Thermoregulatory Disorders
The human thermoregulatory system limits the daily variation in body temperature to ±0.6°C (1). This chapter de-scribes what happens when this system fails, and allows the body temperature to rise or fall to dangerous levels.
I. Heat Stroke
A. Clinical Features
Heat stroke is a life-threatening condition that can be precipitated by environmental temperatures (classic heart stroke) or strenuous exercise (exertional heat stroke). The clinical features include the following (2,3,4):
Body temperature >40°C (104°F)
Altered mentation (e.g., delirium, coma) and seizures
Severe volume depletion with hypotension
Multiorgan involvement, including rhabdomyolysis, acute kidney injury, acute liver failure, and disseminated intravascular coagulopathy (DIC).
The inability to produce sweat (anhidrosis) is typical, but not universal.
B. Management
Management includes volume resuscitation (to replace volume
losses, and reduce the risk of myoglobinuric renal injury from rhabdomyolysis), and cooling measures to reduce the core temperature to 38°C (100.4°F) (4). Thermistor-equipped bladder catheters can be used to monitor core body temperature.
losses, and reduce the risk of myoglobinuric renal injury from rhabdomyolysis), and cooling measures to reduce the core temperature to 38°C (100.4°F) (4). Thermistor-equipped bladder catheters can be used to monitor core body temperature.
External cooling is the easiest and quickest way to reduce the body temperature. This involves placing ice packs in the groin and axilla and covering the upper thorax and neck with ice, then placing cooling blankets over the entire length of the body.
Evaporative cooling is the most effective method of external cooling (3,4), and is typically used in the field. The skin is sprayed with cool water and then fanned to promote evaporation of the water. The evaporation of water from the skin requires body heat, called the heat of vaporization. (This is how sweating reduces body temperature.) This method can reduce the body temperature at a rate of 0.31°C (0.56°F) per minute (3).
The major drawback of external cooling is the risk of shivering, which raises the body temperature.
Internal cooling is easily implemented by infusing cooled (or even room temperature) intravenous fluids. Measures such as cold water lavage of the stomach or bladder are usually not necessary, and heroic measures like cold peritoneal lavage are rarely necessary.
C. Rhabdomyolysis
Skeletal muscle injury (rhabdomyolysis) is a common complication of hyperthermia syndromes, including heat stroke and drug-induced hyperthermia (described in the next sections).
Disruption of myocytes in skeletal muscle releases creatine kinase (CK) into the bloodstream. There is no
standard plasma CK level for the diagnosis of rhabdomyolysis, but CK levels that are five times higher than normal (about 1,000 units/L) have been used in clinical studies of rhabdomyolysis (5).
Skeletal muscle injury also releases myoglobin into the bloodstream, and the myoglobin can damage the renal tubules and produce acute kidney injury (5). This condition is described in Chapter 26, Section III-C.
II. Malignant Hyperthermia
Malignant hyperthermia (MH) is an inherited disorder characterized by excessive calcium release from the sarcoplasmic reticulum in skeletal muscle in response to halogenated inhalational anesthetic agents (e.g., isoflurane) and succinylcholine. The genetic prevalence is about 1 in 2,000 (males >females), and the incidence of MH varies from 1 in 5,000 to 1 in 100,000 exposures to inhalational anesthesia (6).
A. Clinical Features
The clinical manifestations of MH are listed in Table 34.1 (6).
The first sign of MH may be a sudden, unexpected rise in end-tidal PCO2 (from hypermetabolism). This is followed (within minutes to a few hours) by generalized muscle rigidity and rhabdomyolysis.
Trismus is often the first sign of MH from succinylcholine.
The heat generated by the muscle rigidity is responsible for the rise in body temperature (often >40°C or 104°F), which is a late occurrence in MH.
Autonomic instability can lead to cardiac arrhythmias and hypotension.
The mortality rate in untreated MH is 70–80% (6).
Table 34.1 Clinical Features of Malignant Hyperthermia | ||||||||||||||
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B. Management
The first suspicion of MH should prompt immediate discontinuation of the inhalational anesthetic, and administration of the following drug.
1. Dantrolene
Dantrolene sodium is a muscle relaxant that blocks the release of calcium from the sarcoplasmic reticulum. When given early in the course of MH, the mortality rate is as low as 5% (6).
The dosing regimen is 2 mg/kg as an IV bolus, repeated every 5 minutes, if needed, to a total dose of 20 mg/kg (6). Some recommend a maintenance dose of 1 mg/kg IV or 2 mg/kg PO, four times daily for 3 days, to prevent recurrences (7).
Dantrolene is not advised in patients with advanced liver disease (because it can be hepatotoxic), but this applies more to long-term use of the drug.
Side effects of dantrolene, which are uncommon with short-term use, include tissue necrosis from extravasation, muscle weakness, headache, and vomiting (6).
2. Other Measures
Minute ventilation should be increased (by adjustments on the ventilator) to keep the end-tidal PCO2 within normal limits.
Volume resuscitation is often necessary to combat hypotension and reduce the risk of myoglobinuric renal damage. Vasopressor support may also be necessary.
Plasma levels of the following should be monitored: lactate, potassium, creatinine, and creatine kinase.
Cooling measures may not be needed once the muscle rigidity is controlled.
C. Follow-up
All patients who survive an episode of MH should be given a medical bracelet that identifies their susceptibility to MH. Immediate family members should also be tested to identify the gene responsible for MH (6).
III. Neuroleptic Malignant Syndrome
The neuroleptic malignant syndrome (NMS) is similar to malignant hyperthermia in that it is a drug-induced disorder characterized by hyperthermia, muscle rigidity, altered mental status, and autonomic instability (8).
A. Pathogenesis
NMS is typically associated with drugs that influence dopamine-mediated synaptic transmission in the brain.
As indicated in Table 34.2, NMS can be caused by drugs that inhibit dopaminergic transmission (most cases), or
it can be triggered by discontinuing drugs that facilitate dopaminergic transmission.
The incidence of NMS during therapy with neuroleptic agents is 0.2% to 1.9% (9), and the drugs most frequently implicated are haloperidol and fluphenazine (8).Related posts:
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