Martin Možina

Acute poisoning with autumn crocus (Colchicum autumnale L.).

SummaryIntroductionColchicum autumnale, commonly known as the autumn crocus or meadow saffron, contains the antimitotic colchicine, which binds to tubulin and prevents it forming microtubules that are part of the cytoskeleton in all cells.Case reportA 71-year-old woman ate a plant she thought to be wild garlic (Allium ursinum). Ten hours later she arrived at the emergency department complaining of nausea, vomiting and watery diarrhea. Ingestion of a poisonous plant was suspected and she was treated with gastric lavage, oral activated charcoal and an infusion of normal saline. Toxicology analysis with gas chromatography and mass spectrometry revealed colchicine in the patient’s gastric lavage, blood (5 μ/l) and urine (30 μ/l). She developed arrhythmias, liver failure, pancreatitis, ileus, and bone marrow suppression with pancytopenia. Alopecia began in the third week. Treatment was supportive only. Five months later she had no clinical or laboratory signs of poisoning.DiscussionThe patient mistakenly ingested autumn crocus instead of wild garlic because of their great similarity. Colchicine primarily blocks mitosis in tissues with rapid cell turnover; this results in gastroenterocolitis in the first phase of colchicine poisoning, bone marrow hypoplasia with pancytopenia in the second and alopecia in the third, all of which were present in our patient. Colchicine toxicity in tissues without rapid cell turnover caused arrhythmias, acute liver failure and pancreatitis.ConclusionColchicine poisoning can result in gastroenterocolitis followed by multi-organ dysfunction syndrome. In unexplained gastroenterocolitis after ingestion of wild plants as a salad or spice, especially when wild garlic is mentioned, we should always consider autumn crocus. Diagnosis could be confirmed only by toxicology analyses. Management of colchicine poisoning is restricted to supportive therapy.

Prolonged psychosis after Amanita muscaria ingestion

ZusammenfassungAmanita muscaria ist ein Pilz mit einer leuchtend roten oder orangen Kappe mit kleinen weißen Flecken. Er enthält Isoxazol-Derivate, Ibotensäure, Muskimol und Muscazon und andere Toxine, wie etwa Muskarin. Die Dauer der klinischen Symptome nach dem Verzehr von Amanita muscaria ist üblicherweise nicht länger als 24 Stunden. Wir berichten über eine über fünf Tage anhaltende paranoide Psychose nach der Einnahme von Amanita muscaria. Ein 48-jähriger Mann mit völlig blander medizinischer Anamnese sammelte und aß Pilze, die er als Amanita caesarea agnostizierte. Eine halbe Stunde nach der Einnahme begann er zu erbrechen – anschließend schlief er ein. Er wurde komatös mit krampfartigen Zustand aufgefunden. Bei Eintreffen im Spital war er komatös – seine sonstige klinisch physikalische und neurologische Untersuchung ergab einen normalen Befund. Die Creatin-Kinase betrug 8,33 μkat/l. Die übrigen Laborbefunde und das Schädel-CT waren normal. Das toxikologische Screening ergab keinen Hinweis auf Medikamente im Blut und im Harn. Unser Pilzexperte identifizierte Amanita muscaria in den übrig gebliebenen Pilzen. Dem Patienten wurde aktivierte Tierkohle gegeben. 10 Stunden nach Einnahme des Pilzes erwachte er. Zu diesem Zeitpunkt schien er völlig orientiert. 18 Stunden nach der Einnahme verschlechterte sich der Zustand wieder; der Patient wurde verwirrt und zunehmend unkooperativ. Danach trat ein paranoid psychotisches Zustandsbild mit visuellen und akustischen Halluzinationen ein, welches fünf Tage lang anhielt. Ab dem sechsten Tag nach Einnahme begannen die psychotischen Symptome zu verschwinden. Ein Jahr später ist der Patient ohne jede Therapie und ohne Symptome psychiatrischer Erkrankung. Wir folgern daraus, dass eine paranoide Psychose mit visuellen und akustischen Halluzinationen noch 18 Stunden nach Einnahme von Amanita muscaria auftreten und bis zu fünf Tage lang anhalten kann.SummaryAmanita muscaria has a bright red or orange cap covered with small white plaques. It contains the isoxazole derivatives ibotenic acid, muscimol and muscazone and other toxins such as muscarine. The duration of clinical manifestations after A. muscaria ingestion does not usually exceed 24 hours; we report on a 5-day paranoid psychosis after A. muscaria ingestion. A 48-year-old man, with no previous medical history, gathered and ate mushrooms he presumed to be A. caesarea. Half an hour later he started to vomit and fell asleep. He was found comatose having a seizure-like episode. On admission four hours after ingestion he was comatose, but the remaining physical and neurological examinations were unremarkable. Creatine kinase was 8.33 μkat/l. Other laboratory results and brain CT scan were normal. Toxicology analysis did not find any drugs in his blood or urine. The mycologist identified A. muscaria among the remaining mushrooms. The patient was given activated charcoal. Ten hours after ingestion, he awoke and was completely orientated; 18 hours after ingestion his condition deteriorated again and he became confused and uncooperative. Afterwards paranoid psychosis with visual and auditory hallucinations appeared and persisted for five days. On the sixth day all symptoms of psychosis gradually disappeared. One year later he is not undergoing any therapy and has no symptoms of psychiatric disease. We conclude that paranoid psychosis with visual and auditory hallucinations can appear 18 hours after ingestion of A. muscaria and can last for up to five days.

The potential value of the protein S-100B level as a criterion for hyperbaric oxygen treatment and prognostic marker in carbon monoxide poisoned patients.

Carbon monoxide (CO) poisoning resulting in diffuse tissue hypoxia. Cerebral hypoxia is a major cause of morbidity and mortality after CO poisoning. There are some clinical criteria that could help a physician to make a decision concerning the application of hyperbaric oxygenation therapy. However, it would be convenient to discover an objective biochemical serum marker that could help in the grade evaluation of CO poisoning and indication of therapy in CO-poisoned patients. We present two case reports where the established criteria for the CO poisoning were not optimum for the decision regarding therapy. It seems that the S-100B protein could be used as a biochemical marker of CO induced brain injury. S-100B values could perhaps help us to select patients for hyperbaric oxygen therapy and to predict the short and long term outcome.

DRUG POISONING IN SLOVENIA

BACKGROUND The Slovenian Register of Intoxications managed by the Poison Control Centre at LjubljanaUniversity Medical Centre was established in 2001. It offers a continuous review ofpoisoning in Slovenia. Our aim was to study the epidemiology of acute drug poisoning inadult patients admitted to hospitals in Slovenia. METHODS We analyzed the data of reported acutely poisoned patients older than 16 years who weretreated in hospitals in Slovenia between 2001 and 2005. RESULTS A total of 1,838 adult acutely poisoned patients were reported to the Register of Intoxicationsbetween 2001 and 2005, of whom 1,234 (67 %) were poisoned by drugs. 67 % ofpatients poisoned by drugs were women and 76 % of patients ingested drugs at home 85 % of patients ingested drugs in suicide attempts. Anxyolytics, hypnotics, sedatives, antipsychoticsand antidepressants represented 68 % of all ingested drugs due to self-poisoning.Drugs for the musculo-skeletal system and drugs for the cardiovascular system followedpoisoning by these drugs. There were 6 benzodiazepines and related drugs betweenthe 10 most commonly ingested drugs due to self-poisoning. The most common signs ofacute drug poisoning were somnolence and coma (75 %). A gastric lavage was performedin 64 % of patients, active charcoal was given to 73 % of patients and 35 % of patients weretreated with an antidote. CONCLUSIONS Poisoning by drugs for the nervous system, particularly benzodiazepines, is the most commonform of poisoning by drugs in Slovenia. It would be necessary to report all acutelypoisoned patients to the Register of Intoxications, since we need data about all poisoningin Slovenia to improve their prophylaxis and treatment

First aid and emergency treatment after hydrofluoric acid splash

Introduction: Chemicals are used in all kinds of industry and one fifth of workers have dealt with dangerous chemicals. Hydrofluoric acid (HF) is one of the most dangerous inorganic acids; it is used in the electronics, chemical, glass, steel, car and oil industry. HF has a double action, being both corrosive and toxic due to the synergistic action of H+ and F- ions. On contact with the skin and eyes, HF causes severe chemical burns, which allow diffusion of F- into the tissues, and systemic toxicity with cardiac rhythm disturbances due to hypocalcemia. Conclusions: Chemical burns due to HF splashes can be prevented by wearing personal protective gear and immediate decontamination since HF penetration through the epidermis and cornea begins within the first minute. First aid by washing with water followed by topical application of calcium gluconate has several limitations and is unpredictable, while ocular and cutaneous washing with hexafluorine is very effective and can completely prevent chemical burns and systemic toxicity after HF splash.

Adverse drug reactions as a cause of admission to a medical emergency department

Background: Adverse drug reactions (ADRs) have been regarded as a major public health problem as they represent a sizable percentage of admissions to Emergency Departments (EDs). The aim of this study was to evaluate the frequency of admissions to medical EDs and hospitalizations due to ADRs detected by emergency physicians. Methods: The study team of internal medicine specialists reviewed retrospectively 1,000 randomly selected medical records out of 23,000 patients referred to ED of the primary city and tertiary hospitals for ADRs detected by emergency physicians during patient presentation in 2009. Results: The established frequency of ED admissions due to ADRs was 3.7 % of all patients (37/1000). Bradycardia due to verapamil, digoxin and beta-blockers was the most common ADR and represented 20 % of all ADRs. 0.7 % of all patients admitted to the ED (7/1000) were hospitalized due to ADRs caused by beta-blockers, digoxin, diuretics, NSAID, acetylsalicylic acid, clopidogrel and tamoxifen. Conclusion: ADRs cause 3.7 % of all admissions at the medical ED. 0.7 % of all patients admitted to the medical ED are hospitalized due to ADRs, which represents 2.2 % of patients hospitalized through the medical ED at internal medicine departments (7/320).

POISONING WITH GAMMA-HYDROXYBUTYRATE, GAMMA-BUTYROLACTONE AND 1.4-BUTANDIOL

Background. Gamma-hydroxybutyrate (GHB) is a popular recreational drug. GHB overdose typically presents with decreased level of consciousness, miosis, bradycardia, respiratory depression and death. Typically, combativeness, confusion and vomiting occur once the patient begins to recover. Gamma-butyrolactone (GBL) and 1.4-butandiol (1.4-BD) are the prodrugs of GHB and have similar clinical presentation. We present the case of GHB poisoning in Ljubljana. Conclusions. Physicians should suspect GHB poisoning in young ravers who present with CNS depression. Treatment is symptomatic. There is no specific antidote. Gastric lavage is not beneficial but activated charcoal is recommended.