Alterations in fuel metabolism in critical illness: hyperglycaemia.

Hyperglycaemia is common during critical illness and may be viewed teleologically as a means of ensuring an adequate supply of glucose for the brain and phagocytic cells. Under normal conditions, euglycaemia is maintained by neural, hormonal and hepatic autoregulatory mechanisms. Critical illness promotes hyperglycaemia through an activation of the hypothalamic-pituitary-adrenal axis, which in turn increases hepatic glucose production and inhibits insulin-mediated glucose uptake to skeletal muscle. Sustained hyperglycaemia is associated with adverse consequences that demand its control. Appropriate management includes discontinuing causative drugs, correcting hypokalaemia, treating infection and administering insulin. Insulin therapy also appears to be useful for promoting an anabolic response in skeletal muscle.

Metabolic derangements in sepsis and septic shock.

This article examines the spectrum of metabolic alterations in sepsis and septic shock. The clinical manifestations, neuroendocrine control, and bioenergetics of the "ebb" and "flow" phases of sepsis are reviewed. Characteristic alterations in carbohydrate, fat, and protein metabolism induced by sepsis are outlined. Finally, the implications of these metabolic alterations for the nutritional support of patients with sepsis are discussed.

Nutritional support in hepatic encephalopathy.

Hepatic encephalopathy (HE) is a syndrome of global cerebral dysfunction resulting from underlying liver disease or portal-systemic shunting. HE can present as one of four syndromes, depending on the rapidity of onset of hepatic failure and the presence or absence of preexisting liver disease. The precise pathogenesis is unknown but likely involves impaired hepatic detoxification of ammonia as well as alterations in brain transport and metabolism of amino acids and amines. The etiology of malnutrition in hepatic failure is multifactorial. Nutritional deficits may be clinically manifest as marasmus or kwashiorkor, or both. Nutritional support in HE is directed toward reducing morbidity related to underlying malnutrition and concurrent disease. However, reaching nutritional goals is often complicated by protein and carbohydrate intolerance. The use of protein restriction in HE is controversial. Modified formulas that are supplemented in branched chain amino acids may be of value in patients who exhibit protein intolerance with standard feeding solutions or in patients who present with advanced degrees of encephalopathy.

Nutritional support of the hospitalized patient.

Comprehensive care of patients in hospitals includes assessment of nutritional status and provision of appropriate support. This approach is facilitated by knowledge of the essential differences in metabolism between starved and stressed states. Nutritional assessment and care of patients in a hospital are based on answers to the following questions: Who gets it? When do they get it? How much do they get? What route is used to administer it? What kind do they get? What are common complications of enteral and parenteral support? What nutritional aspects are pertinent to common diseases?

Confirmation of spurious hypoxemia using continuous blood gas analysis in a patient with chronic myelogenous leukemia.

Patients with extreme leukocytosis or thrombocytosis who have hypoxemia on arterial blood gas analysis may demonstrate normal oxygen saturation using pulse oximetry. The most commonly invoked explanation for this phenomenon is oxygen consumption in the blood gas sample prior to analysis. However, others have challenged the premise that the hypoxemia is spurious. We describe a patient with extreme leukocytosis and hypoxemia in whom normoxia was confirmed by continuous blood gas analysis.

Reactive hemophagocytic syndrome: a new presentation of disseminated histoplasmosis in patients with AIDS.

We report the cases of six patients with AIDS in whom reactive hemophagocytic syndrome (RHPS) secondary to disseminated histoplasmosis was diagnosed. RHPS was diagnosed by established criteria, including fever (duration of > or = 7 days, with peak temperatures of > 38.5 degrees C), unexplained thrombocytopenia with anemia and/or neutropenia, and bone marrow biopsy findings of hemophagocytic histiocytosis. Disseminated Histoplasma capsulatum infection was diagnosed on the basis of the results of cultures of the bone marrow sample. The serum lactate dehydrogenase (LDH) level was elevated (> 1,000 IU/L) in all patients, and five of six patients had hyperferritinemia (range of ferritin level, 15,848-425,984 ng/mL). Five patients had features resembling severe sepsis with multiorgan dysfunction. Three patients recovered, and the findings of RHPS resolved following therapy with amphotericin B. In patients with AIDS, the combination of fever, cytopenia, elevated serum LDH level (> 1,000 IU/L), and/or hyperferritinemia (ferritin level of > 10,000 ng/mL) is a clue to the diagnosis of RHPS and disseminated histoplasmosis; bone marrow biopsy is valuable in establishing the diagnosis.

Left ventricular outflow tract pulmonary artery fistula in endocarditis.

Patients with infective endocarditis are at risk for the development of a fistulous communication between chambers or great vessels of the heart. The presence of a continuous murmur may suggest the diagnosis. The first case of aortic valve endocarditis complicated by the development of a fistulous communication between the left ventricular outflow tract and the pulmonary artery is reported. Transesophageal Doppler echocardiography did not detect the defect preoperatively. However, pulmonary artery catheterization revealed very high mixed venous oxygen saturation which supported the presence of a left-to-right shunt.

Alterations in carbohydrate metabolism during stress: a review of the literature.

Patients with sepsis, burn, or trauma commonly enter a hypermetabolic stress state that is associated with a number of alterations in carbohydrate metabolism. These alterations include enhanced peripheral glucose uptake and utilization, hyperlactatemia, increased glucose production, depressed glycogenesis, glucose intolerance, and insulin resistance. The hypermetabolic state is induced by the area of infection or injury as well as by organs involved in the immunologic response to stress; it generates a glycemic milieu that is directed toward satisfying an obligatory requirement for glucose as an energy substrate. This article reviews experimental and clinical data that indicate potential mechanisms for these alterations and emphasizes aspects that have relevance for the clinician.