[Circulatory failure after bupropion overdose]. / Allt fler allvarliga förgiftningar med preparatet bupropion.

A case of massive overdose of sustained release bupropion tablets is described. The patient presented with GCS 3, tachycardic and in vasoplegic shock. ECHO and EKG were initially normal. The hemodynamic situation was stabilised with vasopressors, but 18 h after presentation the patient deteriorated with wide complex arrhythmias rapidly progressing to cardiac arrest. The patient was put on VA-ECMO after 35 minutes of CPR. Circulation could be stabilized and ECMO was discontinued after 36 h. The patient was extubated on day 6 and made a complete recovery on discharge two weeks after presentation. At 34h, with ongoing ECMO, 236 tablets (with visible print identifying them as bupropion) were evacuated from the patient's stomach by gastroscopy. The tablets were analysed by NMR (nuclear magnetic resonance) but no longer contained any active substance. Blood levels of bupropion and hydroxybupropion at 36h were 790 and 1300 µg/l. The case illustrates a worrying surge in serious bupropion poisonings as noted by the Swedish Poisons Information Centre during the last 5 years.

Symptoms and signs in interpreting gamma-hydroxybutyrate (GHB) intoxication - an explorative study.

BACKGROUND: Acute poisoning with gamma-hydroxybutyrate (GHB) has been a serious medical and social problem in different parts of the world including Sweden. GHB is a drug of abuse which acts primarily as central nervous system (CNS) depressants. GHB has serious toxicity, although many young users do not recognise GHB as a dangerous drug. The aim of this pilot study was to explore how symptoms with risk of failure in vital functions would be valued among professionals that encounter GHB intoxication in the emergency phase. METHODS: A web-based survey focusing on the assessment of vital clinical signs for possible GHB intoxication using a numeric scale was carried out during April and May 2011. The participants, n 105, are all professionals who encounter GHB intoxicated in the emergency phase, but have different levels of training in GHB intoxication, mainly Registered Nurses (RNs) in southwest Sweden, employed in pre-hospital or emergency departments at somatic and most psychiatric health care facilities, as well as police officers who in their work come into contact with drug users. Responses in the survey were scored according to risk of GHB intoxication with serious failure of vital functions. The score value was then referred to a so-called evidence based priority (EBP) scale and analysed using descriptive statistics and Fisher's exact test. RESULTS: Cardiac arrest, coma, hypoxia, general convulsions, slow respiratory and heart rate and pale skin are symptoms with the highest risk of serious failure in vital physical functions and were predominantly recognised as such. CONCLUSION: Despite the professionals' different levels of training in GHB intoxication, all of them were relatively well aware of and in accordance regarding the most risky symptoms. The interpretation score for the less risky symptoms and signs of GHB intoxication varied depending on their degree of training. The results should be viewed cautiously, as the size of the professional groups and their general knowledge of critical symptoms of GHB poisoning varied.

Use of intravenous lipid emulsion in the resuscitation of a patient with cardiovascular collapse after a severe overdose of quetiapine.

BACKGROUND: Quetiapine is an atypical antipsychotic medication that is increasingly being used in the treatment of psychotic disorders and depression. An overdose of quetiapine is associated with hypotension, sinus tachycardia, and sedation. The clinical effects of its overdose are often mild to moderate, but a severe overdose can cause cardiovascular collapse and death.Intravenous lipid emulsion (ILE) is a proposed treatment for potentially lethal cardiotoxicity after severe overdoses with lipophilic drugs, such as quetiapine, mainly by the sequestration of the lipophilic toxin to an expanded intravascular lipid phase. OBJECTIVES: To report a case where ILE was successfully used in the resuscitation of a patient with cardiovascular collapse after a severe quetiapine overdose. CASE REPORT: A 42-year-old woman was admitted to the Emergency Department after being found unconscious at home, due to an estimated ingestion of 24 g of quetiapine (Seroquel). She was initially cardiorespiratory stable and unresponsive with a Glasgow Coma Scale of 3. The woman was immediately admitted to the Intensive Care Unit, where her condition quickly deteriorated. She was intubated, due to loss of airway. In addition, a gastric lavage was performed and activated charcoal was administered. The patient presented with cardiovascular collapse refractory to vasopressor treatment and volume resuscitation. ILE bolus followed by continuous infusion was administered. Her blood pressure started increasing 5 min after ILE was initiated and within an hour circulation was stabilized. The patient recovered completely without any residual symptoms, after 3 days in the ICU. CONCLUSIONS: ILE may potentially be life-saving in cases of severe quetiapine poisoning and should be considered as a treatment for severe cardiovascular instability resulting from quetiapine poisoning refractory to maximum conventional therapy.

Parallel haemodialysis and surgery saves a life after massive overdose of potassium pills.

Severe poisoning with potassium pills is rare but patients may present with serious cardiovascular symptoms requiring immediate and effective treatment. A 30-year-old healthy woman presented to the emergency department after ingestion of 300 slow-release pills of potassium-chloride with serum potassium of 9.5 mmol/l, and poor cardiovascular function. Gastric lavage was performed with poor outcome. Despite intensive medical treatment serum potassium remained very high around 9 mmol/l. Haemodialysis was initiated but despite ongoing dialysis, potassium increased to 10.3 mmol/l. Hence, a parallel dialysis was started and after 4 h of parallel dialysis, serum potassium decreased to 6.4 mmol/l. An x-ray revealed large amounts of pills remaining in the stomach and the surgeon was able to remove about 200 pills through an acute laparotomy. The patient recovered slowly thereafter, but later developed a gastric stricture and pulmonary embolism.

The clinical toxicology of γ-hydroxybutyrate, γ-butyrolactone and 1,4-butanediol.

INTRODUCTION: Gamma-hydroxybutyrate (GHB) and its precursors, gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-BD), are drugs of abuse which act primarily as central nervous system (CNS) depressants. In recent years, the rising recreational use of these drugs has led to an increasing burden upon health care providers. Understanding their toxicity is therefore essential for the successful management of intoxicated patients. We review the epidemiology, mechanisms of toxicity, toxicokinetics, clinical features, diagnosis, and management of poisoning due to GHB and its analogs and discuss the features and management of GHB withdrawal. METHODS: OVID MEDLINE and ISI Web of Science databases were searched using the terms "GHB," "gamma-hydroxybutyrate," "gamma-hydroxybutyric acid," "4-hydroxybutanoic acid," "sodium oxybate," "gamma-butyrolactone," "GBL," "1,4-butanediol," and "1,4-BD" alone and in combination with the keywords "pharmacokinetics," "kinetics," "poisoning," "poison," "toxicity," "ingestion," "adverse effects," "overdose," and "intoxication." In addition, bibliographies of identified articles were screened for additional relevant studies including nonindexed reports. Non-peer-reviewed sources were also included: books, relevant newspaper reports, and applicable Internet resources. These searches produced 2059 nonduplicate citations of which 219 were considered relevant. EPIDEMIOLOGY: There is limited information regarding statistical trends on world-wide use of GHB and its analogs. European data suggests that the use of GHB is generally low; however, there is some evidence of higher use among some sub-populations, settings, and geographical areas. In the United States of America, poison control center data have shown that enquiries regarding GHB have decreased between 2002 and 2010 suggesting a decline in use over this timeframe. MECHANISMS OF ACTION: GHB is an endogenous neurotransmitter synthesized from glutamate with a high affinity for GHB-receptors, present on both on pre- and postsynaptic neurons, thereby inhibiting GABA release. In overdose, GHB acts both directly as a partial GABA(b) receptor agonist and indirectly through its metabolism to form GABA. TOXICOKINETICS: GHB is rapidly absorbed by the oral route with peak blood concentrations typically occurring within 1 hour. It has a relatively small volume of distribution and is rapidly distributed across the blood-brain barrier. GHB is metabolized primarily in the liver and is eliminated rapidly with a reported 20-60 minute half-life. The majority of a dose is eliminated completely within 4-8 hours. The related chemicals, 1,4-butanediol and gamma butyrolactone, are metabolized endogenously to GHB. CLINICAL FEATURES OF POISONING: GHB produces CNS and respiratory depression of relatively short duration. Other commonly reported features include gastrointestinal upset, bradycardia, myoclonus, and hypothermia. Fatalities have been reported. MANAGEMENT OF POISONING: Supportive care is the mainstay of management with primary emphasis on respiratory and cardiovascular support. Airway protection, intubation, and/or assisted ventilation may be indicated for severe respiratory depression. Gastrointestinal decontamination is unlikely to be beneficial. Pharmacological intervention is rarely required for bradycardia; however, atropine administration may occasionally be warranted. WITHDRAWAL SYNDROME: Abstinence after chronic use may result in a withdrawal syndrome, which may persist for days in severe cases. Features include auditory and visual hallucinations, tremors, tachycardia, hypertension, sweating, anxiety, agitation, paranoia, insomnia, disorientation, confusion, and aggression/combativeness. Benzodiazepine administration appears to be the treatment of choice, with barbiturates, baclofen, or propofol as second line management options. CONCLUSIONS: GHB poisoning can cause potentially life-threatening CNS and respiratory depression, requiring appropriate, symptom-directed supportive care to ensure complete recovery. Withdrawal from GHB may continue for up to 21 days and can be life-threatening, though treatment with benzodiazepines is usually effective.

Severe overdose of quetiapine treated successfully with extracorporeal life support.

BACKGROUND: Quetiapine is a second-generation antipsychotic drug, used mainly in the treatment of psychotic disorders. Overdose is associated with sedation, tachycardia and a prolonged QT-interval on the ECG. Cardiovascular symptoms are uncommon but in severe cases profound cardiovascular depression may occur. OBJECTIVES: To report a case where extracorporeal circulatory support (ECCS) was used successfully in severe quetiapine overdose. CASE REPORT: A 40-year-old woman was admitted to the emergency department (ED) with reduced consciousness apparently due to intoxication. She had a history of schizophrenia and was treated with 900 mg of quetiapine daily. In the ED, she presented with immeasurable low blood pressure, irregular bradycardia, hypothermia and a Glasgow Coma Scale (GCS) of 8. An immunoassay test for tricyclic antidepressive agents (TCA) was positive. Despite resuscitation with intravenous fluids, intensive vasopressor treatment and renal replacement therapy (CRRT) the patient's condition deteriorated. The patient was quickly moved to an intensive care unit where ECCS could be instituted. The patient subsequently recovered after 4 days in the ICU without any residual symptoms. Further laboratory analysis did not confirm the immunoassay finding. CONCLUSIONS: Severe poisoning with quetiapine may imitate tricyclic antidepressant poisoning, and drug screening methods may be falsely positive for TCA. In case of cardiovascular collapse due to quetiapine overdose, ECCS may be life saving.

A case of life-threatening rectal administration of moist snuff.

CASE REPORT: We report a case of self-administration of 75 sachets of moist snuff rectally in a previously healthy, 42-year-old man. He presented with symptoms of nausea, discomfort, and dizziness. He had dry and warm skin, a pulse rate of 53 bpm, a mean arterial blood pressure of 135 mmHg and fluctuations in consciousness. The patient was treated with mechanical ventilation because of respiratory insufficiency. No specific anti-nicotinergic treatment was given. Plasma levels of the nicotine metabolite cotinine were 8,691 µg/L 7 h after admittance and 9,814 µg/L after 12 h. Levels of cotinine in the urine were above >50,000 µg/L. The patient developed a mild pneumonia, but he was uneventfully extubated after 12 h of mechanical ventilation. All physiological parameters were restored and he was discharged from hospital after 36 h. CONCLUSION: Excessive rectal administration of moist snuff may be life threatening. Patients may require intensive care. Long-term sequelae were not seen in this case.

High mortality rates among GHB abusers in Western Sweden.

BACKGROUND: GHB is a drug of abuse and acute poisonings have been an increasing medical problem over the last decade in Sweden. OBJECTIVES: To document all cases of GHB poisonings in Gothenburg during 1995-2004 and to record drug-related deaths to compare the toxicity of GHB with other illicit drugs, such as heroin and amphetamine. METHODS: The number of GHB-poisoned patients treated at the Sahlgrenska University Hospital has been recorded with the help of an in-house database. The number of deaths by illicit drugs was recorded during 2004. Seizures of the drugs GHB, 1,4-butanediol, and GBL were registered between 1996 and 2004. RESULTS: The number of poisoned patients was 259. The number of seizures with GHB was 743, GBL 343, and 1,4-butanediol 236. In 2004 the number of deaths was 6 with heroin, 7 with GHB, 32 with amphetamine, 6 with cocaine, and one with methadone. One patient with GHB poisoning died during hospital care. CONCLUSIONS: Intoxication by GHB has substantial morbidity and abuse of GHB has substantial mortality. The acute prognosis is good but long-term prognosis is insecure with an increased risk for drug dependency and an early death.

[GHB, GBL and butanediol poisonings--a serious problem in Western Sweden]. / GHB-, GBL- och butandiolförgiftningar--ett allvarligt problem i Västsverige.

Acute poisoning with GHB (Gamma-hydroxybutyrate, Gamma-hydroxybutyric acid) has been an increasing medical and social problem during the last decade in Sweden, especially on the west coast. The number of poisonings decreased in the beginning of this millennium but has again increased during the last years. At the same time the number of seizures by the police has increased similarly as well as the number of drug-related deaths. During 2004 the number of GHB-abuse related deaths in western Sweden was seven, approximately the same figures as for heroin. Two other substances which are transformed to GHB in the human body, GBL (gamma-butyrolactone) and 1,4-butanediol, have during the last years presented themselves among the same users as for GHB. Since GBL and butanediol are not classified as illicit drugs the possibilities for the police force to intervene and capture the drugs are severely restricted. Intoxication by GBL and butanediol has shown to be as dangerous as intoxication by GHB. Acute intoxications and abuse of these drugs is still a serious medical and social problem. A legal classification of GBL and butanediol as narcotics appears to be medically motivated.