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B A Mizock

Publications and source records attributed to B A Mizock.

30 records · Page 2Linked to original sources

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.

Animals↗

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.

AIDS-Related Opportunistic Infections↗

Lactic acidosis in critical illness.

PURPOSE: This article reviews the current body of knowledge regarding lactic acidosis in critically ill patients. The classification of disordered lactate metabolism and its pathogenesis are examined. The utility of lactate as a metabolic monitor of shock is examined and current therapeutic strategies in the treatment of patients suffering from lactic acidosis are extensively reviewed. The paper is designed to integrate basic concepts with a current approach to lactate in critical illness that the clinician can use at the bedside. DATA SOURCES: Comprehensive review of the available, basic science, medical, surgical, and critical care literature. CONCLUSIONS: The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.

Acidosis, Lactic↗

Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy.

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.

Ammonia↗

Lactic acidosis.

An understanding of the pathophysiology of lactic acidosis is crucial in facilitating the optimal care of critically ill patients. The relevant biochemistry of lactic acidosis is reviewed, and the more controversial aspects relating to the genesis of the acidosis are highlighted. The current system of classification of lactic acidosis divides etiologies on the basis of the presence or absence of clinical signs of tissue hypoperfusion. Several types of lactic acidosis in which clinical evidence of tissue hypoperfusion is lacking demonstrate hemodynamic evidence of occult hypoperfusion. The diagnostic and therapeutic implications of this observation are discussed. Current diagnostic criteria for lactic acidosis include a pH less than 7.35 and blood lactate concentration greater than 5 to 6 mM/L. An important issue relates to the implications of lactate values that are greater than normal but below this diagnostic range. The use of the oxygen flux test may be valuable in the diagnosis of occult tissue hypoperfusion in patients with low-grade elevations in lactate levels. The current therapy for lactic acidosis involves addressing the primary cause and supportive management. The use of bicarbonate in the therapy for lactic acidosis is controversial due to potential adverse effects on cardiac function. The specifics of this controversy are outlined, and newer therapeutic alternatives are reviewed. The use of blood lactate concentration as a prognostic index may be more useful in patients with shock than without shock.

Acidosis, Lactic↗

Branched-chain amino acids in sepsis and hepatic failure.

The pathophysiologic mechanisms for the metabolism of hepatic failure and severe sepsis are complex, and in many ways similar. The similarities concern abnormalities in peripheral and hepatic protein metabolism. The ability of enteral and parenteral solutions containing increased amounts of branched-chain amino acids to ameliorate many of the derangements observed in these disease states relates to this shared pathophysiology.

Amino Acids, Branched-Chain↗

Computed tomographic brain scan of thrombotic thrombocytopenic purpura.

Computed tomographic (CT) brain scan findings in a patient with severe thrombotic thrombocytopenic purpura (TTP) are described. Multiple scattered lucencies were noted which correlated with thrombotic occlusions found at autopsy. In this patient, the neurologic manifestations of TTP preceded the haemolytic anaemia. In the correct clinical setting, multiple areas of lucency should suggest multiple infarcts secondary to thrombotic vessel occlusions as a diagnostic possibility.

Adult↗

Controversies in lactic acidosis. Implications in critically ill patients.

Lactic acidosis is common in critically ill patients and is usually caused by tissue perfusion that is inadequate to meet metabolic demand. However, it has also been noted in conditions in which tissue perfusion is apparently adequate. Hyperlactatemia can occur in the absence of acidosis, usually in the setting of hypermetabolic disease. Numerous areas of controversy exist regarding the pathogenesis of lactic acidosis, as well as certain of its diagnostic, therapeutic, and prognostic features. Knowledge of these areas of controversy should facilitate the clinician's approach to diagnosis and management.

Acidosis, Lactic↗