Critical care in Africa: A surgical intensivist perspective

Critical care services often fall far outside the focus of mainstream health care agendas. The disease specific list held by many health care stakeholders, including the funding agencies, results in a funneling of political attention and funds predominantly in those directions. Infectious diseases, in particular tuberculosis and HIV/AIDS, are on the fore front of the global public health agendas and rightfully, will remain high on the list for the foreseeable future1. Childhood infectious diseases also represent disease-specific agendas that are a main target of donor funding because of the potential for intervening successfully and the potential of life saved 2,3. The lure of eradication of a disease with a heavy burden on the health of the population as exampled by the Polio campaigns and programs to eradicate guinea worm easily capture the attention of governments and society alike. As a result, crucial life-saving hospital services such as critical care are often overlooked

Adrenocorticotropic hormone and cortisol response to corticotropin releasing hormone in the critically ill—a novel assessment of the hypothalamic-pituitary-adrenal axis

The pathophysiology of adrenal insufficiency, common in surgical intensive care units, has not been fully elucidated. Patients at risk (age > 55 years, in the surgical intensive care unit >1 week, baseline cortisol < 20 μg/dL) were enrolled. After measuring cortisol and adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH) was administered. ACTH and cortisol were measured over 120 minutes. Short and long cosyntropin stimulation tests determined adrenal function. Area under the curve (AUC) and mixed linear models were used to compare cortisol and ACTH responses. Patients were grouped according to survival and response to stimulation testing. Chi-square and t tests were performed, and P values < .05 were considered statistically significant. Six of 25 patients responded poorly to cosyntropin, and 5 died compared with 3 after a normal response ( P < .01). ACTH (AUC) and ACTH peak were increased in nonsurvivors after CRH administration. Cortisol peak and AUC were not different. ACTH responsiveness was increased in nonsurvivors and may predict mortality