Hypothermia

Chapter 166 Hypothermia



Jeffrey Todd, DVM, Lisa Leigh Powell, DVM, DACVECC



KEY POINTS



• Hypothermia causes severe cardiovascular, respiratory, electrolyte, nervous system, acid-base, and coagulation abnormalities.

• Early and aggressive treatment can decrease morbidity and mortality in the critically ill patient.

• Rewarming shock is a common complication, resulting from peripheral vasodilation when the periphery is warmed before the core.

• Therapeutic hypothermia in cardiac arrest and for neuroprotective properties appears promising and is being investigated.1


INTRODUCTION


Hypothermia is a condition in which the core body temperature is below the normal physiologic parameters for an individual species. Any condition or state that causes increased heat loss, decreased heat production, or a disruption of normal thermoregulatory function can lead to hypothermia. Because core temperature fluctuates mildly throughout the day, a range of normal temperatures for dogs and cats of 37.5° to 39.2° C (99.5° to 102.5° F) and 37.8° to 39.5° C (100° to 103.1° F), respectively, has been established.


Hypothermia is a relatively common condition in the emergency setting, with significant deleterious effects to the patient. Cardiovascular, respiratory, electrolyte, nervous system, acid-base, and coagulation abnormalities are commonly noted and should be anticipated. Early and aggressive treatment of hypothermia can decrease morbidity and mortality in the critically ill patient.


Renewed interest in therapeutic hypothermia for the treatment of traumatic brain injury and hemorrhagic shock has shown promising results. Studies in humans have shown that mild therapeutic hypothermia can improve outcome from several ischemic and traumatic insults.2



CLASSIFICATION


Hypothermia is classified as either a primary or secondary condition. Primary hypothermia, or “accidental” hypothermia, is a subnormal temperature caused by excessive exposure to low environmental temperature. Secondary hypothermia is a result of disease, trauma, surgery, or drug-induced alteration in heat production and thermoregulation.3 In animals, severity of hypothermia is classically graded as mild—32° to 37° C (90° to 99° F), moderate—28° to 32° C (82° to 90° F), and severe—less than 28° C (82° F).4 Patients with secondary hypothermia have more profound clinical signs at higher temperatures than do patients with primary hypothermia. Therefore a novel grading system has been proposed to describe patients with secondary hypothermia: mild—36.7° to 37.7° C (98° to 99.9° F), moderate—35.5° to 36.7° C (96° to 98° F), severe—33° to 35.5° C (92° to 96° F), and critical—less than 33° C (92° F).3



THERMOREGULATION REVIEW


A normal core temperature is maintained by an intricate balance of metabolic heat production and heat loss. The main thermostat of the body is the hypothalamus, with temperature changes sensed by the preoptic and anterior hypothalamic nuclei. Secondary temperature sensors are located within the skin and deep body tissues, namely, the spinal cord, abdominal viscera, and great veins.5


Most of the heat generated is by the most metabolically active systems, the brain, truncal organs, and active muscles.5,6 The rate of heat production is dependent on the metabolic rate of the body, maintained by basal and accelerated cellular metabolism. Increased metabolic rate is achieved in response to thyroxine, epinephrine, norepinephrine, sympathetic stimulation, and muscle contraction secondary to shivering.5


Heat production without heat retention would be an ineffective means of increasing and maintaining core body temperature. Therefore heat retention plays an integral role in physiologic homeostasis. Heat retention is achieved by both behavior responses, huddling and curling, and reflex physiologic changes such as piloerection and peripheral vasoconstriction.4 A failure of adequate heat production or retention will lead to hypothermia.


Heat loss is required to prevent hyperthermia, but it can be detrimental to the patient when in excess. There are four main mechanisms of heat loss in the veterinary patient: convection, conduction, radiation, and evaporation.3 In animals, most heat loss is through convection and conduction. This is in contrast to humans, where most heat loss is a result of radiation.7


• Convection is the transfer of heat from the body surfaces to air surrounding the body.

• Conduction is the transfer of heat from body surfaces to objects that come into contact with the body, such as the ground, examination tables, and kennels.

• Radiation heat transfer is the loss of heat to surrounding structures that do not come into direct contact with the body, such as walls.

• Evaporative heat transfer is the loss of heat from moisture on the body surfaces or through the respiratory tract to the environment.3

Many factors contribute to the degree of heat loss. Neonates have large surface areas that accelerate heat loss. Cachectic patients have decreased fat and muscle stores that allow faster heat transfer, because fat is an excellent insulator. Severely debilitated patients have a decreased ability to respond to hypothermia, either due to the inability to seek and retain heat or to mount an appropriate physiologic response.



PHYSIOLOGIC EFFECTS OF HYPOTHERMIA


Hypothermia may cause serious, deleterious effects on the body. These complications can be anticipated based on the degree of hypothermia and the known physiologic effects at those temperatures. It follows that the most serious effects are found in patients with the most profound hypothermia. Cardiovascular, respiratory, neurologic, and metabolic changes are commonly encountered.



Cardiovascular Effects


The cardiovascular changes found in hypothermia include bradycardia, hypotension, cardiac arrhythmias, decreased cardiac output, and asystole. The initial cardiovascular effects with mild hypothermia are an increase in heart rate and arterial blood pressure. This is mediated by catecholamine release secondary to stimulation of the autonomic nervous system.6 As hypothermia progresses, α1-receptor affinity for norepinephrine begins to decrease, leading to a diminished contractile response. At this point, normal vasoconstriction is lost and arterial vasodilation occurs, contributing to hypotension and decreased cardiac output.3


Hypothermia may also cause a shift to the left in the oxygen-hemoglobin dissociation curve, resulting in tissue hypoxia. This, in combination with cutaneous vasoconstriction causing arteriovenous shunting, leads to peripheral hypoxia or dysoxia, causing an increase in systemic vascular resistance.6


Bradycardia develops with mild hypothermia (36° C or 96.8° F), a result of decreased spontaneous depolarization of cardiac pacemaker cells. Consequently, the bradycardia is refractory to atropine administration.6 In humans, hypothermia causes a pathognomonic Osborn, or J, wave, which is an acute ST segment elevation at temperatures of 32° to 33° C (90° to 92° F). This has rarely been documented in small animals.4 Electrocardiographic changes in veterinary patients include lengthened PR intervals, QRS complexes, and QT intervals. As temperatures approach 23.5° C (74.3° F), 50% of dogs demonstrate ventricular fibrillation.8

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Hypothermia

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