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Trevor L. Hoffman, Joseph C. LaManna, Svetlana Pundik, Warren R. Selman, Tim S. Whittingham, Robert A. Ratcheson, and W. David Lust

accumulation of carbon dioxide. 12, 27 Increasing lactacidosis by pretreatment with glucose has been shown to increase the extent of brain damage following an ischemic insult. 21, 22, 25, 26 However, the role of lactacidosis in the evolution of brain damage is not unifactorial, because there is evidence that elevated lactate or acidosis alone do not lead to brain damage unless either condition occurs in conjunction with other insults such as ischemia. 1, 30 There are many reports that have measured energy failure and acidosis during ischemia and the long-term recovery of

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Hiroshi Kuba, Takanori Inamura, Kiyonobu Ikezaki, Masatou Kawashima, and Masashi Fukui

L actic acidosis usually progresses rapidly over 1 or 2 days in the presence of underlying conditions such as diabetes mellitus, myocardial infarction, sepsis, hepatic failure, congenital metabolic disease, or thiamine deficiency. This metabolic disturbance is characterized by a depressed level of consciousness, severe metabolic acidosis, and increased serum lactate concentrations. Some authors have pointed out an increased risk of lactic acidosis due to thiamine deficiency in patients undergoing radiotherapy and chemotherapy for malignant tumors. 6, 8–10, 12

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Michael L. Cannon, Steven S. Glazier, and Loren A. Bauman

with severe adverse events including massive ketonuria, bradyarrhythmia, pulmonary hypertension, severe metabolic acidosis, rhabdomyolysis, myocardial failure, and death. 4, 5, 9, 16, 17, 22, 24 Numerous arguments, both pro and con, have appeared in the critical care and anesthesia literature regarding propofol's long-term use in children. 2, 6, 10, 19, 23 The pediatric patient presented in this report suffered a severe head injury, which in itself could have been fatal, but was sedated by a prolonged infusion of propofol, and began to experience severe metabolic

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Lennart Rabow, Antonio A. F. DeSalles, Donald P. Becker, Mildred Yang, Hermes A. Kontos, John D. Ward, Richard J. Moulton, Guy Clifton, Hanns D. Gruemer, J. Paul Muizelaar, and Anthony Marmarou

A lthough there is a consensus that a high lactate level in the ventricular cerebrospinal fluid (CSF) after a head injury is a grave prognostic sign, the question of causality has not yet been answered. It is our belief that, following mechanical brain injury, generalized and focal brain tissue and ventricular CSF acidosis occur that might irreversibly damage otherwise potentially viable brain cells. 2 Since lactic acid production causes brain acidosis, and since there are various means of correcting this acidosis, such as artificial hyperventilation or

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Kenichi Amagasaki, Tsuneo Shimizu, Yoko Suzuki, and Toshiyuki Kakizawa

T he MELAS syndrome, first described in 1984, 18 presents as a combination of mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes. The disease shares some features with two other mitochondrial diseases, Kearns—Sayre syndrome and MERRF (myoclonus epilepsy and ragged-red fibers) syndrome, and all three manifest as ragged-red fibers on skeletal muscle biopsy. 3 Clinically, MELAS syndrome is characterized by strokelike episodes, nausea, vomiting, encephalopathy, seizures, short stature, headaches, muscle weakness, exercise

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Nam D. Tran, Stefan Kim, Heather K. Vincent, Anthony Rodriguez, David R. Hinton, M. Ross Bullock, and Harold F. Young

development of cerebral acidosis and the formation of cellular or cytotoxic edema. 27 , 28 While both neurons and astrocytes are susceptible to cytotoxic edema, astrocytic contributions are far more important because they outnumber neurons in the brain by ~ 10:1. 24 In vitro, acidotic culture environments can induce pHdependent glial cellular edema. 47 , 50 From the clinical perspective, cerebral acidosis was recently demonstrated to be associated with poorer outcome in patients with severe TBI. 13 Recent studies of pathomechanisms have shown that a major culprit

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Antonio A. F. DeSalles, Hermes A. Kontos, Donald P. Becker, Mildred S. Yang, John D. Ward, Richard Moulton, Hanns D. Gruemer, Harry Lutz, Angelo L. Maset, Larry Jenkins, Anthony Marmarou, and Paul Muizelaar

B rain metabolic acidosis is considered to play an important role in cell damage in various pathological states. 50, 57 We believe that, following mechanical brain injury, subcellular elements may become dysfunctional, causing a focal and generalized brain-tissue acidosis that may be detrimental for potentially viable cells. Many studies have related the degree of brain acidosis, inferred by the levels of cerebrospinal fluid (CSF) lactate and pH, to the outcome after head injury. 9, 11–13, 17, 20, 31, 32, 37, 40, 54, 59, 67 Some of these studies compared the

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Jeffery L. Rush and Eldon L. Foltz

temperature to levels as high as 112° F may begin during or immediately after surgery. Profound metabolic and respiratory acidosis develops early and is often accompanied by hemolysis, hyperkalemia, and myoglobinuria. Cerebral edema, acute renal failure, and consumption coagulopathies with abnormal bleeding cause late morbidity. Recently investigators have substantiated the occurrence of hereditary and sporadic types of MH. 8, 11, 13, 15, 16 The hereditary type may be identified by current laboratory studies. 12 Further distinction between these types is dependent upon

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Pathophysiology and treatment of focal cerebral ischemia

Part II: Mechanisms of damage and treatment

Bo K. Siesjö

cascades of events, are at present the focus of interest. These are the results triggered by calcium overload, by excessive acidosis, and by enhanced production of free radicals. Although I will discuss each in turn, I wish to emphasize that none works in isolation. For example, most if not all effects elicited by a rise in intracellular Ca ++ (Ca ++ i ) result also from energy failure per se . Furthermore, since calcium triggers several reactions leading to the production of free radicals, the question arises whether the damage is calcium- or free radical

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Bo K. Siesjö

corresponding threshold is reported to be about three times as high. 51 Higher CBF thresholds have been reported for other indices of a perturbed cellular metabolism. For example, extra- and intracellular acidosis is observed at CBF values distinctly higher than those associated with energy failure/loss of ion homeostasis. 3, 42, 79, 92, 93 These results are in line with previous studies of progressive hypoxia and ischemia, demonstrating that lactate accumulates in the tissue at far higher arterial pO 2 values or mean arterial blood pressures than those associated with