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Paraneoplastic neurological disorders are a well recognized complication of malignancy. A case report to expand the currently described clinical manifestations of type 1 antineuronal antibody (ANNA-1)-associated paraneoplastic encephalomyelitis to include coma. We present an unusual case of fluctuating coma and rapid fulminant progression to acute respiratory failure from central alveolar hypoventilation caused by ANNA-1 paraneoplastic encephalomyelitis associated with small-cell lung carcinoma. Paraneoplastic infiltration of the brainstem and cerebellum, including respiratory and arousal centers, was documented on autopsy. Paraneoplastic encephalomyelitis should be considered as a possible cause of coma and central alveolar hypoventilation.

In a study of the endovascular cooling system Alsius CoolGard™ combined with the Icy™ venous catheter, Pichon and colleagues concluded the effectiveness and safety of mild induced hypothermia (MIH) after out-of-hospital cardiac arrest resuscitation [1]. We are troubled because the study has reproduced several safety concerns about MIH that have not been confronted. First, the sixfold increase of the nosocomial bloodstream infection rate (13% versus control 2%) is most probably related to insertion of endovascular catheters for MIH [1]. Bloodstream infection in patients with endovascular catheters can become a significant cause of preventable morbidity and mortality [2]. Second, it is unclear why hypokalemia (75% of MIH cases) was dismissed as a factor for the incidence of cardiac dysrhythmia [1]. Temperature changes induce electrolyte shifts and thus influence the depolarization and repolarization times and the conduction velocity of action potentials within the myocardium, promoting aberrant conduction pathways. Electrolyte abnormalities associated with MIH can influence electrophysiological parameters of the myocardium, triggering dysrhythmia [3].

Use of corticosteroids for adrenal supplementation and attenuation of the inflammatory and immune response is widespread in acute critical illness. The study hypothesis was that exposure to corticosteroids influences the mortality and morbidity in acute critical illness. This case–control retrospective study was performed in a single multidisciplinary intensive care unit at a tertiary care institution and consisted of 10,285 critically ill patients admitted between 1 January 1999 and 31 December 2004. Demographics, comorbidities, acute illness characteristics including severity measured by Sequential Organ Failure Assessment, concurrent medications, therapeutic interventions and incidence of infections were obtained from electronic medical records, were examined with multiple regression analysis and were adjusted for propensity of corticosteroid exposure. The primary outcome was hospital death, and the secondary outcome was transfer to a care facility at hospital discharge. Corticosteroid exposure in 2,632 (26%) patients was characterized by younger age, more females, higher Charlson comorbidity and maximal daily Sequential Organ Failure Assessment scores compared with control patients. Corticosteroids potentiated metabolic and neuromuscular sequels of critical illness with increased requirements for diuretics, insulin, protracted weaning from mechanical ventilation, need for tracheostomy and discharge to a care facility. Early exposure to corticosteroids predisposed to recurrent and late onset of polymicrobial and fungal hospital-acquired infections. Corticosteroids increased the risk for death or disability after adjustments for comorbidities and acute illness characteristics. Corticosteroids increased the risk for death or disability in critical illness. Hospital-acquired infections and metabolic and neuromuscular sequels of critical illness were exacerbated by corticosteroids. Careful appraisal of the indications for use of corticosteroids is necessary to balance the benefits and risks from exposure in acute critical illness.