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

Cyanide Poisoningputed tomography scan showed bilateral putaminalhypodensities, which were seen to be hyperintenseon MRI T2-weighted images. Multimodal evoked potentialswere normal.Case Study 11-7. A 19-year-old female survived inhalationalexposure of a large dose (the exact amountwas unknown) as an intended victim of homicide. 173During trial proceedings 8 months after the poisoning,she was noted to be fully recovered with the exceptionof a mild dragging of one leg. No imaging studieswere reported.Case Study 11-8. A 35-year-old female surviveda usually lethal ingestion of KCN. 163 By day 5 shedisplayed agitation and choreoathetotic movementsof all four extremities and the trunk, which was suppressedwhile she was communicating. Deep tendonreflexes were brisk, and both plantar responses werepositive. By week 3, the choreoathetotic movementsabated to a state of akinetic mutism with loss of power,resembling generalized dystonia. She was dysarthricand had limited swallowing. An electroencephalogram(EEG) revealed diffuse, abnormal beta activity, morepronounced in frontal and front-temporal regions, butno focal epileptic activity. Serial evoked potentialstesting revealed central axonal auditory and somatosensorypropagation damage. MRI revealed acuteand subacute damage to the caudate nucleus andglobus pallidus bilaterally and discreet cortical damagelocalized to sensory motor cortex consistent withpseudolaminar necrosis, and functional imaging withβ-CIT SPECT showed loss of nigrostriatal dopaminergicneurons.As contrasted with acute, high-dose survivors,thousands of people survive with lesser overdosesfrom excessive consumption of cyanogenic foods ona chronic basis, particularly in the setting of overallnutritional inadequacy. Such chronic overexposure tocyanide and its metabolite thiocyanate is thought toaccount for prevalent peripheral nervous system disordersand perhaps also for excess goiters found withinsubpopulations of sub-Saharan Africa and Asia. 125,174In summary, most severely poisoned cyanide casualtiesdie in the absence of early intervention. Basedon limited case reports, long-term survivors may developsignificant neurological morbidity arising fromapoptotic demise of neurons of the basal ganglia andsensory-motor cortex. Case series from occupationalsettings where potentially lethal intoxications are typicallyidentified and definitive treatment begun withinminutes of exposure report early return to full duty. 175In addition, it is likely that developing knowledge inthe fields of neuroprotection and resuscitation willafford even gravely ill cyanide casualties better opportunityfor excellent recovery.Cyanide is associated with neuropathies worldwide(but not endemic to Westernized nations) that appearto result from excessive daily dietary cyanide, perhapsin combination with insufficiently varied diets withlow-quality protein content. Bitter cassava root in particularis noted for this association. Cassava is a dietarystaple, but it requires extensive processing to removecyanogens prior to consumption. During food shortagesor civil unrest, preparation is shortened whiledependence on the staple crop increases. The uppermotor neuron disorder konzo notoriously occurs inindividuals—especially children—at these times. 176–178Konzo is a persistent but nonprogressive spastic paraparesis(muscle weakness) that has been studied extensivelyby Rosling and colleagues. 179,180 Konzo sufferersdisplay lower-limb dysfunction, limited mobility, andimpaired fine motor function. 181 Populations recentlyaffected by konzo have been found to have elevatedurinary thiocyanate outputs and decreased inorganicsulfate excretion, consistent with high cyanide intakeand low sulfur-containing amino acids intake.Pediatric ConsiderationsPediatric considerations for any toxicant must bediscussed with awareness of normal development andhow that toxicant interacts with specific stages of development.182 Very little knowledge of cyanide impacton fetal development exists. Because fetal well-being ismost dependent on maternal well-being, the primarytherapeutic consideration for severe acute cyanidetoxicity in a pregnant woman must be urgent restorationof maternal circulatory, respiratory, and neurologicstatus. Chronic excess of thiocyanate is thoughtto be thyrotoxic to both the mother and the fetus 125 ;this situation is endemic in certain parts of the worldwhere maternal-fetal wellness is already threatenedby serious nutritional and socioeconomic problems.Treatment of cyanide intoxication with methemoglobinformers does induce fetal methemoglobinemia. Theamount of fetal methemoglobin formed, however, isnot likely to be clinically important as weighed againstthe necessity to treat the mother. 126Relatively few case reports and no epidemiologicalreports of survival of acute cyanide intoxicationin young children are available. The few publishedcases resulted from consumption of cassava or apricotkernals. Children do seem to be more vulnerable tointoxication through food sources, presumably becauseof lower body weight. 126 In one report, two youngThai children (ages 4 and 1.5 years) became comatose389