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Mild hypothermia (34-35 °C) increases peri-operative blood loss. We have previously demonstrated the beneficial effect of in vitro desmopressin on impairment of primary haemostasis associated with hypothermia. This study evaluated subcutaneous desmopressin in 52 healthy volunteers, randomly assigned to receive either normal saline or desmopressin 1.5, 5 or 15 μg (with 13 in each group). Blood samples were collected before and 2 h after drug administration and incubated at 32 and 37 °C. Platelet function analyser PFA-100(®) closure times were measured. Hypothermia at 32 °C prolonged mean (95% CI) closure times (for adenosine diphosphate/collagen by 11.3% (7.5-15.2%) and for adrenaline/collagen by 16.2% (11.3-21.2%); these changes were reversed by desmopressin. A very small dose was found to be effective (1.5 μg); this dose did not significantly change closure times at 37 °C, but fully prevented its prolongation at 32 °C. Subcutaneous desmopressin prevents the development of hypothermia-induced impairment of primary haemostasis., (© 2011 The Authors. Anaesthesia © 2011 The Association of Anaesthetists of Great Britain and Ireland.)

Summary: Hypothermia and acidosis lead to an impairment of coagulation. It has been demonstrated that desmopressin improves platelet function under hypothermia. We tested platelet function ex vivo during hypothermia and acidosis. Blood samples were taken from 12 healthy subjects and assigned as follows: normal pH, pH 7.2, and pH 7.0, each with and without incubation with desmopressin. Platelet aggregation was assessed by multiple electrode aggregometry. Baseline was normal pH and 36 degrees C. The other samples were incubated for 30 min and measured at 32 degrees C. Acidosis significantly impaired aggregation. Desmopressin significantly increased aggregability during hypothermia and acidosis regardless of pH, but did not return it to normal values at low pH. During acidosis and hypothermia, acidosis should be corrected first; desmopressin can then be administered to improve platelet function as a bridge until normothermia can be achieved.

We proposed that many Intensive Care Unit (ICU) patients would be hypothermic in the early postoperative period and that hypothermia would be associated with increased mortality. We retrospectively reviewed patients admitted to ICU after surgery. We recorded the lowest temperature in the first 24 h after surgery using tympanic membrane thermometers. We defined hypothermia as < 36 degrees C, and severe hypothermia as < 35 degrees C. We studied 5050 consecutive patients: 35% were hypothermic and 6% were severely hypothermic. In-hospital mortality was 5.6% for normothermic patients, 8.9% for all hypothermic patients (p < 0.001), and 14.7% for severely hypothermic patients (p < 0.001). Hypothermia was associated with in-hospital mortality: OR 1.83 for each degree Celsius ( degrees C) decrease (95% CI: 1.2-2.60, p < 0.001). Given the evidence for improved outcome associated with active patient warming during surgery we suggest conducting prospective studies of active warming of patients admitted to ICU after surgery.

A 24-year-old female presented in hospital following self-poisoning with a dose of greater than 30 g of paracetamol (acetaminophen), taken both as co-proxamol (dextropropoxyphene and paracetamol) and paracetamol. She arrived in hospital more than 18 h after ingestion of the drug. On admission, she was profoundly hypothermic, with a rectal temperature of 19 degrees C. Her paracetamol level was 943 mumol.l-1 which, when related to the time of ingestion, implied a very high risk of hepatocellular damage as well as fulminant liver failure, even if she was treated with the antioxidant n-acetylcysteine. The patient's condition was stabilised by initial resuscitation with fluids, vasoactive drugs, and active rewarming. N-acetylcysteine therapy was begun promptly. This patient's liver function tests remained entirely normal in spite of the delay in presentation and she made a rapid and complete recovery. This remarkable clinical course indicates a possible role for therapeutically induced hypothermia in the management of severe paracetamol overdose, particularly in the group of patients who seek medical attention some hours after ingestion of the drug and who therefore remain at high risk, despite treatment with n-acetylcysteine.

A case report is described with successful outcome of prolonged cardiopulmonary resuscitation in a 30-year-old man suffering from acute deep hypothermia. His lowest temperature recorded was 23 degrees C. Continuous external cardiac massage was required for a total of 4.5 h whilst rewarming was instituted. The patient eventually left hospital with no permanent sequelae. A review of hypothermia follows, emphasising some important management principals and pitfalls.

The accuracy of the Nellcor N-100 pulse oximeter was evaluated in hypothermic patients (core temperature less than or equal to 35.0 degrees C) after cardiac surgery. The pulse oximeter overestimated oxygen saturation in comparison to values obtained by direct in vitro oximetry with a mean bias of 0.6% saturation. The 95% predictability limits for individual measurements were +/- 3.9% oxygen saturation. No demonstrable loss of accuracy was caused by skin pigmentation, the concurrent administration of low doses of dopamine or vasodilators, or the intra-operative intravascular administration of Patent Blue V dye.