Poisonings in Laboratory Personnel and Health Care Professionals LOUIS BINDER, MD, LAUREN FREDRICKSON, A case report of an unresponsive chemist presenting to the emergency department is presented; in retrospect, the patient was discovered to have intentionally ingested cyanide. A review of literature regarding ingestions in laboratory and health care personnel weals five common points encountered in these personnel: barbiturates, carbon monoxide, cyanide, azides, and methemoglobin-inducing chemicals. Key diagnostic findings, in the absence of history of exposure, are discussed for these five agents. (Am J Emerg Med lggl;g:ll-15. Copyright 0 1991 by W.S. Saunders Company)

Intentional poisonings occurring in laboratory personnel and health care workers who have access to, and are presumably knowledgeable about, drug effects, toxicities, and potential lethality of various agents, would logically be expected to differ qualitatively from poisonings encountered in laypersons. Data from the 1987 American Association of Poison Control Centers Annual Report’ indicate the most frequently ingested substances in the United States lay population to be cleaning substances, analgesics, and cosmetics. However, review of selected literature suggests a different distribution of poisonings for educated laboratory and health care professionals.2V1’ Ony scant information is available to address the qualitative distribution of poisonings in knowledgeable personnel; this information is potentially useful to the emergency physician faced with a presentation of “unknown poisoning” or “found unresponsive” in such patients. We report such a case of an unresponsive chemist who presented to our institution, along with a review of the available literature on poisonings in laboratory and health care workers.

CASE REPORT A 34-year-old Latin American female chemist employed at the local water plant was found by coworkers “slumped over” and unresponsive at her desk. She was estimated to have been found following 10 minutes of unresponsiveness. No history of antecedent symptoms, trauma, prior medical problems, depression, or suspected ingestion could be elicited from co-workers by the paramedics. She took no medications, and had no allergies. Prehospital care consisted of immobilization, 50 grams dextrose and narcan 0.8 mg intravenously (with no response), and assisted respirations with an

From the Division of Emergency Medicine, Texas Tech University RAHC-El Paso, El Paso, TX. Manuscript received September 11, 1989; revision accepted April 1, 1990. Address reprint requests to Dr Binder: Division of Emergency Medicine, Texas Tech University RAHC-El Paso, 4800 Alberta Ave, El Paso, TX 79905. Key Words: Barbiturate poisoning, carbon monoxide poisoning, cyanide poisoning, methemoglobinemia, suicide in laboratory personnel, suicide in health care personnel. Copyright 0 1991 by W.B. Saunders Company 0735-6757/91/0901-0003$5.00/O

MD

ambu bag (rate lO/min). Additionally, emergency medical service (EMS) personnel provided a list of solvents available in the patient’s laboratory (Table 1) as possible intoxicants. Physical examination showed an unresponsive Latin American woman who was fully immobilized. Vital signs were blood pressure 100160mm Hg, pulse rate 113 beats/min, respirations 4 breaths/min (assisted by paramedics on supplemental oxygen at lO/min), and temperature 99.0”. On arrival to the resuscitation suite, she sustained a respiratory arrest, requiring oral endotracheal intubation with in-line traction and controlled ventilation. Heart, ears, eyes, nose, and throat (HEENT) examination was remarkable for a 2-cm superficial laceration of the left brow with surrounding hematoma. Neurologic examination showed unresponsiveness to verbal and painful stimuli, pupils were 4 millimeters and sluggish bilaterally, comeal and gag reflexes were intact, and extremities were flaccid bilaterally without posturing; the patient was normoreflexic and equal bilaterally with plantar Babinski responses bilaterally. The remainder of the HEENT, neck, cardiac, pulmonary, abdominal, urogenital and musculoskeletal examination were within normal limits. Laboratory and radiographic data showed a white blood count of 17,200/mm3, with 49 polys/47 lymphs/3 monos/l eosinophil; hemoglobin, 13.9 gm/dL; hematocrit, 42.5%; platelet count, 321$00/mm’; sodium was 136 mEq/L; potassium, 3.7 mEq/L; chloride, 99 mEq/L; bicarbonate, 7 mEq/L; glucose 650, mg/dL (following dextrose administration); blood urea nitrogen 9 mg/dL; and creatinine level, 1.4 mg/dL. Prothrombin time was 16.0 seconds and partial thromboplastin time was 26.6 seconds; urinalysis was within normal limits. A portable chest roentgenogram following intubation showed satisfactory endotracheal tube placement, clear lung fields, and a normal cardiac silhouette and mediastinum. Cervical spine series showed no fracture, dislocations, or bony abnormalities. Initial arterial blood gases (ABGs) on 10 liters of oxygen per ambu bag prior to intubation showed PoZ; 63 mm Hg; Pco,, 32 mm Hg; pH, 7.03; bicarbonate, 8.4 mEq/L; 0, saturation, 79%; and carboxyhemoglobin, 2.2%. Second, ABGs following intubation, placement on a ventilator with 100% FiO,, and 1 ampule of sodium bicarbonate intravenously showed PO,, 517 mm Hg; Pco,, 32 mm Hg; pH, 7.07; bicarbonate, 9.4 mEq/L, and 0, saturation 98%. Electrocardiogram and rhythm strip showed a sinus tachycardia of 115 beats/min with no other abnormalities. Serum osmolality was 305 mOsm/kg, serum ketone results were negative, serum ammonia was 48 ymol/L (11 to 35), and serum lactate was 15.3 mmoVL (1.4 to 3.9). A urine toxicology screen for barbiturates, benzodiazepines, antidepressants, amphetamines, cannabinoids, and cocaine was negative. A computed tomography (CT) scan of the head, with and without contrast, was also within normal limits. A large bore nasogastric tube was passed with clear return and no evidence of pill fragments; no unusual odors were noted to the aspirate. The patient’s emergency department diagnosis was respiratory arrest and lactic acidosis of unclear etiology. She remained hemodynamically and neurologically stable both while in the emergency department and in radiology; therapeutic intervention was limited to endotracheal intubation and sodium bicarbonate intravenously. The medicine service was contacted, and the patient was admitted to the medical intensive care unit (MICU). En route to the MICU, the patient began to move spontaneously, and shortly regained consciousness. Repeat ABGs on intermittent mandatory ventilation with 80% FiOZ, 4 hours following admission, were PO,, 420 mm Hg; 11

AMERICAN JOURNAL OF EMERGENCY MEDICINE m Volume 9, Number 1 m January 1991

12

TABLE1.

PotentialSolvent Exposuresand Intoxicants

Sodium hydroxide Sulfuric acid Hydrochloric acid Ethanol

Ammonium molybdenum phosphate Calcium disodium edetate (EDTA) Methanol Nitric acid

Pco,, 30 mm Hg; pH, 7.31; bicarbonate, IS mEq/L; and Oz saturation, 96%; she was subsequently extubated without difficulty. On further questioning, the patient confessed to the ingestion of cyanide powder from her laboratory in a suicide attempt. She remained medically stable throughout her hospital course, and psychiatric consultation was obtained. After 2 days, the patient was discharged to her family and the care of a private psychiatrist. Physical and neurologic examinations at the time of discharge was entirely normal. As no blood was subsequently available from the initial laboratory evaluation, a blood cyanide level was subsequently obtained immediately before discharge; no cyanide was detected in this specimen. Follow-up visitation to the patient’s workplace showed the availability of both potassium cyanide and sodium cyanide, but these chemicals could not be definitively confirmed by coworkers as the ingestant. No other agents were available that would explain either the metabolic acidosis or decreased level of consciousness on initial presentation.

DISCUSSION When faced with an unresponsive or “unknown poisoning” picture in knowledgeable personnel, what poisons should be considered and how might they be recognized in the absence of a history of ingestion? No large series are available that investigate the quantitative distribution of poisonings in knowledgeable personnel. Review of available literature suggests five common poisons encountered in laboratory personnel and health care workers: barbiturates, carbon monoxide, cyanide and its derivatives, azides, and methemoglobin-inducing chemicals. However, laboratory and medical personnel, like laypersons, will often ingest, or succumb to exposure from, whatever is available to them;‘* thus a list of laboratory reagents or pharmaceuticals available to the victim, provided by EMS or coworkers, may be extremely useful to the evaluating physician. In an older series, barbiturates were implicated as the cause of physician suicide in 139 of 203 cases of physician poisoning.‘3 Barbiturate poisoning was more common 10 to 20 years ago when the use of these drugs as tranquilizers was more widespread, but the frequency of barbiturate ingestions has decreased with the advent of numerous other tranquilizers and sedatives, and with the rescheduling of these drugs as controlled substances. They are still commonly used for anticonvulsant therapy and for the induction of anesthesia.14 Thus health care personnel might logically have access to barbiturates as a suicidal poison. Their major site of action is the central nervous system (CNS), where they enhance the action of the inhibitory neurotransmitter y-amino butyric acid (GABA),‘s,‘6 and further act as depressants to metabolism nerve tissue and muscle tissue. Clinically barbiturate toxicity presents with progressive CNS depression, respiratory depression, flaccid muscle tone, pinpoint pupils, bradycardia, hypotension, and hypothermia; the clinical picture is one of profound metabolic depression, consistent with the pharmacology of the drug.14 In the absence of history of barbiturate exposure, the diagnosis may

be difficult, and confused with narcotic overdose or other sedative-hypnotic ingestions, alcohol intoxication, severe CNS insult or herniation, hypothyroidism or myxedema coma, hypothermia, hypoglycemia, hypoxia, or other metabolic encephalopathy (ie, hepatic or uremic).” Diagnosis, in the absence of history of exposure, is supported by a high clinical index of suspicion in the presence of a characteristic clinical presentation in knowledgeable personnel, the presence of pill fragments on gastric lavage, and the exclusion of other potential diagnoses through metabolic work-up and cerebral CT scanning. Confirmation is achieved with an elevated quantitative serum barbiturate concentration, or by rapid turn-around time toxicologic screening. Carbon monoxide poisoning likewise has been implicated in physician suicide,13 and is the single leading cause of toxin-related death in the United States, with 4,908 exposures in 1988,’ and 3,500 accidental and suicidal deaths annuaMy.‘8 Important sources of carbon monoxide result from incomplete combustion of organic fuels such as exhaust fumes from automobiles, fires, furnaces and heaters, wood stoves, and other industrial machinery.18 Thus health care personnel, prehospital health care providers and firemen, and industrial personnel may be knowledgeable about its mode of action and lethality. Carbon monoxide toxicity results from a number of mechanisms, including tissue hypoxia, shifting of the oxygen-hemoglobin dissociation curve to the left, and reversible binding to other hemoproteins (such as cytochrome P450, cytochrome A3, and myoglobin) with development of tissue hypoxia at the cellular level. ‘y-22Clinical findings are relatively nonspecific; in milder exposure, signs of hypoxia (headache, dizziness, giddiness, visual disturbances) predominate,23 whereas at higher levels cardiac toxicity (altered mental status and coma),*’ seizures, and rhabdomyolosis leading to myoglobinemia and acute tubular necrosis.28q’g Diagnosis, if history of exposure is absent. can often be suspected from history of potential exposure (ie, unconscious person, especially physician or other knowledgeable personnel. found unconscious in a car, garage, or at a fire). Other subtle clues to the diagnosis include the new onset of arrhythmias or myocardial ischemia (particularly in a young patient or in knowledgeable personnel); new onset of metabolic (lactic) acidosis, altered mental status, or seizure: equal cherry-red coloration of retinal arteries and veins on funduscopic examination; and an “oxygen saturation gap” of 5% or greater. This gap is calculated by comparing cooximeter measured arterial oxygen percent saturation with calculated oxygen percent saturation derived from nomogram (as reported on arterial blood gases).30*” An elevated carboxyhemoglobin level, once suspected, may confirm the diagnosis. Cyanide and its derivatives have been frequently reported ingestants by these personne1,2-7 presumably because of their rapid action, high lethality, ready availability in most laboratories, and presumed painlessness as a mode of suicide. Cyanide is used as a photographic processing agent, a component in insecticides, a fumigant, a chemical reagent, in industrial processing, and in metallurgy for metal cleaning and extraction of gold and silver, from ore;2.4.3’ hence, persons employed in these fields might logically have access to and be informed about the chemical properties and lethality of cyanide. Eight hundred ten cases of cyanide toxicity were

BINDER AND FREDRICKSON

n POISONINGS

IN LABORATORY

reported in 1987, of which 49 were “intentional”, vocation of victims was not specified.’ Cyanide produces a histotoxic (intracellular) hypoxic poisoning by the binding of cyanide ion to the ferric (Fe+3) iron of mitochondrial cytochrome oxidase, inhibiting cytochrome oxidase activity and resulting in anaerobic metabolism and lactic acid accumulation.2*3’“3 Clinically, cyanide toxicity presents initially as hyperpnea and CNS stimulation, dyspnea, palpitations, headaches, giddiness), followed by bradycardia, hypotension, coma, convulsions, and apnea.3s5.3’*32*34Diagnosis is difficult without the history of cyanide exposure. In these instances the diagnosis may go undetected, but patients frequently recover with aggressive intervention and supportive care, as in this case and as reported previously.5~7~35 Subtle clues to this diagnosis, in the absence of history of exposure, include the patient’s occupation and cyanide availability, the aroma of “bitter almonds” to the gastric aspirate, unexplained and severe lactic acidosis, equal “cherry-red” coloration of retinal arteries and veins on funduscopic examination, a positive Lee-Jones assay of gastric aspirate,35 and an “0, saturation gap” of 5% or greater (as previously described). The azides [sodium azide (NaN,)], potassium azide (KN,), and lead azide (PB(N,),) are water soluble crystals that form hydrazoic acid (HN,), or azoimide, when dissolved in water. Azoimide boils at 37” centigrade (normal human body temperature), producing a colorless and pungent gas that is toxic when inhaled.36-40 The azides have multiple commercial uses, including airbag and airchute inflation [through rapid degradation to nitrogen gas (N2)] in the transportation industry, as an herbicide/fungicide, as a munitions detonator (lead azide), as a petrochemical reagent for sulfur contamination assays of oil, as an antihypertensive pharmaceutical, in automated blood cell counters, and as lab reagents in both physiology (as a mitochondrial poison) and nitrogen donation experiments.3”38.41-43 Hence, laboratory, pharmaceutical, and health care personnel may have access and knowledge of these chemicals, along with professionals in the munitions, petrochemical and agricultural industries. Azide toxicity is relatively infrequent; only seven fatal casess-10,43,44 and several cases of industrial and laboratory exposure 37,38*45-48 have been reported. Six of the fatalities occurred in intentional ingestions by laboratory personne1.8-‘0,43 The azides are toxic to mitochondrial metabolism, thus uncoupling oxidative phosphorylation and inhibiting energy transfer.49*50 This results in lactic acid accumulation, vascular smooth muscle relaxation, increased gastrointestinal and urologic smooth muscle tone, and alternating CNS effects.““@ Clinically, azide toxicity presents initially as CNS stimulation (headache, dizziness, weakness, hyperventilation, visual impairment), gastrointestinal (GI) stimulation (nausea, vomiting, diarrhea), and vascular smooth muscle relaxation (hypotension and reflex tachycardia). This is followed by lactic acidosis, and death.8“0V44 Diagnosis is likewise difflcult without history of azide exposure. Subtle clues to the diagnosis, in the absence of history of exposure, include the patient’s occupation and azide availability, a pungent aroma to the gastric aspirate, unexplained and severe lactic acidosis, the characteristic clinical picture of alternating CNS restlessness and atony coupled with evidence of progressive cellular anoxia (clinical hypoxia, cyanosis, acidosis, apnea, and hypotension), positive ferric chloride testing of gastric

AND HEALTH CARE PERSONNEL

13

aspirate (produces ferrous azide, a red precipitate), and development of mild toxicity (headache, nausea) by members of the resuscitation team. Sodium and potassium azideinduced hydrazoic acid boils at 37”C, and readily volatizes through the lungs, mucous membranes, and skin. Hence azoimide gas given off through exhaled air and gastric aspirate may cause mild impairment of emergency department personnel.’ The methemoglobin-inducing chemicals (nitrites, chlorates, nitro- and amino-aromatic derivatives) include many common laboratory reagents (Table 2).51 They are found in drugs, perfumes, dyes, polishes, many household solvents and cleaners; additionally, amyl- and butyl-nitrate are commonly abused recreationally (“poppers”).1L*52 Thus household and recreational ingestions predominate,51-56 but laboratory and occupational poisonings”*5’~57*58 are an important and frequently unrecognized source of chemically induced methemoglobinemia. Six hundred four cases of chemical and industrial exposure, and 164 cases of recreational exposure were reported in 1987, of which 111 cases were “intentional.“’ These chemicals oxidize hemoglobin (Fe+*) to methemoglobin (FeW3), which cannot reversibly bind with oxygen, resulting in cessation of oxygen transport to tissues, tissue hypoxia, and cyanosis from unoxygenated methemoglobin.5’*52~57 Clinically, methemoglobinemia presents initially with the triad of depressed level of consciousness, cyanosis refractory to supplemental oxygen, and symptoms of tissue hypoxia (headache, tachycardia, dyspnea, vomiting); progressive cyanosis, seizures, and cardiac arrest occur in severe toxicity.5’,J2V57 Even without history of exposure, diagnosis of toxic methemoglobinemia secondary to unidentified poison can often be made presumptively. Key diagnostic findings include the patient’s occupation and TABLE 2.

Substances Producing Methemoglobin

Acetanilid Acetophenetidin (phenacetin) Amy1 nitrite Aniline derivatives Anilinoethanol Antipyrine Benzocaine Bismuth subnitrate Chlorates Chlorobenzene (oral) Chloronitrobenzene (oral) Diaminodiphenylsulfone Dimethylaniline Dinitrobenzene Dinitrophenol Ethyl p-aminobenzoate (idiosyncracy) Hydroquinone (oral) Metachloroaniline Methylene blue (IV) Nitrates (if reduced) Nitrites Nitrobenzene (Dinitrobenzene) Nitrochlorobenzene Reprinted

with permission

Nitrogen oxide Nitroglycerol Pamaquine Para-bromoaniline Para-chloroaniline Para-nitroaniline Pentaerythritol tetranitrate Phenetidin Phenylazopyridine Phenylenediamine Phenylhydroxylamine Piperazaine (also EKG changes) Plasmoquine Prilocaine Primaquine Pyridium Quinones Resorcinol Sulfonamides Sulfones Tetranitromethane Tetronal Trional Toluidine Trinitrotoluene Vegetables (spinach) from Schimelman.5’

14

AMERICAN

JOURNAL

chemicals’ availability, the bitter “petrochemical” smell of certain chemicals, cyanosis refractory to supplemental oxygen administration, and the “chocolate brown” appearance of blood secondary to methemoglobinemia at levels greater than 15%.1’*51*52*57 The specific chemical can be confirmed later on toxicologic analysis. CONCLUSIONS The above case report and literature review suggest five common poisons encountered in laboratory and health care personnel: barbiturates, carbon monoxide, cyanide, azide, and methemogiobin-inducing chemicals. When confronted with a similar case, or a severe symptomatic presentation in these personnel, emergency personnel should undertake meTABLE 3.

Diagnosis of Unknown Poisoning in Knowledgeable Personnel

Poison Barbiturates

Carbon

monoxide

Cyanide

Azides

Methemoglobininducing chemicals

Diagnostic

Clues

Characteristic clinical presentation in knowledgeable personnel. Pill fragments on gastric lavage (refutes other metabolics/CNS diagnoses). Exclusion of other potential diagnoses through metabolic workup and CT scanning. Barbiturate level or tox screen. Hypothermia. Pinpoint pupils, nystagmus. History of potential exposure (found unconscious in car, garage, at fire). New onset of arrhythmias/myocardial ischemia. New onset lactic acidosis, altered mental status, seizure. Equal “cherry-red” coloration of retinal arteries and veins. Oxygen saturation gap > 5%. Availability to victim in workplace or home. Aroma of “bitter almonds” to gastric aspirate. Unexplained “cherry-red” coloration of retinal arteries and veins. Oxygen saturation gap > 5%. Anion gap metabolic acidosis (unexplained). Fire victims. New onset seizures. Pulmonary edema. Availability to victim in workplace or home. Pungent aroma to gastric aspirate. Unexplained and severe lactic acidosis. Alternating CNS restlessness and atony. Positive ferric chloride testing of gastric aspirate (red precipitate). Headache and nausea in resuscitation team members. Availability to victim in workplace or home. Bitter “petrochemical” smell of certain chemicals. Cyanosis refractory to oxygen. “Chocolate brown” appearance of blood.

OF EMERGENCY

MEDICINE

n Volume 9, Number

1 n January

1991

ticulous physical assessment and careful laboratory evaluation in the care of such patients,” and should consider the clinical presentations of these poisons (Table 3) and/or presentations of other poisons known to be accessible to the patient. Additionally, the possibility of other (nontoxicologic) organic illnesses resulting in severe symptomatic presentation must also be considered and investigated. REFERENCES 1. Litovitz TL, Schwitz BF, Matyunas N, Martin TG: 1987 Annual Report of the American Association of Poison Control Centers National Database Collection System. Am J Emerg Med 1988;16:479-515 2. Bonnichsen R, Maehly AC: Poisoning by volatile compounds: hydrocyanic acid. J Forensic Sci 1986;11:516-527 3. Litovitz TL, Larkin RF, Myers RM: Cyanide poisoning treated with hyperbaric oxygen. Am J Emerg Med 1983;1:94-101 4. Winek CL. Fusia E. Collom WD. Shannor SP: Cvanide ooisoning as a mode of suicide. J Forensic Sci 1978;11151-55 * 5. Vogel SN, Sultan TR, Ten Eyck RP: Cyanide poisoning. Clin Toxicol 1981;18:367-383 6. Stewart R: Cyanide poisoning. Clin Toxicol 1974;7:561564 7. Edwards AC, Thomas ID: Cyanide Poisoning (letter). Lancet 1978;1:92-93 8. Abrams J, El Mallakh RS, Meyer R: Suicidal sodium azide ingestion. Ann Emerg Med 1987;16:1378-1380 -9. Emmett EA, Ricking JA: Fatal self administration of sodium azide. Ann Intern Med 1975:83:224-226 10. Albertson TE, Reed S, Siefkin A: A case of fatal sodium azide ingestion. Clin Toxicol 1986;24:339-351 11. Harrison MR: Toxic methaemoglobinaemia. Anaesthesia 1977;32:270-272 12. Hall AH, Rocky Mountain Poison and Drug Center, University of Colorado Health Sciences Center, Denver. CO: personal communication 13. Steppacher RC, Mausner JS: Suicide in male and female physicians. JAMA 1974;228:323-328 14. Baltarowich LL. Sedative hypnotics. In Rosen, Baker, Braen, et al: Emergency Medicine: Concepts and Clinical Practice”. Second Edition, St Louis, MO, Mosby, 1988, pp 21092116 15. Good G, Goodman L, Gillman A (eds). The Pharmacological Basis of Therapeutics”. Sixth Edition, New York, NY, McMillan, 1980 16. Ho IK: Mechanism of Action of Barbiturates. Annu Rev Pharmacol Toxicol, 1981;21:83 17. Huff JS. Coma. In Rosen, Baker, Braen, et al (eds): Emergency Medicine: Concepts and Clinical Practice. Second Edition, St. Louis, MO, Mosby, 1988, pp 250 (table) 18. Reisdorf E, Wiegenstern JG. Carbon Monoxide Poisoning. In Tintinalli, Krome, Ruiz (eds): Emergency Medicine: a Comprehensive Studv Guide. Second Edition, New York. NY. McGrawHill, 1988, pp’809-813 19. Douglas CG, Haldane JS, Haldane JBS: The Laws of Combination of Hemoglobin with Carbon Monoxide and Oxygen. Physiology (Lond) 1912;44:275 20. Hinshaw HC, Murrah JF: Chemical, Radiation, Thermal, and Aspiration Injuries. In Hinshaw (ed): Diseases of the Chest. Fourth Edition, Philadelphia, PA, Saunders, 1980, p. 767 21. Coburn RF: Mechanisms of Carbon Monoxide Toxicity. Preventive Medicine 1979;8:310 22. Debias DA, et al: Effects of carbon monoxide inhalation on ventricular fibrillation. Arch Environ Health 1976;31:38 23. Myers RAM, Linberg SF, Cowley RA: Carbon Monoxide Poisoning: The Injury and its Treatment”. JACEP 1979;8:479 24. Aronow WS, lsbell MW: Carbon monoxide effect on exercise-induced angina pectoris. Ann Int Med 1973;79:392 25. Anderson FR, Allensworth DC, DeGroot WJ: Myocardial toxicity from carbon monoxide poisoning”. Ann Int Med 1967;67:1172 26. Shafer NM, Smiley MG, and MacMillan FP: Primary myo-

BINDER AND FREDRICKSON n POISONINGS IN LABORATORY AND HEALTH CARE PERSONNEL

cardial disease in man resulting from acute carbon monoxide poisoning. Am J Med 1967;36:316 27. Garland H, Pearce J: Neurological complications of acute carbon monoxide poisoning. Cl J Med 1967;34:445 26. Linton AL, Adams JH, Lawson DH: Muscle necrosis and acute renal failure in acute carbon monoxide poisoning. J Postgrad Med 1966;44:336 29. Loughridge WL, Leader LP, Bowen DAL: Acute renal failure due to muscle necrosis in acute carbon monoxide poisoning. Lancet 1965;2:349 30. Dinerman N, Huber JA. Inhalation injuries. In Rosen, Baker, Braen, et al (eds): Emergency Medicine: Concepts and Clinical Practice. Second Edition. St Louis. MO. Mosbv. 1988. DO 31. Hall AH, Rumack BH: Clinical toxicity of cyanide. Ann Emerg Med 1986;15:1067-1074 32. Krieg A, Saxena K: Cyanide poisoning from metal cleaning solutions. Ann Emerg Med 1987;16:582-584 33. Chen KK, Rose CL: Nitrate and thiosulfate therapy in cyanide poisoning. JAMA 1952;149:113-119 34. Wright IH, Vesey CJ: Acute poisoning with gold cyanide. Anaesthesia 1986;41:936-939 35. Graham DL, Laman D, Theodore J, Robin ED: Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema. Arch Intern Med 1977;137:1051-1055 36. Kleinhofs A, Owais WM, Nilan RA: Azides. Mutat Res 1978;55:165-195 37. Haas JM, Marsh WW: Sodium azide: a potential hazard when used to eliminate interferences in the iodometric determination of sulfur. Am Ind Hyg Assoc J 1970;31:318-321 36. Fairhall CT, Jenrette WV, Jones SW, et al: The toxicity of lead azide. Public Health Rep USA 1943;58:607-617 39. Graham JDP: Actions of sodium azide. Br J Pharmacol 1949;41:1-4 40. Kocher Z: “Ein Fall von Stickstoffwasserstaffauervergiftung.” Klin Wochenschr 1930;9:2160-2161 41. Ketcherside ML, Merkle MG: Dissipation and phytotoxicity of sodium azide in soil. Weed Sci 1976;24:312-315 42. Parochetti JV, Warren GF: Behavior of potassium azide in the soil. Weed Sci 1970;18:555-560 43. Klein-Schwartz W, Gorman RL, Oderda GH, et al: Three fatal sodium azide poisonings”. Med Toxicol 1989;4:219-227

15

44. Kozlicha-Gajdzinska H, Brzyski J: A case of fatal intoxication with sodium azide”. Arch Toxicol 1966;22:160-163 45. Richardson SGN, Giles C, Swan CHJ: Two cases of sodium azide poisoning by accidental ingestion of isoton. J Clin Pathol 1975;28:350-351 46. Burger E, Bauer HE: Akuter Vergiftungsfall durch versehantliches Trinken von Natriumzidlosung. Arch Toxicol 1965;20:279-283 47. Stern R: Uber toxische Wirkengen der Stickzoftwasserstoffsaure. Klin Wochenschr 1927:6:304-305 48. Gonni A: Tre casi di intossicazione de sodiozaide. Med Lav 1967;58:297-300 49. Boqucka K, Wojteza KL: Effect of sodium azide on oxidation and phosphorylation processes in rat liver mitochondria. Biochem Biophys Acta 1966;122:381-392 50. Palmieri F, Klingenberg M: Inhibition of respiration under the control of azide uotake bv mitochondria. Eur J Biochem 1967;1:439-449 ’ . 51. Schimelman MA, Soler JM, Muller HA: Methemoglobinemia: nitrobenzene ingestion. JACEP 1978;7:406-408 52. Rosen PJ, Johnson C, McGehee WG, Beuter E: Failure of methvlene blue treatment in toxic methemoglobinemia. Ann Intern Med 1971;75:83-86 53. Smith M, Stair T, Rolnick MA: Butyl nitrite and a suicide attempt. Ann Int Med 1980;92:720-721 (letter) 54. Shesser R, Dixon D, Allen Y, et al: Fatal methemoglobin from butyl nitrite ingestion. Ann Intern Med 1980;92:131-132 (letter) 55. Laaban JP, Bodenan P, Rochemaure J: Amyl nitrite poppers and methemoglobinemia. Ann Intern Med 1985;103:804805 (letter) 56. Osterloh J, Olson K: toxicities of alkyl nitrites. Ann Intern Med 1986;104:727 (letter) 57. Harris JC, Rumack BH, Peterson RG, et al: Methemoglobinemia resulting from absorption of nitrates. JAMA 1979; 242:2869-2871 58. Fleetham JA, Tunnicliffe, Munt PW: Methemoglobinemia and the oxides of nitrogen. N Engl J Med 1978;298:1150 (letter) 59. Olson KR, Pentel PP, Kelley MT: Physical assessment and differential diagnosis of the poisoned patient. Med Toxicol 1982;2:52-81