Hypothermia and hyperthermia

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Chapter 32 Hypothermia and hyperthermia

David Lewis-Driver

Although Canadians write more about hypothermia and Saudis write more about hyperthermia, in fact neither condition is rare in Australia. Heat waves and fun runs occur every year in every Australian city. At the opposite end of the spectrum hypothermia is a regular accompaniment to injury and disease throughout the year, and can occur in summer—for example when nursing home patients are left scantily clothed under the air conditioner to cool them. It is important too to remember that the average multiple trauma patient in any country will become hypothermic unless specific preventive steps are taken.

PHYSIOLOGY

Temperature control requires a functioning hypothalamic centre, adequate cardiovascular function to be able to dissipate or conserve heat, adequate muscle bulk to generate heat, intact skin and sweat glands, and sufficient commonsense and mobility to escape the heat or cold. All of these may be affected by disease, trauma or environmental factors.

In both hyperthermia and hypothermia, skin circulation is a problem. Overheating cold skin induces vasodilation which feels good but may overwhelm the pumping capacity of a cold heart, resulting in ‘rewarming shock’. Ice on hot skin induces vasoconstriction, which may limit heat transfer.

HYPOTHERMIA

This condition is defined as a core temperature < 35°C. It is classified in Table 32.1.

Table 32.1 Classification of hypothermia

Temperature (°C)	Grade	Signs
35–32	Mild	Shivering/apathy
32–28	Moderate	Confusion ↓PR ↓BP
< 28	Severe	CV failure

Physiology

The body responds to a fall in temperature by attempting to seek warmth and by shivering. If these efforts fail because of environmental factors or drugs, injury or disease and the temperature falls, an initial rise in respiration, pulse and blood pressure is followed by a gradual slowing of all body systems, with death due to cardiovascular failure. CNS slowing results in apathy and confusion, and cardiovascular system (CVS) slowing proceeds to death in asystole, unless an irritable heart is jolted into ventricular fibrillation (VF). In general, slow warming and gentle handling are appropriate. Vigorous attempts at external rewarming can result in skin burns or death from ‘rewarming shock’, an ill-understood phenomenon that can best be considered as shunting of needed blood to the surface while the core is still too cold to cope with the demand. Core temperature lags behind surface temperature during rewarming, and healthy volunteers start to feel better when rewarmed while their core temperature is still falling due to continued cold penetration. An ‘undressing phenomenon’ is also well described, where failure of skin vasoconstriction as a terminal event allows return of skin circulation and leads to a sensation of warmth so that victims are found to have undressed themselves as a last act before death.

Diagnosis and differential diagnosis

If temperature is not a routine observation on every patient, ensure it is taken in those patients who are potential hypothermia candidates, as outlined in Table 32.2.

Table 32.2 Conditions associated with hypothermia

Conditions associated with accidental hypothermia

Trauma that limits protective mechanisms, e.g. neck of femur (NOF)

Overdose

Alcoholism

Conditions that may cause hypothermia

Sepsis

Myxoedema or adrenal insufficiency

Parkinsonism (failure to shiver)

Wernicke’s encephalopathy

Drugs, e.g. phenothiazines; beta-blockers; clozapine; sedatives

Hypoglycaemia; diabetic ketoacidosis (affect the thermostat)

Pancreatitis

Myocardial infarction or other cause of low CO

Malnutrition/anorexia

Burns; extensive skin rashes (excessive heat loss)

Conditions that hypothermia may be mistaken for

Cerebrovascular accident (CVA)

Dementia; confusion in the elderly; delirium

Hypoglycaemia

Myocardial ischaemia

Drunk and disorderly

Myxoedema

If the temperature is < 36°C on a standard instrument, use a low reading thermometer. The tympanic thermometers commonly used in emergency departments will generally read down to 26°C and are thus adequate to suggest the diagnosis. However, they are not accurate enough to guide treatment. Use an electronic probe—rectal in an awake patient and oesophageal in an intubated patient.

Investigations and management

Mild hypothermia (35–32°C)

1. Stop further heat loss. The most powerful way to prevent heat loss in any emergency department patient is to stem conduction and radiation loss—i.e. remove wet clothes and provide a blanket or space blanket. This is also called passive external rewarming, because prevention of heat loss allows the patient’s own metabolism to raise body temperature.

2. Treat the underlying cause (Table 32.2).

3. Monitor temperature. A rise of above 0.5°C per hour is acceptable.

4. Apply a Bair Hugger, if available. This method of active external warming using hot air is commonly available and unlikely to cause rewarming shock or burns. Active warming, however, is not vital unless the patient is incapable of generating heat because of systemic disease or a condition (e.g. CVA) that has reset the temperature centre. If a Bair Hugger is used, do not exceed a rise of 2°C/h. It is probably better to leave the arms exposed because the main risk is that sequestered cold blood will be restored to the circulating pool by skin vasodilation, causing an afterdrop in the core temperature. This risk is less from the trunk than the limbs.

5. Give O₂ and monitor O₂ saturation. If the saturation monitor will not read because of vasoconstriction, warm the finger or even do a digital block to overcome vasospasm.

6. Set up IV access and take blood for:

• Blood sugar level (BSL). Physiologically, hypothermia causes firstly a rise in BSL due to catecholamine-induced glycogenolysis, then reduced insulin secretion. Finally (below 30°C) insulin stops working. But there is a high association with hypoglycaemia in alcoholics, and elderly or malnourished patients may have exhausted glycogen stores by the increased metabolism of shivering. Treat hypoglycaemia but not hyperglycaemia. If rewarming does not correct hyperglycaemia, exclude haemorrhagic pancreatitis (a complication of hypothermia) or diabetic ketoacidosis (a cause of hypothermia).

• Urea and electrolytes. Fluid shifts and renal dysfunction mean that Na and K can go in either direction. Minor changes in the initial results do not require treatment and can simply be observed during rewarming. Significant changes should be treated and may be a clue to the underlying cause of the hypothermia.

• Lipase. Pancreatitis is both a cause and a result of hypothermia.

• Full blood examination (FBE). Expect the haematocrit to be high (due to cold diuresis—an attempt to compensate for central fluid overload due to peripheral vasoconstriction) and the WCC and platelets to be normal or low (due to sequestration). A normal Hb/Ht may indicate anaemia and a normal WCC does not rule out infection. Thus the main reason for doing the tests is that a high WCC increases suspicion of an underlying disease process.

• Troponin. Patients who become hypothermic during surgery have a higher incidence of myocardial events. Subendocardial infarctions have been found at autopsy in the absence of ECG changes. In elderly patients, repeat troponin after rewarming.

• CK. May be a clue to rhabdomyolysis in overdose or injury.

• Not coagulation screens. Hypothermic patients bleed more after surgery and trauma and this is generally attributed to failure of one or more of the enzymes in the coagulation cascade and qualitative platelet dysfunction. However, coagulation screens will generally be normal because these tests are done in the lab at room temperature. Rewarming is the best treatment. It is not generally possible either to get the lab to re-do the tests at the patient’s temperature or to make fresh frozen plasma (FFP) work while the patient is still cold.

7. Give fluid. 500–1000 mL of dextrose/saline or normal saline (warmed!). Hartmann’s is contraindicated because the cold liver cannot metabolise the lactate. Assume that the patient is dehydrated due to third space shifts and cold diuresis. Some fluid is required to compensate for the return of skin flow during rewarming, but when the patient is warmer the third space fluid will return. Elderly patients require cautious fluid replacement but younger patients can have the full litre fairly quickly.

8. Do an ECG. Hypothermia increases conduction times and often causes a slow atrial fibrillation which reverses with rewarming. The classical ECG change is the appearance of a J wave between the QRS complex and the T wave. Some computerised ECG programs interpret this wave incorrectly as myocardial infarction.

9. Institute cardiac monitoring. Ventricular fibrillation is the terminal event in a significant number of hypothermia deaths, and is commonly thought to be provoked by jostling or rescue or treatment procedures. It is unlikely above 29°C though.

10. Monitor BP. If it drops, turn off the Bair Hugger if it is being used (rewarming shock due to skin vasodilation).

11. Take an ABG and use the result, which is uncorrected for temperature. Expect hypoxia (due to ventilation/perfusion defects plus shift in oxyhaemoglobin curve plus increased haematocrit) and a lactic acidosis due to shivering. Below 32°C a respiratory acidosis due to slowed respiration will be added. Try to keep the uncorrected pH close to normal, but only by warming and ventilation. HCO₃^– is not indicated.

12. Measure urine output. Use an indwelling catheter (IDC) if required. Neither PR, BP nor urine output will be reliable indicators of hydration status, but urine output will be the best of the three.

13. Keep nil by mouth until 35°C is reached (poor gut motility).

14. Consider central venous pressure (CVP). It may be the only way to measure fluid replacement requirements in the elderly, but the risk of coagulopathy is a strong disincentive. If a CVP catheter is introduced, it should stop well above the R atrium to avoid an arrhythmia in the irritable heart.

15. Do a chest X-ray (CXR). Cold induces bronchorrhoea and reduces ciliary activity and resistance to infection, making bronchopneumonia more likely.

16. Give thiamine to alcoholic or malnourished patients, because of the association between Wernicke’s encephalopathy and hypothermia.

17. Confirm that the patient can protect his airway, cooperate with treatment, maintain a satisfactory pO₂ on oxygen, and has a fairly stable pulse, BP and cardiac rhythm. If not, proceed to the more aggressive measures in the next section.

Moderate hypothermia (32–28°C)

Treatment should not be based on temperature alone, particularly since core temperature may not initially reflect the rewarming that has been commenced. BP, pulse, O₂ saturations and ability to protect the airway all influence treatment decisions. Because VF is a frequent complication in this temperature range, patients with frequent ventricular ectopic beats (VEBs) merit vigorous rewarming.

In addition to the measures above, most moderately hypothermic patients will need:

1. Intubation. The patient will be hypoventilating and having problems dealing with copious bronchial secretions. Use standard drugs and dosages. Pharmacokinetics and pharmacodynamics are altered by hypothermia, but there is no specific information to guide dosing. Below 30°C, most drugs do not work at all, and ‘cold’ intubation may be required. At higher temperatures, if the drugs work, they will generally have a longer half-life. Insert a heat-moisture-exchanger into the circuit. Seventy per cent of respiratory heat loss goes into humidifying expired air. Most emergency departments do not have mechanisms for heating inspired air, and this additional effort brings marginal benefit.

2. Nasogastric tube (NGT). Cold reduces gastric motility and distension is likely.

3. Active external rewarming. If a Bair Hugger is not available, put hands and feet in warm water or use radiant heat or hot water bottle. Be careful of burning poorly vascularised and insensitive skin.

Severe hypothermia (< 28°C)

1. Most of these patients will need active core rewarming and ICU admission. Heated gastric lavage and/or bladder irrigation through the NGT and IDC are non-invasive but not as effective as peritoneal lavage (one or two catheters) or thoracic lavage (two catheters). The most effective rewarming procedure is extracorporeal rewarming using cardiopulmonary bypass or haemodialysis machines.

2. Give broad spectrum antibiotic prophylaxis because of the high incidence of sepsis due to impaired resistance.

If there is no cardiac output

Death from hypothermia will be preceded by slow pulse and respirations, so more care than usual in seeking signs of life is indicated. Unfortunately, the muscular rigidity associated with severe hypothermia is similar to rigor mortis, so the clinical diagnosis of death is difficult without an ECG. But there are also cases of cold asystolic people recovering or being resuscitated, so the axiom ‘no one is dead until they are warm and dead’ creates a dilemma in the emergency department, particularly if CPR has been started pre-hospital.

Some guidelines are:

• T < 15°C, or K > 12 mmol/L is unsalvageable.

• 32°C is a reasonable level to achieve. Once it has been reached, if resuscitation has not already been successful, it probably will not be.

• T < 32°C, if cardiopulmonary bypass is available, use it. If it is not available, use warmed fluids through two intercostal catheters while CPR continues. VF may not respond to either drugs or defibrillation < 32°C.

Pre-hospital care

Shivering is a very effective method of heat production, so simply rescuing and drying the patient is a good start. A warm carbohydrate drink provides core rewarming and energy for more shivering. Warm blankets stop shivering but are now considered to do no harm and they make the patient feel better.

Jostling a severely hypothermic patient (including unnecessary CPR) may precipitate VF. This makes the decision about whether to commence CPR very difficult. If the victim has no pulse or respirations, bag them with oxygen for a few minutes. This may improve output enough for a carotid pulse to be detected. (Wait at least 60 seconds before declaring it absent.) If there is still no pulse, CPR will not make things any worse. Start CPR unless:

• it will endanger rescuers by evacuation delays

• there are obvious lethal injuries

• airway is blocked with ice

• chest is too rigid to be compressed.

HYPERTHERMIA

Hyperthermia is technically different to fever. It is an increased body temperature due to failure of the temperature regulation systems. Unlike hypothermia, it is not possible to say that the diagnosis is defined by temperature. However, it is reasonable to say that below 40°C urgent treatment is unlikely to be needed. Above 42°C, cellular damage is likely whatever the cause—fever or hyperthermia.

Definitions

In fever, the body’s temperature regulation is reset to a new level. Re-setting the temperature control with antipyretics may help.

Heat stress is a sense of discomfort in a hot environment.

Heat exhaustion is thirst, weakness, dizziness etc, plus a normal or mildly elevated temperature due to water or salt depletion.

Heat stroke is a medical emergency described below.

Heat stroke

This is defined as collapse plus CNS abnormalities plus T > 40°C occurring once temperature regulation is overwhelmed. In athletes it occurs despite sweating (exertional heat stroke), but in sedentary elderly or frail people (classical heat stroke) it usually occurs after sweating stops. There is a risk of multi-organ failure from the combination of hyperthermia and an exaggerated acute phase response. Once this response has started, temperature correction may not be enough to avert death.

Key clinical features are:

• CNS disturbances, including altered behaviour, delirium, convulsions

• dry skin (when sweating eventually fails)

• hypotension

• muscle rigidity, rhabdomyolysis

• coagulopathy, petechiae

• renal failure.

Diagnosis

Diagnosis is easy if a patient has been exercising in hot conditions, but the presentation may be more subtle. Refer to Table 32.3 for a list of situations that predispose to hyperthermia.

Table 32.3 Conditions predisposing to hyperthermia

Condition	Reason
Advanced age	Impaired adaptation/mobility
Infancy	Immature sweating
Cardiac disease/drugs	Unable to increase CO
Dehydration/diuretics	Less circulating fluid
Anticholinergics/skin disease	Reduced sweating
High humidity	Reduced evaporative cooling
Hyperthyroidism/stimulant drugs	Increased heat production

As with hypothermia, surface temperature may not reflect core temperature. Tympanic infrared thermometers are technically capable of detecting high temperatures but may be unreliable due to technique. As with hypothermia, the diagnosis should be confirmed with a rectal probe if suspected.

Management

Heat stroke is a medical emergency. If the diagnosis is suspected, commence treatment immediately.

1. Cool the patient. Remove clothing as far as modesty permits, place a fan at each end of the bed, and continuously spray the patient with water at room temperature (or warmer) using a misting device. This evaporative cooling is the most effective cooling mechanism. If the temptation to use ice is irresistible, try to confine it to strategic areas (groin and axilla). Aim to reduce the temp to 39°C within 30 minutes. Stop cooling when 39°C is reached.

2. Give oxygen.

3. Intubate if hypoxic or unable to protect the airway.

4. Give normal saline. Marathon runners can have 1 L stat and 1 L in the first hour. Other patients should have half this. If BP and urine output are not restored, use CVP to monitor further replacement. Pulmonary oedema is a risk because of renal failure and cardiovascular compromise.

5. Insert an IDC. Monitor urine output. If myoglobinuria is present, alkalinise the urine with HCO₃ and give mannitol.

6. Consider sedation. Use a benzodiazepine to sedate the patient if agitated or confused and to control seizures.

7. Do not use aspirin or paracetamol. In theory they will not work: aspirin will exacerbate bleeding and paracetamol will require metabolising by a deranged liver. In fact, pyrogenic cytokines have been implicated in heat stress, but there have been no controlled trials of antipyretics.

8. Consider chlorpromazine 25 mg IVI if shivering is impeding cooling, but do not use it routinely because it may lower BP and impair sweating.

9. Use FFP and platelets if bleeding is a problem. Disseminated intravascular coagulation (DIC) may be present but treatment with heparin is controversial. Coagulation defects should correct with time and cooling.

If symptoms and blood abnormalities do not correct with cooling, ICU admission will be required. Heat stroke has a significant mortality rate.

Pre-hospital considerations

Cooling, rest and fluids are the cornerstones of pre-hospital care. Fans and evaporative cooling are preferred for the frail elderly. Fun runners and athletes can be put into an ice slurry bath. Despite inducing vasoconstriction and shivering, this is effective and has been shown to be safe in young people.

Malignant hyperthermia

This is a rare complication of anaesthesia that usually occurs soon after anaesthesia, but may be delayed up to 11 hours. Most anaesthetic agents (including succinylcholine) can cause it. Temperature is 41–45°C. Treatment is similar to heat stroke but with the addition of dantrolene 2–3 mg/kg/day.

Neuroleptic malignant syndrome

This is an idiosyncratic reaction occurring in about 0.2% of patients given neuroleptics. Haloperidol is the commonest offender. Dopamine receptor blockade leads to skeletal muscle spasticity (generating heat) and impaired hypothalamic regulation (interfering with response). The patient has T > 41°C plus muscle rigidity plus altered consciousness plus autonomic instability. Treatment is as for heat stroke. Both dantrolene and bromocriptine are thought to be helpful, although there have been no controlled trials.

PEARLS AND PITFALLS

• Rapid rewarming may be dangerous. 0.5–2°C per hour is enough.

• Bair Huggers are safe and effective but generally not essential if the temperature is above 32°C.

• If the sats monitor will not read because the finger is too cold, a digital block may help.

• Hypothermia interferes with the coagulation cascade, but coagulation tests will be normal when the blood is warmed in the lab. There is no need to order the test.

• The classic triad of heat stroke is hyperthermia plus neurological abnormalities plus dry skin.

• Aspirin and paracetamol will not lower the temperature in heat stroke.

CONTROVERSIES

Will intubation precipitate ventricular fibrillation in the cold heart? There are isolated reports, but a multicentre study that collected 117 intubated hypothermic patients (Ann Emerg Med 1987; 16:1042–1055) showed no problems.

RECOMMENDED READING

Auerback P. Field guide to wilderness medicine, 3rd edn. St Louis: Mosby; 2008.

Bouchama A., et al. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 11(3), 2007. R54

Epstein E., Anna K. Accidental hypothermia. BMJ. 2006;332:706-709.

Sessler D. Complications and treatment of mild hypothermia. Anaesthesiology. 2001;95(2):531-543.

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