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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One-hundred twenty-nine patients with carotid artery injuries were analyzed to compare the results of revascularization with those of ligation or occlusion. In patients who present with central neurologic deficit short of coma (Grades 1 to 4), revascularization is clearly the operative method of choice. Revascularization in patients with preoperative coma (Grade 5) is also indicated when ischemia has only been present for a short period of time before surgery. Controlling cerebral edema and minimizing infarct size in patients with severe deficits may be essential to optimize the chance of recovery of these patients.
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PMID:Carotid artery injuries. 714 36

Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.
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PMID:Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia. 721 9

We conducted serial neurologic examinations on 500 patients in nontraumatic coma to identify factors predicting recovery. Overall, 81 patients (16%) led an independent life at some point within the first year; the remainder either died without recovery from coma (61%), never improved beyond the vegetative state (12%), or regained consciousness but remained dependent on others for daily activities (11%). Functional recovery did not depend on age but was to some degree related to the cause of coma (subarachnoid hemorrhage and other cerebrovascular disease having the worst recovery; hypoxia-ischemia, intermediate; and hepatic and miscellaneous causes, best) and especially to early clinical signs of brain dysfunction. Even within hours of the onset of coma, only one of 120 patients lacking two of corneal, pupillary, and oculovestibular responses ever regained independent function. The study identifies clinical features of comatose patients that appear within the first week and that are important for predicting recovery and designing future therapeutic trials.
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PMID:Prognosis in nontraumatic coma. 722 76

To clarify the physiopathologic mechanism leading to a marked increase in aromatic amino acids (AAA) in acute hepatic failure (AHF), we compared two experimental models of AHF. Ten pigs were submitted to one-stage hepatic devascularization (group A); in eight other pigs total hepatectomy was performed (group B). The animals were maintained under constant glucose infusion. The mean survival time in group A was 23 +/- 2 hours; after hepatectomy it was 30 +/- 4 hours. Hepatic coma progressively deepened from 8 +/- 3 hours in Group A animals and was delayed until 17 +/- 5 hours in the anhepatic pigs. AAA, methionine, and tryptophan immediately increased markedly in pigs with liver ischemia. In group B animals, AAA showed a slight increase only 18 hours after hepatectomy, whereas there were no significant differences in methionine and tryptophan. The different amino acid patterns in the two groups of animals demonstrate that hepatocyte necrosis is a major source of plasma amino acids after liver devascularization. The slight increase in AAA after total hepatectomy suggests that a release mechanism from muscular mass is involved in the later stages of the experiment. The onset of coma is related to the increase in AAA rather than to alterations in blood ammonia that did not differ in either group of animals.
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PMID:Plasma amino acid patterns in experimental acute hepatic failure: comparison between hepatectomy and liver devascularization in pigs. 726 30

Recent research has contributed to the understanding of nontraumatic rhabdomyolysis. In cases associated with coma, the pathophysiology is secondary to local pressure necrosis caused by compression from the patient's own body. The local pressure results in an edema-ischemia cycle concluding with compartmental tamponade and muscle breakdown. Myoglobin released by the damaged muscle indirectly induces the acute renal failure via its breakdown product, ferrihemate, which poisons renal tubular cells. Uric acid nephropathy may also play a role. Radionuclide scanning has assumed a significant role as a diagnostic tool to determine the extent of soft tissue injury. Early volume expansion and administration of sodium bicarbonate and mannitol are recommended as prophylaxis against renal failure. Fasciotomy appears to have a role both in the prevention of limb damage and in the diminution of the systemic toxic effects produced by muscle breakdown.
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PMID:Rhabdomyolysis secondary to drug overdose and prolonged coma. 740 37

Following severe head injury, derangements of the cerebral vasculature and cerebral blood flow (CBF) often occur, rendering the brain at risk of secondary ischemia. Therefore, monitoring of CBF in head-injured patients is considered useful for understanding the pathophysiology and effects of therapy, although such monitoring has not yet become part of routine patient management in most centers. In this article, we review the current research on CBF in head injury. Understanding of the physiologic relationship between CBF and cerebral oxygen metabolism (CMRO2) is crucial in the interpretation of CBF values obtained in comatose head injured-patients. Although CMRO2 is reduced with coma, there is ample evidence to suggest that vulnerability of the brain to ischemia is in fact enhanced after traumatic injury. It is now well established that cerebral ischemia (CBF < or = 18 mL/100 g/min) is present in approximately 30% of cases within the first 6 hrs postinjury. In addition, early ischemia has been found to correlate with poor outcome and early mortality. Notably, early ischemia was present even with normal or restored blood pressure and arterial oxygenation, which suggests that other, nonsystemic causes of cerebral ischemia after traumatic brain injury exist. Although spasm of the larger cerebral arteries has been postulated as a possible cause of ischemia, recent measurements of cerebral blood volume are more compatible with compromise of the microcirculation, possibly due to perivascular swelling, with endothelial injury and leukocyte stasis. Disturbances of cerebrovascular CO2 reactivity and autoregulation appear to be less frequent than previously assumed. However, when present, such derangements do have consequences for therapy, in particular the management of blood pressure and cerebral perfusion pressure. Potential implications for patient management are discussed.
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PMID:Cerebral blood flow in severe clinical head injury. 749 46

Knowledge of cerebral metabolic variables increases the information available for managing the head-injured patient. This article reviews normal cerebral metabolism and describes the derangement of metabolism observed in patients with head trauma. Cerebral metabolism is globally decreased by one third to one half in the severely head-injured patient, usually because of the lower metabolic expenditure associated with coma, but sometimes because of superimposed hypoxia/ischemia, primarily due to secondary insults. Measurement of jugular venous oxygen saturation has become the most useful method for monitoring cerebral metabolism in the ICU. Although jugular venous oxygen saturation does not provide quantitative information about either cerebral blood flow or cerebral metabolism, it reflects the ratio between these two variables. To maintain a sufficient level of available oxygen and energy production at the cellular level, there are two therapeutic strategies: a) hemodynamic and b) metabolic. Treatments can be directed at both increasing oxygen delivery and integrating hemodynamic handling, and at various pharmacologic or physical methods intended to reduce the cerebral metabolic demand. The latter strategy is designed to depress either the basal or activation components of cerebral metabolism. This strategy includes manipulations of brain temperature and the use of central nervous system-depressant, barbiturate, and similar drugs.
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PMID:Cerebral metabolic management. 749 49

Rhabdomyolysis caused 28 out of 903 (3.1%) of cases of severe acute renal failure (ARF) treated at Leeds General Infirmary over a 14-year period (1980-1993). The commonest cause of rhabdomyolysis was muscle compression, usually due to drug- or alcohol-induced coma. Other causes included fits, infection, acute limb ischemia, trauma, and heat stroke. Prognosis was relatively good, with a 78.6% survival rate and recovery of renal function to normal in all survivors who were followed up. The creatinine/urea ratio was higher in ARF due to rhabdomyolysis than in an unselected group of patients with other causes of ARF but not when the comparison was with sex- and age-matched controls with ARF. This suggests that this previously described feature of rhabdomyolysis simply reflects the increased muscle mass of a younger group of patients, rather than a specific effect of muscle damage. Clinical features of muscle damage were often absent and so the possibility of rhabdomyolysis should be considered in appropriate settings if the diagnosis is to be made early enough to administer treatment that may prevent ARF and the consequences of the compartment syndrome.
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PMID:The clinical and biochemical features of acute renal failure due to rhabdomyolysis. 756 17

Anesthesiological errors after clinical death during narcosis for strumectomy are considered. These errors were continuation of surgery after systole, inadequate management of the systemic arterial pressure and cerebral circulation after global ischemia, early switch-off of artificial ventilation of the lungs. All these steps led to prolonged coma, development of the apallic syndrome, and invalidism of the patient.
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PMID:[Course of apallic syndrome after clinical death during anesthesia]. 773 72

Regional cerebral metabolism of glucose (rCMRglu) was evaluated in patients who were in a coma and vegetative state to determine the level of brain function during these conditions. rCMRglu was measured in 17 discrete brain regions with (/-) [18F] -fluoro-2-deoxy-D-glucose (FDG) and positrn emission tomography (PET) in 15 patients with ;brain pathology subsequent to cardiorespiratory arrest (CA), head trauma (HT), or brain ischemia (BI) resulting from cerebrovascular accident or brain surgery. Five comatose patients (Coma group, n = 5), and 10 vegetative state patients (VS, patients awake but not aware) were studied. The VA patients were subdivided, according to the length of their VS condition, into a VS group (n = 6, < 3 months if CA or BI patients, or < 12 months if HT patients) and a persistent vegetative state group (PVS, n = 4, > 3 months if CA or BI patients of > 12 months if HT patients.) Ten normal age-matched subjects served as control. Global CMRglu was 6.72 +/- 0.93 (+/-SD) mg/100 g/min in control subjects. It was significantly (p < - 0.001) reduced to 3.70 +/- 61 in coma, to 3.45 +/- in VS, and to 2.33 +/- 0.34 mg/100 g/min in PVS patients. rCMRglu was significantly reduced (p < - 01001) from control values in all the 17 structures surveyed in every patient. In the Coma and VS groups, there was an overlapping of rCMRglu in the majority of the brain structures. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral metabolism of glucose in comatose and vegetative state patients. 777 63


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