valuable clue. However, because respiratory depression or pulmonary damage are likely to occur in such patients, and because inspired oxygen concentrations may vary, a normal venous or mixed venous pO2 level in a given setting may be unknown.
For smoke-inhalation victims, 100% oxygen should be administered immediately and IV access established.
The biologic half-life of carbon monoxide using 100% oxygen is 60 to 90 minutes. If hypotension, bradycardia, or acidosis persist, cyanide poisoning is likely, and antidote should be administered. Methemoglobin levels should be monitored carefully throughout nitrite therapy. Blood pressure also should be monitored and the nitrite infusion rate slowed if hypotension occurs.
The two major side effects of sodium nitrite from the antidote kit are excessive methemoglobinemia and hypotension. Methemoglobinemia is due to the oxidation of ferrous (+2) iron in hemoglobin to ferric (+3) by nitrite, and, therefore, care must be taken to avoid excessive nitrite doses. Hypotension results from the vasodilating action of nitrite.
Short-term sequelae of patients acutely poisoned by cyanide may include tremors and convulsions. Longer-term effects may include posthypoxic brain damage and myocardial lesions.
The long-term sequelae in persons chronically exposed to cyanide depend on exposure level and duration. In occupational settings, mild abnormalities in vitamin B12, folate, TSH levels, and thyroid function have been reported. Enlarged thyroid, dyspnea on exertion, psychosis, encephalopathy, and myocardial lesions have also been noted but may be due to multiple episodes of subacute poisoning rather than true chronic exposure. In populations consuming large quantities of cassava, endemic goiter, neuropathies, and cretinism have been noted, although dietary deficiencies may have contributed to these effects. Retrobulbar optic neuritis in heavy smokers has also been linked to chronic, low-level cyanide exposure from cigarette smoke.
Whether the neighbors described in the case study who have had chronic cyanide exposure through drinking water will experience long-term effects is difficult to predict. The level of cyanide in their drinking water (212 ppb) is close to what the EPA will propose in 1990 (200 ppb). The amount of cyanide ingested through cassava consumption in the Mozambique population is unknown, and comparisons are not warranted. Persons chronically exposed to low levels of cyanide have not been adequately studied. However, if neurologic, ophthalmologic, and thyroid examinations are normal, reassurance should be given that no ill effects from consumption of the water are evident. The local or state health department could be consulted to obtain assistance with possible control measures to remove cyanide from the well water.
More information on the adverse effects of cyanide and the treatment and management of cyanide-exposed persons can be obtained from ATSDR, your state and local health departments, and university medical centers. Case Studies in Environmental Medicine: Cyanide Toxicity is one of a series. For other publications in this series, please use the order form on the back cover. For clinical inquiries, contact ATSDR, Division of Health Education, Office of Director, at (404) 639–6204.