This was a retrospective chart review of consecutive obese patients admitted to the medical intensive care unit. Patients were divided into 2 groups: mild to moderately obese (group 1, body mass index =30-40 kg/m(2)) and morbidly obese (group 2, body mass index >40 kg/m(2)). Acute Physiology and Chronic Health Evaluation II scores were not significantly different between the 2 groups. Morbidly obese patients (group 2) had higher rates of mortality and nursing home admission. They also showed higher rates of intensive care unit complications including sepsis, nosocomial pneumonia, acute respiratory distress syndrome, catheter infection, tracheostomy, and acute renal failure. Their median length of mechanical ventilation was longer (2 days, range 2-12 vs 9 days, range 1-37,P = .009). In a logistic regression analysis, morbid obesity remained a significant predictor of death or disposition to nursing home even after controlling for age (P = .019, odds ratio = 7.60, 95% confidence interval = 1.39-41.6). Morbidly obese patients (body mass index >40 kg/m(2)) admitted to intensive care units have higher rates of mortality, nursing home admission, and intensive care unit complications and have longer stays in the intensive care unit and time on mechanical ventilation.

These results indicate that prolonged and sustained PAP therapy is effective in restoring some of the deficiencies in patients with OSAH, particularly in terms of memory, depression, anxiety and increased psychological pathology.

Two cases of optic neuropathy associated with cimetidine therapy are reported. Recovery occurred in both after drug withdrawal. Rechallenge with the same agent totally reproduced the condition in the first case. Cimetidine exerts an unequivocal toxicity on the central and peripheral nervous systems. Since its introduction in 1976, it has been used in over 100 million patients, but only 3 cases of optic neuropathy have been reported as far as we know. Although the mechanism of toxicity is still unclear, cimetidine is a well-recognized zinc chelator, and zinc deficiency has been implicated in causing optic neuropathy. Hence, it can be concluded that cimetidine produced this toxicity through its mechanism of zinc chelation. However, close ophthalmic follow-up of such patients is unnecessary, but an unexplained visual deterioration should prompt immediate drug withdrawal.

No abstract