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Background: At least a third of the world's population consumes alcohol regularly. Patients with alcohol use disorders (AUDs) are frequently hospitalized for both alcohol-related and unrelated medical conditions. It is well recognized that patients with an AUD are thiamine deficient with thiamine replacement therapy being considered the standard of care. However, the incidence of vitamin C deficiency in this patient population has been poorly defined., Methods: In this retrospective, observational study, we recorded the admission vitamin C level in patients with an AUD admitted to our medical intensive care unit (MICU) over a 1-year period. In addition, we recorded relevant clinical and laboratory data including the day 2 and day 3 vitamin C level following empiric treatment with vitamin C. Septic patients were excluded from this study., Results: Sixty-nine patients met the inclusion criteria for this study. The patients' mean age was 53 ± 14 years; 52 patients (75%) were males. Severe alcohol withdrawal syndrome was the commonest admitting diagnosis (46%). Eighteen patients (26%) had cirrhosis as the admitting diagnosis with 18 (13%) patients admitted due to alcohol/drug intoxication. Forty-six patients (67%) had evidence of acute alcoholic hepatitis. The mean admission vitamin C level was 17.0 ± 18.1 μmol/l (normal 40-60 μmol/l). Sixty-one (88%) patients had a level less than 40 μmol/l (subnormal) while 52 patients (75%) had hypovitaminosis C (level < 23 μmol/l). None of the variables recorded predicted the vitamin C level. Various vitamin C replacement dosing strategies were used. A 1.5-g loading dose, followed by 500-mg PO q 6, was effective in restoring blood levels to normal by day 2., Conclusion: Our results suggest that hypovitaminosis C is exceedingly common in patients with an AUD admitted to an intensive care unit and that all such patients should receive supplementation with vitamin C in addition to thiamine. Additional studies are required to confirm the findings of our observational study and to determine the optimal vitamin C dosing strategy.

The combination of thiamine, ascorbic acid, and hydrocortisone has recently emerged as a potential adjunctive therapy to antibiotics, infectious source control, and supportive care for patients with sepsis and septic shock. In the present manuscript, we provide a comprehensive review of the pathophysiologic basis and supporting research for each element of the thiamine, ascorbic acid, and hydrocortisone drug combination in sepsis. In addition, we describe potential areas of synergy between these therapies and discuss the strengths/weaknesses of the two studies to date which have evaluated the drug combination in patients with severe infection. Finally, we describe the current state of current clinical practice as it relates to the thiamine, ascorbic acid, and hydrocortisone combination and present an overview of the randomized, placebo-controlled, multi-center Ascorbic acid, Corticosteroids, and Thiamine in Sepsis (ACTS) trial and other planned/ongoing randomized clinical trials.

The early detection and treatment of sepsis are the most important factors in improving the outcome of patients with this condition. However, many patients admitted to hospital experience a long delay in the diagnosis of sepsis. Furthermore, it is not uncommon for febrile patients to be sent home from the Emergency Department or the physician's office with the diagnosis of 'flu' only to return hours or days later in overt septic shock. The early diagnosis of sepsis may be challenging as many of the signs and symptoms are non-specific. Clinical studies suggest that early diagnosis of sepsis requires a high index of suspicion and comprehensive clinical evaluation together with laboratory tests, including a complete blood count with differential, lactate and procalcitonin levels.

Stress hyperglycemia is common in critically ill patients and appears to be a marker of disease severity. Furthermore, both the admission as well as the mean glucose level during the hospital stay is strongly associated with patient outcomes. Clinicians, researchers and policy makers have assumed this association to be causal with the widespread adoption of protocols and programs for tight in-hospital glycemic control. However, a critical appraisal of the literature has demonstrated that attempts at tight glycemic control in both ICU and non-ICU patients do not improve health care outcomes. We suggest that hyperglycemia and insulin resistance in the setting of acute illness is an evolutionarily preserved adaptive responsive that increases the host's chances of survival. Furthermore, attempts to interfere with this exceedingly complex multi-system adaptive response may be harmful. This paper reviews the pathophysiology of stress hyperglycemia and insulin resistance and the protective role of stress hyperglycemia during acute illness.

An intact hypothalamic-pituitary-adrenal (HPA) axis with effective intracellular glucocorticoid anti-inflammatory activity is essential for host survival following exposure to an infectious agent. Glucocorticoids play a major role in regulating the activity of nuclear factor-kappa- B, which has a crucial and generalized role in inducing cytokine gene transcription after exposure to an invading pathogen. Severe sepsis is, however, associated with complex alterations of the HPA axis, which may result in decreased production of cortisol as well as glucocorticoid tissue resistance.

The definition of what constitutes a 'normal' adrenal response to critical illness is unclear. Consequently, published studies have used a variety of biochemical criteria to define 'adrenal insufficiency'. These criteria have been based on the baseline cortisol level or the increment in cortisol following corticotropin administration. However, in critically ill patients there are a number of confounding factors that make interpretation of these tests difficult. Furthermore, in those patients who are most likely to benefit from treatment with low-dose glucocorticoids, there is no evidence that treatment should be based on adrenal function testing. In those patients in whom the diagnosis of adrenal insufficiency may be important, this diagnosis may best be made based on the free cortisol level or the total cortisol level stratified by serum albumin.

Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.

Hypertension is an extremely common clinical problem, affecting approximately 50 million people in the USA and approximately 1 billion individuals worldwide. Approximately 1% of these patients will develop acute elevations in blood pressure at some point in their lifetime. A number of terms have been applied to severe hypertension, including hypertensive crises, emergencies, and urgencies. By definition, acute elevations in blood pressure that are associated with end-organ damage are called hypertensive crises. Immediate reduction in blood pressure is required only in patients with acute end-organ damage. This article reviews current concepts, and common misconceptions and pitfalls in the diagnosis and management of patients with acutely elevated blood pressure.

Background: Our objective was to evaluate the impact of gastric versus post-pyloric feeding on the incidence of pneumonia, caloric intake, intensive care unit (ICU) length of stay (LOS), and mortality in critically ill and injured ICU patients., Method: Data sources were Medline, Embase, Healthstar, citation review of relevant primary and review articles, personal files, and contact with expert informants. From 122 articles screened, nine were identified as prospective randomized controlled trials (including a total of 522 patients) that compared gastric with post-pyloric feeding, and were included for data extraction. Descriptive and outcomes data were extracted from the papers by the two reviewers independently. Main outcome measures were the incidence of nosocomial pneumonia, average caloric goal achieved, average daily caloric intake, time to the initiation of tube feeds, time to goal, ICU LOS, and mortality. The meta-analysis was performed using the random effects model., Results: Only medical, neurosurgical and trauma patents were enrolled in the studies analyzed. There were no significant differences in the incidence of pneumonia, percentage of caloric goal achieved, mean total caloric intake, ICU LOS, or mortality between gastric and post-pyloric feeding groups. The time to initiation of enteral nutrition was significantly less in those patients randomized to gastric feeding. However, time to reach caloric goal did not differ between groups., Conclusion: In this meta-analysis we were unable to demonstrate a clinical benefit from post-pyloric versus gastric tube feeding in a mixed group of critically ill patients, including medical, neurosurgical, and trauma ICU patients. The incidences of pneumonia, ICU LOS, and mortality were similar between groups. Because of the delay in achieving post-pyloric intubation, gastric feeding was initiated significantly sooner than was post-pyloric feeding. The present study, while providing the best current evidence regarding routes of enteral nutrition, is limited by the small total sample size.