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

Somatosensory evoked potentials (SEP) were used intraoperatively 25 cerebral aneurysm cases during the temporary occlusion of the parent artery of the aneurysm under moderate hypothermia. This technique of vascular occlusion is very useful in facilitating the dissection of difficult aneurysms as well as in reducing the risk of intraoperative rupture. Middle cerebral artery (MCA) cases in Hunt & Hess's grade III, undergoing early surgery, who had shown a transient neurological deficit at the time of subarachnoid haemorrhage or where vasospasm was evident in intraoperatively were prominent among 6 cases where the median nerve SEP was lost within 13 minutes of temporary MCA occlusion at 28.6 degrees C to 31.1 degrees C. A transient neurological deficit was seen in one of these and a permanently increased deficit in the other. In contrast, the SEP was well maintained during occlusion times of upto 52 minutes in 8 cases in the absence of any of the above circumstances. The SEP was lost after 7 minutes in one of 5 cases of internal carotid artery occlusion; this was followed by a paresis of a few hours' duration. The posterior tibial nerve SEP was absent for one minute in one of 5 cases of bilateral A1 segment occlusion; none of these cases showed a postoperative deficit. It is concluded that 1. appropriate SEP monitoring can make a major contribution to patient safety in aneurysm surgery, 2. substantially longer cerebrovascular occlusion times are permissible during hypothermia than at normal temperatures and 3. the employment of additional cerebral protective measures should be considered in cases at high risk from ischaemic damage.
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PMID:Somatosensory evoked potentials in cerebral aneurysm surgery. 339 99

A 31-year old primigravida was admitted at 31 week gestation for subarachnoid haemorrhage. Cerebral angiography revealed an aneurysm on the left middle cerebral artery. Eleven days later, the aneurysm was clipped off. General anaesthesia was induced with thiopentone, pancuronium and fentanyl, and maintained with fentanyl (40 micrograms.kg-1) and isoflurane in air/O2 with a non-rebreathing circuit. The patient was mechanically ventilated to maintain mild hypocapnia. Arterial hypotension was induced by increasing the inspired isoflurane concentration from 1 to 3 vol%. The response was immediate and a mean arterial pressure of 60 mmHg was maintained for 80 min with an inspired isoflurane concentration of 2.5 vol%. Foetal heart rate was monitored before, during and after general anaesthesia. Loss of beat to beat variation was observed after induction, and foetal heart rate slowly decreased from 150 to 115 b.min-1 at the end of the operation. Postoperative state was good, except for transitory aphasia. At 35 week gestation, the patient went into premature labour, with hypothermia of 39.5 degrees C; an emergency caesarean section was performed. The 2,340 g female infant had a 10 min Apgar score of 8. One month later, clinical examination of the mother and daughter was quite normal. The precautions and anaesthetic management of patients suffering from ruptured cerebral aneurysm during the end of pregnancy are reviewed. Hypotensive agents are discussed.
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PMID:[Hypotension induced by isoflurane for the treatment of intracranial aneurysm in late pregnancy]. 343 89

We describe a 30 year old man who developed chronic adipsic hypernatraemia and hypothermia following a subarachnoid haemorrhage from an anterior communicating artery aneurysm. Anterior pituitary function tests were normal. Hypothermia was demonstrated over 4 years with loss of the ability to control heat conservation despite body temperatures as low as 30 degrees C. He failed to experience thirst despite plasma sodium concentrations of up to 187 nmol/l and plasma osmolalities of up to 397 mOsm/kg. The slope of the plasma vasopressin-plasma osmolality curve indicated loss of the osmoreceptor. There was an absent vasopressin response to insulin-induced hypoglycaemia but a normal response to apomorphine. The apomorphine-stimulated immunoreactive vasopressin was shown to behave identically to the synthetic peptide on HPLC and was bioactive.
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PMID:Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage. 377 77

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

Temporary vessel occlusion is an effective technique used by microvascular surgeons to facilitate dissection and permanent clipping of cerebral aneurysms; however, several questions remain regarding the overall safety of this technique. To identify technical and patient-specific risk factors for perioperative stroke, the authors examined a series of patients in whom induced hypertension and mild hypothermia and intravenous mannitol administration were used as protection during temporary vessel occlusion for aneurysm clipping. The study comprises a nonconcurrent prospective analysis of 132 consecutive aneurysm clippings performed with the aid of temporary vascular occlusion and a specific antiischemic anesthetic protocol at the Massachusetts General Hospital from 1991 to 1993. Factors studied included duration of the temporary clip application, number of occlusive episodes, patient age and neurological status, presence of preoperative subarachnoid hemorrhage (SAH), and intraoperative aneurysm rupture ("forced" temporary clipping), as well as whether proximal vessel occlusion or complete aneurysm trapping was used. In a univariate analysis, patient age, intraoperative aneurysm rupture, temporary clipping lasting more than 20 minutes, clipping between the 4th and 10th day after SAH, and multiple clipping episodes were all significantly associated with stroke outcome. Multivariate logistic regression revealed that intraoperative aneurysm rupture (relative risk 5.6, p = 0.02) and a duration of temporary clip application that lasted more than 20 minutes (relative risk 9.4, p = 0.04) were independently associated with stroke outcome. Overall, 5.2% of the patients had postoperative clinical strokes. Based on their findings the authors conclude that temporary clipping is a safe adjunct to aneurysm surgery, particularly when the duration of clipping is short.
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PMID:Temporary vessel occlusion for aneurysm surgery: risk factors for stroke in patients protected by induced hypothermia and hypertension and intravenous mannitol administration. 862 52

Direct surgical management of giant or large cerebral aneurysms remains one of the most challenging topics in the neurosurgical field. Surgical results have remained unsatisfactory. We review 22 cases of large or giant aneurysms with intraluminal thrombus and/or atherosclerotic thickening of the aneurysmal neck that have received direct surgical management in our department during the period from 1984 to 1996. As initial symptoms, ten patients presented with mass effect, five with ischemic attack, and three with subarachnoid hemorrhage. Sixteen aneurysms were supratentorial and six were in the posterior fossa. Direct neck clipping was attempted in sixteen cases. Two giant basilar aneurysms among them were clipped under deep hypothermia with cardiac arrest. Simple trapping of the parent artery was performed in three aneurysms and trapping with bypass graft was also carried out in three aneurysms. Ten patients made an excellent clinical recovery. Eleven patients suffered mild to severe disability. One death resulted from brain stem infarction, not directly related with surgical management. Appropriate preoperative assessment and intraoperative management of the associated thrombus and atherosclerotic change of the aneurysmal neck are essential for obtaining acceptable surgical results of large or giant cerebral aneurysms.
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PMID:[Direct surgical management of giant and large intracerebral aneurysms, associated with intraluminal thrombus and/or atherosclerotic thickening of aneurysmal neck]. 938 65

In order to optimize therapy for the injured brain it is desirable to continuously monitor substrate delivery in the critically ill patient. Interruption of substrate delivery is a major factor of the great vulnerability to ischemic damage, which affects a majority of patients after severe head injury, stroke or subarachnoid hemorrhage. An approach to protecting the brain during ischemia is to increase the delivery of oxygen via residual blood flow through ischemic tissue. Hypothermia is also an important means of protecting brain cells from the deleterious effects of ischemia, after severe head injury, because it reduces metabolic demands. In this study we continuously measured brain oxygen, brain CO2, brain pH and brain temperature, as well as hourly brain glucose and lactate. A multiparameter sensor was inserted into brain tissue, via a three lumen bolt, along with a ventriculostomy catheter and a microdialysis probe in 60 severely head injured patients. Brain oxygen delivery was increased by stepwise increase of inspired oxygen (FiO2) from 30% to 60% to 100% over a period of 6 h, in order to test the effect of enhanced oxygen tension, on tissue oxygen. In most patients brain oxygen was initially low, and progressively increased, over the monitoring period, to a steady state level, around 30-40 mmHg. In those who died or remained vegetative, brain oxygen fell to anerobic levels. Episodes of increased ICP (n = 25), hypotension (n = 15), and respiratory difficulties (n = 9) caused an immediate increase in brain CO2. Multiple logistic regression analysis showed brain oxygen to be the strongest predictor for outcome in these patients. By increasing FiO2, an increase in oxygen delivery of more than 100%, and a simultaneous decline in lactate production was seen (p < 0.01). Brain temperature was closely related to rectal temperature, brain oxygen, and cerebral blood flow. Patients who were spontaneously hypothermic had a poor outcome (p < 0.01). A fuller understanding of dynamic factors affecting brain metabolism and substrate delivery may be obtained with extended neuromonitoring.
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PMID:Extended neuromonitoring: new therapeutic opportunities? 958 32

The injured brain may be damaged by primary impact, secondary injury from secondary damage due to initiation of destructive inflammatory and biochemical cascades by the primary injury or secondary ischemic injury following secondary insults that initiate or augment these immunological and biochemical cascades. Cerebral ischemia will arise whenever delivery of oxygen and substrates to the brain fall below metabolic needs. Many factors lead to the development of secondary insults to the injured brain during initial resuscitation, transport, surgery, and subsequent intensive care. Continuous monitoring of cerebral oxygenation (jugular oximetry, brain tissue PO2) and cerebral blood flow velocity (transcranial Doppler ultrasonography) in patients with brain trauma reveals multiple episodes of transient hypoperfusion with an adverse relationship between incidence and outcome. Secondary brain insults arise through systemic or intracranial mechanisms that reduce cerebral blood flow from compromised CPP, vascular distortion or cerebrovascular narrowing or lower oxygen delivery from hypoxemia associated with airway obstruction, pulmonary pathology, or anemia. Secondary brain ischemia remains a common pathway to secondary brain damage in most critically ill neurosurgical patients. In the future prevention of secondary brain injury may well hinge on giving a cocktail of novel agents that modify destructive biochemical and inflammatory pathways, each having a potential therapeutic window possibly in a subgroup of patients. To date, phase 3 clinical trials of several agents including PEGSOD and tyrilizad mesylate have failed to show relevant efficacy after brain trauma or subarachnoid hemorrhage. The therapeutic role of calcium channel blockers in traumatic subarachnoid hemorrhage is currently under investigation following the results of subgroup metaanalysis. Several phase 3, NMDA receptor antagonist studies are underway in brain trauma with results expected soon. Although we know that secondary insults promote excitotoxic secondary brain damage there is currently no pharmacological intervention with proven efficacy and, therefore, detection and correction of secondary insults appear to offer the best therapeutic strategy. After brain trauma, systemic hypotension, compromised CPP, raised ICP, elevated temperature, hypoxemia, and jugular bulb venous desaturation are associated with poor prognosis. Clinical trials of moderate hypothermia following brain trauma are ongoing. Following adult brain trauma maintenance of CPP above at least 65 mmHg (probably > 40 mmHg in children below 8 years) seems important to improve outcome indicating the need for continuous ICP monitoring during intensive care of brain-injured patients.
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PMID:Mechanisms and prevention of secondary brain damage during intensive care. 970 38

A new hypothermia bed system was used to induce mild hypothermia (33-35 degrees C) in six patients with stroke due to subarachnoid hemorrhage, hypertensive intracerebral hemorrhage, or embolic internal carotid artery occlusion. The system bed contained all necessary equipment including a respirator, a cooling unit, physiological monitors, and a storage battery. Surface cooling of the patients was performed using water-circulating blankets, and core temperature was maintained based on bladder temperature and a feedback computer program. During hypothermic therapy, patient transfer and radiological examination including computed tomography and positron emission tomography could be easily and safely performed. Differences between the measured bladder temperature and the target temperature were approximately +/- 0.1 degree C. The proposed hypothermia system bed may be useful for serial radiological examination of patients with stroke.
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PMID:Hypothermia bed system for stroke patients. Technical note. 1039 24

Acidosis, hypoxia, and hypoglycemia rapidly and transiently appear after reduction of cerebral blood flow. Acidosis also accompanies head trauma and subarachnoid hemorrhage. These insults result in necrotic and apoptotic loss of neurons. We previously demonstrated that transient acidification of intracellular pH from 7.3 to 6.5 induces delayed neuronal loss in cultured hippocampal slices (49). We now report that acidosis induced both necrotic and apoptotic loss of neurons. Necrosis and apoptosis were distinguished temporally and pharmacologically. Necrosis appeared rapidly and was dose dependent with the duration of the acidosis treatment. Apoptosis was delayed with maximal number of apoptotic cells seen with a 30-min acidosis treatment. Apoptotic neuronal loss was accompanied by DNA fragmentation and was blocked by inhibitors of protein and RNA synthesis, ectopic expression of the anti-apoptotic gene bcl-2, or an inhibitor of caspases, proteases known to be activated during apoptosis. Necrotic neuronal loss was unaffected by these treatments. Hypothermia, a treatment known to attenuate neuronal loss following a variety of insults, blocked both acidosis-induced necrosis and apoptosis. These results indicate that acidosis is neurotoxic in vitro and suggest that acidosis contributes to both necrotic and apoptotic neuronal loss in vivo.
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PMID:Acidosis induces necrosis and apoptosis of cultured hippocampal neurons. 1071 84


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