Carbon monoxide poisoning in wood pellet storerooms.

Background: Carbon monoxide is the leading cause of mortality from unintentional poisoning in Slovenia. It has been shown that carbon monoxide levels can rise in wood pellet storerooms because of chemical degradation of pellets, even at room temperature. We present a case of lethal carbon monoxide poisoning with first responder carbon monoxide exposure. Aims: To highlight the dangers rescuers face during interventions in pellet storerooms and the need for preventive precautions. Case report: Paramedics and firemen were called to help an unconscious man in a wood pellet storeroom. Firemen immediately evacuated the victim and paramedics began cardiopulmonary resuscitation. Soon after, rescuers complained of dizziness and developed headache, nausea and fatigue. A carbon monoxide level of 600 ppm was detected. Three rescuers were treated with 100% oxygen. Blood carboxyhaemoglobin levels were up to 8% on arrival at the emergency department. The victim died and autopsy confirmed carbon monoxide poisoning. Conclusions: First responders have to be aware of the dangers of carbon monoxide in wood pellet storerooms. Basic precautions and safety instructions should be followed before entering a wood pellet storeroom. Carbon monoxide should be measured before entering and self-contained breathing apparatus should be used. Wood pellet storerooms require continuous ventilation and should be equipped with carbon monoxide detectors.

Chlorobenzylidene malononitrile tear gas exposure: Rinsing with amphoteric, hypertonic, and chelating solution.

OBJECTIVE: Chlorobenzylidene malononitrile (CS) is the tear gas used by the police. The aim was to evaluate an amphoteric, hypertonic, and chelating rinsing solution in CS exposure. METHODS: The first (CS) group of six police officers was exposed to CS only. The second (preexposure) group of eight sprayed their faces with an aqueous, hypertonic, amphoteric, and chelating solution before CS exposure. The third (postexposure) group of eight sprayed their faces with an aqueous, hypertonic, amphoteric, and chelating solution after CS exposure. The time between exiting the CS cloud and arriving at the "ready for action" checkpoint was measured. Their facial pain both inside the CS cloud and at the checkpoint was assessed (0-10 points). RESULTS: The pain level inside the CS cloud was significantly lower in the preexposed group (5.6 ± 1.1; p = 0.01) than in the CS group (9.7 ± 0.5) and in the postexposure group (9.1 ± 0.4) where it was similar. The time interval between CS exposure and arrival at the checkpoint in the preexposure group (1:26 ± 0:44 min) was significantly shorter than both in the CS group (2:28 ± 0:25 min; p = 0.04) and postexposure group (2:30 ± 0:48 min; p = 0.02) where it was not different. The residual pain at the checkpoint in the preexposure (1.1 ± 0.4) and postexposure (1.4 ± 0.7) groups was similar with a significant lower pain level than in the CS group (2.3 ± 0.5; p = 0.02). CONCLUSION: CS decontamination with an aqueous, hypertonic, amphoteric, and chelating solution reduces facial pain, whereas prevention with it reduces pain and recovery time.

S100B protein in benzodiazepine overdose.

BACKGROUND: Severe benzodiazepine overdose can result in coma and respiratory depression that might cause brain hypoxia, necrosis and delayed post-anoxic leucoencephalopathy with permanent neurological sequelae. The aim of this study was to assess the possible role of S100B, a structural protein of astroglial cells, as a biochemical marker of brain injury in acute benzodiazepine overdose. METHODS: Serum S100B determination was performed in 38 consecutive patients admitted to the emergency department (ED) in Ljubljana with benzodiazepine overdose. The level of consciousness and respiratory insufficiency on the scene were assessed by responsiveness to a verbal stimulus and pulse oximetry. Blood samples were taken immediately after arrival at the ED and S100B concentrations were measured with a commercial immunoluminometric assay. 20 healthy sex- and age-matched volunteers formed a control group. RESULTS: There were significant differences in S100B levels between the control group and the patients with benzodiazepine overdose according to their responsiveness to a verbal stimulus. Post hoc test results showed that S100B levels in patients with benzodiazepine overdose who were unresponsive to a verbal stimulus were significantly higher than those in patients responsive to a verbal stimulus (median 0.31 vs 0.11 microg/l; p = 0.001). Both groups of patients with benzodiazepine overdose had significantly higher S100B levels than the control group (median 0.07 microg/; both p = 0.001). Arterial oxygen saturation of patients with benzodiazepine overdose unresponsive to a verbal stimulus was significantly lower than in patients responsive to a verbal stimulus (median 83% vs 94%; p = 0.001). There was no significant difference in the systolic blood pressure of patients with benzodiazepine overdose responsive or unresponsive to a verbal stimulus. CONCLUSION: Raised levels of S100B protein are associated with depressed levels of consciousness and respiratory insufficiency in patients with benzodiazepine overdose.

Poisoning with 1-propanol and 2-propanol.

1-Propanol and 2-propanol are isomers of an alcohol with three carbons. They are colorless liquids with a sweet odor. 1-Propanol is metabolized by alcohol dehydrogenase to propionic acid and presents with metabolic acidosis and elevated anion gap, whereas 2-propanol is metabolized by alcohol dehydrogenase to acetone and presents with rapidly developing (within 3-4 h after exposure) ketosis and ketonuria but without metabolic acidosis. We report a patient who simultaneously ingested a lethal dose of 1-propanol and 2-propanol as a hand disinfectant in hospital. The patient lost consciousness and stopped breathing within half an hour after ingestion. He was intubated and artificially ventilated. Initial laboratory results showed mixed acidosis with elevated anion gap, but ketonuria appeared only 12 h after admission and 6 h following the regaining of consciousness. Therefore, laboratory results in simultaneous poisoning with two isomers of alcohol are not just a sum of laboratory results obtained in isolated poisoning with each isomer because they influence each other's metabolism: 1-propanol retards the metabolism of 2-propanol to acetone. In conclusion, 1-propanol and 2-propanol poisoning presents early with mixed acidosis and elevated anion gap and only later with ketonuria.

Butanol ingestion in an airport hangar.

1-Butanol is a colourless organic solvent with a rancid sweet odour. 1-Butanol ingestion may result in vomiting, abdominal pain, headache, drowsiness and unconsciousness. We present a 47-year-old male with no previous medical history, who was found comatose and soiled after having vomited while unconscious. On arrival, he had a Glasgow coma scale of 3, tachycardia, hypotension, shallow tachypnoic breathing, hypotonic muscles, absent myotatic reflexes and aromatic odour. The patient was intubated and treated with oxygen, dopamine and volume replacement therapy. Gastric lavage was performed and activated charcoal was given. His initial laboratory test revealed hypokaliemia, renal failure, acidosis with elevated lactate and hypercapnic respiratory insufficiency. Twelve hours after admission, the patient started to respond to a painful stimulus and 4 h later he was conscious. He was extubated 23 h after admission. All pathological laboratory results gradually returned within normal limits. The subsequent toxicological examination of gastric content and urine sample by gas chromatography revealed 1-butanol. On awakening, he confirmed ingestion of a solvent stored in an airport hangar. In conclusion, we describe a patient who ingested - a posteriori with suicidal intention - an unknown dose of 1-butanol. Symptoms were headache, vomiting, abdominal pain, coma, muscular hypotonus, hypotension, respiratory insufficiency and mixed acidosis. The patient totally recovered after supportive therapy over 30 h. In future cases, intravenous administration of ethanol or even hemodialysis can be considered analogous to the treatment of methanol and ethylene glycol poisoning.