Controlled hypothermia is indicated for neuroprotection after cardiac arrest, neonatal asphyxia, and neonatal encephalopathy, with improved outcome in the intensive care unit setting. It has been shown that decreasing core temperature is protective when there is a risk of ischemia and hypoxia. The brain has high metabolic demands, requiring a constant glucose and oxygen supply, which make it highly vulnerable to injury. Hypothermia is applied intraoperatively in neurosurgical and cardiac surgeries, both of which are associated with high risk of tissue hypoxia and ischemia. Cardiac surgery requiring cardiopulmonary bypass (CPB) exposes multiple organ systems, including the brain, to the risk of hypoxia and ischemia. Hypothermia during CPB reduces whole body oxygen consumption. However, routine application of induced hypothermia continues to be controversial.
When applied, the controlled hypothermia target temperature is usually 32–34°C. There are several ways to cool a patient, including the following:
Endovascular cooling is accomplished by inserting a heat-exchanging catheter into the inferior vena cava via the femoral vein. This can cool a patient at the rate of 4°C/h, and is the most rapid method available. CPB is a more sophisticated variation of endovascular cooling that allows for rapid cooling.
Administration of cold, intravenous fluids peripherally is the second most effective way to induce hypothermia. Temperature can decrease at 0.5°/L. However, this risks fluid overload as it requires 4 L to reach the goal temperature of 34°C.
Forced-air blankets are easily accessible to cool a patient but do not rapidly decrease the core body temperature. It can take up to 2.5 hours to cool a patient to 33°C.
Submersion in ice water or external ice bag application.
Passive cooling is the slowest method.
Hypothermia reduces the tissue metabolic rate by 8% per °C. This change is beneficial when there is a risk for ischemia and hypoxia during surgery where the arterial blood flow is disrupted for surgical exposure.
Glucose and insulin homeostasis is also altered during hypothermic therapy. There is decreased glucose consumption, decreased insulin secretion, and resistance to exogenous insulin therapy. Glucose should be monitored actively in this setting; however, glucose regulation typically resolves with normothermia.
Shivering is a common side effect of hypothermia that requires treatment. It is even more likely to occur after hypothermic therapy. Shivering increases metabolic oxygen requirements by increasing the heart rate, blood pressure, and stress. There is a threefold increase in myocardial ischemia with shivering. Forced-air warming blankets are useful in this setting.
Hypothermia has been found to increase bleeding, as it affects coagulation. Proteins necessary for coagulation are particularly sensitive to temperature, thus affecting factors in the coagulation cascade. Mild hypothermia to temperatures < 35°C induces platelet dysfunction. Consequently, the need for transfusion may increase during intraoperative hypothermia secondary to increased bleeding.
Infections are a common complication of hypothermia. Immune function and perfusion are impaired, increasing the risk of wound infection. Prolonged hypothermia in the ICU is associated with pneumonia.