Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 12: Cyanide Toxicity
Case Study 12: Cyanide Toxicity
Pages 312-331
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From page 312... ...
Ed Cyanide poisoning is a hazard in many enclosed-space f res, and its occurrence in smoke-inhalafior' victims may be underestimated. Acute cyanide exposure results primarily in CNS, cardiovascular, and respiratory effects; thyroidfunction abnormalities also have been noted in persons chronically exposed.
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From page 313... ...
The woman's vital signs include BP 70/50 mm Hg, pulse 1 20/min, respiration rate 30/mint She is being administered 100% oxygen via face mask. The child's vital signs include BP 50/20 mm Hg, pulse 50/min, respiration rate O/min.
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From page 314... ...
and cyanide salts (potassium cyanide, sodium cyanide, calcium cyanide) , which can combine with acid to release HCN.
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From page 315... ...
, an illicit street drug, may contain cyanide if improperly manufactured. For the general population, the single largest source of airborne cyanide exposure isvehicle exhaust.
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From page 316... ...
Smokers generally have higher blood cyanide levels than nonsmokers and are at increased risk of cyanide's nervous system effects, particularly tobacco amblyopia and retrobulbar optic neuritis.
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From page 317... ...
Clinical cases of cyanide poisoning after dermal exposure are rare and most often have involved burns with molten cyanide salts or immersion in cyanide solutions. Once cyanide is absorbed, it is rapidly distributed by the blood throughout the body.
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From page 318... ...
Survival in any specific case often depends upon the rapidity and scope of treatment. Acute Exposure An acute cyanide exposure affects primarily the central nervous system, initially producing stimulation, which may be followed quickly by depression.
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From page 319... ...
Delayed onset Paricinsonlike syndromes have been described after severe cyanide poisoning as well as after carbon monoxide poisoning, implying that the basal ganglia are sensitive to the neurotoxic effects of both agents. Chronic Exposure Central Nervous System An epidemic of spastic paraparesis in Mozambique was attributed to consumption of the cyanogenic vegetable, cassava.
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From page 320... ...
Clinics/ Eva/uation History and Physical Examination Pertinent history may include occupation and hobbies, medications, diet, smoking habits, and drinking water source. Physical examination of chronically exposed patients should include particular attention to neuropsychiatric and ophthalmologic examinations, and cardiovascular system and thyroid functioning.
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From page 321... ...
Severe metabolic acidosis results from anaerobic metabolism with increased lactic acid production. Cardiovascular signs include initial transient hypertension with reflex bradycardia and sinus dysrhythmia, followed by tachycardia with hypotension and cardiovascular collapse.
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From page 322... ...
Characteristics of patients with significant cyanide poisoning secondary to smoke inhalation may include the following: Persistent hypotension Coma Seizures Cardiac dysrhythmias Cardiac ischemia Chronic Exposure Long-tem, effects of chronic cyanide exposure Include cardiovascular, respiratory, and thyroid function abnormalltles. O Whole blood cyanide levels can be used to confirm diagnosls.
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From page 323... ...
Other. Wheneversmoke inhalation isthe potential sourceofcyanide exposure, carboxyhemoglobin and methemoglobin levels should also be obtained.
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From page 324... ...
Whether HBO offers any added clinical advantage over 100% normobaric oxygen and the cyanide antidote kit is unknown. Smoke inhalation is frequently associated with chemical pneumonitis, skin burns, carbon monoxide poisoning, and cyanide poisoning; HBO has theoretical or documented benefit in the treatment of all four conditions.
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From page 325... ...
If excessive methemoglobinemia occu rs, methylene blue treatment can be used. Since this treatment can cause deterioration by re-establishing high cytochrome ferro cyanide levels, it should be administered only by highly trained professionals experienced in managing cyanide poisoning.
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From page 326... ...
(12) What are possible side effects of the cyanide antidote kit?
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From page 327... ...
Standards and regulations for cyanide . Agency Focus Leered Comments Hi_ ACGIH Air-Workplace 4.7 ppm Advisory; TWAt for cyanides, based on skin absorption NIOSH Air -Workplace 5 mg/m Advisory; 10-minute ceiling limit OSHA Air -Workplace 10 ppm Regulation; PEL§ for HCN 5 mgim 3 Regulation; PEL§ for cyanide salts EPA Air-Environment N/A Regulation: to tee covered under the Clean Air Act Water-Environment N/A Regulation; drinking water standard to be proposed in 1990 3.5 ppb Advisory; 24-hour coverage to protect aquatic life Food 25 ppm Regulation; residual HCN, when used as a postharvest fumigant in dried beans, peas, and nuts; 250 ppm in spices ACGIH ~ American Conference of Governmental Industrial Hygienists; EPA = Environmental Protection Agency; NIOSH = National Institute for Occupational Safety and Health; OSHA Occupational Safety and Health Administration t TWA (Time-Weighted Average)
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From page 328... ...
Food EPA tolerances for HCN in foods when used as a postharvest fumigant range from 25 ppm in dried beans, peas, and nuts, to 250 ppm in spices. Reference doses were extrapolated from studies of rats fed cyanide salts for 2 years at levels resulting in no observable effect.
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From page 329... ...
Gupta BN, Bhargava SK, Clerk SH, Mahendra PN. Chronic cyanide exposure biochemical and industrial hygiene study.
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From page 330... ...
(4) Causes of an elevated blood cyanide level might include occupational exposure, heavy cigarette smoking, ingestion of large quantities of cyanogenic plants, nitroprusside therapy, smoke inhalation, or a possible laboratory error.
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From page 331... ...
Whetherthe neighbors described in the case study who have had chronic cyanide exposurethrough drinking water will experience long-term effects is difficult to predict. The level of cyanide in their drinking water (212 ppb)
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