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

The major problems in the treatment of open fractures with high blood loss are hypothermia acidosis and coagulopathy. By improving the standards of polytrauma management and using massive transfusion systems, which should help to avoid those complications, the indication for primary limb salvage under hypovolemic shock conditions is greatly increased. The following case of an grade 3 open fracture of the femur with severe soft-tissue damage, including vascular lesions, with consecutive massive transfusion, should demonstrate that the cardiac-respiratory system can still be stabilized, even if a surgical solution seems impossible.
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PMID:[Saving the extremity by massive transfusion in grade III open femoral fracture with vascular lesion. A case report]. 934 Jul 85

For 25 years aggressive prehospital fluid administration in trauma patients has been common practice. Recent studies suggest that this may increase mortality in patients with hypovolaemic shock. These studies include retrospective analysis of patient survival, computer modelling of volume loss and replacement, controlled animal experiments, and clinical studies of trauma patients. Fluid resuscitation before definitive haemostasis has been achieved, may accelerate blood loss, cause hypothermia and result in a dilutional coagulopathy. Further studies are needed to establish optimum volume replacement in trauma patients with hypovolaemic shock.
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PMID:Early fluid resuscitation in haemorrhagic shock. 942 44

In a previous study with this dog model, post-insult hypothermia of 31 degrees C for 5 h prevented secondary intraventricular pressure (IVP) rise, but during 35 degrees C or 38 degrees C, one-half of the dogs developed delayed IVP rise to brain death. We hypothesized that 31 degrees C extended to 48 h would prevent brain herniation. Using epidural balloon inflation, we increased contralateral IVP to 62 mm Hg for 90 min. Controlled ventilation was to 72 h and intensive care to 96 h. Group 1 dogs (n = 10) were normothermic controls (37.5 degrees C). Group 2 dogs (n = 10) were surface-cooled from 15 to 45 min of balloon inflation and maintained at moderate hypothermia (31 degrees C) to 48 h. Rewarming was from 48 to 72 h. Four additional dogs of hypothermia Group 2 had to be excluded from analysis for pneumonia and/or bleeding diathesis. After balloon deflation, IVP increased to 20 mm Hg or greater at 154 +/- 215 (range 15-720) min following the insult in Group 1 and at 1394 +/- 1191 (range 210-3420) min in Group 2 (p = 0.004), still during 31 degrees C but without further increase during hypothermia. Further IVP rise led to brain death in Group 1 in 6 of 10 dogs at 44 +/- 18 (range 21-72) h (all during controlled ventilation); and in Group 2, in 6 of 10 dogs at 87 +/- 11 (range 72-96) h (p = 0.001), all after rewarming, during spontaneous breathing. Survival to 96 h was achieved by 4 of 10 dogs in Group 1, and by 7 of 10 dogs in Group 2 (NS). Three of the six brain deaths in Group 2 occurred at 96 h. The macroscopically damaged brain volume was only numerically smaller in Group 2. The vermis downward shift was 6.8 +/- 3.5 mm in Group 1, versus 4.7 +/- 2.2 mm in Group 2 (p = 0.05). In an adjunctive study, in 4 additional normothermic dogs, hemispheric cerebral blood flow showed post-insult hypoperfusion bilaterally but no evidence of hyperemia preceding IVP rise to brain death. In conclusion, in this model, moderate hypothermia during and for 48 h after temporary epidural brain compression can maintain a low IVP during hypothermia but cannot prevent lethal brain swelling after rewarming and may cause coagulopathy and pulmonary complications.
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PMID:Moderate hypothermia for 48 hours after temporary epidural brain compression injury in a canine outcome model. 960 47

As a component of a staged laparotomy for trauma, perihepatic packing can be lifesaving in the patient with exsanguinating liver injury who, due to hypothermia and coagulopathy, is unable to tolerate a more extensive procedure. However, if intra-abdominal pressure increases, the manoeuvre has been reported to compromise cardiopulmonary stability. Patients who suffer the adverse consequences of intra-abdominal hypertension are commonly managed with a loose temporary closure, frequently using an artificial material to bridge the skin defect across the incision. A case is reported where these two seemingly contradictory options were combined to achieve a successful outcome.
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PMID:Packing and temporary closure in a liver injury. 962 65

A 63-year-old woman presenting with thrombocytepenia and signs of intravascular coagulation (prothronbin time, 59%: FDP, 100 micrograms.ml-1) due to a giant hemangioma of the liver (Kasabach-Merritt syndrome) was scheduled for the resection of the right lobe of the liver. In order to protect the liver on occlusion of the right hepatic artery and portal vein, we induced mild hypothermia technique with vasodilation and surface cooling by convecting warming device together with hepatoprotective agents of PGE1 and ulinastatin. Severe, acute massive bleeding occurred due to the injury of the middle hepatic vein and from the resected surface of the liver. Her rectal temperature was 31.9 degrees C during massive bleeding. Her hemoglobin decreased to 3.9 g.dl-1. Total estimated blood loss was 22,000 ml. The weight of the resected liver was 2.5 kg. The maximum postoperative levels of T-Bil and GOT were 2.47 mg.dl-1 and 171 IU.l-1, respectively. The liver seemed to have been well preserved and no other complications were observed. The hemangioma was completely removed by excision of the right lobe of the liver. Subsequently, all coagulation parameters returned to normal, indicating a complete reversibility of the coagulopathy. Surface-induced mild hypothermia is a useful and valuable method for protecting the liver during severe massive bleeding.
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PMID:[Surface-induced mild hypothermia anesthesia for hepatectomy in a patient with a giant hemangioma of the liver (Kasabach-Merritt syndrome)]. 985 99

Thermoregulation is impaired during anesthesia for cardiac surgery. Redistribution of body heat and heat loss to the environment result in mild hypothermia before cardiopulmonary bypass. Maintenance of normothermia, rather than hypothermia, may facilitate early tracheal extubation. Hypothermia alters the distribution and decreases the metabolism of most drugs, including anesthetic drugs and muscle relaxants, thus prolonging recovery. Postoperative shivering increases metabolic rate and potentially leads to myocardial ischemia; prevention is therefore critical to the success of early tracheal extubation after cardiac surgery. Coagulopathies, increased incidence of surgical wound infection, and perioperative cardiac morbidity are other potential risk factors identified in noncardiac patients. Hypothermia, however, does have potential benefits to the patient, including protection from cerebral ischemia and hypoxemia. Mild core hypothermia (approximately 34 degrees C) may represent the optimal balance between risks and benefits for fast-track patients.
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PMID:The implications of hypothermia for early tracheal extubation following cardiac surgery. 991 65

With the organization of trauma systems, the development of trauma centers, the application of standardized methods of resuscitation, and improvements in modern blood banking techniques, the ability to aggressively resuscitate patients in extremis has evolved. The concept of the "golden hour" has translated into unprecedented speed and efficiency of trauma resuscitation with the ultimate goal of short injury-to-incision times. As the shift in care of patients in extremis has continued to move from the street to the emergency department and beyond, the focus of trauma resuscitation has shifted to the operating room and ultimately to the intensive care unit. The "new" golden hour may well be the time in the operating room before the patient reaches the physiologic limit, defined as the onset of the triad: hypothermia, acidosis and coagulopathy. Critical care nurses must understand this triad, because it forms the basis and underlying logic on which the damage control philosophy has been built. This article explores the pathogenesis and treatment of acidosis, hypothermia, and coagulopathy as it applies to the exsanguinating trauma patient.
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PMID:The trauma triad of death: hypothermia, acidosis, and coagulopathy. 1034 89

The triad of hypothermia, acidosis, and coagulopathy during initial operative and resuscitation efforts has been recognized as a significant cause of death in patients with traumatic injuries. A staged surgical approach with a brief initial laparotomy, subsequent intensive care unit resuscitation, and a planned reoperation is an emerging technique used in trauma surgery, with application to a variety of other surgical challenges. Successful damage control therapy requires a coordinated multidisciplinary team effort by a trauma team experienced in the process of damage control operations, intensive care unit priorities, and potential complications of this innovative surgical approach.
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PMID:Damage control surgery. 1034 90

Hypothermia occurs commonly in severely injured patients and is associated with a high mortality rate. It perturbs the normal homeostatic response to injury and affects multiple organ systems and physiologic processes. In trauma patients, hypothermia-induced coagulopathy often leads to marked bleeding diathesis and frequently provides a challenge for the surgeon. Once hypothermia occurs, it is often difficult to correct. Efforts to prevent and treat hypothermia in trauma patients should be instituted in the field and continued as an integral part of the resuscitation process. Hospital personnel and physicians at various levels caring for trauma patients from the initial injury and thereafter should bear in mind that a patient's temperature is as important as any other vital sign. Appropriate measures for preventing and treating hypothermia should be instituted promptly and tended to with utmost vigilance.
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PMID:Hypothermia in trauma patients. 1035 64

"Damage control" is a surgical strategy for the staged repair of severe trauma that aims to avoid an irreversible physiologic insult marked by a self-propagating combination of hypothermia, coagulopathy, and acidosis. The point beyond which the physiologic insult becomes irreversible, however, remains ill-defined. The aim of this study was to address this problem by means of a dynamic computer model of heat loss during laparotomy for exsanguinating hemorrhage. A single compartment model was developed using a graphic modeling tool and was implemented to calculate the time interval from the beginning of laparotomy to a core temperature of 32 degrees C, which is a marker of irreversible physiologic derangement in injured patients. A series of simulation runs showed that the exposed peritoneum is the dominant factor contributing to heat loss; the bleeding rate has a less marked effect. Elevation of the ambient temperature and rapid abdominal closure are effective interventions available to the surgeon to modify the heat loss curve. This study shows that during a "damage control" laparotomy for exanguinating hemorrhage the window of opportunity for salvage before the onset of an irreversible physiologic insult is no longer than 60 to 90 minutes.
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PMID:Computer simulation of hypothermia during "damage control" laparotomy. 1044 28


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