Medical Aspects of Chemical Warfare (2008) - The Black Vault

Long-Term Health Effects of Chemical Threat Agentsfrom headache and dizziness to death (although onlyone person died, and this individual was in extremiswhen found). All individuals in the report who hadvital signs at the time of discovery recovered. Most ofthe victims inhaled cyanide fumes for 30 to 90 secondsand became unconscious with irregular respirations orapnea. All these patients received supportive care ofbagged oxygen and amyl nitrite within 5 minutes. Onesurviving patient required intravenous antidotes aswell as amyl nitrite, and the rest recovered with amylnitrite and artificial ventilation alone. Nearly all thepatients recovered quickly, and some were even sentback to work after a few hours of observation. No longtermeffects were reported. These cases demonstratethe efficacy of simple field treatment if implementedwithin a few minutes of exposure. It is noteworthythat patients who remained conscious after inhalationof cyanide recovered with supplemental oxygen andno antidotes. 147Medical reports from severe ingestions include variousoutcomes. Many patients responded to treatmentand experienced complete recovery. Other outcomeswere difficult to discern because the patients may havedeveloped global deficits from prolonged hypoxia. Insome severe casualties, a distinct pattern of neurologicalimpairment occurred. The basal ganglia appearedto be particularly vulnerable to insult from cyanide,with frequent involvement of the globus pallidus andputamen. 148 Symptoms reported were parkinsonian,with bradykinesia, shuffling gait, rigidity, and othersymptoms resembling a generalized dystonia. Cognitivefunction sometimes remained intact. 149 In all caseswith long term sequelae, the patients experiencedsignificant delays of 30 minutes to hours before antidoteadministration. (There are several excellent caseexamples in Chapter 11, Cyanide Poisoning.)Long-Term ExposureLong-term exposure to cyanide contributes to anumber of conditions, although the different diseasesusually have several features in common. First, they areprimarily neurological diseases. Second, they involvedprolonged exposures to cyanide-containing food ormedication. Third, those affected tend to subsist on amonotonous diet with insufficient protein.The most common dietary exposure is bitter cassavaroot, Manihot esculenta Crantz, which is widelyconsumed in the tropics and sub-Saharan Africa, whereit ranks fourth in nutritional importance after rice,wheat, and maize. Cassava is a staple during times offamine because it can grow in poor soil and climateconditions. Cassava’s cyanogenicity confers immunityto pests. Procedures such as prolonged soaking, smashing,or boiling are necessary to remove cyanogeniccompounds such as linamarin. Fresh cassava roots cancontain up to 1,500 mg hydrogen cyanide equivalentper kilogram. 145 Acute intoxications, even death, haveresulted from consumption of raw cassava, thoughlong-term exposures from incompletely processedcassava are more likely.Konzo (“tied legs”) is a form of spastic paraparesisfound among poor rural populations of central andeast Africa who primarily consume cassava. It affectsindividuals of all ages. Konzo is symmetrical, isolated,and permanent. It is associated with sensations ofheaviness and weakness in legs that can cause theinability to stand. It is often present in entire familiesand varies in severity from a mild toe-scissor gait, torequiring a walking stick, and to the point where walkingis not possible. Those at risk for konzo have ankleclonus and lower extremity hyperreflexia. 150 Konzo isalso associated with optic neuropathy. 151 Individualswith konzo are noted to have very high levels of urinarythiocyanate. They are also protein deficient, with agreat deal of ingested amino acid sulphur diverting tocyanide detoxification. 152 Linamarin has been identifiedas a specific toxic factor in this disease. It is also thoughtthat overwhelmed detoxification mechanisms and anabrupt increase in metabolites over their chronic levelslead to the sudden clinical presentation of konzo. 153Tropical ataxic neuropathy is a distinct cyanide-relateddisease with several other names that is classicallyassociated with prisoners of war or middle-agedand elderly persons in southwestern Nigeria. It is apolyneuropathy associated with bilateral optic atrophy,bilateral neurosensory deafness, and sensory gaitataxia. This condition was widespread in Nigeria untilan improved diet resulting from the 1970s oil boomrelegated this condition to rural areas. 154 Tropical ataxicneuropathy is a gradual onset, permanent conditionassociated thiocyanate, cyanate, and a monotonouscassava diet. 155Smokers are known to have blood cyanide levelssignificantly higher than the nonsmoking population.156 Tobacco amblyopia is caused by chronic cyanidelevels sometimes coupled with malnutrition andalcoholism. Symptoms are loss of color perceptionand decreased vision, which is often recoverable afterdiscontinuation of smoking or even administration ofcyanide antidotes. This once-common syndrome hasbecome rare in the United States. 157Another cyanide-related disorder is Leber hereditaryoptic neuropathy (LHON). LHON, first describedin 1871, is a maternally inherited disease of highly variablepenetrance that impairs oxidative phosphorylation.LHON is the model disease for mutations of themitrochondrial genome. The disease is heteroplasmic,323