Chapter 020. Hypothermia and Frostbite (Part 5)

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Hypothermia: Treatment When a patient is hypothermic, target organs and the cardiovascular system respond minimally to most medications. Moreover, cumulative doses can cause toxicity during rewarming because of increased binding of drugs to proteins, and impaired metabolism and excretion. As an example, the administration of repeated doses of digoxin or insulin would be ineffective while the patient is hypothermic, and the residual drugs are potentially toxic during rewarming. Achieving a mean arterial pressure of at least 60 mmHg should be an early objective. If the hypotension does not respond to crystalloid/colloid infusion and rewarming, low-dose dopamine (2–5 µg/kg per min) support...

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Chapter 020. Hypothermia and Frostbite (Part 5) Hypothermia: Treatment When a patient is hypothermic, target organs and the cardiovascular system respond minimally to most medications. Moreover, cumulative doses can cause toxicity during rewarming because of increased binding of drugs to proteins, and impaired metabolism and excretion. As an example, the administration of repeated doses of digoxin or insulin would be ineffective while the patient is hypothermic, and the residual drugs are potentially toxic during rewarming. Achieving a mean arterial pressure of at least 60 mmHg should be an early objective. If the hypotension does not respond to crystalloid/colloid infusion and rewarming, low-dose dopamine (2–5 µg/kg per min) support should be considered. Perfusion of the vasoconstricted cardiovascular system may also be improved with low-dose IV nitroglycerin.
Atrial arrhythmias should initially be monitored without intervention, as the ventricular response will be slow, and unless preexistent, most will convert spontaneously during rewarming. The role of prophylaxis and treatment of ventricular arrhythmias is problematic. Preexisting ventricular ectopy may be suppressed by hypothermia and reappear during rewarming. None of the class I agents has proved to be safe and efficacious. When available, bretylium tosylate was the class III ventricular antiarrhythmic of choice. There is no evidence that amiodarone is safe. Initiating empirical therapy for adrenal insufficiency is usually not warranted unless there is a history suggesting steroid dependence, hypoadrenalism, or a failure to rewarm with standard therapy. The administration of parenteral levothyroxine to euthyroid patients with hypothermia, however, is potentially hazardous. Because laboratory results can be delayed and confounded by the presence of the sick euthyroid syndrome (Chap. 335), historic clues or physical findings suggestive of hypothyroidism should be sought. When myxedema is the cause of hypothermia, the relaxation phase of the Achilles reflex is prolonged more than the contraction phase. Hypothermia obscures most of the symptoms and signs of infection, notably fever and leukocytosis. Shaking rigors from infection may be mistaken for shivering. Except in mild cases, extensive cultures and repeated physical examinations are essential. Unless an infectious source is identified, empirical
antibiotic prophylaxis is most warranted in the elderly, neonates, and immunocompromised patients. Preventive measures should be discussed with high-risk individuals, such as the elderly or people whose work frequently exposes them to extreme cold. The importance of layered clothing and headgear, adequate shelter, increased caloric intake, and the avoidance of ethanol should be emphasized, along with access to rescue services. Frostbite Peripheral cold injuries include both freezing and nonfreezing injuries to tissue. Tissue freezes quickly when in contact with thermal conductors such as metal or volatile solutions. Other predisposing factors include constrictive clothing or boots, immobility, or vasoconstrictive medications. Frostbite occurs when the tissue temperature drops below 0°C. Ice crystal formation subsequently distorts and destroys the cellular architecture. Once the vascular endothelium is damaged, stasis progresses rapidly to microvascular thrombosis. After the tissue thaws, there is progressive dermal ischemia. The microvasculature begins to collapse, arteriovenous shunting increases tissue pressures, and edema forms. Finally, thrombosis, ischemia, and superficial necrosis appear. The development of mummification and demarcation may take weeks to months. Clinical Presentation
The initial presentation of frostbite can be deceptively benign. The symptoms always include a sensory deficiency affecting light touch, pain, and temperature perception. The acral areas and distal extremities are the most common insensate areas. Some patients complain of a clumsy or "chunk of wood" sensation in the extremity.Deep frostbitten tissue can appear waxy, mottled, yellow, or violaceous-white. Favorable presenting signs include some warmth or sensation with normal color. The injury is often superficial if the subcutaneous tissue is pliable or if the dermis can be rolled over boney prominences. Clinically, it is most practical to classify frostbite as superficial or deep. Superficial does not entail tissue loss. Classically, frostbite is retrospectively graded like a burn. First-degree frostbite causes only anesthesia and erythema. The appearance of superficial vesiculation surrounded by edema and erythema is considered second degree (Fig. 20-1). Hemorrhagic vesicles reflect a serious injury to the microvasculature and indicate third-degree frostbite. Fourth-degree injuries damage subcuticular, muscular, and osseous tissues. Figure 20-1