Complications
May occur due to the effect of cold temperatures on the heart. All types of cardiac arrhythmias are known to occur, the most common being atrial fibrillation and ventricular fibrillation. Atrial fibrillation may resolve spontaneously as the patient is re-warmed. Ventricular fibrillation may be refractory to treatment and may require defibrillation.[3][24][33] If defibrillation fails, it may be appropriate to defer further defibrillation until the patient is rewarmed above 86°F (30°C).[3]
The hypothermic heart is very sensitive to movement, so movement should be minimised.
Requires treatment with 50 mL of a 50% dextrose intravenous push.
With ECG changes, hyperkalaemia requires prompt treatment with calcium gluconate to stabilise the myocardium, and an insulin dextrose infusion. Sodium bicarbonate infusion is required if the hyperkalaemia is the result of acidosis.
May occur in those exposed to the cold for a prolonged time and/or enduring a crush injury. The symptoms are often non-specific. Up to 15% of patients develop acute kidney injury.[51] This is a direct result of mechanical obstruction of the renal tubules by myoglobin precipitate and is associated with a high morbidity and mortality. The release of vasoactive kinins by the damaged muscles interferes with the renal haemodynamics. A creatine kinase (CK) level of ≥16,000 units is associated with the development of acute kidney injury.[51] As a direct consequence of rhabdomyolysis, hypocalcaemia, hyperkalaemia, cardiac arrhythmias, cardiac arrest, acute compartment syndrome (day 3 to day 5 of presentation), and disseminated intravascular coagulation may occur.
The objectives are to alkalinise the urine to a pH >6.5 and to ensure flushing of myoglobin. Forced diuresis with sodium bicarbonate infusion may prevent acute kidney injury. Urine output must be maintained at a rate of >300 mL/hour and normal saline infusion is given at rate of 1.5 L/hour until the myoglobinuria stops or the CK level is <1000 units/L. Serial CK levels should be monitored.
At temperatures <34°C (<93.2°F), intestinal motility is impaired resulting in paralytic ileus. Punctate hemorrhages and gastric erosions, known as Wischnewski ulcers, may occur, but are clinically insignificant.[52]
Hepatic impairment can develop, probably due to the reduced cardiac output. Pancreatitis is discovered in 20% to 30% of autopsies performed on hypothermic patients.[53]
Hypothermia leads to coagulopathy due to platelet dysfunction, enhanced fibrinolytic activity, and changes in enzymatic activity. Inhibition of thromboxane B2 production causes a decrease in platelet aggregation. Hypothermia also causes a release of a heparin-like substance, which induces disseminated intravascular coagulation, characterised by prolonged prothrombin time and PTT and an increase in D-dimer. Hypothermia alters enzymatic activity such that the Hageman factor and thromboplastin fail to act effectively. Prolonged bleeding and clotting times result. Patients may require treatment with clotting factors and platelets.
Intravenous fluid resuscitation may dilute available clotting factors; these patients may require transfusion with clotting factors and/or platelets. Treatment is often not successful until the associated acid and base derangement is corrected.
Usually reversible if the patient survives the hypothermic injury. Requires treatment with an indwelling catheter.
Cold-induced local injuries may vary in severity, from blistering to skin necrosis due to profound vasoconstriction. Severe injuries may require prolonged supportive management, escharotomy, skin grafting, or amputation. If not interfering with movement, blisters should not be drained. If blisters have ruptured, the dead skin must be excised and the wound covered with topical antibiotic ointment.
Frostbite is a local cold-induced injury typically affecting exposed body parts such as the face and extremities. The injuries may vary in severity, and may warrant extensive hospitalisation and surgical intervention. Typically, in superficial injury, the damage is to the skin and subcutaneous tissue and can be easily recognised on re-warming by the presence of a clear blister. Deep frostbite, on the other hand, affects the bone and on re-warming is associated with haemorrhagic blisters. Tetanus prophylaxis should be given in patients with extensive injury.
Reduced coronary perfusion may occur during active external re-warming especially if the extremities are re-warmed concurrently. Cardiac arrhythmias may result.[3][11][21][23] The hypothermic heart is very sensitive to movement, so movement of the patient should be minimised.
Even with treatment, management of ventricular fibrillation may be problematic. The hypothermic heart may be unresponsive to defibrillation; however, there is an absence of robust supporting data.[24][33] If defibrillation fails, it may be appropriate to defer further defibrillation until the patient is re-warmed above 30°C (86°F.[3] Most other arrhythmias will improve with re-warming.[3]
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