RENAL AND NEUROPSYCHIATRIC MANIFESTATIONS OF CARBON MONOXIDE POISONING

Carbon Monoxide Poisoning

Abstract

INTRODUCTION

Carbon monoxide (CO) is a highly toxic, odorless, colorless, tasteless, and nonirritating gas. The most common causes of CO exposure are fires, faulty combustion heating systems, exhaust from internal combustion engines, and heating gases. When breathed in, CO competes with oxygen in the blood, binding to hemoglobin in place of the oxygen and interfering with the oxygenation of tissues. The affinity of CO to hemoglobin is approximately 200 times greater than that of oxygen, making it a very effective mechanism to displace oxygen [1]. Although the neurotoxicant effect of CO exposure was initially believed to be a result of hypoxia secondary to the displacement of oxygen, it is now believed that additional mechanisms are involved, including the suppression of mitochondrial oxidative respiration and cardiomyopathy, with the associated hypotension and systemic acidosis. The clinical signs and symptoms of carbon monoxide poisoning vary, but in general, symptom severity correlates with carboxyhemoglobin (COHb) level. Symptoms can manifest suddenly but are relatively nonspecific (eg, headache, dizziness, weakness, nausea, visual disturbances, and confusion) [2]. The brain and heart are very sensitive to carbon monoxide poisoning; other organs are also affected. Studies support the fact that delayed neuropsychiatric symptoms may occur 3 to 240 days after exposure, after apparent recovery from acute intoxication [3,4].  Diagnosis of CO toxicity is based upon history of exposure to the source, physical examination and COHb levels if facility is available. We are reporting the first case from any hospital of Armed forces.