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At least 19 recordsLinked to original sources
PubMed2000

Therapeutic hypothermia for head injury.

BACKGROUND: Mild to moderate induced hypothermia has been used in the treatment of head injury for over 50 years, although few randomised controlled trials have been performed. Recent encouraging results from small, single-centre trials and consistent findings of a cerebral protection effect of cooling in laboratory models of global ischaemia has led to a renewed interest in the area. OBJECTIVES: To determine whether the use of mild therapeutic hypothermia in the treatment of moderate and severe head injury improves short-term control of intracranial pressure (ICP) and long-term functional outcome. SEARCH STRATEGY: Electronic searches of the Injuries Group trial registry and EMBASE for any relevant randomised trials, supplemented by hand searching of conference proceedings and reference lists of relevant articles. SELECTION CRITERIA: All randomised controlled trials of mild hypothermia versus control (open or normothermia) in the treatment of patients with any closed head injury requiring hospitalisation. Mild hypothermia was defined as local or systemic cooling to a target temperature of at most 34-35 degrees Celsius for a period of at least 12 hours. Outcome was all-cause mortality and death or severe disability at the end of the scheduled follow-up period. All trials were assessed by two reviewers, and included or excluded on a consensus basis. DATA COLLECTION AND ANALYSIS: Eleven potential trials of therapeutic hypothermia for head injury were found, of which two are ongoing and one is awaiting assessment. The eight remaining trials were included in the systematic review. Data on death, GOS score at final follow-up, complications and ICP were sought and extracted, either from published material or by contact with the investigators. Mantel-Haenzel odds ratios and 95% confidence intervals were calculated for death and death and severe disability for each trial on an intention-to-treat basis. No quantitative synthesis of data on either complications or ICP was attempted. Trials of immediate and deferred hypothermia were analysed separately. MAIN RESULTS: Active immediate hypothermic treatment was associated with a 33% non-significant (p=0.16) reduction in the odds of death at the end of treatment or final follow-up, (OR 0.67, 95% confidence interval 0.38 to 1.17), and a 61% reduction (p=0.004) in the odds of being dead or severely disabled, (OR 0.39, 95% confidence interval 0.20 to 0.74). Similar effect sizes were found for delayed hypothermia. These results are, however, based on a few small trials each of less than 100 patients. A multi-centre trials of hypothermia versus control in 392 patients will be reporting results in 1999, providing substantially more evidence than is currently available. REVIEWER'S CONCLUSIONS: Although this review would suggest a strong positive effect of therapeutic hypothermia, the results are based on several small trials carried out in single, specialist centres. The results of a large multi-centre trial are expected in 1999 and will more than treble the available evidence. Until these results have been released, it would be inappropriate to make any short-term recommendations for clinical practice or research.

Craniocerebral Trauma↗
PubMed2003

After spontaneous hypothermia during hemorrhagic shock, continuing mild hypothermia (34 degrees C) improves early but not late survival in rats.

BACKGROUND: Spontaneous hypothermia is common in victims of severe trauma. Laboratory studies have shown benefit of induced (therapeutic) mild hypothermia (34 degrees C) during hemorrhagic shock (HS). Clinical data, however, suggest that hypothermia, which often occurs spontaneously in trauma patients, is detrimental. Because critically ill trauma patients are usually cool, the clinical question, which has not been explored in the laboratory with long-term outcome, is whether maintaining hypothermia or actively rewarming the patient improves outcome. We hypothesized that after spontaneous cooling during HS, continuing mild therapeutic hypothermia during resuscitation is beneficial compared with active rewarming. METHODS: In study A, under light isoflurane anesthesia, 24 Sprague-Dawley rats were bled over 10 minutes to, and maintained at, mean arterial pressure (MAP) of 40 mm Hg until reuptake of 30% of maximal shed blood volume was needed. Rectal temperature (Tr) decreased spontaneously to, and was then maintained at, 35 degrees C during HS. Fluid resuscitation included the remaining shed blood and up to 400 mL/kg of lactated Ringer's solution with 5% dextrose over 4 hours. During resuscitation, three groups (n = 8 each) were studied: normothermia (rapid rewarming to Tr 37.5 degrees C at the beginning of resuscitation); hypothermia-2 h (cooling to Tr 34 degrees C to resuscitation time 2 hours); and hypothermia-12 h (cooling to Tr 34 degrees C to 12 hours). Rats were observed to 72 hours. In study B, more severe HS than in study A was studied. HS was induced with 3 mL/100 g blood withdrawal over 15 minutes followed by maintenance of MAP of 40 mm Hg until 50% of maximal shed blood volume was needed. Two groups (n = 8 each) were studied: normothermia and hypothermia-12 h. Data are presented as mean +/- SD or median (range). RESULTS: In study A, both hypothermia groups had higher MAP and lower heart rates during resuscitation than the normothermia group (p < 0.01). Survival to 72 hours was achieved in three of eight rats in the normothermia group and two of eight in each hypothermia group. Thirteen of 17 deaths occurred after 24 hours. In study B, for resuscitation, the hypothermia group needed less fluid (53 +/- 6 mL vs. 79 +/- 32 mL, p < 0.05), but had higher MAP (p < 0.01), lower heart rate (p < 0.01), and lower lactate level (p = 0.06). All rats died before 72 hours. The hypothermia group had longer survival time (24.5 [13-48.5] hours) than the normothermia group (7.5 [1.5-19] hours) (p = 0.003 by life table analysis). CONCLUSION: After spontaneous cooling during moderately severe HS, mild, controlled hypothermia during resuscitation does not seem to affect long-term survival. After more severe HS, hypothermia increases survival time. Hypothermia supports arterial pressure during resuscitation from severe HS.

Animals↗
PubMed2003

Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia.

OBJECT: This study was performed to determine whether moderate hypothermia (31 degrees C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34 degrees C). METHODS: Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31 degrees C, the volume of intravenous fluid infusion was increased significantly from 1.9 +/- 0.9 to 2.6 +/- 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 +/- 3.1 to 8.2 +/- 4.4 microg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 +/- 13.1 to 85.1 +/- 10.5 mm Hg (p < 0.01) and from 92.2 +/- 13.8 to 72.2 +/- 14.3 beats/minute at (p < 0.01) at 34 and 31 degrees C, respectively. Arterial base excess was significantly aggravated from -3.3 +/- 4 at 34 degrees C to -5.6 +/- 5.4 mEq/L (at 31 degrees C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31 degrees C decreased significantly compared with those at 34 degrees C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients. ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. CONCLUSIONS: The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.

Adolescent↗
PubMed1977

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. IV. Topical atrial hypothermia in normothermic beating hearts.

This study compares (1) the effects of slowing heart rate by topical hypothermia in hearts perfused at 37 degrees C. with bradycardia produced by perfusion hypothermia (28 degrees C.) and (2) the consequences of counteracting the bardycardic effects of perfusion hypothermia by atrial pacing. Topical atrial hypothermia (myocardial temperature 37 degrees C.) produced a level of bradycardia comparable to perfusion hypothermia (82 vs. 71 beats per minute), but reduced myocardial oxygen requirements 25 per cent more than perfusion with 28 degrees C. blood. Myocardial oxygen uptake per beat did not change with topical atrial hypothermia but increased 40 per cent with perfusion hypothermia. Counteracting the bradycardic effects of perfusion hypothermia with atrial pacing (to 130 beats per minute) reduced subendocardial flow 25 per cent, caused a redistribution of flow away from the subendocardium, and produced evidence of ischemia on the intracavitary electrocardiogram. This study shows that (1) topical atrial hypothermia with systemic normothermia reduced myocardial oxygen demands as effectively as perfusion hypothermia and (2) subendocardial ischemia develops in beating empty hearts when the expected bradycardia of hypothermia does not occur.

Animals↗
PubMed2002

Systemic hypothermia, but not regional gut hypothermia, improves survival from prolonged hemorrhagic shock in rats.

BACKGROUND: Extracorporeal blood perfusion of the gut or enterectomy can improve survival during hemorrhagic shock (HS), suggesting that the gut may be of primary importance in resuscitation. We hypothesized that cooling the gut alone could improve survival in a rat HS model and avoid potential deleterious effects of systemic hypothermia. METHODS: Thirty-two Sprague-Dawley rats were anesthetized with halothane. The gut (small intestine, cecum, and colon) was exteriorized. The right atrial (T ), rectal, and gut (T ) intraluminal temperatures were monitored. HS was induced by withdrawal of 2 mL of blood per 100 g body weight over 10 minutes. Mean arterial pressure was then maintained at 35 to 40 mm Hg to HS 90 min. From HS 20 min to resuscitation time 1 h, rats were randomized into four groups (n = 8 each): normothermia (T and T approximately 38.0 degrees C), gut-25 degrees C (T approximately 38 degrees C, T approximately 25 degrees C, induced by rinsing the gut with cooled saline), gut-33 degrees C (T approximately 38 degrees C, T approximately 33 degrees C), and systemic hypothermia (T approximately 33 degrees C, T approximately 25 degrees C). At HS 90 min, shed blood and Ringer's solution were infused to restore normotension. Survival, metabolism, and tissue damage were observed to 72 hours. RESULTS: Blood pressure was not different between groups. Compared with the normothermia group, the systemic hypothermia group had lower base deficit and lactate, and needed less fluid during resuscitation for normotension (p < 0.05), but these values were not different in the gut hypothermia groups. In addition, there were no significant improvements in tissue protection induced by regional gut hypothermia, whereas the systemic hypothermia group had lower plasma potassium, lower ornithine carbamoyltransferase (marker of liver injury), and higher glucose levels after HS (all p < 0.05). All rats in the systemic hypothermia group survived to 72 hours, whereas there was only one survivor in the normothermia group, two in the gut-33 degrees C group, and none in the gut-25 degrees C group (all p < 0.05 vs. systemic hypothermia). CONCLUSION: Cooling the gut alone does not improve acute survival from HS, suggesting that early deaths are not secondary to gut ischemia. Mild systemic hypothermia allowed 100% survival from prolonged HS.

Animals↗
PubMed1992

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

BACKGROUND AND PURPOSE: Mild cerebral hypothermia (34 degrees C) induced immediately after cardiac arrest improves outcome. Deep postarrest hypothermia (15 degrees C) has not been studied. METHODS: We used our dog model of normothermic ventricular fibrillation (no blood flow) of 12.5 minutes, reperfusion by brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 72 hours. Head surface cooling and bypass cooling were performed from start of reperfusion to 1 hour. Five groups of six dogs each were compared: group I, normothermic controls; group II, deep hypothermia (15 degrees C); group III, moderate hypothermia (30 degrees C); group IV, mild hypothermia (34 degrees C); and group V, mild hypothermia with head surface cooling begun during no flow. RESULTS: In control group I, five dogs remained comatose (overall performance category [OPC] 4) and one severely disabled (OPC 3). In group II, four dogs achieved OPC 4 and two dogs OPC 3 (NS versus group I). Compared with group I, OPCs were better in group III (p less than 0.05), group IV (p less than 0.05), and group V (p less than 0.05). Neurological deficit scores were also better in groups III, IV, and V than in groups I or II (p less than 0.05). Total brain histological damage scores were better in group III (p = 0.02), group IV (p = 0.06), and group V (p less than 0.05) than in group I. In group II, OPC and neurological deficit scores were the same and histological damage scores numerically worse than in group I and all were worse than in groups III, IV, and V (p less than 0.05). Cardiovascular complications and myocardial morphological damage in groups II and III were worse than in groups I, IV, and V (p less than 0.05). CONCLUSIONS: Mild or moderate cerebral hypothermia induced immediately after cardiac arrest improves cerebral outcome, more likely when initiated during arrest, whereas deep postarrest hypothermia can worsen cerebral and cardiac outcome.

Animals↗
PubMed1991

Profound hypothermia (less than 10 degrees C) compared with deep hypothermia (15 degrees C) improves neurologic outcome in dogs after two hours' circulatory arrest induced to enable resuscitative surgery.

Deaths from uncontrollable hemorrhage might be prevented by arresting the circulation under protective hypothermia to allow resuscitative surgery to repair these injuries in a bloodless field. We have shown previously that in hemorrhagic shock, circulatory arrest of 60 minutes under deep hypothermia (tympanic membrane temperature, Ttm = 15 degrees C) was the maximum duration of arrest that allowed normal brain recovery. We hypothesize that profound cerebral hypothermia (Ttm less than 10 degrees C) could extend the duration of safe circulatory arrest. In pilot experiments, we found that the cardiopulmonary system did not tolerate arrest at a core (esophageal) temperature (Tes) of less than 10 degrees C. Twenty-two dogs underwent 30-minute hemorrhagic shock (mean arterial pressure 40 mm Hg), rapid cooling by cardiopulmonary bypass (CPB), blood washout to a hematocrit of less than 10%, and circulatory arrest of 2 hours. In deep hypothermia group 1 (n = 10), Ttm was maintained at 15 degrees C during arrest. In profound hypothermia group 2 (n = 12), during cooling with CPB, the head was immersed in ice water, which decreased Ttm to 4 degrees-7 degrees C. The Tes was 10 degrees C in all dogs during arrest. Reperfusion and rewarming were by CPB for 2 hours. Controlled ventilation was to 24 hours, intensive care to 72 hours. In the 20 dogs that followed protocol, best neurologic deficit scores (0% = normal, 100% = brain death) at 24-72 hours were 23% +/- 19% in group 1 and 12% +/- 8% in group 2 (p = 0.15). Overall performance categories and histologic damage scores were significantly better in group 2 (p = 0.04 and p less than 0.001, respectively). We conclude that profound cerebral hypothermia with CPB plus ice water immersion of the head can extend the brain's tolerance of therapeutic circulatory arrest beyond that achieved with deep hypothermia.

Animals↗
PubMed1978

Influence of moderate hypothermia and deep local hypothermia with or without cardioplegia on intramyocardial oxygen tension during ischemic cardiac arrest.

The effect of ischemic cardiac arrest on intramyocardial oxygen tension (MpO2) in hearts of dogs under normothermia, moderate hypothermia as well as in heart in deep local hypothermia and in hearts subjected to deep local hypothermia combined with Bretschneider cardioplegia was examined. In the last mentioned condition the myocardial oxygen depletion was slowest and even at the end of 30 minutes of anoxia MpO2 was significantly higher in comparison with the other groups. Release of myocardial ischemia resulted in an immediate rise of MpO2 to overshoot levels in animals in normothermia and with deep local hypothermia alone, while in animals in moderate hypothermia and with combination of local hypothermia with cardioplegia reversed only to preanoxic values. On the basis of MpO2 measurements and of postischemic recovery of cardiac function the authors conclude that the combination of deep local hypothermia with cardioplegia is superior for myocardial protection to other used techniques.

Animals↗
PubMed2000

Mild resuscitative hypothermia to improve neurological outcome after cardiac arrest. A clinical feasibility trial. Hypothermia After Cardiac Arrest (HACA) Study Group.

BACKGROUND AND PURPOSE: Recent animal studies showed that mild resuscitative hypothermia improves neurological outcome when applied after cardiac arrest. In a 3-year randomized, prospective, multicenter clinical trial, we hypothesized that mild resuscitative cerebral hypothermia (32 degrees C to 34 degrees C core temperature) would improve neurological outcome after cardiac arrest. METHODS: We lowered patients' temperature after admission to the emergency department and continued cooling for at least 24 hours after arrest in conjunction with advanced cardiac life support. The cooling technique chosen was external head and total body cooling with a cooling device in conjunction with a blanket and a mattress. Infrared tympanic thermometry was monitored before a central pulmonary artery thermistor probe was inserted. RESULTS: In 27 patients (age 58 [interquartile range [IQR] 52 to 64] years; 7 women; estimated "no-flow" duration 6 [IQR 1 to 11] minutes and "low-flow" duration 15 [IQR 9 to 23] minutes; admitted to the emergency department 36 [IQR 24 to 43] minutes after return of spontaneous circulation), we could initiate cooling within 62 (IQR 41 to 75) minutes and achieve a pulmonary artery temperature of 33+/-1 degrees C 287 (IQR 42 to 401) minutes after cardiac arrest. During 24 hours of mild resuscitative hypothermia, no major complications occurred. Passive rewarming >35 degrees C was accomplished within 7 hours. CONCLUSIONS: Mild resuscitative hypothermia in patients is feasible and safe. A clinical multicenter trial might prove that mild hypothermia is a useful method of cerebral resuscitation after global ischemic states.

Brain↗
PubMed2001

A multicenter prospective randomized controlled trial of the efficacy of mild hypothermia for severely head injured patients with low intracranial pressure. Mild Hypothermia Study Group in Japan.

OBJECT: The criteria for the use of mild hypothermia (34 degrees C) in severely head injured patients have not been standardized. A prospective randomized controlled trial was conducted to determine whether mild hypothermia is essential in the treatment of severely head injured patients with low intracranial pressure (ICP). METHODS: At 11 medical centers, 91 severely head injured patients with an admission Glasgow Coma Scale score of 8 or less in whom ICP could be maintained below 25 mm Hg by conventional therapies were divided randomly into two groups: the mild hypothermia group (HT group, 45 patients) and the normothermia group (NT group, 46 patients). Patients in the HT group were exposed to mild hypothermia (34 degrees C) for 48 hours, followed by rewarming at 1 degrees C per day for 3 days, whereas patients in the NT group were exposed to normothermia (37 degrees C) for 5 days. The two groups were similar with respect to prognostic factors, and there was no difference in clinical outcome at 3 months postinjury. During treatment, there was a significantly greater use of neuromuscular blocking agents in the HT group (p = 0.011). During the initial 2 weeks postinjury, the incidences of pneumonia, meningitis, leukocytopenia, thrombocytopenia, hypernatremia, hypokalemia, and hyperamylasemia were significantly higher in the HT than in the NT group (p < 0.05). CONCLUSIONS: Mild hypothermia should not be used for the treatment of severely head injured patients with low ICP because this therapy conveys no advantage over normothermia in such patients.

Adolescent↗
PubMed1987

Techniques of aortic arch replacement: profound hypothermia versus moderate hypothermia with innominate artery perfusion.

Aortic arch resection remains a challenging problem. At present, the most reliable technique appears to be profound hypothermia and circulatory arrest, although long cardiopulmonary bypass times and coagulopathy remain significant problems. Interest in alternative procedures continues. Herein, we report our experience of aortic arch replacement in eight patients using profound hypothermia (12 to 17 degrees C) and circulatory arrest in six patients (Group I) and moderate (20 degrees C) hypothermia with low flow (200 ml/min), pressure-monitored (100 mm Hg) innominate artery perfusion by way of a 14 Ga. cannula in 2 (Group II). Arch repair was by patch graft in two, and tube graft in six. Concomitant ascending aortic replacement was performed in five, aortic valve replacement in four, and coronary bypass in two. Circulatory arrest times ranged from 15 to 71 minutes in Group I and were 15 minutes and 35 minutes in Group II. All patients survived. One patient in Group I had a neurologic injury of moderate severity, probably due to a hypoxic postoperative cardiac arrest. We have found low flow pressure-monitored innominate artery perfusion and moderate hypothermia to be simple and expedient, and we will continue use of this technique.

Aged↗
PubMed2003

Closing the audit loop--prevention of perioperative hypothermia: audit and reaudit of perioperative hypothermia.

BACKGROUND AND OBJECTIVE: Perioperative hypothermia is generally regarded as undesirable, but its incidence rate in the elective procedures in our hospital and the effect of the preventative measures taken against it were unknown. An initial audit indicated that postoperative hypothermia occurred. Therefore, changes in practice were implemented to address the problem. A further audit was then undertaken to assess the impact of these measures. METHODS: The first audit recorded data from 177 patients undergoing major elective surgical procedures. Variables recorded were: ASA classification, duration of operation, use and description of preventative measures for hypothermia, blood loss, intravenous fluids, and core and peripheral temperatures on arrival and discharge from the recovery room. The subsequent audit included 158 patients undergoing major general, orthopaedic or vascular surgical procedures. Patients had core temperatures measured preoperatively, immediately upon arrival in the recovery room, and just before discharge back to the ward. Core temperatures in both audits were measured using an infrared temperature probe. RESULTS: The mean body temperature on arrival in the recovery room of patients in the initial audit was 35.5 degrees C (range 32.2-37.2, SD +/- 0.74), and in the subsequent audit 36.6 degrees C (33.6-38.2, +/- 0.72). These differences reached significance (P < 0.0001). This was despite an average duration of surgery of 133.5 (25-330) min in the initial study compared with 154.7 (90-480) min subsequently. CONCLUSIONS: We found that with simple but consistently implemented changes in practice, postoperative hypothermia in elective patients could largely be eradicated.

Anesthesiology↗
PubMed1998

Mild hypothermia: an alternative to deep hypothermia for achieving neuroprotection.

The role of excitotoxins in the ischemic cascade that results in ischemic neuronal death has been clearly defined and has brought about attempts to halt the progression of neurologic damage. Improved understanding of this process has allowed for the development of interventions to optimize neurologic outcome following periods of ischemia. Deep hypothermia (15-22 degrees C) has long been recognized as one method of achieving neuroprotection, but is not without serious implications and risks to the patient. Mild hypothermia (32-34 degrees C) is evolving as an alternative neuroprotective measure that has been shown to improve neurologic outcome in experimental models of ischemia and head injury, as well as in recent head injury clinical trials. It has been safely used intraoperatively in a large series of patients undergoing craniotomy. Mild hypothermia is a technique that may soon be commonly employed alone or in conjunction with other methods of neuroprotection. Nurses caring for patients undergoing this technique must be aware of the practice implications associated with this procedure and adapt their care accordingly.

Brain Ischemia↗
PubMed2003

Pediatric nonenvironmental hypothermia presenting to the emergency department: Episodic spontaneous hypothermia with hyperhidrosis.

Cases of pediatric nonenvironmental hypothermia are uncommon. When presenting to the emergency department, these patients are often evaluated for possible sepsis/shock, brain tumors, endocrine disorders, and drug ingestions. We report a case of a 5-year-old girl who presented to the pediatric emergency department on two occasions with hypothermia and lethargy. She was found to have an unusual cause of her symptoms: episodic spontaneous hypothermia with hyperhidrosis.

Child, Preschool↗
PubMed1984

Acid-base control during hypothermia. Acid-base control in children during hypothermia without temperature correction of pH and PCO2.

In 28 children undergoing cardiopulmonary bypass with deep hypothermia for open heart surgery, an attempt was made to maintain pH at 7.4 not corrected for temperature by varying the CO2 concentration supplied to the oxygenator so that the PaCO2 was 5.33 kPa, not corrected for temperature. One to two percent CO2 gave satisfactory results. Five percent CO2 had previously been given. No adverse clinical side effects were noted, and the acid-base status remained stable for 24 hours in 16 patients. There are strong theoretical reasons for maintaining a pH of 7.4, uncorrected for temperature, during hypothermia and a clinical impression was gained of better myocardial function and improved systemic and cerebral perfusion.

Acid-Base Equilibrium↗