The role of corticosteroid therapy in the management of septic shock has been debated for half a century. Results from large, well-designed, randomized clinical trials demonstrate no benefit, and perhaps harm, associated with short duration, high-dose methylprednisolone or dexamethasone administered at the onset of septic shock. Based on evidence of "relative adrenal insufficiency" and steroid-responsive adrenergic receptor desensitization in sepsis, administration of modest doses (200 to 300 mg/d) of hydrocortisone for 1 to 3 weeks has been investigated. A multicenter, placebo-controlled clinical trial demonstrated improved survival rates and faster cessation of vasopressors among patients with septic shock who have a poor response to corticotropin injection, consistent with relative adrenal insufficiency. However, concerns regarding a trend for higher mortality among corticotropin responders and the possibility that patients with true adrenal insufficiency may have been enrolled in this placebo-controlled trial, potentially skewing results, should be considered.

Effective management of hemorrhagic shock depends on titration of therapies against reliable resuscitation end points. Conventional clinical and laboratory indexes of shock are often slow to respond to progressive circulatory compromise. GI mucosal ischemia resulting from redistribution of blood flow may, however, precede uncompensated shock and may compound the initial hemorrhagic insult by touching off cascades of inflammatory responses. Trauma patients with evidence of subclinical GI ischemia have been shown to have poor outcomes. Gastric tonometry, by detecting the presence of gastric intramucosal acidosis as a proxy of splanchnic hypoperfusion, may facilitate more timely and rational shock resuscitation. This article reviews the development and validation of gastric tonometry and summarizes the clinical studies that have used this modality to guide the management of shock in trauma patients.

There is a general consensus that antimicrobial resistance in the hospital setting has emerged as an important variable influencing patient outcome and resource utilization. Hospitals worldwide are faced with increasingly rapid emergence and spread of antibiotic-resistant bacteria. Both antibiotic-resistant Gram-negative bacilli and Gram-positive bacteria are reported as important causes of hospital-acquired infections. Few antimicrobial agents are available for effective treatment. Selective digestive decontamination (SDD) is a technique aimed at selectively eliminating aerobic Gram-negative bacilli and yeast from the mouth and stomach to reduce the occurrence of hospital-acquired infections, including ventilator-associated pneumonia. Unfortunately, the application of SDD has been associated with emergence of antibiotic-resistant bacterial strains, limiting its overall utility.

Despite decades of research, the morbidity and mortality of sepsis and septic shock remain very high. To further compound the problem, results from all investigative trials (with one exception) have shown that tested immunotherapies aimed at modulating the excessive expression of key cytokines, such as the interleukins and tumor necrosis factor, have been either equivalent or inferior to placebo. While controversy prevails in terms of continuing such investigative trials, study designs can be held accountable for inherent flaws. Testing for the wrong hypothesis, errant study design, using the wrong agent, focusing on an inappropriate target group, excessive expectations, and uncontrolled variables have potentially obscured the real efficacy such agents might have to offer. By standardizing protocols and reducing uncontrolled variables, research can be more precisely targeted so as to unmask the real benefits to the patient.

Low-dose dopamine administration (ie, doses < 5 microg/kg/min) has been advocated for 30 years as therapy in oliguric patients on the basis of its action on dopaminergic renal receptors. Recently, a large, multicenter, randomized, controlled trial has demonstrated that low-dose dopamine administered to critically ill patients who are at risk of renal failure does not confer clinically significant protection from renal dysfunction. In this review, we present the best evidence and summarize the effects of low-dose dopamine infusion in critically ill patients. We review the history and physiology of low-dose dopamine administration and discuss the reasons why dopamine is not clinically effective in the critically ill. In addition to the lack of renal efficacy, we present evidence that low-dose dopamine administration worsens splanchnic oxygenation, impairs GI function, impairs the endocrine and immunologic systems, and blunts ventilatory drive. We conclude that there is no justification for the use of low-dose dopamine administration in the critically ill.