växer på murken ved. Kan förväxlas med tofsskivling)
  • Toppig giftspindling (toppig giftspindelskivling) (växer i mossig granskog. Kan förväxlas med trattkantareller)
  • Stenmurkla (växer i skogshyggen, även i sandig mark). Kan förväxlas med toppmurkla.

Giftsvampar grupperas vanligen efter vilka toxin de innehåller. Huvudgrupperna av toxiner utgörs av: cytotoxin, neurotoxin och mag-tarmirriterande toxin (se Tabell 1).


Till cytotoxinerna räknas de giftiga ämnena orellanin, amatoxin och gyromitrin. Cytotoxiska svampar är exempelvis stenmurkla, vit flugsvamp, lömsk flugsvamp, gifthätting och toppig giftspindling. Vit och lömsk flugsvamp (amatoxin) är mycket giftiga och orsakar varje år flera allvarliga förgiftningar, ibland även dödsfall. Toppig giftspindling är främst njurskadande (orellanin). Amatoxin och orellanin orsakar cellskada i ff a i lever, tarm och njurar. Svamparna innehåller även hemolysiner som kan orsaka blödningar i hud och tarm.

Förtäring av cytotoxiska svampar är vanligen förenat med längre latenstid mellan intag och symtomdebut än neurotoxiska och mag-tarmirriterande svampar. Tiden mellan förtäring och uppkomst av symtom kan ge vägledning om vilken typ av förgiftning som inträffat. Cytotoxiska svampar ger i allmänhet en latenstid på 8-24 timmar från intag till symtomdebut. I vissa fall kan latenstiden vara längre när symptomen beror på organskada, symptomen kan debutera först efter 3-7 dygn.


Till denna toxintyp räknas exempelvis ämnena muskarin, ibotensyra, muskimol, muskazon, psilocybin och psilocin. Neurotoxiska substanser finns bl a i trattskivlingar, trådskivlingar, slätskivlingar och flugsvamp (röd, brun, panterfläckig). Bland de mest kända neurotoxiska svamparna bör nämnas Röd flugsvamp som innehåller både muskimol, ibotensyra, muskazon och muskarin samt Gifttrattskivling som innehåller muskarin. Gifttrattskivling kallas även giftig trattskivling samt ängstrattskivling. Rödbrun rottryffel kan ge upphov till yrsel, kräkningar och synhallucinationer.

Neurotoxiska svampar orsakar i första hand centralnervösa och sensoriska symtom. Muskarin ger upphov till kolinerga symtom som ökad salivsekretion och bronkobstruktivitet medan ibotensyra, muskimol och muskazon förorsakar antikolinerga symtom. Latenstiden från intag till uppkomst av symtom är kortare för neurotoxiner än för cytotoxiner; vanligen ½-2 timmar, men ibland längre. Röd och brun flugsvamp och panterflugsvamp ger i första hand symtom som hjärtklappning, stora pupiller och illamående. Halten av muskimol och ibotensyra är som högst under vår och försommar. Muskarina svampar ger ökad svettbildning, låg puls och andningssvikt.

Svampar med hallucinogena effekter kan användas som berusningsmedel på samma vis som narkotiska droger. Vanligast är olika slätskivlingar som innehåller psilocybin eller psilocin. En del hallucinogena svampar växer naturligt i Sverige, t ex röd flugsvamp och toppslätskivling. Hallucinogena svampar kan inhandlas via internet och levereras med vanlig postförsändelse. En del användare intar svampar samtidigt med andra droger, t ex cannabis, LSD eller ecstasy. Svampförgiftningar kan förorsaka akut psykos med kraftiga hallucinationer och ett utagerande beteende. Fallbeskrivningar finns med bisarra inslag.

Mag-tarmirriterande toxiner

Det finns ett stort antal mag-tarmirriterande toxiner bland svamparna som mest ger gastrointestinala symtom. Dessa är dom vanligaste svampförgiftningarna. De förekommer bl a i bolmörtskivling (Entoloma sinuatum), giftchampinjon, kastanjemusseron och giftkremla. Symtomen utgörs ff a av illamående, buksmärtor, magkramper, kräkningar och diarré.

Latenstiden från intag till symtomdebut är i allmänhet kort, 2-4 timmar (d v s betydligt kortare tid än för cytotoxinerna) och symtomen avklingar oftast inom ett dygn. Observera att en del neurotoxiner även har mag- och tarmirriterande effekt, exempelvis muskarin och muskazon.


Ett fåtal toxiner faller inte in under någon av de tre huvudgrupperna ovan. Viktigast av dessa är koprin (och koprinliknande toxiner) som kan orsaka en antabusliknande reaktion med “flush” (rodnad), svettning, takykardi och blodtrycksfall vid samtidigt intag av alkohol. Koprin finns t ex i grå bläcksvamp (Coprinus atramentarius).

Pluggskivling kan ge upphov till en allergisk reaktion efter upprepad förtäring. Intag av vissa asiatiska svampar (Ekmussling – Lentinus edodes (Shiitake)) kan ge upphov till ett migrerande erytem över bål och extremiteter 12 timmar till 5 dagar efter intag.

Bensodiazepines and similar drugs

BensodiazepineBrand nameFormula
DiazepamStesolid, Diazepam, (Valium Apozepam - unreg)Tablet, rectal solution
KlonazepamIktorivil, RivotrilTablet, injektionslösning, oral solution
LorazepamTemesta, LorazepamTablet
MidazolamDormicum, Midazolam, BuccolamInjection solution, blend
NitrazepamNitrazepam, Mogadon, ApodormTablet
FlunitrazepamFlunitrazepam, (Fluscand, Rohypnol - unreg)Tablet
OxazepamSobril, OxascandTablet
AlprazolamXanor, Xanor depot, Alprazolam, XanacTablet, Tablet extended release
ZolpidemStilnoct, Zolpidem, EdluarTablet
ZopiklonImovane, Zopiklon, Zopiclon, ZopicloneTablet
ZaleplonSonata (unreg. 2015)Tablet

Approximate equipotent doses and clearance times of different benzodiazepines

BensodiazepineEquivalent dose (mg)Terminal half-life (h)


Vid misstanke om akut svampförgiftning är det angeläget att identifiera svampen tidigt. Utan ingående kunskap om svampar krävs i allmänhet hjälp av en svampexpert för både makroskopisk och mikroskopisk identifiering. Kontaktuppgifter kan fås från Giftinformationscentralen i Stockholm eller de botaniska institutionerna vid universiteten runt om i landet.

Länk till: SvampGuiden med bilder på olika gift- och matsvampar

Anamnesen är mycket viktig i det akuta omhändertagandet, särskilt avseende svampidentifikation och uppskattning av förfluten tid mellan svampintag och symtomdebut. Anamnesen bör sträcka sig en längre tid tillbaka; latenstiden för en del cytotoxiner kan som ovan nämnts vara upp till 2-3 veckor.

Om en grupp personer ätit samma anrättning, men endast vissa blivit sjuka utesluter detta inte svampförgiftning. Exempelvis toppig giftspindling är så pass giftig att enstaka exemplar räcker för att de personer som får i sig bitar insjuknar, medan övriga förblir friska. Toxinet i toppig giftspindling är i likhet med en del andra toxiner värmestabila och tål både kokning och frysning.


Symtom vid svampförgiftning:

  • magont
  • magkramper
  • illamående
  • kräkningar
  • diarré, ofta kraftig, kan vara blodtillblandade
  • grumlat medvetande, vakenhetssänkning
  • hjärtklappning
  • stora pupiller
  • huvudvärk
  • allmän sjukdomskänsla, matthet
  • led- och muskelvärk
  • ångest, oro
  • nedstämdhet


  • Amatoxininnehållande svampar förorsakar buksmärtor, illamående, kräkningar och profus vattentunn diarré (koleraliknande) 6-12 timmar efter intag. Dessa symtom varar vanligen upp till 24 timmar. Efter 2-3 dagar uppkommer symtom på leverskada. Denna kan progrediera till fulminant leversvikt inom 3-7 dagar.
  • Latenstiden vid förgiftningar med cytotoxin är längre än för de övriga toxinerna, vanligen 8-24 timmar.
  • Symtomen kan komma smygande (efter 2 dagar upp till flera veckor) till följd av sekundär organskada med akut leversvikt eller uremi.
  • Förgiftning med stenmurkla kan förorsaka pyridoxinbrist med CNS-påverkan. Även slemhinnor, lever och njurar kan påverkas och akut hemolys kan uppstå.


  • Illamående, berusning, omtöckning, eufori, förvirring, grumlat medvetande, hallucinationer, excitation, hyperreflexi och i allvarliga fall generella kramper.
  • Ångest, oro och nedstämdhet är vanligt förekommande.
  • Symtom/tecken från muskarina effekter såsom; mios, bradykardi, hyper/hypotension, flush, svettning, bronkobstruktivitet, ökad salivation, bronkorré och i uttalade fall lungödem. Särskilt intag av vissa tråd- och trattskivlingar (släktena Inocybe och Clitocybe), t ex gifttrattskivling (= ängstrattskivling, giftig trattskivling) och pudrad trattskivling, kan ge upphov till denna kliniska bild.

Mag-tarmirriterande toxin

  • Gastrointestinala symtom, i uttalade fall ihärdiga kräkningar och diarré.
  • Symtomen är många gånger väldigt besvärande, men snabbt övergående, vanligen inom 24 timmar.
  • I allmänhet är sjukhusvård sällan indicerat om isolerat intag av mag-tarmtoxininnehållande svamp kan fastställas.
  • En del toxin, t ex det i bolmörtsskivling, är uteslutande mag-tarmirriterande, medan en del andra, t ex muskarin, är både neurotoxiskt och mag-tarmirriterande.
  • Det är viktigt att ha i minnet att gastrointestinala symtom efter svampförtäring inte alltid är uttryck för en akut svampförgiftning. Svampar angrips lätt av bakterier och parasiter och kan precis som andra livsmedel orsaka matförgiftning. Många människor insjuknar varje år efter förtäring av gammal eller felaktigt behandlad matsvamp.


  • Svettning
  • Flush
  • Blodtrycksfall


  • Identifiering av svampen (tillkalla expert)
  • Alla allmänpåverkade patienter bör behandlas på sjukhus
  • Ta Hb, LPK, CRP, trombocyter, PK/INR, kreatinin, leverstatus och urinsticka. Vid behov sätt dropp, t ex Ringer-acetat.
  • Adekvat vätsketillförsel, sätt minst en PVK och ge riklig rehydrering (2-3 liter Ringer-Acetat) med sikte på god diures.
  • Noggrann monitorering av vätskebalans, elektrolytstatus, njurfunktion och leverstatus. Korrigera elektrolytrubbningar.
  • Ventrikelsköljning kan ev. utföras vid tidigt omhändertagande (inom 6-8 timmar efter svampintag, helst inom en timme). Bör inte utföras vid ihållande kräkningar.
  • Medicinskt kol (Carbomix) p.o., 50 g x 4 (10-25 g till barn) kan ges upp till 2-3 dygn efter förtäring av giftig svamp. Kol ges i upprepade doser under ett dygn.
  • Silibinin (Legalon Sil, licenspreparat från Madaus/Schering-Plough), ges vid förgiftning med vit flugsvamp, lömsk flugsvamp och gifthätting. Dosering: 20 mg/kg/dygn i 2 dygn uppdelat på 4 doser (5 mg silibinin/kg per infusion). Infusionen ges under 2 timmar med 4 timmars mellanrum. Silibinin är ett extrakt från växten Carduus marianus, Mariatistel, Mjölktistel eller St. Marys tistel (Eng: Milk thistle).
  • Bensylpenicillin (bensylpenicillin) i hög dos (5 g x 4) i 3 dygn vid förgiftning med vit flugsvamp, lömsk flugsvamp och gifthätting) om inte silibinin finns tillgängligt
  • Acetylcystein (Acetylcystein) i.v. vid förgiftning med lömsk flugsvamp. Inhalationsvätska acetylcystein 200 mg/ml ges långsamt intravenöst under 1 timme 150 mg/kg i 200 ml glukosinfusionsvätska 50 mg/ml. Därefter 50 mg/kg under 4 timmar och därefter 100 mg/kg under de följande 16 timmarna (uppblandad i likadan glukoslösning som ovan). Totalt ges alltså 300 mg/kg under 20 timmar. Det finns visst vetenskapligt stöd för att acetylcystein skall ges i minst 48 timmar vid förgiftning med amatoxin.
  • Antiemetika ges vid illamående, t ex Zofran (ondansetron) 4 mg x 1 eller Kytril (granisetron) 1 mg x 1
  • Bensodiazepiner vid oro eller kramper (inj. Stesolid (diazepam) 5-10 mg i.v. vb)
  • Atropin (atropin), 1-2 mg i.v. vid kolinerga symtom. Observera att vanliga doser om 0,5-1 mg oftast är otillräckligt. Ibland behövs mer än 1-2 mg, symtomatologin styr. Undvik atropin vid förgiftning med isoxazolderivat.
  • Acidoskorrektion, buffra med natriumbikarbonat
  • Vid hemolys alkalinisering av urinen med natriumbikarbonat
  • Pyridoxinhydroklorid (Pyridoxin) vid intag av stenmurkla. Dosering: 1,5-2 g per dygn (25 mg/kg) i.v. som engångsdos eller två-dosförfarande beroende på symtom
  • Hemoperfusion (hemodialys med kolfilter), alternativt forcerad diures kan övervägas i tidigt skede (inom 36 h) vid förgiftning med toppig giftspindling.
  • Behandling av njursvikt.
  • Behandling av leversvikt, Fytomenadion (Konakion) 10 mg x 2 i.v. Överväg MARS-behandling vid akut leversvikt. Överväg levertransplantation i allvarliga fall av leversvikt.
SubstanceBrand NameMechanism of ActionSort of InhibitionHalf timeDiscontinuation time before planned operation
Abciximab ReoproGPIIb/IIIa Irreversible30 min 48 hours
Salicylic AcidTrombylCOX-1 Irreversible30 min 3 days
low dose (75-350 mg) as primary prophylaxis
(ASA in high dose - see table below)
30 min 3 days
as a secondary prophylaxisPatients with high thrombotic risk using ASA secondary prophylactically may continue with ASA, alternatively, abstain from ASA on the day of operation, after individual assessment.
Argatroban NovastanThrombinReversible1 hour2 2–4 hours
Bivalirudin Bivalirudin ThrombinReversible30 min4 hours
Cilostazol Cilostazol, PletalPDE3 Reversible10,5 hours5 days
Dabigatran PradaxaThrombin Reversible 12–17 hours24 hours3
Dipyridamol Dipyridamol, AsasantinAdenosineReversible10–12 hoursDiscontinuation not needed
Eptifibatid IntegrilinGPIIb/IIIa Reversible2,5 hours8 hours
Fondaparinux ArixtraFactor Xa Reversible17–21 hours36 hours
Heparin Heparin Factor IIa, IXa, Xa Reversible1–2 hours4 hours4
Iloprost Ilomedin, VentavisProstacycline analogue Reversible30 minuter 2 hours
Clopidogrel PlavixADP-receptor (P2Y12) Irreversible6–8 hours 5 days
Prasugrel EfientADP-receptor (P2Y12) Irreversible7 hours(2–15) 5 days
Rivaroxaban XareltoFactor Xa Reversible7–11 hours24 hours
Tirofiban AggrastatGPIIb/IIIa Reversible1,5 hours8 hours
Warfarin WaranProthrombine, Factor VII, IX, XReversibleR-warfarin 37–89 hours
S-warfarin 21–43 hours
3 days5
Low molecular weight heparin (therapy doses, subcutaneous), high intensity treatment
Dalteparine (>5000 E) FragminFactor IIa, Xa Reversible3–4 hours6 24 hours
Enoxaparine (>40 mg) KlexaneFactor Xa Reversible4 hours6(repeated dose, 7 hours) 24 hours
Tinzaparine (>4500 E) InohepFactor Xa Reversible3–4 hours624 hours
Low molecular weight heparin (therapy doses, subcutaneous), low intensity treatment
Dalteparine (≤5000 E) FragminFactor IIa, Xa Reversible3–4 hours6 10 hours
Enoxaparine (≤40 mg) KlexaneFactor Xa Reversible4 hours6 (repeated dose, 7 hours)10 hours
Tinzaparine (≤4500 E) InohepFactor Xa Reversible 3–4 hours6 10 hours
1 Patients with high thrombotic risk who use ASA secondary prophylactically may continue with ASA, alternatively, abstain from ASA on the day of operation, after individual assessment.
2 The efficacy of liver disease is greatly prolonged.
3The variation is large between different subpopulations
4Applies to the condition that the aPTT is normalized after the specified release time.
5Applies to therapeutic INR 2-3 and target INR prior to surgery <1.4.
6The task relates to anti-Xa activity.

Ventrikelsköljning och administrering av medicinskt kol är de viktigaste initiala åtgärderna vid svampförgiftning, men måste ges kort tid efter svampintag för god effekt (var god se ovan för detaljer). Kol är atoxiskt och ofarligt att dricka för den som inte är medvetandesänkt.

Aktiva antidoter finns mot förgiftning med vit flugsvamp, lömsk flugsvamp, gifthätting, stenmurkla och muskarinhaltiga svampar (se tabell 2 ovan).

Silibinin (Legalon Sil) anses förhindra toxinupptag i levercellerna och minskar risken för leverskada. Möjligen ökar även nivåerna av glutation i levern. Acetylcystein bör ges vid leverskada efter förgiftning med amatoxininnehållande svampar. Biverkningar utgörs ff a av värmekänsla och flush. Även bensylpenicillin reducerar risken för leverskada och bör ges om silibinin inte finns tillgängligt vid förgiftningar med vit flugsvamp, lömsk flugsvamp eller gifthätting Observera att bensylpenicillin i högdos kan ge upphov till generella kramper. Ett alternativ till bensylpenicillin är cefuroxim (Zinacef). Behandlingen i övrigt är i huvudsak symtomatisk.

Vid förgiftning med neurotoxiska svampar (t ex psilocybesarter) bör patienten vårdas i ett lugnt och stilla rum. Förvirring och andra psykiska symtom behandlas symtomatiskt med sedativa och neuroleptika, t ex olanzapin eller droperidol.

Njurskador efter svampförgiftning leder inte sällan till manifest njursvikt med uremi som behandlas med dialys eller njurtransplantation. Akut leverskada kan leda till fulminant leversvikt med dålig prognos 3-7 dagar efter intag av giftsvamp. Fulminant levercellskada efter svampförgiftning har varit fall för akut levertransplantation. Akut leversvikt efter svampförgiftning behandlas på sedvanligt sätt men observera möjligheten av antidotbehandling. Behandling med dialys och kolfilter i ett MARS system kan prövas. Patienter med njur- eller leverskador efter svampförgiftning bör behandlas på en intensivvårdsavdelning.

Dödsfall till följd av svampförgiftning är mycket sällsynt, men förekommer även bland små barn, oftast sekundärt till akut leversvikt.

Uppföljning efter allvarlig svampförgiftning bör planeras med kontroll av leverfunktion och njurfunktion.


  • Toxisk effekt av förtärd svamp T62.0


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Venomenous fish and fish poisoning

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21


Ett stort antal fiskar, blötdjur, anemoner och andra marina organismer kan orsaka en toxisk reaktion vid kontakt med människor. Av havets cirka 27 000 kända arter bedöms omkring 1 700 som mer eller mindre giftiga. Det är fler än alla kända giftiga ryggradsdjur tillsammans. Förgiftning av marina arter kan uppträda efter förtäring av giftig fisk men kan även inträda efter sting eller beröring, vanligen genom gifttaggar. De vanligaste förgiftningarna efter förtäring av fisk är scombroidförgiftning, ciguateraförgiftning och fuguförgiftning (blåsfisk), varav fuguförgiftning är den allvarligaste med flera inträffade dödsfall.

Det blir allt vanligare att svenskar dyker eller badar i tropiska vatten och exponeras för olika giftiga marina arter. Förtäring av giftiga exotiska fiskar har blivit vanligare i Europa genom import. Flera fall av ciguateraförgiftning har inträffat i Tyskland under senare år.

För information om andra giftiga havslevande djur och alger, var god se behandlingsöversikt:
Maneter, alger och giftiga havslevande djur

FJÄRSING (Trachinus draco)

Fjärsing (”Taggig drake”, eng. Greater weever) är en ätlig fisk som förekommer längs med den svenska västkusten ända ner till Öresund, vanligast är den i Bohuslän.


Fjärsingen är långsmal, ser hoptryckt ut och blir vanligen några decimeter lång. Den är tecknad i skimrande grönt, gult och svart på en gulgrön botten, munnen är uppåtriktad, fjärsingen ser lite trulig ut.

På ryggen och gälfenorna har fjärsingen gifttaggar. Den kan injicera ett gift vid sting, främst från ryggfenorna. Fisken har två ryggfenor och det är den främre som är giftig. Toxinet är både hemorragiskt, neurotoxiskt och nekrotiserande. Fjärsingen attackerar inte, till skillnad från t ex Drakfiskar, utan sticker endast i självförsvar.
Extern länk till bild på fjärsing från Havs och Vattenmyndighetens webbplats

Risk för sting

Fjärsingen kommer in mot kusten fram på våren och finns invid stränderna under sommaren, då flest sting inträffar. Fjärsingen ligger gömd i sanden på botten där den ligger och väntar på byten. Den har då bara ögonen och munnen synliga.

  • Det vanligaste är att sting uppkommer i samband med att fiskare rensar sina garn efter fångst av fjärsing och råkar komma mot gifttaggarna med fingrarna.
  • Det är riskabelt att kroka av en fjärsing från en fiskekrok då man lätt kan bli stungen. Observera att även gälfenorna har gifttaggar, inte bara ryggfenorna!
  • Sting i foten kan inträffa om man råkar trampa på en fjärsing.

Fjärsingens gift är aktivt även när fisken är död efter fångst. Ett sting av fjärsing leder till en kraftig inflammation med smärta, svullnad och domningar. Fjärsingen är trots sitt gift en fin matfisk (smakar i stil med sjötunga) som går att inhandla i fiskhandeln.

Mindre fjärsing (Echiichtys vipera)

Längs med Danmarks västkust i Atlanten finns en variant av fjärsing kallad liten fjärsing eller mindre fjärsing. Denna fisk finns även i Engelska kanalen, Ostatlanten, längs Frankrikes västkust, i Svarta havet och Medelhavet.

Liten fjärsing anses vara Europas farligaste fisk. Fisken är cirka 15 cm lång och sandfärgad. Ryggfenan med gifttaggarna är helt svart. Taggarna är så pass vassa att de kan gå igenom en våtdräkt eller en “flip-flop”-sandal. Den lilla fjärsingens toxin innehåller mer serotonin än sin större släktings, vilket anses förklara varför smärtan blir mer uttalad vid sting av denna fisk.
Extern länk till foto på liten fjärsing


Vanliga symtom vid sting av fjärsing är:

  • intensiv smärta
  • svullnad
  • domningar
  • känselbortfall
  • missfärgning av huden

Även generella symtom kan tillstöta, såsom:

  • illamående
  • allmänt obehag
  • huvudvärk
  • yrsel
  • frossa
  • svettningar
  • dåsighet
  • generella kramper (i sällsynta fall)

Stinget är normalt inte livshotande, men en bakteriell infektion kan tillkomma lokalt i afficierad hud och komplicera förloppet.

Känselbortfall efter sting av fjärsing är vanligen övergående, men kan bli långdraget och bestående i sällsynta fall. Svullnaden kan kvarstå under lång tid, oftast upp till en månad, i enstaka fall ända upp till ett år! Toxinet finns dock inte kvar mer än i högst 48 timmar.


  • Angripen kroppsdel bör omedelbart efter stinget sänkas ner i hett vatten (minst 40 grader). Då inaktiveras toxinet (proteinet denatureras) och man uppnår omedelbar och effektiv smärtlindring. Vattnet bör hålla en temperatur runt 45 grader och det är förstås viktigt att man inte skållar sig. Angripen kroppsdel bör hållas i det varma vattnet tills varaktig smärtlindring har uppnåtts. Uppvärmningen bör pågå i minst 30 minuter, men ända upp till en och en halv timma kan behövas. Man får fylla på med nytt hett vatten under behandlingen och helst mäta temperaturen med en vattentermometer.
  • Rester av en eventuell gifttagg som kan finnas kvar i såret bör avlägsnas. Om man måste bör detta göras kirurgiskt. Svårfunnen gifttagg kan ibland hittas med hjälp av ultraljudsundersökning!
  • Angripen kroppsdel ska i övrigt lämnas i fred och såret hållas rent.
  • Antibiotika ges enbart om sekundär infektion tillstöter vilket inte är ovanligt.

I händelse av följande bör sjukvård uppsökas:

  • Om generella symtom tillstöter.
  • Vid besvärlig långvarig smärta.
  • Om kirurgiskt avlägsnande av en gifttagg krävs. Ultraljud!


STENFISK (Synanceia verrucosa)

Stenfisk är en mycket giftig fisk med utbredning i de tropiska delarna av Indiska oceanen och Stilla havet. Stenfisken blir 30-60 cm lång och är en stormunnad kindpansrad rovfisk som lever av att blixtsnabbt attackera och äta småfisk. Stenfisken skadar människor genom sting av gifttaggar.

Stenfisken tillhör släktet skorpionfiskar (scorpenidae) och är sannolikt den giftigaste av alla fiskar. Flera dödsfall finns beskrivna, några redan inom en timma efter stinget. Flera olika underarter av synanceia finns, förutom Synanceia verrucosa också till exempel Synanceia erosa och Synanceia trachynis i olika storlekar.


Stenfisken är en synnerligen ful fisk med välutvecklat kamouflage. Det gör den ytterst svår att upptäcka i havet även om man tittar just där fisken ligger. Fisken ligger ofta gömd i sanden med endast mun och ögon synliga. Den vårtliknande täckningen gör den helt lik omgivande stenar och alger på botten. Stenfisken har 13 gifttaggar på ryggfenorna som den omedelbart reser om man närmar sig fisken, vidrör den eller råkar trampa på den. Giftet är mycket komplext och innehåller neurotoxiner och myotoxiner såväl som proteiner som förorsakar en kraftig antigenreaktion. Antiserum mot stenfiskgift finns tillgängligt för systemisk behandling vid allmänsymtom efter sting.
Extern länk till en bild på en Stenfisk


Toxinet från stenfisken är mycket giftigt och ett sting ger upphov till omedelbara mycket svåra smärtor.

Vanliga symtom är:

  • intensiv smärta
  • svullnad
  • domningar
  • känselbortfall
  • missfärgning av huden

Även generella symtom kan tillstöta, såsom:

  • illamående
  • allmänt obehag
  • huvudvärk
  • yrsel
  • frossa
  • svettningar
  • blodtrycksfall och kramper (i sällsynta fall)
  • cirkulations- och andningspåverkan, i uttalade fall

Toxinet kan vara dödligt med ett allvarligt insjuknande inom ett fåtal minuter. Dödsfall har inträffat inom en timma efter stinget.


  • Angripen kroppsdel bör omedelbart sänkas ner i hett vatten vid sting. Då inaktiveras toxinet (proteinet denatureras). Vattnet bör hålla en temperatur runt 45 grader. Angripen kroppsdel bör hållas i det varma vattnet i 30-90 minuter, tills varaktig smärtlindring uppnås.
  • Immunglobulin mot tetanus, 250 IE i.m. om tetanusskydd saknas, annars tetanusvaccin s.c. (rekommenderas, men med tveksamt vetenskapligt underlag, stelkrampsfall finns dock beskrivet).
  • Vid uttalade allmänsymtom eller chock ges behandling med specifikt immunserum mot stenfiskgift.


DRAKFISK (Pterois volitans)

Drakfisk är en vacker zebraliknande fisk som lever bland koraller i Indiska oceanen och västra delarna av Stilla havet. Drakfisken kan ge upphov till förgiftning genom sting. Den förekommer också längs med USA:s östkust. I Sverige förekommer drakfisken enbart som akvariefisk.

Drakfisken tillhör släktet drakhuvudfiskar, en undergrupp till skorpionfiskarna – Scorpenidae.


Fisken blir upp till 38 cm och kan väga upp till ett kilogram, men är vanligen något mindre. Drakfisken är en vacker fisk, tvärrandig i brunt och vitt, och kallas även för lejonfisk.

Drakfisken jagar fisk och kräftdjur på natten och ligger och gömmer sig bland koraller på dagen. Den har stora bröstfenor, bukfenor och en ryggfena som den rör sakta likt vackra slöjor.

Drakfiskar har ett toxin som utsöndras från de tre första ryggfenorna. Toxinet är i första hand neurotoxiskt. Både lokalsymtom och generella symtom kan utvecklas. Toxinet innehåller inflammatoriska substanser som prostaglandiner och tromboxan B2.

Drakfisken kan attackera och sticka angriparen aktivt med sina ryggfenor. Sting är vanligast på nedre extremiteten. Skador i Sverige rapporteras i första hand från personer som arbetar med akvariefiskar.
Extern länk till bild på drakfisk, Wikipedia


Giftkörtlarna på drakfisken är mindre än på stenfisken. Toxinet är mycket giftigt och ett sting ger upphov till omedelbar svår smärta.

Vanliga symtom, utöver smärtan, är:

  • svullnad
  • domningar
  • känselbortfall
  • missfärgning av huden

Även generella symtom kan tillstöta, såsom:

  • illamående, kräkningar
  • allmänt obehag
  • huvudvärk
  • yrsel
  • frossa
  • svettningar
  • dåsighet
  • cirkulations- och andningspåverkan (i sällsynta fall)

Dödsfall är mycket ovanligt, men förekommer. Toxinet är aktivt även efter att fisken är död, och tål frysning. Sekundärinfektioner är vanliga efter sting.


Angripen kroppsdel bör omedelbart sänkas ner i hett vatten. Då inaktiveras toxinet (proteinet denatureras). Vattnet bör hålla en temperatur av minst 40 grader, helst mellan 45 och 50 grader. Man bör hålla angripen kroppsdel i det varma vattnet i 30-90 minuter, tills varaktig smärtlindring uppnås. Sök efter gifttaggar med ultraljud och avlägsna eventuella rester kirurgiskt.

PRICKIG KOFFERTFISK (Lactophrys bicaudalis)

Den prickiga koffertfisken (eng: Trunk fish) är en korallfisk som utsöndrar ett ciguateratoxin vid beröring från körtlar på ryggen. Toxinet är endast farligt vid förtäring av fisken, så det finns ingen omedelbar fara för dykare vid beröring. Dock kan hajar dö som ett resultat av att de äter en koffertfisk. Även muränor liksom många andra korallfiskar kan vara rikliga på cigueteragift vid förtäring.


Konsumtion av fisk av arten scombroidae och scomberesocidae kan ge upphov till ett förgiftningssyndrom kallat scombrotoxism eller scombroidförgiftning. Vanligen uppkommer syndromet efter förtäring av olika arter av tonfisk eller makrill, t ex Skipjack Tuna eller Bonito. Dessa fiskar konsumeras vanligen i sallader, bl a i medelhavsområdet.

Scombrotoxism uppkommer efter att man ätit fisk kontaminerad med bakterier som frisätter rikliga mängder histidin. Bakterierna är av arten E. Coli, Proteus, Klebsiella eller Aerobacter. I dessa bakterier produceras histamin och histaminliknande ämnen (histidin) av enzymet histidindekarboxylas.

Scombrotoxism är inte någon allergisk reaktion, men symtomatologin är likartad.


Symtom uppträder vanligen inom en timma efter konsumtion. Symtomatologin är relaterad till histaminfrisättning och utgörs av:

  • svettning
  • illamående
  • kräkningar
  • diarré
  • huvudvärk
  • hjärtklappning
  • flush (rodnad)
  • urtikaria
  • yrsel
  • svullnad i ansiktet med svullna läppar och svullen tunga (i sällsynta fall)

Andningsproblem kan uppstå med bronkobstruktivitet och blodtrycksfall. Symtomen är vanligen kortvariga och övergående inom 8-10 timmar.


  • Behandling med antihistaminer som blockerar H1– och H2-receptorer rekommenderas, t ex cimetidin (Tagamet) 400 mg x 2.
  • Kortison är inte indicerat utan kan tvärtom förlänga förloppet.
  • Allvarliga förlopp måste behandlas med intravenös vätska, antihistaminer och adrenalin.



Förgiftning kan uppstå efter konsumtion av fiskar som hör till släktet ciguatera. Dessa fiskar finns främst i Västindien och i Karibiska havet. Hit räknas napoleonfisk, papegojfisk, barracuda, tropisk havsaborre, röd snapper, amberjack, kingfish och andra exotiska fiskar som lever runt korallrev. Ciguateraförgiftning är vanligt i och runt Dominikanska republiken. Papegojfisk kan även innehålla tetrodotoxin som är betydligt värre.

Ciguateragift kommer från toxinbildande alger som finns i korallrev och som passerat uppåt i näringskedjan. Fisken luktar och smakar normalt. Koncentrationen av toxin är högst i lever och inälvor i fisken.


Vanliga symtom är:

  • illamående
  • kräkningar
  • diarré
  • allmän sjukdomskänsla, trötthet och sömnighet
  • myalgi, nackont
  • frossa och svettningar
  • neurologiska bortfallssymtom (polyneuropati), parestesier, domningar och känselbortfall i extremiteterna, främst de nedre men även kranialnervspåverkan kan förekomma
  • smärta, värk och muskelsvaghet
  • metallsmak i munnen
  • smärta vid beröring av kyla, allodyni
  • blodtrycksfall, bradykardi
  • koma i uttalade fall

Gastrointestinala symtom varar i 1-2 dagar, övriga symtom varar upp till en vecka. Neurologiska bortfallssymtom kan bli långdragna och i enstaka fall bestående. Man talar om kronisk ciguateraförgiftning. Detta tillstånd kan ge allodyni och ett kroniskt smärttillstånd. Utredning med klinisk neurofysiologi kan påvisa nedsatt nervledningsförmåga i affekterad extremitet.

Diagnosen ställs genom anamnes och klinisk bild. Analys av ciguateragift på människa är under utveckling men är ännu inte någon etablerad metod. Fiskrester kan dock analyseras och bekräfta förekomsten av ciguateragift, Detta bör göras om flera personer blivit förgiftade och hälsovårdsmyndigheten bör kopplas in.


I huvudsak symtomatisk med vila och vid behov intravenös vätska. Mannitol givet intravenöst (1 g/kg) har i flera fallbeskrivningar visats ge god effekt mot neurologiska och muskulära symtom om behandlingen ges inom 48 timmar efter insjuknandet. Det vetenskapliga underlaget för mannitolbehandling är dock svagt och behandlingen har ifrågasatts. Annan specifik behandling saknas. Antihistaminer kan hjälpa liksom vanliga analgetika typ paracetamol (Alvedon) mot värk.


I Japan och en del andra asiatiska länder konsumeras blåsfisk, Fugu som rätt anredd anses vara en delikatess. Några olika arter av blåsfisk är Takifugu rubripes, Lagocephalus och Sphoeroides. Blåsfisken lever i Stilla havet, Röda havet och Indiska oceanen. Fisken finns främst kring Japan, Kina, Filippinerna och Taiwan men finns även i Västindien och Mexico. Blåsfisken kallas även knotig tetraodontitfisk eftersom den är knotig och har fyra kraftiga tänder. Förgiftning inträder efter förtäring.

Länk till bild på Fugu

Fisken har ett potent gift, tetrodotoxin, som kan ge upphov till mycket allvarlig neuromuskulär förgiftning, även dödsfall. Tetrodotoxin är ett neurotoxin som kan orsaka förlamningar. Toxinet binder till natriumkanaler i perifera nervceller och blockerar neurotransmissionen. Tio milligram anses vara en dödlig dos. Det passerar inte blodhjärnbarrriären utan ger huvudsakligen upphov till perifer förlamning, inklusive andningsförlamning. Tetrodotoxin finns även i andra marina arter som den blåringade bläckfisken, papegojfisk och vissa grodarter (pilgiftsgrodor). Toxinet finns anrikat i fiskens inälvor, främst i levern men även i tarmarna, gonaderna (ovarierna) och i skinnet. Blåsfiskens taggar är inte giftiga men toxinet finns i hela fisken.

Från 1974 till 1983 rapporterades 646 fall av Fuguförgiftning i Japan med 179 dödsfall. Vid allvarlig förgiftning har mortaliteten uppskattats till nära 50 % i paralytiska förlamningar med andningsförlamning. Den förgiftade patienten kan utveckla total förlamning men ändå vara vaken och medveten nära inpå döden. Döden inträder vanligen inom 4-6 timmar efter förtäring, med ett intervall från 20 minuter till 8 timmar. Patienterna dör genom andningsförlamning och asfyxi. Vid behandling med artificiell ventilation har mortaliteten sänkts till runt 5 %. Någon antidot finns inte. Giftet bildas sannolikt av olika bakterier som fisken äter, t ex Vibrio alginolyticus.


Vanliga symtom vid Fuguförgiftning är:

  • bedövningskänsla kring munnen och läpparna
  • tilltagande känselbortfall i ansiktet, armar och ben
  • känsla av domningar och frånvarokänsla (”lightheadness”)
  • huvudvärk
  • magsmärta
  • illamående
  • diarré
  • tilltagande neuromuskulär paralys
  • hypoventilation
  • hypoxi
  • hyperkapné
  • kramper
  • mental avtrubbning
  • hjärtarytmier
  • kardiovaskulär kollaps


Specifik antidot saknas. Behandlingen är huvudsakligen symtomatisk med inriktning på artificiell ventilation och följer generella intensivvårdsprinciper. Eftersom neuromuskulär paralys är vanligt är det viktigt att understödja andningen och insätta mekanisk ventilation och respiratorbehandling så snabbt som möjligt. Behandling med intravenös vätska och hjärtstärkande (inotropa) läkemedel följer gängse intensivvårdsprinciper.


Denna vackra fisk har givit upphov till ett antal farliga förgiftningar genom sting med svansfenan, oftast av alltför närgångna dykare. Stingrockan är en broskfisk och en sötvattenfisk som förekommer i Sydamerikas floder. Skador uppkommer oftast när man råkar trampa på en rocka, den angriper vanligen inte människor. Ett sting kan ge upphov till smärta, svullnad, ömhet och inte sällan sekundära infektioner. Muskelkramper och generella symtom kan uppträda. Stinget är vanligtvis inte livshotande om inte vitala organ skadats. En del av fenan kan finnas kvar i såret och bör avlägsnas kirurgiskt. Behandling kan prövas med hett vatten (45 grader i 30 min) som vid andra marina sting av affekterad kroppsdel.


  • Fiskförgiftning orsakad av ciguatera T61.0
  • Fiskförgiftning orsakad av scombroid T61.1
  • Toxisk effekt av kontakt med fisk T63.5


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Jellyfish and algiers

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Ett stort antal fiskar, blötdjur, anemoner och andra marina organismer kan utlösa en toxisk reaktion vid närkontakt med människa, vanligen genom sting. Av havets cirka 27 300 kända arter bedöms omkring 1 700 som mer eller mindre giftiga. Det är fler än alla kända giftiga ryggradsdjur tillsammans. Cirka 9000 olika marina arter är nässeldjur s k Cnidaria, benämnt från grekiskans ”stinga”. Till gruppen cnidaria hör maneter, koralldjur och hydror. Alla nässeldjur är en typ av rovdjur som lever på att tillfångata och äta byten.

Man beräknar att minst 80 000 människor varje år drabbas av olika åkommor orsakade av giftiga havsdjur. Flertalet av dessa utgörs av hudirritation efter kontakt med nässelceller (nematocyster) då ett inflammatoriskt toxin frisatts från nässeldjur.

Detta PM beskriver de vanligaste giftiga organismerna, undantaget fiskar, som finns i svenska vatten och några av dem vi kan komma i kontakt med på exotiska breddgrader. Det blir allt vanligare att svenskar dyker eller badar i tropiska vatten och exponeras för olika giftiga marina arter. I medelhavet finns ett stort antal maneter som ökat dramatiskt i antal under senare år.

För mer information om giftiga fiskar, se även:

Visa översikt: Fjärsingstick och andra giftiga fiskar

Nässeldjur delas in i fyra klasser: anthozoer (Anthozoa), maneter (Scyphozoa), kubmaneter (Cubozoa) och hydrozoer (Hydrozoa).

  • Anthozoa: koralldjur som saknar medusaform. Solitära eller kolonibildande polyper.
  • Scyphozoa: maneter, polyper i medusaform, ringmaneter, lungmaneter och skivmaneter.
  • Cubozoa: kubmaneter med flera olika underarter.
  • Hydrozoa: en artrik och mycket varierad undergrupp av nässeldjur. Kolonibildande, t ex Portugisisk örlogsman.

MANETER (Scyphozoa)

Maneter är frisimmande medusor, klock- eller tallriksformade med en krans av tentakler under sig. Munnens kanter på undersidan är förlängda till muntentakler eller armar som hänger (trålar) under djuret. Ett litet antal olika maneter förekommer naturligt i svenska havsvatten. Öronmanet, röd brännmanet och blå brännmanet förekommer längs västkusten, i Kattegatt och Skagerack. Även kompassmanet och lungmanet kan ses här. Av dessa förekommer endast öronmaneten i Östersjön.

I våra farvatten är det främst röd brännmanet som ger upphov till skador på människor, men även blå brännmanet och kompassmanet har nässelceller som kan ge upphov till hudirritation. De i Sverige förekommande maneterna förorsakar mest bara lokalsymptom i form av en brännskadeliknande hudirritation. I tropiska länder finns betydligt mer giftiga maneter som kan orsaka generella symptom förutom uttalade lokalsymptom.


Maneter är en typ av ryggradslösa, mjuka nässeldjur som i huvudsak består av bundet vatten med ett geléliknande skal. Överdelen av manetens kropp utgör klockan och under klockan sitter flera munarmar och tentakler. Från klockan hänger och pendlar ett stort antal bränntrådar.

Maneter simmar fram genom rytmiska sammandragningar av klockan, vilket orsakar en propulsiv jetstråle, men i huvudsak följer maneterna passivt vattenströmmarna. De långa tentaklerna trålar efter kroppen och har till uppgift att fånga byten som fångas in, bränns, sönderdelas och digereras till föda.

Maneterna förekommer framför allt under sommaren och hösten i svenska havsvatten. Maneter lever i två faser, först som polyper fastvuxna till botten och härefter som fritt simmande medusor. Den fritt simmande fasen inleds under våren när maneten knoppas av från sin polypösa fas, härefter lever maneten i medusaform i cirka ett år.

Röd brännmanet kallas på engelska för “Lejonmansmanet” – Lion’s mane jellyfish, vilket talande beskriver utseendet. Den största röda brännmaneten som hittats hade en diameter på 2,3 meter och 36,5 meter långa trådar. Väldigt stora röda brännmaneter förekommer mest ute i öppet hav på Atlanten, invid kusten blir de sällan mer än 50 cm i diameter. Normal storlek är cirka 20-30 cm i diameter. Röd brännmanet trivs i kallt vatten. Om vattentemperaturen stiger för mycket (över 20 grader) drar sig maneten ner på djupare och kallare vatten.


Det finns runt 200 olika typer av maneter (Scyphozoa), varav runt 14 arter i Sverige. Dessa indelas i fyra huvudgrupper:

Röd brännmanet Cyanea (Cyanea capillata) och blå brännmanet (Cyanea lamarckii)

Öronmanet Aurelia (Aurelia aurita)

Kompassmanet Chrysaora (Chrysaora hysoscella)

Lungmanet Rhizostoma (Rhizostoma octopus)

Bland de giftigaste arterna runt om i världen finns Portugisisk örlogsman (Blåsmanet, Physalia physalis, eng. “Man-of-War“), Kubmanet (Chironex fleckeri) och Irukandjimanet (Carukia barnesi). Dessa maneter orsakar varje år massvis av svåra sting (“stingers”) med allvarliga förgiftningstillbud, till och med dödsfall. Se ytterligare information om respektive manet nedan.

Portugisisk örlogsman (Blåsmanet, klass: Hydrozoa)

Den portugisiska örlogsmannen (Physalia physalis) har stor spridning i tropiska och varmtempererade hav, vanligast är den utanför Floridas kust och sydost i den mexikanska golfen. Blåsmaneten är egentligen inte en äkta manet, scyphozoa utan manetliknande kolonial organism (kolonibildande nässeldjur) och kategoriseras som hydrozoa. Den finns också längs Afrikas kuster och en närbesläktad art förekommer i Australien (Physalia utriculus). Blåsmaneten består av ett kluster av olika organismer som lever i symbios. Överdelen är geléliknande och gasfylld, innehållande bl a koldioxid och kvävgas. Överdelen fungerar som ett segel som ligger över vattenytan och driver blåsmaneten framåt.

Den portugisiska örlogsmannen är sannolikt den manet som orsakar flest allvarliga sting av alla arter, även dödsfall har förekommit. Direkt kontakt med trådarna ger svår smärta, svår feber och kraftig inflammation i huden. Maneten blir cirka 30 cm i diameter och flyter omkring uppe på ytan med meterlånga tjocka tentakler trålande långt under ytan, klockan ligger delvis över vattenytan.

Följ länken för en bild på en portugisisk örlogsman:

Kubmanet (klass: Cubozoa)

Den australiska kubmaneten, s k ”Box Jellyfish” (Chironex fleckeri), är en mycket farlig manet. Kubmaneten har en transparent blåskimrande kubformad klocka. Man beräknar att den har orsakat ett sextiotal dödsfall, framför allt längs med Australiens norra och västra kust. Det finns ca 40 kända underarter, många är betydligt mindre än den stora kubmaneten. Maneten kan väga upp till 2 kg, klockan kan vara stor som en salladsskål och tentaklerna blir upp till 2 m långa. Den kubiska klockan har fyra långa tentakler rikligt täckt med farliga nässelceller.

Kubmaneten förflyttar sig relativt fort och tentaklerna trålar i vattnet. Varje tentakel innehåller flera miljoner nässelkapslar (nematocyster) som kan orsaka allvarliga brännskador och mycket svår smärta vid kontakt. Sammanlagt beräknas den ha inte mindre än 5 miljarder nematocyster.

Irukandjimanet (klass: Cubozoa)

Irukandjimaneten (Carukia barnesi) är en farlig liten ”stinger” som är betydligt mindre än kubmaneten med en klocka stor som en vanlig armbandsurtavla (ca 2 cm i diameter). Den förekommer mest i Australien, särskilt i norra Queensland. Irukandjimaneten håller vanligtvis till på djupare vatten, men kan komma in mot stränderna efter stormar. Maneten kommer gärna i stim eller flockar.

Kontakt med Irukandjimaneten kan ge mer generella symptom med illamående, allmänpåverkan och omtöckning. Toxinet frisätter katekolaminer varför puls och blodtryck stegras markant, även hjärtarytmier förekommer. Symptomen kan debutera 30 minuter efter kontakt med en intensiv smärta som stegras långsamt. Smärtan blir gradvis värre och värre och angripen kroppsdel svullnar påtagligt.

I norra medelhavet längs med Spaniens, Frankrikes och Italiens kuster finns ett stort antal maneter som kan ge upphov till olika grader av brännskada. Här följer en kort beskrivning av några av dem.

  • Lysmanet (Pelagia noctiluca) Lysmaneter (Spanska: ”Clavel de mar” – Havsnejlika) är rosa eller blåskimrande (violetta) och transparanta med multipla mörkare prickar i klockan och tentaklerna. Klockan är halvsfärisk med en diameter på 5-10 cm. Den har 4 större centrala munarmar och 16 perifera tentakler. De mörkröda tentaklerna liknar bläckfiskarmar och är rikligt täckta av nässelceller. Klockan har illuminerande celler som ger ett fascinerande ljussken i vattnet nattetid eller vid kontakt. Lysmaneter ger en relativt kraftig brännskada vid kontakt med hud.

  • Medelhavsmanet (Cotylorhiza tuberculata) Medelhavsmaneter kallas vanligen för ”stekta ägg” för att de helt enkelt liknar stekta ägg (Sp: ”Aguacuajada” eller ”Huevo frito”). Medelhavsmaneter är gula med en platt kompakt klocka med en central halvsfärisk rund gul upphöjning med en diameter på 20-35 cm. Under klockan finns 8 inverterade munarmar som ger maneten ett kompakt utseende. Botten av plattan med munarmarna är vitaktig med mörka eller blåsvarta prickar. Klockan är indelad i 16 lober. Medelhavsmaneter ger en lätt till måttlig brännskada vid kontakt med hud.

  • Lungmanet (Rhizostoma pulmo) Lungmaneten (Sp: ”Aguamala”) är besläktad med den som förekommer i svenska vatten. Maneten är stor med en vitaktig violett halvsfärisk klocka med ett blått kantband. Klockan kan bli upp till en meter i diameter (90-100 cm). Klockan har blåvioletta lober utan bränntrådar men med 8 sammansatta munarmar. Munarmarna formar en vitaktig fast munbotten. Lungmaneter ger endast en lätt brännskada vid kontakt med hud.

  • Kompassmanet (Chrysaora hysoscella) Kompassmaneter förekommer både i medelhavet och i nordligare havsvatten (Sp: Compases). Den har en vit till gulaktig halvtransparent klocka med en diameter upp till 30 cm. Klockan har mörkare centrifugala linjer som gör att utseendet liknar en kompass. Kompassmaneter ger en relativt kraftig brännskada vid kontakt med hud.

  • Bidevindseglare (Velella velella) Bidevindseglare är små, 1-5 cm tjocka eller breda maneter som har en geléartad kropp som den använder som segel ovan vattenytan för att förflytta sig (Sp: ”Velero”). Seglet är täckt av en vitaktig hinna. Klockan är violett eller blåaktig och halvtransparent. Runt kroppen finns en blåviolett ring av relativt korta trådar. Den liknar men är ej att förväxla med den betydligt farligare portugisiska örlogsmannen. Bidevindseglaren är ofarlig vid kontakt med hud.

  • ”Vattenmanet – kristallmanet” (Aequorea forskalea) Kristallmaneter är transparenta blåvioletta svagt färgade maneter. Kroppen är halvsfärisk med centrifugala (radiala) linjer (kanaler) och en central uppklarningszon. I uppklarningszonen finns ett triangulärt kondenserat område. Klockan mäter upp till 15-30 cm i diameter. Under klockan hänger långa trådliknande tentakler. Kristallmaneter är vanligare i Atlanten än i medelhavet. Dessa maneter ger ingen brännskada vid kontakt med hud.

Maneter ger upphov till toxiska skador genom kontakt mot människans hud med sina tentakler och bränntrådar. På tentaklerna och bränntrådarna finns nässelceller med små blåsor, nematocyster. I dessa nematocyster finns hullingförsedda trådar som vid hudkontakt skjuter in genom huden likt en harpun och frigör ett toxin. Nematocystorna fastnar i tusentals i huden och kan ge upphov till fortsatta reaktioner om huden gnuggas eller om nematocysterna lyserar. Tidig avspolning av huden syftar till att avlägsna icke-utlösta nematocyster. Toxinet som frigörs ger upphov till en inflammatorisk reaktion.

Manetens toxin är komplext sammansatt och innehåller en rad inflammationsbefrämjande substanser, bland annat:

  • Bradykinin
  • Hemolysin
  • Serotonin
  • Histamin
  • Prostaglandiner

Vid kontakt uppstår en varierande grad av hudinflammation som vid en brännskada. Toxinet orsakar ett ökat inflöde över cellmembranet i olika vävnader av kalcium, kalium och natrium som är icke-sensitivt för organiska kanalblockerare. Reaktionen uppstår genom ökad permeabilitet över cellmembranet och inte genom bildning av porer.

I Sverige är det främst röd brännmanet som ger upphov till skador men även blå brännmanet och kompassmanet har nässelceller med nematocyster som kan ge upphov till hudirritation.

Den portugisiska örlogsmannen och den australiska kubmaneten kan ge upphov till mycket kraftig inflammation med långa piskrappsliknande rodnader över de hudpartier som angripits.

Toxinet från kubmaneten är både neurotoxiskt, hemolytiskt och kardiotoxiskt. Kontakt med mer än 1,2 meter tentakler anses vara livshotande beträffande den australiska kubmaneten.

Den portugisiska örlogsmannen har tentakler som kan vara mer än 10 meter långa, tentaklerna kan även lossna från maneten och sväva fritt i vattnet. Toxinet är huvudsakligen neurotoxiskt och kan ge upphov till respiratorisk paralys. Tentaklerna är fulla med nematocyster. Inflammationen kan bli så pass kraftig att bestående ärr kan uppkomma med hudkontrakturer som efter brännskador. Även Irukandjimanetens toxin är neurotoxiskt.

Symptom vid kontakt med maneter i svenska vatten är främst lokala hudsymptom, såsom:

  • Klåda, ofta ihållande
  • Rodnad
  • Svullnad
  • Lätt till måttlig smärta

I enstaka fall kan mer generella symptom tillstöta, främst:

  • Generell ihållande klåda
  • Svår smärta
  • Illamående, kräkningar
  • Dåsighet, somnolens

Öronmanet och lungmanet ger endast upphov till lättare hudirritation.

Kontakt med kubmaneten kan förorsaka en så snabb inflammation att andnöd och andningsstopp med chock kan uppträda momentant följt av kardiovaskulär kollaps. Flera fall finns beskrivna där omedelbar hjärtlungräddning invid vattenlinjen varit livräddande.

Kubmaneten och den portugisiska örlogsmannen ger vid hudkontakt upphov till omedelbar mycket svår smärta och mer generella symptom, som:

  • Illamående
  • Frysningar
  • Muskelvärk
  • Huvudvärk
  • Andningspåverkan
  • Cirkulationskollaps


Vid angrepp av maneter i svenska vatten, främst röd brännmanet (Cyanea capillata):

  • Skölj av det affekterade området med rikliga mängder havsvatten, dock inte med kranvatten. Tag 3 spänner med havsvatten och skölj över huden. Man rekommenderar saltvatten i första hand, då sötvatten får nematocysterna i bränntrådarna att lysera och därigenom frisätta mer toxin. Undvik att duscha direkt efter brännskadan.
  • Man kan prova att badda angripen hud med kylbalsam. Undvik att få manettrådar på händerna. Undvik vinäger då detta lyserar bränntrådarna.
  • Rester av manettrådar kan skapas bort, t ex med ett kreditkort. Man kan även dra bort trådar med hjälp av en bred tejp, t ex silvertejp. Man bör däremot inte gnugga huden eftersom det kan frigöra toxiner. Även raklödder och rakhyvel kan effektivt få bort manettrådar.
  • Om symptom kvarstår kan man även pröva att sänka ner angripna kroppspartier i varmt vatten (40-45 grader) för att neutralisera toxiner. Man bör pröva ett hett bad i 30-60 minuter efter spolning med saltvatten!
  • Vid kontakt med ögonen bör man skölja rikligt och långvarigt med kranvatten eller helst fysiologiskt saltvatten (minst 15 minuter).
  • Antihistaminer per os, t ex cetirizin (Zyrlex) 10 mg per os (ej till barn < 6 år) eller loratadin (Clarityn) 10 mg x 1, till barn under 2 år och mindre än 30 kg ges 5 mg x 1. Till barn under 30 kg rekommenderas Clarityn sirap (1 mg/ml) snarare än tabletter.
  • Huden kan smörjas med kortisonkräm t ex Hydrokortison CCS eller Mildison eller kylbalsam för att dämpa den inflammatoriska reaktionen och klådan. Man kan även pröva acetylsalicylsyra i kräm eller salva.
  • Iskyla eller lidokain-kräm över smärtsamma partier kan lindra smärtan. Applicera inte iskuber (kranvatten) direkt på huden, applicera i stället isen i en plastpåse.
  • Symptomatisk behandling i övrigt.
  • Vinäger, som ibland rekommenderats till baddning av huden har visat sig lysera nässelceller i hög utsträckning och rekommenderas därför inte vid sting av röd brännmanet, däremot rekommenderas det vid sting av en del exotiska maneter i andra länder (vetenskapligt oklart).

Vid angrepp av kubmanet och portugisisk örlogsman i utländska vatten:

  • Vid skada av kubmaneter eller portugisisk örlogsman bör man omedelbart söka sig till närmaste sjukvårdsinrättning.
  • Kubmanet kan ge upphov till andningsstopp och hjärtstopp.
  • Smärtan vid kontakt med kubmaneten och den portugisiska örlogsmannen kan vara extremt kraftig och är mycket svårbehandlad. Regional anestesi är en möjlig väg att blockera smärtan med hjälp av perifera blockader och lokalbedövningsmedel.
  • Vid angrepp av kubmaneten rekommenderas från vissa håll att man smörjer huden rikligt med vinäger. Vinäger uppges förhindra lysering av bränntrådar men hjälper inte mot redan uppkommen skada. Behandling med vinäger är kontroversiell och inte vetenskapligt belagd.
  • Man bör sänka ner angripna kroppspartier i varmt vatten (40-45 grader) för att neutralisera toxiner. Man kan pröva ett hett bad i 30-60 minuter vid utbredda brännskador!
  • Man skall undvika att gnugga huden liksom att applicera alkohol över huden.
  • Det finns en antidot till kubmaneten i form av ett immunserum utvecklat med hjälp av immuniserade får. Tre ampuller med immunserum ges intravenöst så snabbt som möjligt efter angrepp av kubmaneten, om allmänsymptom eller chocksymptom föreligger.


Alger tillämpar fotosyntes, men är inga växter utan en typ av mikroorganismer klassificerade som växtplankton. Giftiga alger förekommer i Sverige främst i sött eller bräckt vatten, d v s mest i Östersjön. Dessa alger kan producera toxiska cyanobakterier som kan orsaka akut förgiftning. De giftproducerande algerna tål inte saltvatten och finns därför inte längs Västkusten, i Kattegatt eller Skagerack. Det finns en icke-verifierad hypotetisk koppling mellan cyanobakterier och neurologiska sjukdomar som ALS, Alzheimer och Parkinsons sjukdom genom en ökad bildning av beta-N-metylamino-L-alanin (BMAA) och ökad glutamataktivitet i CNS. Kopplingen är endast hypotetisk och viss forskning i detta fält pågår.

Algblomning förekommer ute till havs, längs med kusten, i sjöar och vattendrag med stillastående vatten. Algblomning innebär en stark tillväxt av toxinbildande alger, vanligen av en och samma art.

Algblomning sker främst vid soligt och vindstilla väder när vattnet är i obalans, men också vid övergödning, främst med fosfor och nitrater. Rikligt med solljus behövs för algblomning. Blomningen av toxinproducerande alger sker främst vid en vattentemperatur mellan 15 och 23 grader.

Algmängder under 10 000 celler per ml vatten kategoriseras vanligen inte som algblomning. Vid omfattande algblomning finns mer än en miljon celler per milliliter vatten.

Algblomning kan oftast, men inte alltid, konstateras med ögat och näsan. Tecken på algblomning:

  • Vattnet blir grumligt med en påtaglig färgförändring. Denna kan skifta i gulgrönt, blågrönt, gulvitt, rödbrunt eller rabarberliknande.
  • I allmänhet är vattengrumlingen ytnära och ej förekommande på djupet.
  • Smak och doft av vattnet kan vara påverkat, vattnet luktar oftast illa med en påtagligt frånstötande doft.

Algerna kan blomma under alla delar av året, men vanligen sker toxiska algblomningar under juli och augusti. De kan dock äga rum ända in i november. Ofta förekommande vår- och höstblomningar är inte toxinproducerande och därför ofarliga för människan.

Algblomning kan leda till produktion av förruttnelsebakterier med påföljande syrebrist i vattnet, vilket i sin tur kan leda till fiskdöd.

Exposition för toxiska alger sker främst genom bad varvid kontakt äger rum genom huden och slemhinnor, men också genom nedsväljning av vatten.

Giftproducerande alger utgörs av blågröna alger, vilka är en variant av växtplankton. I själva verket produceras toxinerna av bakterier (eubakterier), men klassificeras som växtplankton.

Det finns minst åtta olika typer av toxinproducerande alger i Sverige. Några av dessa är Microcystis aeruginosa, Anabaena sperica, Oscillatoria och Nodularia Spumigena (katthårsalg).

Toxinerna klassificeras främst i tre olika kategorier:

  • Neurotoxiska toxiner
  • Hepatotoxiska toxiner
  • Tarmtoxiska toxiner

De kan även ge upphov till irritation i hud och slemhinnor vid direktkontakt. Förutom rent toxiska symptom kan de ge upphov till allergiska symptom.

I den kliniska bilden efter närkontakt ingår vanligen hudutslag och mag-tarmbesvär. Uttalade symptom uppkommer främst om man svalt vatten genom upprepade kallsupar eller av misstag druckit kontaminerat vatten. Det sistnämnda drabbar främst djur, ff a hundar.

Symptomen uppkommer vanligen inom några timmar efter bad, sällan senare än efter 12 timmar, och är i regel övergående inom något dygn. I uttalade fall kan symptomen vara i 2-3 dygn.

Risk för leverpåverkan och njurpåverkan finns vid kraftig exposition. En indikation på stark exposition är generella symptom som muskelvärk och ledvärk. Diagnos ställs genom anamnes och klinisk bild.

Även andra djur än människa löper risk att bli sjuka vid kontakt med toxiska alger; främst hundar löper risk för allvarliga symptom efter bad bland alger eller genom nedsväljning av kontaminerat vatten.

Vanliga symptom vid förgiftning med toxiska alger:

  • Klåda
  • Utslag
  • Ögonirritation
  • Illamående
  • Kräkning
  • Diarré
  • Magont
  • Magkramper
  • Feber
  • Muskelsmärtor
  • Ledsmärtor
  • Rinnande näsa
  • Astmaliknande besvär, bronkobstruktion

Någon specifik behandling finns inte. Behandlingen är i huvudsak symptomatisk.

  • Om man badat bland giftiga alger skall man skölja kroppen noggrant med duschvatten och därefter tvätta sig med tvål och vatten över hela kroppen.
  • Vid ögonsymptom bör man skölja rent ögonen med rinnande vatten.
  • Har man svalt stora mängder vatten och upplever allmänpåverkan bör man uppsöka sjukhus. På sjukhus bör man kontrollera lever- och njurfunktion med vanliga rutinprover.
  • Hundar som badat bland giftiga alger bör initialt dricka rikligt med friskt vatten.


Det är allt vanligare att svenskar reser till tropiska länder och dyker eller badar i tempererade, subtropiska och tropiska vatten. Här kan man stöta på havsanemoner, koraller och nässeldjur som kan ge upphov till toxiska reaktioner vid kontakt med nässelceller. Man bör därför undvika att ta i eller bryta av koraller och havsanemoner.

Framför allt orsakar dessa organismer lokalsymptom genom sina nässelceller, men en del av dem kan även ge upphov till generella symptom. Nässelcellerna frisätter ett toxin för att organismen skall kunna paralysera sitt byte som den sedan konsumerar.

Anemoner tillhör gruppen sexstråliga koralldjur och är en typ av polyp med tentakler. De hudirriterande anemonerna tillhör stammen Cnidaria som är en typ av nässeldjur med toxinfrisättande nässelceller (nematocyster). Nedan nämns några toxiska anemon- och korallarter. Klicka på rödmarkerad extern länk för bild.

Actinodendron plumosum (bild) är en toxisk havsanemon, den har rikligt med nematocyster som frisätter ett irriterande toxin.

Andra starkt brännande anemoner är Bolocera tuediae (bild) och eldkorallen (Millepora dichotoma, bild). Sting från eldkorallen kan förorsaka uttalad brännskada med bestående ärrbildning.

Behandlingen är i huvudsak symptomatisk och liknar den vid angrepp av brännmaneter.

  • Skölj först av det skadade området med saltvatten.
  • Undvik värme och solexponering.
  • Applicera en kortisonkräm eller ytanestesimedel innehållande Xylocain.
  • Antihistamin per os kan dämpa den inflammatoriska reaktionen, t ex Tavegyl 1-2 mg p.o.

Det är ovanligt med generella symptom.


Vid hantering av saltvattensakvarier kan vissa implanterade koraller avge ett toxin, ett s k palytoxin. De koraller som främst är aktuella är palythoakoraller och protopalythoakoraller, även vissa anemoner kan avge detta toxin. Palytoxin är ett potent toxin och har gett upphov till allvarliga förgiftningar. Man kan bli exponerad för palytoxin via hudkontakt, ögonkontakt, förtäring eller inhalation. Toxinet är en kraftig vasokonstriktor och kan ge upphov till kärlischemi, även kardiell ischemi.

Symptom vi palytoxinförgiftning kan ge symptom liknande överdosering med lokalanestesimedel men ger främst respiratoriska symptom som hosta och bronkobstruktivitet, gastrointestinala symptom med illamående och kräkningar samt feber. Långdragna obstruktiva besvär har beskrivits (1-3 mån). Symptom som kan uppträda är:

  • Metallsmak i munnen
  • Takykardi
  • Andnöd, hosta
  • Bronkobstruktivitet
  • Feber
  • Bröstsmärta
  • Blodtrycksfall
  • EKG-förändringar
  • Muskelspasm
  • Svår smärta
  • Kräkningar
  • Kramper

Vid hantering av dessa koraller rekommenderas användning av skyddsglasögon, visir och långa handskar för att undvika stänk! Behandlingen är huvudsakligen symptomatisk och understödjande men man kan pröva vasodilaterande behandling med t ex papaverin eller nitroglycerin. Man bör undvika att koka koraller från dylika akvarier då ångorna kan ge respiratoriska besvär.

KÄGELSNÄCKA (Conus geographus)

Kägelsnäckan är en typ av rovdjurssniglar som lever av att attackera och äta fiskar. Kägelsnäckan är stor, har ett konformat fläckigt (leopardliknande), hårt och tjockt skal och kan uppnå en längd av 25 cm. Den har oftast ett vackert mönstrat skal som gör den attraktiv som samlarobjekt och turistattraktion. Den förekommer främst i Stilla havet och Indiska oceanen. Snäckan har en munarm som den kan skjuta ut som en harpun ur sitt skal och på så sätt paralysera och fånga byten. Även människor har skadats genom kontakt med kägelsnäckan.

Kägelsnäckan injicerar ett neurotoxiskt gift (konotoxin) som ger upphov till smärta, parestesier och domningar men även generella symptom som muskelslapphet, koordinationssvårigheter och försämrat tal, hörsel och syn. Även enstaka dödsfall finns rapporterat.


(Chloeia Flavia)
Dessa små maskar (Eng: Bristle worms/Fire worms) simmar fritt i tropiska och varma vatten och kan ge upphov till brännande smärta vid hudkontakt med dykare. Eldmaskarna tillhör gruppen polychaete som innehåller ett stort antal olika arter. Maskarna har nässelceller som kan ge upphov till lokal rodnad, smärta och klåda. Nematocysterna kan avlägsnas med tejp (silvertejp) från affekterad hud. Därefter bör man skölja av huden, stryka in vinäger och sedan applicera en kortisonkräm eller ett lokalanestetikum. Antihistamin kan dämpa klådan något.


Blåmussla är en art i klassen musslor av typen blötdjur. Blåmusslan är blåsvart och normalt ovalt formad. Den blir vanligen cirka 6 centimeter lång, men kan bli upp till två decimeter. Den ätbara muskeln är gul/gulvit.

Blåmussla fiskas intensivt och odlas i stor skala. Musslor säljs färska, konserverade eller frysta. Blåmusslor är en vanlig matvara efter kokning. De har bäst smak på våren.

Blommande växtplankton som är toxinproducerande kan påträffas i blåmusslor. Dessa kan då bli otjänliga som födoämnen. Ett släkte växtplankton (Alexandrium) har påträffats i sådana mängder bland blåmusslor i Bohuslän att de kan ge upphov till allmänna sjukdomssymptom.

Det är ytterst sällsynt med förgiftning från blåmusslor. Vanligtvis stiger toxinhalten under hösten och är som högst under vintern.
Bild: Skal från blåmussla

Symptom vid konsumtion av toxiska blåmusslor är i huvudsak gastrointestinala:

  • Diarré
  • Illamående
  • Kräkningar


I normalfall behöver man inte uppsöka sjukvården, då symptomen är relativt beskedliga och snabbt övergående. I uttalade fall kan vätska behöva ges intravenöst. I övrigt gäller symptomatisk behandling.

PSP “Paralytic Shellfish Poisoning”

Mer allvarlig förgiftning efter konsumtion av blåmusslor har förekommit då musslorna är kontaminerade, bl a av Gonyulax catenella. Det vanligaste toxinet som orsakar PSP är ett saxitoxin. Saxitoxinet kan härbärgeras i musslor i flera veckor eller längre. Toxinet produceras av mikroskopiska alger som filtrerats genom blåmusslan, t ex efter algblomning. Andra toxiner som kan ge upphov till förgiftningssymptom är neosaxiton och gonyautoxin. Samtliga toxiner är i huvudsak neurotoxiska.

Initiala symptom är illamående och kräkningar men detta toxin kan även ge upphov till yrsel, koordinationsstörning, talsvårigheter, torr mun, sväljningssvårigheter, andningssvårigheter, tilltagande muskelsvaghet och paralys. Det förekommer även blodtrycksfall, hjärtsvikt och kardiovaskulär kollaps. Enstaka dödsfall finns rapporterade. Barn och immunosupprimerade personer är mer känsliga för dessa toxiner.

Behandlingen av PSP är i huvudsak symptomatisk. I svåra fall kan respiratorbehandling på en intensivvårdsavdelning behöva tillgripas.

CSP (Ciguatera shellfish poisoning)

I Franska Polynesien har rapporterats om ciguateraliknande symptom efter konsumtion av skaldjur, bl a ostron.


  • Illamående
  • Kräkningar
  • Asteni
  • Myalgi
  • Parestesier
  • Dysestesier
  • Ihållande hicka


Behandlingen är i huvudsak symptomatisk men mannitol intravenöst har prövats som vid ciguateraförgiftning.


Annan fisk- och skaldjursförgiftning T61.2
Toxisk effekt av kontakt med andra marina djur T63.6


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Smoke inhalation injuries

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Förgiftning efter exponering för retande gaser uppkommer oftast efter bränder men kan även uppkomma efter kemiska olyckor. Brandrök kan innehålla uppemot 60 olika kemiska ämnen som kan irritera luftvägar och bronker men i huvudsak är det svart sot som irriterar luftvägarna i samband med brand. I tillägg till skadlig rök vid brand kan luftvägarna skadas av extrem värme, het ånga, giftiga gaser och hypoxi. Svedda ögonbryn, ögonfransar, näshår och skägg, konjunktivit, ökat tårflöde, ljusskygghet, brännskada i ansiktet, upphostningar av sot, ödem i svalg och näsöppningar är symtom på inhalationsskada. Larynx kan svullna kraftigt efter termiska skador och sot kan obstruera luftvägarna rent mekaniskt. Sot kan plugga igen bronkträdet och ge upphov till avstängda luftvägar med auto-PEEP.  Andra symptom kan vara hosta, heshet, stridor samt obstruktiv andning. Om kraftigt ödem föreligger i luftvägarna bör patienten intuberas akut och vårdas på en intensivvårdsavdelning.

Retande gaser kan orsaka trakeit, bronkit och bronkiolit med hyperemi, bronkospasm, riklig slemsekretion och ödem. I svåra fall kan en ARDS-bild utvecklas med tilltagande lungfibrotisering. Inspektion av farynx och larynx före intubation bör göras om sot och ödem förekommer genom tunn fiberskopi via näsan under lätt sedering.

Gaser kan utöva direkt toxicitet, exempelvis cyanvätegas (blockerar cellandningen), kolmonoxid (blockerar syretransporten) eller klorgas (slemhinneirriterande). Andra gaser kan orsaka allvarlig hypoxi genom att ersätta syret i inandningsluften, exempelvis metan-, koldioxid- och butangas.

Inhalation av svart sot ger snabbt upphov till kraftig andnöd, luftvägsirritation, ödem och hosta. Primär åtgärd vid exponering för retande gaser blir naturligtvis att undkomma expositionen och andas frisk luft. Om expositionen varit kortvarig hämtar sig de flesta snabbt utan att behöva söka sjukvård men känsliga personer kan inkomma med kvarstående bronkobstruktion och luftvägsirritation. Kraftig exposition för brandrök kan ge upphov till allvarliga symtom som kan ge långdragna besvär. Vid inhalation av brandrök är det främst inhalation av kolmonoxid och cyanväte som ger allvarliga förgiftningssymtom.

Retande gaser

Lättlösliga gaser

Egenskaper för lättlösliga gaser i vatten är att de löser sig lätt i fuktiga slemhinnor, exempelvis i övre luftvägar och ögon. De lättlösliga gaserna ger därför omedelbara symtom.

Exempel på lättlösliga gaser är:

  • Alkali
  • Ammoniak
  • Fenacylklorid
  • Fluorvätegas
  • Formaldehyd
  • Gasformiga syror
  • Svaveldioxid
  • Väteklorid (saltsyra)
  • Zinkklorid (i försvarets rökgranater)

Medelhög löslighet

Gaser med medelhög löslighet i vatten ger symtom både från de övre och nedre luftvägarna.

Exempel på gaser med medelhög löslighet är:

  • Fenol
  • Svaveldioxid

Svårlösliga gaser

Egenskaper för svårlösliga gaser i vatten är att gaserna har svårt att lösa sig i de fuktiga slemhinnorna. Därmed når gaserna de nedre luftvägarna och ända ner till lungblåsorna. De svårlösliga gaserna ger därför fördröjda symtom; från 30 minuter upp till 48 timmar efter exponering, med risk för sent lungödem. Omfattningen av skadan i luftvägarna beror på koncentrationen av gasen, tiden för expositionen och gasens löslighet. Svårlösliga gaser ger mer djupgående skador som i högre grad riskerar att ge bestående men som bronkiolit, granulation med fibros och ARDS. Fosgen och nitrösa gaser kan ge beskedliga initialsymptom som förvärras efter hand.

Exempel på svårlösliga gaser är:

  • Fosgen
  • Isocyanater
  • Klor
  • Klordioxid
  • Kvicksilverånga
  • Kvävedioxid
  • Nitrösa gaser
  • Svavelväte (vätesulfid)
  • Ortoklorbensalmalononitril (tårgas)

Exempel på några ämnen som kan ge allvarliga symtom efter exposition av gaser eller rök


  • (CS-gas) – används som inkapaciterande medel i samband med demonstrationer och upplopp
  • Innehåller vanligen 2-klorbensenmalonsyradinitril.

Ämnet används som en aerosol löst i aceton. Tårgas är kraftigt luftvägsirriterande och ger kraftig sveda och klåda i ögon och slemhinnor med ymnig tårsekretion. Tårgas ger vanligen inga uttalade förgiftningssymptom men enstaka dödsfall har förekommit. Svensk polis använder numera i stället företrädesvis pepparspray som innehåller kapsaicin som är en beståndsdel från pepparfrukt.


  • Färglös, flyktig, brännbar vätska
  • Lösningsmedel i lacker och plaster
  • Kan orsaka huvudvärk och i värsta fall medvetslöshet


  • Färglös, giftig och mycket brandfarlig vätska
  • Omvandlas till cyanid i kroppen
  • Symptomen kommer gradvis under flera timmar
  • Finns i plaster och nitrilgummi
  • Ger sveda i ögonen, irriterar huden och kan ge kräkningar och huvudvärk
  • Bör behandlas med cyanidantidoten natriumtiosulfat


  • Färglös gas vid rumstemperatur
  • Förekommer i kylanläggningar och i kemisk industri
  • Irriterar ögon och luftvägar redan i små mängder. Kan vid höga halter leda till kvävning.


  • Färglös giftig vätska, finns bl.a i kylskåp
  • Används vid tillverkning av färgämnen, läkemedel och antioxidationsmedel.
  • Blockerar hemoglobinets syrebärande kapacitet så att det varken kan avge syre eller ta upp koldioxid i cellerna


  • Färglös, mycket brännbar vätska
  • Lösningsmedel för fett
  • Cancerframkallande, kan påverka benmärgen


  • En grupp aromatiska kolväten som bildas vid ofullständig förbränning, till exempel i bilmotorer
  • Starkt cancerframkallande och reproduktionsstörande


  • Färglös, lättflyktig och extremt giftig vätska eller gas. Luktar bittermandel.
  • Har använts vid avrättningar i vissa länder och vid framställning av metakrylat, aminosyror och cyanidföreningar.
  • Blockerar cellernas förmåga att ta upp syre.
  • Ger kramper, hjärtpåverkan och medvetslöshet.
  • Höga doser dödar mycket snabbt


  • Starkt frätande och giftigt ämne som bildar färglösa kristaller.
  • Tillverkning av bland annat plaster, färgämnen, sprängmedel, läkemedel och tvättmedel.
  • Flera fenoler kan bidra till cancer. Ett gram har orsakat dödsfall.


  • Färglös gas som utvinns ur metanol. Lättlöslig i vatten.
  • Används vid framställning av plaster, desinfektionsmedel och insektsgift.
  • Luftvägsirriterande, skadar flimmerhåren. Kan vara cancerframkallande.


  • Silvervit, mjuk metall som finns i jordskorpan. Mycket giftigt.
  • Finns i batterier och legeringar.
  • Kan skada luftvägar och lungor. Kan vara cancerframkallande.


  • Kraftigt slemhinneirriterande både i ögon, munhåla och svalg samt övre och nedre luftvägarna
  • Omvandlas till syra och ger upphovande till kraftig slemhinneskada
  • Dödlig i starka koncentrationer


  • Färglös giftig gas.
  • Tillverkning av PVC-plaster
  • Kan vara cancerframkallande.


  • Finns i färger och plaster
  • Kan ge hudallergier
  • Förångas och kan bilda giftiga gaser vid temperaturer över 160 grader
  • Var det ämne som i huvudsak orsakade mer än 2000 dödsfall i samband med läckage från en industri i Bhopal i Indien 1984.

SYMTOM efter inhalation av giftiga gaser

Inhalation av brandrök och andra retande gaser ger oftast kraftig irritation i luftvägarna med ihållande hosta, andnöd, kraftig slemsekretion och luftvägsobstruktivitet (bronkospasm). Hypoxi, cyanos och hyperkapné kan följa. Övriga kliniska symptom kan vara agitation, oro, dyspné, ångest, tachypné, näsvingeandning, vakenhetssänkning, medvetslöshet och intercostala indragningar. Observera att vissa giftiga gaser kan vara toxiska utan att vara retande i luftvägarna, t ex kolmonoxid.

Laryngospasm i sig kan ge kraftig hypoxi, svimning och medvetslöshet. När laryngospasmen släpper kan ett reflektoriskt lungödem framträda. Vid exponering för svårlösliga gaser eller nitrösa gaser kan ett toxiskt lungödem uppkomma sent i förloppet och patienten behöver därför övervakas i minst 24 timmar.


Generell behandling

Patienter som inhalerat giftig gas eller brandrök behandlas vanligen både med kortison och bronkdilaterande medel i inhalation.

Budesonid (Pulmicort) samt terbutalin (Bricanyl) eller salbutamol (Ventoline) ges i upprepade inhalationer. Combivent och Sapimol innehåller både ipratropium och salbutamol. Kortikosteroider kan behöva ges i upprepade doser i inhalation, ges vanligen inte systemiskt. Ge behandling med betastimulerare före behandlingen med kortikosteroider för att förbättra möjligheten för steroiderna att nå ut till fler lungsegment.

I fall med mycket medtagna patienter är det bättre att säkra luftvägen akut genom intubation med kontrollerad andning och vård i respirator. Andningsstopp kan komma plötsligt hos en utmattad patient. Bronkoskopi bör utföras för diagnostik och rensugning av slem och sot. Sot i luftvägarna kan plugga igen bronkträdet och bör utförskaffas via bronkoskopi med lavage. Observera risken för tidigt eller sent lungödem. Vid brännskada över jugulum försiktighet med tracheotomi.

Vaken patient

  • Lugn och ro
  • Efter inandning av retande gaser, giftiga gaser eller brandrök skall patienten helst vila i sittande, s k hjärtläge, gärna med syrgas på tättslutande mask.
  • Vid kraftig exposition med svullnad av luftvägarna eller förekomst av sot bör luftvägarna inspekteras med fiberskopi.

Medvetslös patient

  • Patienten läggs i vänster sidoläge, alternativt i framstupa sidoläge.
  • Initialt ges 100 % syrgas på mask och akut intubation med kontrollerad ventilation bör utföras snabbt vid medvetslöshet. Föreligger hjärtstillestånd efter rökgasförgiftning är det stor risk för global anoxisk hjärnskada.
  • Vid kraftig exposition med svullnad av luftvägarna eller förekomst av sot bör luftvägarna inspekteras med fiberbronkoskopi, liberal indikation för intubation.


Initialt ges 100 % syrgas på tättslutande mask med reservoarblåsa tills man bestämt CO-Hb och uteslutit allvarlig kolmonoxidförgiftning. Om CO-Hb är lägre än 10 % kan syrgas i fortsättningen ges via halvöppen andningsmask, Optiflow-system eller grimma. Via näsgrimma ges 4-6 liter/min för att nå SaO2 ≥ 90 %. Svårigheter kan uppkomma med maskventilation när patienten har ett stort behov av hosta. Hostan kan dämpas med morfin och teofyllamin.


Inhalationsbehandling ges tidigt med betastimulerare och steroider. Upprepade behandlingar är ofta nödvändigt.

Beta 2-stimulerare

  • Bricanyl Turbuhaler 0,5 mg/dos 2-3 inhalationer så snart som möjligt alternativt
  • Salbutamol (Ventoline) 5 mg/ml, 1-2 ml inhalationslösning i nebulisator. Ovanstående inhalation kan kombineras med 2 ml ipratropiumbromid (Combivent, Sapimol, Atrovent) inhalationsvätska 0,25 mg/ml vid påtaglig slemsekretion.
  • Om patienten inte kan inhalera, kan beta 2-stimulerare ges parenteralt. Injektionslösning terbutalin (Bricanyl) 0,5 mg/ml, 0,5-1,0 ml subkutant. Vid svåra anfall spädes 1 ml av injektionslösningen med 10 ml NaCl och ges långsamt (över 5 minuter) intravenöst.


  • Indikation för kortisonbehandling föreligger om patienten har haft uttalade retsymtom med intensiv besvärande hosta eller andningspåverkan, obstruktivitet eller varit exponerad för fosgen eller nitrösa gaser.
  • Steroider ges i första hand som inhalation via nebulisator. Budesonid (Pulmicort) suspension för nebulisator 2 mg x 2 (4 ml x 2).
  • Vid allvarliga symtom initialt 10 inhalationer samt vid behov 4-5 inhalationer x 1-2 inom första timmen. Efter varje inhalation bör man hålla andan i cirka 10 sekunder. Nästa inhalation görs efter ett par normala andetag. Vid återkommande symtom ges ytterligare 2-3 behandlingar första dygnet. Till barn halveras doserna.
  • Steroidbehandling parenteralt (intravenöst) rekommenderas normalt inte. Om steroider inte kan ges i inhalation kan systemisk tillförsel övervägas (intravenöst/intramuskulärt).


Motståndsandning med CPAP kan prövas med 100 % syrgas (BiPAP). Motståndet varieras mellan 5 och 10 cm H2O. Starta aldrig på 10 cm H2O utan normalt på 5 cm H2O. Observera dock att det innebär ett extra andningsarbete och kan innebära en enorm påfrestning för patienten. Ofta krävs sedering. Vid CPAP-behandling måste det finnas omedelbar beredskap för intubation. En utmattad patient bör inte behandlas med CPAP. Intubation och kontrollerad ventilation är betydligt säkrare och bättre om patienten är medtagen.


Ett optiflowsystem kan med fördel användas om patienten har uttalad hosta då det är besvärligt att hosta i en tättslutande mask. Optiflow ger ett ökat motstånd i utandningen och bidrar till uppluftning av atelektaser.


Vid riklig slemsekretion ges ett antikolinergikum intravenöst.

Atropin 0,5 mg/ml, 2 ml i.v. eller Robinul 0,2 mg/ml, 1-2 ml i.v. Observera att i sällsynta fall vid förgiftning med organofosfater, isocyanid samt vissa insekticider och pesticider kan betydligt större doser atropin behöva ges (SIC-doser). Behandlingen styrs efter den kliniska bilden med slemsekretion i luftvägarna eller andra kolinerga symtom.


Kan ges vid uttalad andningssvårighet eller ihållande hosta. Ge 10 ml (23 mg/ml) teofyllamin långsamt (10 minuter) i.v. Aldrig i central ven. Överdosering kan ge livshotande arytmier. Sätt därefter 20 ml teofyllamin i 500 ml 5 % glukos över 12 timmar. Kontrollera gärna teofyllaminkoncentration i serum.

Specifik behandling

Cyanidförgiftning – inhalation av cyanväte

Antidotbehandling mot cyanidförgiftning kan påbörjas på skadeplatsen i samband med exponering för brandrök men vanligen räcker det med att starta behandlingen efter ankomst till sjukhus med vägledning av en arteriell blodgas där man mäter SvO2 och laktat. Cyanid går vanligtvis inte att mäta. Antidot mot cyanidförgiftning ges om den skadade varit eller är medvetslös och har dragits ut från ett brinnande hus samt har sot i näsöppningarna eller hostar sot. Laktatvärden mindre än 10 mmol/l indikerar att allvarlig cyanidförgiftning inte föreligger och inte behöver behandling med antidot. Allvarlig cyanidförgiftning är vanligen förenad med svimning och medvetslöshet. Om patienten är vaken är således allvarlig cyanidförgiftning mindre sannolikt. Hydroxokobolamin (Cyanokit) ges intravenöst vid förgiftning med cyanväte (brandrök) eller andra cyanidföreningar.

Behandling med hydroxokobolamin (Cyanokit):

  • Vuxna: 5 g ges i.v. som infusion under 15-30 minuter, upprepas vid behov
  • Barn: 70 mg/kg kroppsvikt

Observera efter behandling med hydroxokobalamin blir huden, urinen och andra kroppsvätskor starkt rödfärgade. Detta bör meddelas personal och patienten som annars kan bli förvånade och oroliga. Färgen kan påverka kemiska analyser som är baserade på kromatografi.

Om Cyanokit inte finns tillgängligt kan behandling även ges med natriumtiosulfat.

  • Vuxna: natriumtiosulfat 150 mg/ml: 15 g (100 ml) ges i.v. under 5- 10 minuter. Kan eventuellt upprepas
  • Barn: 375 mg (= 2,5 ml)/kg kroppsvikt


Kolmonoxidförgiftning är vanligt efter exponering för brandrök. Kolmonoxid ger vakenhetssänkning och andningssvikt. Överväg tryckkammarbehandling (HBO) och akut transport till tryckkammare om patienten är medvetslös eller har varit medvetslös. Rådfråga Giftinformationscentralen vid tveksamhet. CO-Hb värden över 25 % indikerar allvarlig kolmonoxidförgiftning. Behandlingen utgörs i första hand av syrgas på tättslutande andningsmask (NBO, normobar oxygenterapi). Laktatvärden överstiger sällan 10 mmol vid ren kolmonoxidförgiftning.

Visa behandlingsöversikt: Kolmonoxidförgiftning

Kutan exposition

Har patienten råkat ut för en kemisk olycka med kutan exponering (förgiftning genom huden) av kemikalier, ibland i kombination med en brännskada, skall patienten saneras. Tag av alla kläder (använd rejäla skyddshandskar vid kontakt med kemiska vätskor). Skor och smycken skall också tas av. Spola eller duscha patienten med rikliga mängder vatten. Använd varmt vatten och se till att patienten inte blir nedkyld. Vid kemisk exponering skall patienten om möjligt först saneras en gång utomhus och därefter en gång inomhus. Var noggrann med ögonen. Är patientens kläder torra behöver man i regel inte sanera. Tvätta exponerad hud med tvål och vatten. Proceduren skall dock inte överdrivas.

En del saneringslokaler ligger i halvslutna rum, typ ett ambulansintag. Där är i regel temperaturen låg och det gäller att snabbt ge patienten varma kläder och filtar för att undvika nedkylning. Vid exponering av starkt alkaliska kemikalier skall sköljningen bedrivas under lång tid. Gas och lukt från giftiga kemikalier blåses bort alternativt sugs ut med fläktsystem – se till att luften är varm!

Om personalen exponerats för retande gaser kan även dessa behöva behandling med kortisoninhalationer! Observera om någon gett patienten mun-till-munandning.


Om sveda, klåda eller rodnad förekommer i ögonen skölj så snabbt som möjligt med rinnande vatten i 5-15 minuter. Håll ögonlocken brett isär så att spolningen blir effektiv. Exempel på ögonirriterande ämnen är klorgas, lut eller syror av olika slag. Exposition för dessa ämnen kan kräva längre tids spolning än 15 min. Ögonirritation är vanligt bland badande i samband med tekniska simbassängsolyckor med utsläpp av klor.


Uppföljning av patienten som exponerats för brandrök är viktigt då luftvägsbesvären och andnöden kan ge långdragna besvär och i vissa fall bestående men. Remiss till lungmedicinsk klinik är angeläget. Anmälan om arbetsskada måste också utföras i relevanta fall.


  • Gaser, rök och ångor, ospecificerade T59.9
  • Bronkit och pneumonit orsakad av kemikalier, gaser, rök och ånga J68.0
  • Inflammation i övre luftvägarna orsakad av kemikalier, gaser, rök och ånga som ej klassificeras annorstädes J68.2


  1. Toxic smoke inhalation: Cyanide poisoning in fire victims. Jones J, McMullen J, Dougherty J. Am J of Emerg Med. Volume 5, Issue 4, July 1987, Pages 317-321, Länk.
  2. Toxic smoke inhalation and cyanide poisoning. Merril A, Cohen MD, Lawrence J, Guzzardi MD. The American Journal of Emergency Medicine Volume 6, Issue 2, March 1988, Pages 203-204, Länk.
  3. Chlorine Gas Exposure and the Lung: A Review Rupali Das, Paul D. Blanc. Toxicology and Industrial Health Vol 9, Issue 3, 1993, Länk.
  4. The Role of Bronchoscopy in Pulmonary Complications due to Mustard Gas Inhalation. Freitag L, Firusian N, Stamatis G, Greschuchna D. Chest Volume 100, Issue 5, November 1991, Pages 1436–1441, Länk.
  5. Behandlingsanvisningar vid händelse med kemiska ämnen. Fastställt av RKMK 206-05-10. Reviderade 2011.
  6. Wang J, Winskog C, Edston E, Walther SM. Inhaled and intravenous corticosteroids both attenuate chlorine gas-induced lung injury in pigs. Acta Anaesthesiol Scand 2005;49:183–190.
  7. Wang J, Zhang L, Walther SM. Inhaled budesonide in experimental chlorine gas lung injury: influence of time interval between injury and treatment. Intensive Care Med 2002;28:352–357.


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB

Bite and Sting

By Kai Knudsen, Senior Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.
Updated 2018-12-21

Symtom från bett och sting uppträder framför allt sommartid när människor ute i naturen kommer i kontakt med knott, mygg, bin, getingar, fästingar, maneter m m.

De flesta bett och sting i Norden är av godartad natur och orsakar endast lindriga till måttliga symtom. En del sting kan ge upphov till allvarligare symtom och antalet sjukvårdsrelaterade fall kan räknas i tusental varje sommar. Dödsfall är mycket sällsynta, men enstaka fall förekommer varje år, främst i form av allergiska reaktioner efter bistick med anafylaktisk chock som följd där man räknar med 2-3 dödsfall per år. Dödsfall efter ormbett förekommer endast sporadiskt, runt ett fall per årtionde i Sverige.

Ett antal sjukdomar som överförs från insekter till människor (zoonoser) kan ge mycket allvarliga symtom. Nedan följer en kort sammanfattning av bett och sting av olika genes.

SYMTOM (insektsbett)

  • Smärta
  • Svullnad
  • Rodnad
  • Klåda
  • Missfärgning
  • Måttliga allmänsymptom


  • Rengör bettstället med tvål och vatten
  • Applicera avkylande och avsvällande lokalbehandling, t ex ispackning. Alternativt kan man applicera avkylande gel eller särskild insektsgel (t ex Mygga – innehåller bl a mentol och eucalyptusolja).
  • Undvik att klia på bettstället.
  • Avlägsna om möjligt kvarvarande tagg eller mundelar med en pincett. Undvik att klämma sönder biets gadd.
  • Lokalanestesimedel i salva lindrar klåda, t ex Xylocain salva 5 %.
  • Antihistaminer per os, t ex cetirizin (Zyrlex) 10 mg per os (ej till barn < 6 år) eller loratidin (Clarityn) 10 mg x 1. Till barn över 2 år med kroppsvikt under 30 kg ges 5 mg x 1. Till barn med en kroppsvikt under 30 kg rekommenderas Clarityn sirap 1 mg/ml snarare än tabletter.
  • Hydrokortisonkräm lokalt, t ex Hydrokortison CCS eller Mildison vid svullnad.
  • Antiseptisk kräm lokalt, t ex LHP 1 % som innehåller väteperoxid.



Myggbett är vanligt förekommande varje sommar i samband med fukt och värme, särskilt kvälls- och nattetid i skogsmark eller i närheten av vattendrag. Det finns mer än 30 000 olika sorters myggor varav ca 2000 i Sverige. I huvudsak förekommer två typer av stickmyggor, skogsmyggor (Aedes communis) och översvämningsmyggor (Aedes sticticus). Det är enbart honmyggan som suger blod.


  • Skogsmyggor är främst aktiva i gryningen och på kvällen. De tar tid på sig innan de sticker, och kan flyga högst två kilometer från kläckningsplatsen. Det är enbart honorna som sticker för att suga blod. Myggorna kan leva i upp till två månader.
  • De flesta bett uppkommer perifert på extremiteterna, d v s runt fotleder och handleder.
  • Myggorna är aktiva från juni, är flest runt midsommar och blir färre under juli.


  • Översvämningsmyggor är aktiva under hela den ljusa delen av dygnet, de kan stickas även mitt på dagen i solsken.
  • Översvämningsmyggorna är mer aggressiva och sticker direkt vid kontakt med människor.
  • Kan flyga upp till två mil från kläckningsplatsen och är aktiva t o m september.


  • Olika människor attraherar mygg i olika utsträckning men lockas framför allt av varm och svettig hud. Alkoholpåverkan som ökar blodgenomströmningen ökar risken för bett. Människors dofter och svettningsbenägenhet spelar viss roll medan blodgruppen spelar mindre roll. Enligt en japansk studie på tigermyggor så föredrar dessa myggor personer med blodgrupp 0.
  • Myggbett svullnar och rodnar, men blir sällan infekterade om man inte själv rivit och kliat sönder huden och på så vis fått in bakterier från hudfloran i såret.
  • Vid pågående myggbett låt myggan suga klart för att den avslutningsvis skall kunna aspirera sin saliv vilket möjligen efterlämnar mindre klåda.
  • Myggbett kan i viss mån förebyggas genom bärande av ljusa och svala kläder eller genom att applicera kräm eller salva från ett myggstift som håller myggorna borta (“repellenter” – spray eller gel). Repellenter innehåller bl a DEET (N,N-diethyl-meta-toluamide).
  • Symptomen efter myggbett kan lindras med kyla, t ex en ispackning eller kylbalsam. En mängd olika huskurer av varierande kvalitet finns beskrivna, t ex att applicera filmjölk eller lime på huden. För medicinsk behandling, se ovan.
  • Myggbett i Sverige ger mycket sällan upphov till farliga sjukdomar. Fall av myggburen tularemi (harpest) förekommer. Harpest orsakas av bakterien francisella tularensis. Också broms, fästingar och knott kan sprida denna bakterie. Harpest kan ge hög feber, illamående och huvudvärk. Ett smetigt sår uppträder efter myggbettet, lymfkörtlarna blir ömmande och förstorade. Infektionen behandlas med antibiotika, t ex doxycyklin eller streptomycin.
  • Ockelbosjukan, tidigare kallad bärplockarsjukan eller Pogostasjukan beror på ett virus kallat sindbisvirus som överförs med myggor. Symptomen utgörs av utslag, ledvärk, trötthet och feber. Symptomen är vanligtvis måttliga och övergående men ledvärk har i en del fall blivit långdraget. Sjukdomen är vanligast under sensommaren och tidig höst. Utslagen är finprickiga och värk har beskrivits från bl a händer och fötter.
  • Ingåvirus har främst förekommit i Finland. Sjukdomen beror på ett virus kallat bunayvirus som sprids med myggor.  Infektionen är vanligen subklinisk men kan gå med en meningitbild.
  • Under 2015 och 2016 utfärdades globala larm om det farliga Zikaviruset som kan överföras med myggor. Sjukdomen förekommer i Syd- och Centralamerika, Sydostasien samt Afrika. Allvarlighetsgraden beror på misstanke om allvarliga neurologiska anläggningsmissbildningar på foster om smittan överförs under tidig graviditet. Flera barn har fötts med mikrocephali. Själva sjukdomsförloppet har varit relativt godartat med milda influensaliknande besvär, ibland helt asymptomatiskt. Sjukdomen kan gå med ett makulopapulärt exantem, klåda, ledvärk, konjunktival injektion och lymfadenopati. Misstankar om kopplingar till fosterdöd, placentainsufficiens, tillväxthämning och Guillain-Barré finns också.
  • Flera andra sjukdomar kan spridas med myggor i exotiska länder, däribland kan nämnas malaria, West-Nilenvirus och visceral leishmaniasis. Malariamyggor förekommer även i Sverige men de är inte bärare av malariaparasiten.

Knott (svidknott, ”svidingar”)

  • Knott (Simuliidae) är en typ av små myggor (2-5 mm) med rundad höjd rygg och breda flugliknande vingar. Det finns omkring 35 olika arter i Sverige. Knott bits, därav trivialnamnet ”svidingar”. Bett av knott inträffar liksom myggbett främst på sommaren, framför allt i de nordligare delarna av Sverige och på högre höjd, såsom i fjällvärlden.
  • Knottangrepp ger ofta upphov till ett stort antal bett samtidigt.
  • Liksom mygg dras knott till varm och fuktig hud. Knottbett orsakar samma symtom som vanliga myggbett, även själva bettet kan smärta.
  • Undvik att fjällvandra med bara hudpartier, undvik kortärmat och kortbyxor. Behandlingen är densamma som för myggbett.


  • Broms/blinning är en typ av tvåvingad fluga som kan bita människor och suga blod. Observera att bromsar inte sticks utan bits. Blinning är ett trivialnamn som bygger på att flugan inte verkar se eller reagera när man försöker vifta bort den. Bromsar liknar flugor, men är vanligtvis något större och klumpigare. Bromsar flyger ljudlöst och överaskar med plötsliga nedslag på bara hudpartier. De irriterar framför allt hästar och kor som går ute i beteshagar, men biter även människor.
  • Det finns inga kemikalier som skyddar mot bromsar. Betten ger ofta upphov till ett större affekterat hudområde jämfört med myggbett. Rodnad med inslag av blödning (ekymoser) gör att det bildas ett blåmärke, vilket kan bli stort som en handflata. Blödningen beror på att bromsen injicerar koagulationshämmande enzymer i huden när den biter.
  • Behandlingen är i huvudsak symtomatisk med klådstillande krämer samt avkylande och desinficerande lösning, t ex alsolsprit.


  • Älgflugan är en 5-7 mm lång lusfluga (Lipoptena cervi) som kan bita människor. Normalt biter den och suger blod från älgar och andra pälsbärande hjortdjur. Flugan har kloliknande fötter som den håller sig fast med efter nedslag och som gör den svår att få bort. När den fastnat tappar den sina vingar, biter och suger blod. Älgflugan förekommer mest under sensommaren och tidig höst i skogsnära terräng.
  • Parfymer och andra dofter som karaktäriserar människor kan hålla älgflugan borta. Vid nedslag på människa kan det förekomma bett av ett tjugotal flugor samtidigt.
  • Betten ger upphov till klåda och svullnad. Normalt medför den inga sjukdomar men kan vara bärare av bakterier, t ex Bartonella schoenbuchensis.
  • Behandlingen är i huvudsak symtomatisk med klådstillande krämer samt avkylande och desinficerande lösning, t ex alsolsprit.


  • Det finns ca 42 000 kända arter av spindlar varav ca 600 i Sverige. De flesta är helt ofarliga för människor, men spindlar väcker ändå starkt obehag och rädsla hos en del. Vanliga spindlar i Sverige är husspindel, vargspindel, korsspindel, mörkrumsspindel, harlekinspindel, sektorspindel och fettspindel. Spindlarna varierar i storlek och färg, men känns igen på de åtta benen som sitter i fyra benpar.
  • Alla spindlar är rovdjur och kan följaktligen bitas, men bett på människor är sällsynt. Korsspindelns bett kan orsaka lokal rodnad och svullnad, men bettet är ofarligt och besvären är normalt snabbt övergående. En svagt giftig spindelart som förekommer i södra Sverige är luffarspindeln (Tegenaria agrestis). En spindel som kan ge mer obehag vid bett är den taggiga säckspindeln (Cheiracanthium punctorium); dess bett orsakar besvär ungefärligen i paritet med ett getingstick. Taggig säckspindel förekommer huvudsakligen på Öland.

Utländska spindlar

  • I andra delar av världen, främst i Afrika, Sydamerika och Australien, finns flera giftiga arter varav några t o m kan vara dödliga för människor.
  • Den mest kända giftspindeln är svarta änkan (Latrodectus mactans), där honan har en karaktäristiskt röd timglasformad fläck över ryggen. Svarta änkan bär på ett potent gift, latrotoxin. Dock injiceras så litet av giftet att effekterna på människa sällan är allvarliga, dödsfall förekommer men är mycket sällsynt. Bettet är smärtsamt och smärtan ökar i intensitet efter ett par dagar för att därefter klinga av. Svarta änkan förekommer framför allt i södra och mellersta USA, men släktingar till svarta änkan förekommer över stora delar av världen.
  • I Australien förekommer ett antal giftiga spindlar som kan orsaka allvarliga reaktioner på människa. Bland de farligaste är den rödryggade spindeln (Red back spider, Latrodectus hasselti), vilken är en typ av änkespindel som rör sig relativt långsamt. Den farligaste spindeln är Sydney Funnel Web Spider (Atrax robustus), vilken är en typ av trattminörspindel. Spindeln är relativt stor (ca 3 cm lång) och blir lätt aggressiv. Den gömmer sig gärna i skor! Spindeln är utrustad med två kraftiga käkar och kan injicera relativt mycket gift som kan vara farligt för människor. Serum för behandling av bett av den rödryggade spindeln och Sydney funnel web spider finns tillgängligt i Australien och ges till patienter som utvecklar allmänsymtom efter bett. Dödsfall förekommer sporadiskt bland människor, men är mycket sällsynt. Sedan serum utvecklades 1981 har inget dödsfall registrerats i Australien.

Bistick och getingstick

  • Det finns mer än 100 000 olika arter under ordningen steklar.
  • Bistick ger vanligtvis upphov till lokal smärta och svullnad som normalt klingar av och försvinner inom ett par dygn. Ett bistick är betydligt mer smärtsamt än ett myggbett. Bin och getingar sticker vanligen endast i självförsvar när de känner sig hotade.
  • Allergi mot bistick kan utvecklas i alla åldrar. Vanligtvis kommer allergin först efter flera harmlösa stick.
  • Barn blir oftast stungna mer än vuxna men systemiska reaktioner sker endast hos cirka 1 % av barnen. Ett fåtal personer reagerar kraftigare på dessa sting och kan utveckla allmänsymtom med allmän sjukdomskänsla, oro, ångest och andnöd.
  • Bin injicerar vanligen mer gift än getingen varför dess bett irriterar mer. Biets gadd har hullingar medan getingens saknar hullingar. Biets gadd fastnar därför lättare i huden. Försök att avlägsna kvarvarande gadd. Skrapa bort gadden utan att klämma ihop den.
  • Bistick kan orsaka anafylaktisk chock som kan bli livshotande. Även stick på känsliga ställen, såsom tunga och svalg, kan bli livshotande p g a svullnad och bör därför behandlas med kortison i.v. eller i.m. för att undvika andningshinder.
  • Ett okomplicerat bistick kan behandlas lokalt med avkylande ispackning eller kylomslag och därefter med klådstillande medel eller lokalanestetika, t ex en hydrokortison kräm eller Xylocain salva 5 % 10 gr
  • Perifer venkateter (PVK) sätts och vätska ges i form av kristalloid lösning vid allmänsymptom, t ex Ringer-Acetat 1000 ml.
  • Allmänreaktioner bör behandlas med antihistaminer och kortikosteroider.
  • Antihistamin, t ex T. Aerius (desloratidin) 10 mg munlöslig p.o. eller loratidin (Clarityn) 10 mg p.o.
  • Allvarlig anafylaktisk reaktion måste behandlas med adrenalin, epinefrin (t ex Epipen) 500/300/150 µg i.m. i lårets utsida. Till vuxen över 60 kg rekommenderas 500 µg i.m. Till vuxna och barn mellan 20 och 60 kg rekommenderas 300 µg i.m. Till barn som väger 10-20 kg rekommenderas 150 µg i.m. Beta-stimulerare (t ex salbutamol) ges i inhalation vid bronkobstruktivitet.
  • Anafylaxi behandlas och övervakas på sjukhus. Se även Anafylaxi – vuxna och Anafylaxi – barn.

Man bör undvika att attrahera bin och getingar genom att placera matvaror och sötsaker (särskilt saft) öppet i närheten av deras bon eller samhällen. Vid närvaro av bin eller getingar bör man undvika att vifta eller angripa insekterna då detta lockar till anfall. Vid angrepp av en hel svärm är flykt att föredra. Tobaksrök och annan rök innehållande kolmonoxid dämpar bins aktivitet påtagligt.


  • Fästingbett är vanligt förekommande efter barbent promenad i skogs- eller ängsmarker, särskilt i högt gräs. Den i Sverige förekommande fästingen (Ixodes ricinus) biter sig obemärkt fast i huden och växer sedan genom att suga blod, från några få mm till ca 10 mm i storlek.
  • Fästingbett ger vanligtvis inte upphov till särskilt stora besvär i sig, men kan överföra farliga sjukdomar, såsom Borrelia, Rickettsia, TBE (Tick-Borne Encephalitis) och Anaplasmos (Ehrlichia).
  • Fästingar kan bära på flera olika arter av patogena mikroorganismer.
  • Om man upptäcker en fästing på huden bör denna avlägsnas så snart som möjligt genom att fatta fästingen runt huvudet med en finspetsig pincett (eller med en särskild fästingpincett) och dra den rakt ut. Man bör försöka avlägsna alla insektsdelar. Att applicera fett runt fästingens huvud rekommenderas inte längre. Bettstället bör tvättas med tvål och vatten eller alsolsprit efter att fästingen avlägsnats.
  • Om en enstaka rodnad (erythema migrans) större än en femkrona uppkommer bör denna behandlas med antibiotika i form av fenoximetylpenicillin (PcV), t ex Kåvepenin (1 g x 3 i 10 dagar). Utsådd av rodnader bör behandlas med antibiotika med bättre penetration till CNS, t ex doxycyklin 200 mg x 1 i 10 dagar. Rodnader under en femkronas storlek behöver inte behandlas med antibiotika om inte allmänsymtom föreligger. Uppkommer symtom tydande på TBE bör patienten handläggas av infektionsläkare.

Borrelia (Lyme borrelios)

  • Borrelia orsakas av en grupp bakterier (borrelia burgdorferi) som sprids med fästingar. Fästingarna får ofta i sig bakterierna från infekterade smågnagare. Infektionen är ovanligare norr om Dalälven.
  • Inkubationstiden varierar från tre dygn upptill en månad. Ca 10 000 personer beräknas få borrelia varje år i Sverige. Störst risk föreligger i Sveriges södra och mellersta delar, samt längs med kuster och insjöar.
  • Merparten av de borreliadrabbade får endast lokalsymtom i form av rodnad och lättare svullnad kring bettstället. Rodnaden är oftast rundad och ringformad, men kan även vara asymmetrisk. Vanligen sprider rodnaden sig ringformat utåt från bettstället och bleknar centralt.
  • Borrelia bör behandlas med antibiotika i form av PcV eller tetracykliner (doxycyklin) i 10-21 dagar. Doxycyklin väljs om neurologiska symtom föreligger. Vaccin finns ännu inte att tillgå. Felaktig diagnostik av borrelia är vanligt.
  • Borrelia kan obehandlat orsaka encefalit med allvarliga symtom i form av allmän sjukdomskänsla, feber, vakenhetssänkning och kraftnedsättning.
  • Se separat behandlingsöversikt om borrelia.

TBE (Tick-Borne Encephalitis)

  • TBE orsakas av flavivirus som sprids med fästingar. Varje år rapporteras 150-200 fall i Sverige. TBE förekommer främst i södra och mellersta delarna av landet och är vanligast i de östra delarna kring Mälaren, i Uppland och Södermanland.
  • TBE yttrar sig som en encefalit med hög feber, svår huvudvärk, emellanåt med kramper och utveckling av perifer neuropati med domningar, parestesier och bortfallssymtom. Merparten av de drabbade blir helt återställda men ca 30 procent får långdragna eller bestående men med kronisk trötthet, svaghet och minnesstörningar.
  • Specifik behandling mot flavivirus saknas och behandlingen är i huvudsak symtomatisk.
  • TBE kan förebyggas genom vaccination. Vaccination rekommenderas till särskilda riskgrupper, t ex personer som bor permanent i högriskområden och personer som genom sina vanor ofta blir fästingbitna.
  • Se separat behandlingsöversikt om TBE.


  • Rickettsioser orsakas av bakterier som sprids med fästingar, klädlöss, loppor och kvalster. Rickettsior är små gramnegativa bakterier som förökar sig intracellulärt. Idag finns ett tjugotal kända rickettsior, varav två förekommer i Sverige. Av dessa är Rickettsia helvetica (som sprids med fästingar) den mer studerade. Dess betydelse som sjukdomsalstrare är inte helt klarlagd.
  • Symtomen utgörs av hög feber, huvudvärk, muskelvärk, svettningar, hudutslag, hörselbortfall och i svåra fall myokardit. Fall med dödlig utgång sekundärt till myokardit finns beskrivet.
  • Behandla med doxycyklin (T Doxyferm) 100 mg 2 x 1 i 10 dagar.
  • Se separat behandlingsöversikt om rickettsioser.



I Sverige orsakas manetsting vanligtvis av brännmaneter (Cyanea capillata), men även kompassmaneter (Chrysaora hysoscella) kan ge upphov till sting, ibland även rodnad och svullnad. Den röda brännmaneten är vanlig utmed västkusten från juni och framåt under sommarhalvåret. Symtomen vid sting av brännmanet utgörs av ihållande klåda och sveda. Maneter är nässeldjur och skadan orsakas av miljontals nematocyster i manetens bränntrådar.

Se separat behandlingsöversikt om bl a manetsting.

Behandling av manetsting

  • Skölj först av affekterade hudpartier med rikligt med havsvatten från en hink.
  • Undvik kontakt med sötvatten primärt, undvik att duscha.
  • Applicera en kylpackning över huden, t ex isbitar i en påse. Applicera inte is direkt på huden.
  • Undvik att gnida eller gnugga huden, t ex med en handduk.
  • Försök att ta bort kvarvarande manettrådar genom att skrapa huden med ett kreditkort eller raka huden med rakhyvel och raklödder.
  • Har en uttalad reaktion uppstått kan man pröva att sänka ner den angripna kroppsdelen i hett vatten (ca 45 grader) i ca 20-30 minuter.
  • Applicera en mild hydrokortisonkräm eller Xylocain salva 5 % 10 gr.


Bett av ormar orsakas i Sverige vanligtvis av huggormar under sommarhalvåret, främst i kustnära terräng. Bett av tropiska ormar är mer sällsynt, men förekommer när ormar hanteras ovarsamt i privata eller offentliga terrarier. Huggormsgift är nekrotiserande och hemorragiskt.

Se separat behandlingsöversikt om ormbett.


  • Smärta
  • Svullnad
  • Missfärgning (hemorragier)
  • Domningar
  • Förlamningar, paralys
  • Parestesier
  • Nekroser
  • Blödningar, ekymoser
  • Kompartmentsyndrom


  • Alla ormbitna patienter bör behandlas på sjukhus
  • Sätt minst en PVK. Ta Hb, LPK, trombocyter, PK/INR, APTT och urinsticka. Vid behov sätt dropp, t ex Ringer-acetat
  • Lägg in alla barn samt allmänpåverkade patienter på sjukhus i minst ett dygn.
  • Opåverkade patienter bör observeras i minst 6-8 timmar.
  • Kortison (t ex Solu-Cortef 100-200 mg x 1-3 i.v. eller i.m.). Vetenskapliga belägg är bristfälliga för behandling med steroider vid huggormsbett men utgör en väl beprövad rutin och rekommenderas främst vid allergiska symtom eller efter behandling med serum framställt på häst. Är sannolikt även av nytta vid påtaglig inflammatorisk reaktion.
  • Antihistaminpreparat (t ex Tavegyl 1 mg i.v. x 1-2).
  • Serumbehandling bör övervägas vid allmänsymtom. Serum är den viktigaste delen av behandlingen vid allvarliga ormbett. Bäst effekt uppnås inom fyra timmar efter bettet men det kan ges även senare vid allmänsymptom.
  • Immobilisering av biten kroppsdel, helst i högläge. Vid bett i handen häng upp armen högt i en mitella till en sängstolpe eller liknande.
  • Morfin/Ketogan (5-10 mg i.v.) vid smärtor.
  • Antitetanus. Tidigare rekommenderades att alla som inte vaccinerat sig på 5 år skulle få en antitetanus boosterdos. Denna rekommendation har väldigt svagt vetenskapligt stöd men bygger på att byten som ormen nyss tagit, typ sorkar kan bära på tetanusbakterier från underjordiska gångar (0,5 ml diTeBooster im x 1).
  • Vid allergiska/anafylaktiska reaktioner eller bronkospasm, ge adrenalin (1 mg/ml, 0,3-0,5 ml i.m. i lårets utsida) och kortison.
  • Vid cirkulatorisk chock kan 0,1-0,5 mg adrenalin ges i.v. – dosen titreras efter blodtrycket.
  • Ge adekvat vätskesubstitution, t ex Ringeracetat, eller Macrodex.
  • Om dextran inte ges bör annan trombosprofylax övervägas, t ex Fragmin i lågdos (2500-5000 enheter s.c.) alt Klexane 40 mg s.c. oavsett vikt.
  • Inotropt stöd och övrig chockbehandling ges på sedvanliga indikationer vid cirkulatorisk svikt, t ex infusion noradrenalin.
  • Syrgas på grimma eller via näskateter.
  • I allvarliga fall kontrollera Hb, LPK, TPK, CRP, myoglobin, PTK/APTT, S-haptoglobin, kreatinin, leverstatus, TNT och LD.


  • Icke giftigt insektsbett, ospecificerat T14.0D
  • Insektsbett, giftigt, UNS T63.4X
  • Toxisk effekt av gift från spindel T63.3
  • Getingstick, bistick T63.4A
  • Toxisk effekt av kontakt med andra marina djur T63.6
  • Toxisk effekt av ormgift T63.0


  1. Insektsgiftallergi – diagnostiken kan vara svår men bra behandling finns. Theo Gülen,
  2. Janne Björkander, Läkartidningen. 2016;113:D7CI
  3. P Brasil, et al. N Engl J Med. ZIKA virus. Epub 4 mar 2016 doi: 0.1056/NEJMoa1602412
  4. Moutailler S, et al. PLoS Negl Trop Dis. Epub 17 mar 2016. Doi: 10.1371/journal.pntd.0004539
  5. Dotevall L, Hagberg L. Successful oral doxycycline treatment of Lyme disease associated facial palsy and meningitis. Clin Infect Dis 1999:28;569-574.
  6. Hagberg L. Fästingburen Borreliainfektion. Läkartidningen 1995;92:8:729-731.
  7. Jaenson TG, Pålsson K, Borg-Karlson AK. Evaluation of extracts and oils of mosquito (Diptera: Culicidae) repellent plants from Sweden and Guinea-Bissau. J Med Entomol. 2006 Jan;43(1):113-9.
  8. Jensenius M, Fournier PE, Rauolt D. Rickettsiosis and international traveler. Clin Inf Disease 2004;15:39(10)1493-99.
  9. Karlsson et al. Comparison of intravenous penicillin G and oral doxycycline for treatment of Lyme neuroborrelios. Neurology 1993;43:169-175
  10. Karlson-Stiber C, Persson H, Heath A, Smith D, Al-Abdulla IH, Sjöström L. First clinical experiences with specific sheep Fab fragments in snake bite. Report of a multicenter study of Vibera berus envenoming. J Intern Med 1997; 241: 53-8.
  11. Persson H, Karlson-Stiber C. Huggormsbett – klinik och behandling. Läkartidningen 1995; 92: 2906-10.
  12. Reunala T, Brummer-Korvenkontio H, Karppinen A, Coulie P, Palosuo T. Treatment of mosquito bites with cetirizine. Clin Exp Allergy 1993; 23: 72-5.


Kai Knudsen

Anestesikliniken, Sahlgrenska Sjukhuset, Göteborg

Publicerat med tillstånd av Internetmedicin AB