Sudden death: a clinicopathological study.

OBJECTIVE: To ascertain the causes of sudden death (SD) by autopsy examination. METHODS: All cases of sudden death were subjected to a postmortem examination. In addition previous postmortem reports of sudden death over a two years were also included. Postmortem findings were correlated to clinical state and the cause of death was ascertained. The information was analyzed to find out the cause of sudden death in our patients. RESULTS: Out of a total of 130 autopsies there were 13 cases of SD. All were males (age 23 to 50 years). Death was within one your of onset of symptoms in five (38.5%) cases and within 24 hours in eight (61.5%) cases. Death was due to coronary artery disease (CAD) in 10 (76.93%) cases, aortoarteritis, cardiomyopathy and cerebrovascular accident (CVA) in (7.69%) case each. Amongst CAD patients triple vessel disease (TVD) was seen in eight cases (which included one case of cardiomyopathy), two vessel disease (DVD) in two and single vessel disease (SVD) in one. No specific preponderance of right or left coronary artery was seen. One patient of 21 year who died following exertion showed anomalous origin of coronary arteries. His right and left coronary artery originated from aortic arch 1.5 cm above the aortic valve. Right coronary artery was ill developed and had atheromatous plaque. The case of cardiomyopathy also had TVD. In the case of aortoarteritis all vessels were affected (carotids, renal and coronary). In one case of CVA bleeding was from an arterio-venous malformation in right temporal lobe. Nine out of 11 cases of CAD had atheromatous plaque without coronary thrombosis. CONCLUSIONS: Coronary artery disease (Triple vessel disease) contributed to maximum number of cases of SD. Aortoarteritis, cardiomyopathy and cerebrovascular accident (CVA) was the cause of death in one case each. Postmortem identified the cause of death in all cases.

Carbon monoxide poisoning.

OBJECTIVES: We studied the clinical profile and autopsy findings of carbon monoxide (CO) poisoning encountered at a hospital located at the altitude of 5,000 ft above mean sea level. METHODS: Clinical and postmortem findings in 25 and 15 cases of accidental CO poisoning respectively were evaluated. The diagnosis was made on circumstantial evidences, definite history of "Bukhari" burning and positive Kunkel's test for carboxyhaemoglobin (COHb). Detailed routine investigations including pulse oxymetry, X-ray chest and electrocardiographical monitoring was carried out in all the 25 patients. Oxygen (100%) via an endotracheal tube in all the comatosed patients and by conventional non-rebreathing plastic face masks was the mainstay of treatment. All patients were monitored and followed up for any delayed neurological sequelae. RESULTS: Most of the patients were young adults and the duration of exposure varied between three to eight hours. The initial diagnosis was stroke in three, seizure in one, encephalitis in two and ischaemic heart disease (IHD) in four. Neurological and respiratory signs and symptoms were noted in 19 and 18 of 25 patients respectively. SPO2 measured by pulse oxymetry was normal in all cases. ECG was suggestive of IHD in four patients. No delayed neurological sequelae was noted in any patients. Autopsy revealed deep red discoloration of skin and serous membranes in 80%, pulmonary oedema in 100% and cerebral oedema with widespread multiple pin point haemorrhages mainly in thalamus and globus pallidus in 40%. CONCLUSION: A high level of suspicion and routine history about the kind of indoor heating, specially in cold climate areas during winter will help in early diagnosis and decrease the incidence of misdiagnosis of CO poisoning. Oxygen (100%) or hyperbaric oxygen, if available should be administered without waiting for COHb levels to decrease morbidity and mortality.