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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients who were deeply unconscious (GCS = 4) following head injuries, sustained whilst intoxicated with alcohol, became hypothermic due to cold exposure. Despite negative prognostic factors both underwent craniotomy and evacuation of large acute subdural haematoma. After intensive postoperative management and rehabilitation both have made satisfactory recoveries. The contribution of hypothermia to their unpredicted favourable outcome is discussed, and the importance of recording temperature in head-injured patients is emphasized.
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PMID:Hypothermia and severe head injury. 292 40

Cerebral hypothermia treatment of critical brain injury patients was studied based on the management and control of cerebral thermo-pooling, synaptic excitation, hypermetabolic demand, and the systemic critical condition of the metabolic reserve. The initial pathophysiological changes after trauma included a progressive increase in brain tissue temperature. Such cerebral thermo-pooling, which reached a maximum of 43.8 degrees C, can change or damage the vascular proteins directly. The brain tissue temperature was influenced by four factors: 1. the cerebral metabolism, 2. the systemic excess energy metabolism, 3. the CPP that carries the systemic energy to the brain tissue, and 4. the cerebral blood flow that leads to washout of brain tissue temperature. Mild cerebral hypothermia (32-33 degrees C) managed by the whole body compartment cooling technique in the critical conditions of diffuse brain injury patients (GCS < 4) produced a good recovery in 8 of 10 patients. Continuous monitoring of the jugular venous oxygen saturation and BTT/TMT was effective for evaluating cerebral ischemia and oxygen metabolic disturbances even during cerebral hypothermia treatment.
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PMID:Systemic management of cerebral edema based on a new concept in severe head injury patients. 797 43

Eleven patients with severe head injuries were treated by artificial moderate hypothermia (32.0-33.0 degrees C). Measurement of the serum levels of anterior pituitary hormones (LH, FSH, TSH, and PRL) and the response of these hormones to the respective releasing hormones was done in the 11 patients before and during hypothermia. All 11 patients were under GCS 5. Those with brain death during hypothermia were excluded. Moderate hypothermia was performed for 3-7 days and involved cooling to 32.0-33.0 degrees C (Jugular venous blood temperature). The peak value of LH, FSH, TSH and PRL to administration of TRH or LH-RH during hypothermia were significantly lower than those before hypothermia, while basal values of those hormones were not affected by this treatment. These findings suggested that anterior pituitary function were suppressed by moderate hypothermia.
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PMID:[Anterior pituitary functions in patients with severe head injuries treated with moderate hypothermia]. 904 26

We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-D-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF (n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). As part of an ongoing study, patients were randomized within 6 hours after injury to either hypothermia (32 degrees C) or normothermia (37 degrees C) treatments for 24 hours. Otherwise, patients received standard neurointensive care. Quinolinic acid was measured by mass spectrometry. Univariate and multivariate analyses were used to compare CSF quinolinic acid concentrations with age, gender, GCS, time after injury, mortality, and treatment (hypothermia versus normothermia). Quinolinic acid concentration in CSF increased maximally to 463 +/- 128 nmol/L (mean +/- SEM) at 72 to 83 hours after TBI. Normal values for quinolinic acid concentration in CSF are less than 50 nmol/L. Quinolinic acid concentration was increased 5- to 50-fold in many patients. There was a powerful association between time after TBI and increased quinolinic acid (P < 0.00001), and quinolinic acid was higher in patients who died than in survivors (P = 0.003). Age, gender, GCS, and treatment (32 degrees C versus 37 degrees C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinic acid concentration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.
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PMID:Quinolinic acid is increased in CSF and associated with mortality after traumatic brain injury in humans. 962 84

We have presented a new concept of brain hypoxia oriented brain hypothermia treatments. All severe brain injury patients (148 cases) were GCS < 6. The masking brain hypoxia by brain thermo pooling, catecholamine surge induced cardiac dysfunction and intestinal vasodilatation, reduction of Hb-2.3 diphosphoglyserate were major target of initial treatment. These specific brain hypoxia was only controlled by brain hypothermia (34-32 degrees C), oxygen delivery > 800 ml/min. and AT-III > 100%. 2. The brain hypothermia were very successful to prevent masking brain hypoxia, selective radical attack to A10 dopamine nervous system, and brain edema. However, metabolic shift to lipid metabolism and lower growth hormone related immune crisis were recorded as a negative factors. Clinical results were so advanced. The mortality were 44 in 148 cases (30%), good recovery were 59 in 148 cases (40%), mild disability were 20 in 148 cases (13%) and vegetate state were only 15 in 148 cases (10%). The combination of brain hypothermia and replacement of cerebral dopamine were very successful to prevent the vegetation in severe brain injury.
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PMID:[The brain hypothermia therapy for prevention of vegetation after severe brain injury]. 1048 50

The neuroprotective action and effect of hypothermia on the neurochemical system is not well understood. The present study was performed using six patients with GCS scores of 5 or less to clarify the relationship between monitored brain temperature, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and oxygen saturation of the jugular venous blood (SjO2). Changes in concentration of excitatory amino acids, glutamate (GLU) and aspartate (ASP), and NO2 were studied using intracerebral microdialysis as well as in jugular venous blood and cerebrospinal fluid (CSF). Changes in brain temperature, CPP and SjO2 resulting from hypothermia and brain death associated with markedly higher concentrations of and fluctuations in the concentrations of GLU, ASP and NO2 were observed in the dialysate than in the jugular venous blood or CSF. Hypothermic treatment significantly reduces excitatory amino acid and NO2 concentrations, a finding which was associated with an improvement in CPP and SjO2. Measurement of GLU and ASP using intracerebral microdialysis is a clinically useful method for clarifying abnormal neurochemical events associated with severe head injury and for evaluating the effects of hypothermia.
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PMID:Neurochemical monitoring in the management of severe head-injured patients with hypothermia. 1109 69

A nationwide survey of the management of severe head injury was carried out in 1988 by sending the questionnaires to 1,088 main neurosurgical hospitals in Japan. The items of the survey included annual number of patients with closed severe head injury (GCS score of 8 or less), place of patients' care, type of neuromonitorings, medical and surgical treatments, severity and outcome measures. Out of 1,088 questionnaires, 457 (42% response rate) were collected and analyzed. Characteristic features of the management status were the scarcity of patients annually in each institution, limited use of specific neuromonitorings, and variety of the actual managements. Aggressive managements such as hyperventilation, barbiturate and/or hypothermia have been employed in many hospitals to control high ICP. External and internal decompression are also used widely for intradural hematomas. These results clarified not only present status of Japan but also the problems to be solved in the actual managements.
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PMID:Result of nationwide survey of the management of severe head injury in Japan. 1178 52

OBJECTIVE: To summarize the therapeutic experience of 24 patients of traumatic head injuries with GCS score of 3. METHODS: Twenty-four most severely head-injured patients with GCS score of 3 who were admitted to our department from Jan 1995 to Mar 1998 were retrospectively analyzed. RESULTS: Twelve cases (50.0%) survived, of which 7 cases (29.2%) had good recovery or moderate disability and 5 cases with severe deficits (20.8%), and the other 12 died (50.0%) after therapy. CONCLUSIONS: The prognosis of most severely head-injured patients with GCS score of 3 could be improved by early intracranial hematoma removal with large decompressive craniotomies, early moderate hypothermia therapy, early assistant ventilation and effective prevention and treatment of complications.
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PMID:Clinical experience of the management for the most severely head-injured patients with GCS score of 3. 1190 Jun 58

Although therapeutic hypothermia for patients with head injury has improved the outcome, the results in the most severe cases (GCS 3-6) have not been satisfactory so far. We induced hypothermia in head injury patients within 3 hours after the trauma, and compared the outcome of the treatment without hypothermia. Fourteen patients with GCS less than 6 were entered into this study (age range 13 to 58, mean 27.0 years). Seven of them were treated by hypothermia and 6 by the conventional method. The patients undergoing hypothermia were cooled to 34 degrees C within 3 hours after injury, kept at 32-34 degrees C for 48 hours, and then rewarmed. The outcome was evaluated at 6 months post-trauma, and the results were compared in the two groups. Therapeutic hypothermia dramatically suppressed brain swelling on CT in 3 of 7 patients. Four patients including these 3 showed a favorable outcome (good or moderate disability) and 3 died in the hypothermia group. In the conventional treatment group, only 1 patient was moderately disabled and 6 exhibited an unfavorable outcome (severely disabled, vegetative, or death). Early induction of hypothermia can improve the outcome in patients with severe head injury by reducing the severe brain swelling.
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PMID:Effect of early induction of hypothermia on severe head injury. 1216 65

Striking gender differences have been reported in the pathophysiology and outcome of acute neurological injury. Greater neuroprotection in females versus males may be due, in part, to direct and indirect sex hormone-mediated antioxidant mechanisms. Progesterone administration decreases brain levels of F(2)-isoprostane, a marker of lipid peroxidation, after experimental traumatic brain injury (TBI) in male rats, and estrogen is neuroprotective in experimental neurological injury. In this study, we evaluated the effect of gender on lipid peroxidation, as assessed by cerebrospinal fluid (CSF) levels of F(2)-isoprostane, after severe TBI in humans. Lipid peroxidation was assessed in CSF from 68 adults enrolled in two randomized controlled trials evaluating the effect of therapeutic hypothermia after severe TBI (Glasgow coma scale [GCS] score </= 8). Patients treated with hypothermia (n = 41, 12 females, 29 males) were cooled to 32-33 degrees C (within approximately 6 h) for either 24 or 48 h and then re-warmed. F(2)-isoprostane levels were assessed by ELISA in ventricular CSF samples (n = 199) on day 1, 2, and 3. The association between age, GCS score, time, gender, treatment, duration of treatment, core temperature at the time of CSF sampling, secondary hypoxemia, and CSF F(2)-isoprostane level was assessed by multivariate and dichotomous analyses. F(2)-isoprostane was approximately 2-fold higher in males than females (145.8 +/- 39.6 versus 75.4 +/- 16.6 pg/mL, day 1 p = 0.018). An effect of time after injury (p = 0.007) was reflected by a marked early peak in F(2)-isoprostane (day 1). CSF F(2)-isoprostane was also associated with hypoxemia (p = 0.04). Hypothermia tended to decrease F(2)-isoprostane levels only in males on d1 after TBI. To our knowledge, this is the first study showing gender differences in lipid peroxidation after clinical TBI. Lipid peroxidation occurs early after severe TBI in adults and is more prominent in males vs females. These results established that gender is an important consideration in clinical trial design, particularly in the case of antioxidant strategies.
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PMID:Marked gender effect on lipid peroxidation after severe traumatic brain injury in adult patients. 1498 60


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