Thermal Disorders

KEY POINTS

1 Body temperature is the net result of balance between heat generated and heat lost. Usually heat loss is a much more efficient process than heat generation when environmental stresses act to displace body temperature from normal.

2 The method of temperature measurement is important in recognizing fever or hypothermia. Many thermometers cannot detect hypothermic range temperatures or those above 40°C. A pulmonary artery monitoring catheter sampling core temperature is the most accurate but risky method. Oral and axillary temperatures are much less accurate because of problems of tachypnea and poor thermometer-body contact, respectively. The most practical reliable temperature monitoring site in the ICU patient is the rectum.

3 Hypothermia is usually multifactorial in origin, in which patients with infection, hypothyroidism, or drug or alcohol use are exposed to cool ambient temperatures. Although controversial, passive external rewarming is probably the best treatment for most patients with initial temperatures at or above 32°C. Passive rewarming can be supplemented by warmed gastric lavage, heated humidified ventilator gas, and warmed IV fluids. Peritoneal lavage or cardiopulmonary bypasses are rarely necessary.

4 Exertional and nonexertional heatstrokes, though due primarily to environmental stress, often are complicated by underlying cardiovascular diseases and medication and illicit drug use. Lowering the ambient temperature and spraying the patient with a wind-blown mist of tepid water are the most efficient methods to achieve rapid cooling. Fluid replacement is adjunctive; deficits are much more prominent in patients with exertional heatstroke than classic heatstroke.

5 Malignant hyperthermia, a potentially lethal syndrome, precipitated by the use of inhalational anesthesia and neuromuscular blockade, must be considered as a cause of fever in the perioperative period. When the characteristic muscle rigidity and high fever are recognized, precipitating drug exposure must be terminated and a combination of external cooling and dantrolene initiated.

6 Neuroleptic malignant syndrome, another chemical-induced hyperthermic disease, can be caused by neuroleptic drug use or withdrawal of dopaminergic agents. Onset may occur at any time during drug exposure but is more common with the initiation of therapy or with a dosing increase. Termination of the offending drug and dantrolene therapy are indicated.

▪ NORMAL TEMPERATURE REGULATION

Body temperature is normally tightly regulated between 36°C and 37.5°C. The net temperature is the result of the balance between heat generated and that lost. Heat dissipation occurs primarily by radiation and evaporation at the skin surface with a lesser contribution from exhaled gas. When heat production rises (e.g., exercise) or heat loss declines (e.g., environmental exposure), sweating, cutaneous vasodilation, and hyperventilation attempt to return temperature toward normal. Behavioral responses (shedding clothing, drinking cool liquids, cessation of exercise, etc.) also serve to lower the temperature. If compensatory mechanisms fail to keep pace with heat generation, body temperature rises. Significant reductions in body temperature are usually the result of exposure to low ambient temperatures. Vasoconstriction and behavioral responses (donning extra clothing, seeking a warm environment, etc.) attempt to counteract excessive heat loss, but exercise and shivering are the only effective compensatory methods for raising heat production. In general, the body is much better adapted to losing excess heat than it is to rapid heat production.

Aging impairs the ability to sense temperature extremes and blunts thermoregulation, thus the elderly are at highest risk for most temperature disorders. When cold, older patients are less able to generate heat because of decreased body weight and fat stores, decreased exercise and shivering capacity, and a reduced ability to vasoconstrict peripheral vessels. When hot, the elderly have impaired vasodilation. Older patients are also more likely to develop diseases that can either induce temperature changes (e.g., sepsis, hypothyroidism, renal failure) or impair their ability to respond to thermal challenges (e.g., peripheral vascular disease, depression, heart failure, and stroke). These very same conditions are likely to be treated with medications that further impair temperature sensing, regulation, and compensation. Finally, the elderly are most prone to financial barriers preventing environmental heating or cooling.

▪ TEMPERATURE MEASUREMENT

Types of Measuring Devices

The technique used to measure temperature is critical in detecting fever or hypothermia. Mercury thermometers are usually unable to detect temperatures less than 34.4°C (94°F) or greater than 40.6°C (105°F) and fail to record values below the initial “shaken” level. Mercury thermometers respond slowly to temperature changes, making use of an electronic device or thermocouple (e.g., on a pulmonary artery catheter or indwelling urinary catheter) preferable when recording temperature extremes and rapid fluctuations. Infrared-sensing ear canal probes capable of accurate estimation of core temperature within seconds are now quite accurate. Plastic-strip thermometers have limited accuracy and recording range.

Sites of Measurement

Regardless of which site is chosen, it is important to be consistent in location and units. If throughout the day the temperature is sometimes measured orally, other times in the axilla, and occasionally using an indwelling pulmonary artery catheter and is sporadically recorded in Fahrenheit and other times Centigrade degrees, confusion about temperature trends is sure to ensue.

Measured oral temperatures are routinely less than their true value when respiratory rates exceed 18 breaths/min. Rectal temperatures avoid the artifacts of oral recordings because of varying respiratory rates, poor thermometer-patient contact, and aberrations caused by smoking or drinking hot or cold liquids. Although usually accurate, rectal temperatures may be spuriously low in patients with colonic impaction and may be slow to respond when rewarming the hypothermic patient if the temperature probe is lodged in cold stool. Axillary temperatures often underestimate core temperature because of poor thermometer-skin contact and wide differences between skin and core temperature. Obviously, a significantly elevated axillary temperature indicates fever. Esophageal measurement is an accurate “noninvasive” way to measure core temperature not commonly used because it requires specialized equipment. Infrared sensing of external ear canal temperature closely parallels core temperature and is not subject to influence by eating, drinking, or smoking as is oral temperature. The temperature of pulmonary artery blood may be continuously monitored using a thermistortipped pulmonary artery catheter and that of urine can be measured in the bladder using a thermistorequipped indwelling catheter.

▪ HYPOTHERMIA

Definition and Problems in Detection

Patients with uremia, hypothyroidism, malnutrition, and congestive heart failure often have mildly reduced (1°C to 2°C) basal temperatures. In these patients, a “normal” or slightly increased temperature may represent fever. Clinical hypothermia, a core temperature below 35°C, frequently escapes detection because symptoms are nonspecific and because most thermometers fail to record in the appropriate range.

Etiology

Hypothermia can occur at any time of the year and is usually multifactorial in origin. Outdoor adventurers and the destitute are at highest risk. Among the latter group, environmental exposure following intoxication or a neurological event is a common sequence of events. It is important to know that extreme ambient cold is not necessary to cause hypothermia, and a substantial number of cases occur at mild temperatures. Hypothermia may also be caused by medications that (a) alter the perception of cold, (b) increase heat loss through vasodilation, or (c) inhibit heat generation. (Phenothiazines and barbiturates are frequent offenders.) Common contributing metabolic conditions include adrenal
insufficiency, hypoglycemia, and myxedema. Because hypothyroidism decreases heat production, blunts the shivering response, and impairs temperature perception, it is an etiologic factor in up to 10% of cases of hypothermia. Hypopituitarism, severe sepsis, diabetic ketoacidosis, malnutrition, and mass lesions of the central nervous system (CNS) may also induce hypothermia. (The topic of hypothermic sepsis is discussed in Chapter 27.) An intact skin covering and the ability to vasoconstrict are essential to the regulation of core temperature. Hence, both burns and spinal cord injuries impair the ability to conserve heat. Hypothermia is commonly observed during and immediately after general anesthesia because of the exposure of the body to low ambient temperatures and the use of drugs that blunt the vasoconstrictor response (e.g., neuromuscular blockers).

Clinical Manifestations

Because physiologic changes are not precisely linked to specific temperature landmarks, it is best to classify hypothermia in broad categories: mild (32°C to 35°C), moderate (28°C to 32°C), and severe (<28°C). Vasoconstriction to conserve heat and shivering to generate heat are important initial compensatory mechanisms to prevent hypothermia. Unfortunately, both responses are blunted by a variety of underlying diseases or drugs and by profound hypothermia. Progressive hypothermia depresses metabolism of essentially all organ systems. Common physiologic events occurring during hypothermia are illustrated in Figure 28-1.

Cardiovascular

Mild hypothermia initially increases heart rate, blood pressure, and cardiac output through sympathetic stimulation. As temperature falls, heart rate and cardiac output decline as vasoconstriction maintains blood pressure. Moderate hypothermia decreases cardiac conduction and slows repolarization prolonging all measured electrocardiographic (ECG) intervals, eventually causing atrioventricular (AV) nodal blockade. Characteristic deformations of the J point (Osbourn waves) may be seen on the ECG but are neither sensitive nor specific indicators of core temperature. In advanced hypothermia, disproportionate reductions of cardiac output and blood pressure often result in metabolic acidosis. Myocardial irritability, manifest by any number of arrhythmias, increases at temperatures less than 28°C, but eventually asystole supervenes as temperatures fall below 20°C.

▪ FIGURE 28-1 Benchmarks in hypothermia.

Neurological

Cerebral oxygen consumption is roughly halved for each 10°C (18°F) decline in temperature, greatly increasing the CNS’s tolerance of reduced perfusion. Initial CNS responses to hypothermia include decreased respiratory drive, lethargy, confusion, and fatigue. As temperatures fall below 32°C, hallucinations and a reduced level of consciousness are seen. Coma usually develops when core temperatures fall below 28°C, and at slightly lower temperatures, the EEG may even become electrically silent. Concurrent with the loss of consciousness, deep tendon reflexes disappear and the pupils become fixed. Asymmetric neurological deficits rarely result from hypothermia, unless an independent CNS event (trauma or stroke) is the precipitant. Complete neurological recovery is possible following an hour or more of asystolic cardiac resuscitation of patients with hypothermia.

Renal

Early in hypothermia, the combination of increased cardiac output, vasoconstriction, and renal tubular unresponsiveness to antidiuretic hormone produces a “cold diuresis.” The resulting large-volume dilute urine output (often with an osmolarity < 60mOsm/L) leads to intravascular volume depletion. Later in the course of hypothermia, volume contraction, a low cardiac output, and
arterial vasoconstriction profoundly decrease the renal blood flow. At temperatures below 27°C, most patients become anuric.

Respiratory

Hypercarbic respiratory drive generally decreases parallel to reductions in temperature and metabolic rate. Hence, a suppressed hypercarbic drive often allows respiratory acidosis to develop, even though hypoxic drive is preserved. As temperature approaches 30°C, oxygen consumption and CO₂ production are roughly halved. Early in hypothermia, the oxyhemoglobin dissociation curve shifts leftward, decreasing tissue oxygen delivery. This effect is offset by increasing lactic acidosis resulting from hypoxia and reduced cardiac output. Despite these derangements, net oxygen delivery is often adequate, given the profound reductions in consumption. Altered consciousness and an increased volume of respiratory secretions warrant a low threshold for intubation.

Unnecessary controversy exists with regard to interpreting arterial blood gas (ABG) values in hypothermia. Standard practice is to warm ABG samples to 37°C for analysis. When this is done, higher partial pressures of oxygen (PaO₂) and carbon dioxide (PaCO₂) and lower pH are observed than those that exist in vivo. (PaCO₂ and PaO₂ tensions are elevated by 4% to 7% per 1°C, and the pH is reduced by approx. 0.02 units per 1°C fall in temperature.) To the naïve physician, the reported ABG values may prompt poor clinical decisions: (a) the use of sodium bicarbonate to treat an artifactual acidosis, (b) overventilation in response to artifactual hypercarbia, and (c) withholding supplemental oxygen because reported PaO₂ values appear adequate. Hence, even though there is no need to “correct” the blood gas values for temperature, making sure that adequate oxygen is administered is important.

Hematologic

Hypothermia-induced diuresis decreases plasma volume, causing hemoconcentration (approx. 2% rise in hematocrit per °C) and increased serum viscosity. The resulting sluggish blood flow predisposes to deep venous thrombosis. Total leukocyte counts are usually normal or slightly increased, but isolated granulocytopenia may be seen. Thrombocytopenia, a common finding, is believed to result from platelet sequestration. Hypothermia impairs coagulation enzyme activities leading to impaired intrinsic and extrinsic clotting function.

Other Complications

Hyperglycemia is common as cold impairs pancreatic insulin release and increases counterregulatory hormone levels, including those of cortisol, epinephrine, glucagon, and growth hormone. Because it is relatively frequent and easily diagnosed and treated, hypothyroidism should be sought. Skeletal and cardiac muscle enzymes may increase in response to membrane dysfunction or rhabdomyolysis. Because hypothermia increases gastric acid production, it is sound to prescribe an acid-suppressing medication. Pancreatitis, ileus, and venous thrombosis are common. Although venous thrombosis often complicates hypothermia, subcutaneous heparin is poorly absorbed. Thus initially, pneumatic compression devices may be the best option for prophylaxis. Coexisting or precipitating infections (particularly pneumonia and meningitis) complicate as many as 40% of hypothermia cases. Cold-induced stiffness of the abdominal wall or neck often confounds clinical interpretation by simulating acute abdomen or meningitis.

Treatment

General Principles

Many hypothermia deaths are iatrogenic. Overly aggressive treatment, including excessive catecholamines, and prophylactic pacemaker insertion should be avoided; rewarming, close observation, gentle patient handling, and a search for underlying causes are key factors in successful therapy. Because patients with mild-to-moderate hypothermia already have maximal vasoconstriction, exogenous vasoconstrictor drugs often only serve to induce arrhythmias. With profound hypothermia (<28°C), vasoconstrictors may be useful to restore vascular tone. Fluids should be replaced as necessary to maintain blood pressure and vital organ perfusion. Central venous catheters are preferred for fluid and drug administration because peripheral intravenous lines are difficult to place (because of vasoconstriction) and allow only sluggish infusion. Catheters should not be advanced into the right atrium or ventricle, where they may stimulate life-threatening arrhythmias. (In most situations, it is probably best to avoid pulmonary artery catheterization.)

Serum amylase should be measured to detect pancreatitis—a complication seen in 20% to 30% of severe cases. Hypothyroidism, a common precipitant of hypothermia, should also be sought. Because many patients either have infection as a precipitating cause or develop an infection as a result of the
hypothermia, it is prudent to obtain cultures of blood, urine, sputum, and spinal fluid if clinically indicated and then begin empiric antibiotics. Empiric coverage should probably include that for pneumonia and bacterial meningitis if suspected. (Fortunately, such regimens will treat essentially all skin and urinary tract infections.) A gently inserted nasogastric tube is useful in management to counter gut hypomotility and can be used for rewarming gastric lavage. Because many medications have prolonged actions in hypothermia, all drugs must be given cautiously, particularly those that are hepatically degraded. Finally, it should be emphasized that prolonged resuscitative efforts (hours) can prove successful in hypothermia. Therefore, patients with hypothermia must be rewarmed to temperatures exceeding 29°C (85°F) before death is declared.

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