This is defined as a core temperature of <35°C.¹ Hypothermia is classified on the basis of severity. The reason for this classification is that it influences the rewarming mechanisms that are most often deployed. It is also related to the physiological ability of the patient to compensate for hypothermia. An easy way to remember these temperature ranges is:

• acceptable low temperature: 2°C below 37°C (>35°C);

• true mild hypothermia: 3°C below that (32–35°C);

• moderate hypothermia: 4°C below that (28–32°C);

• severe hypothermia: anything below that (<28°C).

Tables 22.4.1 and 22.4.2 show the main consequences of hypothermia at a given temperature.^1,^3,⁶ Much of our understanding of this pathophysiology comes from controlled hypothermia in cardiac surgery. Note that there is a huge variation of the onset of certain clinical signs based on temperature level. For instance, some patients may exhibit confusion at higher temperatures compared with others. Note that in children clinical manifestations of altered consciousness may be subtle.

Mild (32–35°C) Moderate (28–32°C) Severe (<28°C)

Increased basal metabolic rate by shivering

Vasoconstriction peripherally, leading to fluid shift

Mild tachycardia

Cold diuresis (see text)

Apathy, ataxia, amnesia, dysarthria

Limits of increasing basal metabolic rate reached

Shivering stops

Decreasing cerebral blood flow, causing delirium and gradual decreased level of consciousness

Decreased rate of neural impulse transmission, causing clumsiness and numbness

Muscle rigidity due to increasing acidosis

Complete loss of thermoregulation

Dysrhythmias, initially slow atrial fibrillation then ventricular fibrillation

Appearance of death at < 25°C with asystole

Falling blood pressure

See text for more specific changes

Table 22.4.2 Findings at low body temperatures
Temperature (°C)	Findings
27	Reflexes absent, no response to pain, comatose
25	Cerebral blood flow one-third of normal, cardiac output one-half of normal
23	No corneal reflex, ventricular fibrillation risk is maximal
19	Asystole, flat EEG
15	Lowest temperature survived from accidental hypothermia

Note that only during severe hypothermia does protection from hypoxia occur, due to decreased demand for oxygen by tissues, and even then only at extremely low temperatures (patients <20°C can tolerate anoxia for up to 60 minutes). Metabolic processes slow by approximately 6% for each 1°C drop in body temperature.¹ Thus at 28°C the basal metabolic rate is about 50% of normal. This leads to hypoventilation and hypoxia. However, at this temperature the decreased cellular metabolism affords some protection against hypoxia.

Cold diuresis is an initial brisk diuresis; this is due to decreased tubular reabsorption and also a decreased production of antidiuretic hormone. There is also an increased central blood circulating volume as blood is shunted away from the periphery, thus presenting the kidneys with an apparent increased blood volume for filtration.¹

History

Important points in history are:

• approximate time of exposure, if known;

• environment in which patient was found;

• resuscitation at the scene, including duration of time with no cardiac output (‘downtime’);

• pre-existent illnesses (e.g. thyroid disease);

• drugs, medications, allergies, and immunisation status.

Examination

• Full primary and secondary assessment of patient.

• Accurate measurement of core body temperature.

Diagnosis

This requires only two essentials:¹

• a thermometer able to record low core temperatures accurately;

• a high index of suspicion.

Core temperatures can be measured best with oesophageal or rectal probes. The most direct method of measurement is with a cardiac catheter such as a Swan–Ganz, but this is impractical in the emergency setting. Rectal probes are often used,⁷ but care must be taken when using these. The probe must be at least 10 cm into the rectum in older children (more than 8 years old) and 5 cm in younger children. Inaccuracies may occur due to the presence of faecal material,¹ and the probe must be left in until the temperature equilibrates. Tympanic measurements are well known to be unreliable in the very young,⁷ but they are a good indicator of therapy progression in the older child. Oral and axillary temperature probes are unreliable and impractical in the setting of true hypothermia.

Treatment

Pre-hospital treatment

This is mainly the realm of passive external rewarming methods (see below). Patients should be carefully removed from the precipitant cold environment to a dry, sheltered area. If clothes are wet, they should be removed, and the patient dried and covered with a warm dry blanket. All patients should be gently handled, especially during transport, as there is evidence that sudden movements to a body in severe hypothermia can precipitate arrhythmias, particularly ventricular fibrillation.⁶ While this is occurring, one should attend to the patient’s airway, breathing, and circulation, as per any resuscitation.

Active rewarming should be avoided until the patient reaches the emergency department. This is because of the complications of rewarming, namely ‘after-drop’ and shock.^1,^6,⁸

Treatment in the emergency department

Once in the emergency department, the patient should be triaged to an appropriate area, which is warm. In the very young, a radiant warmer bed and heating lamps should be available when the patient presents.^4,⁹ Patients should have their airway, breathing, and circulation reassessed and appropriate resuscitation commenced. Appropriate monitoring should be instituted, including electrocardiogram (ECG), and core temperature, either by rectal or oesophageal means. Oxygen saturation monitoring should be attempted, whilst understanding that initial vasoconstriction will give inadequate readings. Urine output should be monitored. Gentle handling should be continued to avoid precipitation of arrhythmias.⁶ Patients should continue 100% oxygen on arrival in emergency.

Blood tests taken should include arterial blood gas (ABG); full blood count; electrolyte, urea, creatinine (EUC); liver function tests; amylase; comprehensive metabolic panel (CMP); glucose; thyroid function tests (TFTs); coagulations; tests for infection; and, if suspected, a screen for sedative drugs and ethanol. Hypothermia causes measured pH to fall and pO₂ and pCO₂ to be higher. It is recommended that these ABG values should not be corrected for temperature to better reflect the physiological state of the patient.⁶

A 12-lead ECG should be taken. Classic changes include the presence of a J (Osborn) wave, interval (PR, QRS, QT) prolongation, atrial dysrhythmias, and ventricular dysrhythmias.¹⁰ Other less well-known changes include abnormalities similar to myocardial infarction. Hypothermia can also blunt the ECG changes with hyperkalaemia.⁶ Note that all these are not present in all hypothermic patients.

Once temperature is measured, the severity of hypothermia determines the methods of rewarming. Specific methods of rewarming are classically divided into four categories:^6,^8,¹¹

• passive external rewarming;

• active external rewarming;

• active internal (core) rewarming;

• extracorporeal rewarming.

Due to the child’s larger surface area to weight ratio,^1,⁵ emergency physicians should start to institute limited active external rewarming methods, such as radiant light warmers and forced warm air blankets, even in mild hypothermia.¹¹ If the child is unable to produce extra heat, then the institution of simple active internal rewarming methods (warm humidified oxygen and warmed IV fluids) is appropriate.

In older children, asking them to drink some warm liquids (hot chocolate or soup) will in effect give them the effects of a warm gastric lavage. However, patients should only have warmed fluids if they are fully conscious, can protect their airway, and have no evidence of gastroparesis.

Moderate hypothermia (28–32°C) should have all active external rewarming techniques instituted except immersion in warm bath therapy, which is limited to localised cold injury in the emergency setting (see frostbite below). It is almost impossible to adequately monitor patients while they are in an immersion bath. Forced air warming blankets can increase core temperature by up to 1.5°C hr^–1. Patients should also have warmed IV fluids and heated humidified oxygen for inhalation. Together, they can increase core temperature by 1–2°C hr^–1. Normal saline bags can be safely warmed in a microwave oven. The optimum operating system for warming 500-mL bags of crystalloid is 400-W microwave for 100 seconds or 800-W microwave for 50 seconds.¹² Alternatively, if a heat infusion pump is available, this should be used. Intravenous infusion tubing should be as short as possible, as longer tubing loses more heat to the atmosphere.

Severe hypothermia requires institution of invasive core-rewarming techniques. All can raise core temperature by 2°C every 5 minutes.⁶ In cardiac arrest, cardiopulmonary resuscitation (CPR) should be commenced until core temperature has reached 35°C, and then a further assessment of the patient done (see Controversies). Note that, according to criteria for diagnosing brain death as quoted from the Australian and New Zealand Intensive Care Society,¹³ the patient must have a core temperature above 35°C, whereas other sources say 32°C.¹⁴

The decision of who to rewarm continues to evolve. There is a case report of a 26-month-old patient with a core temperature of 15°C who, after rewarming, recovered neurologically intact.¹⁵ For patients without submersion, extreme duration of exposure is not incompatible with life. In immersion patients, successful recovery is very rarely seen unless patients are immersed in ice-cold water (< 10°C) for long periods of time (see Chapter 22.2). However, further attempts to resuscitate after failure to restore a circulating cardiac rhythm within 30 minutes of rewarming to above 32°C are likely to be ineffective.¹⁴ In most Australian cases, however, the adage ‘you’re not dead till you’re warm and dead’ does not apply. The above only relates to patients that are ‘snap frozen’ in snowy weather.

With the recent evidence of inducing hypothermia for out-of-hospital arrests, it would make sense for patients who present hypothermic due to out-of-hospital arrests to be warmed to 34°C. In this way, hypothermia has been treated, whilst giving the patient admitted to the paediatric intensive care unit an opportunity to recover with the best possible neurological outcome.¹⁶

Neonatal resuscitation

In neonatal resuscitation, a warm ambient environment for the newborn child is prepared. A heated room with an overhead warmer is required. Warmed towels and blankets are used to rapidly dry the newborn to prevent evaporative heat loss. Unwell neonates should be admitted to special care nurseries or neonatal intensive care within humidicribs or transport cribs with radiant heat. If ventilated, humidified warm gases should be used.^4,⁵

There is now increasing evidence that in neonates suffering hypoxic ischaemic encephalopathy a period of hypothermia may be beneficial (see Controversies). Some centres in Australia have already changed their practice to cool such neonates. The reader is advised to consult local guidelines and their referring neonatal intensive care unit for more information, and the latest resuscitation guidelines of their country which were released following the latest ILCOR guidelines released in late 2010.

Complications

Complications can be classified as due to the hypothermia itself and complications as a result of rewarming.

Complications from hypothermia include:^1,³

• cardiac: arrhythmia;

• haematological: platelet dysfunction, thrombocytopenia and disseminated intravascular coagulopathy;

• pulmonary: pneumonia, pulmonary oedema and (adult) acute respiratory distress syndrome;

• infection: immune complex suppression;

• renal: acute tubular necrosis and rhabdomyolysis;

• neurological: cerebral oedema, prolonged coma and slow neurological recovery (up to 6 months);

• gastrointestinal: pancreatitis;

• biochemical and metabolic derangements (including glucose, sodium and potassium).

There are two main complications that result directly from the rewarming of patients: after-drop and shock.^1,^6,⁸ After-drop is a drop in core temperature after rewarming therapies have commenced. There are two proposed mechanisms for after-drop:

Cold peripheral blood re-enters the circulation once peripheral vasodilatation occurs with rewarming.

After-drop is due to ongoing conduction of heat from the warmer core into colder peripheries and surface layers of the body.

In reality, after-drop is most probably a combination of the two mechanisms described. This can be minimised by ensuring that rewarming only occurs over the core of the body, while the peripheries of the body are not actively rewarmed. For instance, a forced warm air blanket is placed over the patient’s body, but their hands and feet are left outside the blanket.

Shock occurs from the same mechanism, where peripheral vasodilatation increases the intravascular space to be filled, causing a consequent drop in blood pressure and rise in heart rate. In addition, the cold diuresis experienced has already decreased the circulating blood volume (up to 35%). In immersion patients, there is also a hydrostatic squeeze effect, which further decreases blood volume. Rewarming should therefore occur only once vascular access is established and warmed normal saline is instituted if active rewarming occurs, starting with usual shock doses of 20 mL kg^–1. Insertion of a central venous pressure (CVP) line would be useful; however, this needs to be balanced against the increased rough handling of the body during insertion.

Medications in hypothermia behave unpredictably. Metabolism of most drugs will be slowed due to hypothermia. Some drugs have decreased effectiveness; others, such as morphine, have increased effects. Drugs not used in treatment include sodium bicarbonate, insulin, corticosteroids, empirical antibiotics, and ethanol (contrary to popular belief).^3,⁶

Electrical defibrillation and antiarrhythmics may be administered at any temperature, but most efforts do not succeed until the temperature reaches above 28–30°C.³

Disposition

A patient with mild hypothermia, once treated, may be observed in the emergency department for a few hours before discharge if the patient is well. Moderate and severe hypothermia are an indication for ward or intensive care unit admission, depending on if cardiac abnormalities are present during assessment. Discharge should include education to patients on prevention of further occurrences, for example the proper use of clothing, checking weather reports, etc.¹

Localised cold injuries

Frostbite is the most severe of the injuries, but others include chilblain (perniosis), cold-induced fat necrosis (panniculitis), frost nip, and trench foot.^17,¹⁸

Frost nip is transient blanching and numbness of peripheries that resolves with rewarming. Only the skin surface is damaged. No ice crystals form within tissues, as opposed to frostbite (see below).

Trench foot, also known as immersion foot, is historically the most interesting, with the most famous cases occurring at Napoleon’s failed invasion of Russia in the winter of 1812. It is due to prolonged exposure to wet and cold, most common in the feet when poorly ventilated cold shoes are worn. There is peripheral neurovascular damage, but no ice crystal formation within tissues.

Perniosis or chilblain is injury due to repeated exposure to dry cold. Bullae form 12 hours post injury. These bullae burst to form ulcers, which are painful and pruritic. It is possibly due to repeated vasoconstriction. Common areas involved are the feet, lower legs and face.

Panniculitis consists of red lesions due to cold. Treatment is with non-steroidal anti-inflammatory drugs (NSAIDs), and the lesions resolve in 10–21 days.

Frostbite

Frostbite is the most dangerous of the local cold injuries. It is caused by freezing and ice crystal formation within the interstitial and cellular spaces due to prolonged exposure to freezing temperatures. It tends to occur more if the skin is directly exposed to temperatures less than –10°C. Several pathogenic phases evolve, called the frostbite injury cascade:^8,¹⁸

Prefreeze phase. Superficial tissue cooling occurs, which leads to increased blood viscosity, microvascular constriction, and endothelial plasma leakage.

Freeze phase. Ice crystals form in the extracellular space, leading to disruption of endothelium, disruption of cell anatomy, and hyperosmolality within cells due to crystals osmotically drawing water out of cells. This leads to protein denaturation and DNA synthesis inhibition.

Vascular stasis. There is arteriovenous shunting within damaged tissue, leading to stasis coagulopathy and thrombus formation.

Late progressive ischaemic phase. The thrombus induces inflammation, distal hypoxia, and anaerobic metabolism, which eventually leads to tissue necrosis.

Clinical features and diagnosis

Symptomatically, frostbite begins as an initial coldness of the skin. It then progresses to a stinging or burning pain, then to an anaesthetic limb, loss of fine motor function, loss of gross motor function, and finally severe joint pain. Examination of the affected limb will reveal varying degrees of frostbite.¹⁸ In the past, they have been classified similarly to burns, from first-degree to fourth-degree injury. It is much easier to classify them as superficial or deep.⁸ Superficial injuries go only to the skin and subcutaneous tissues, whereas deep frostbite also affects bones, joints, and tendons.

Most investigations are unhelpful. However, a full blood work up with full blood count, EUC, liver function tests, glucose, and creatine kinase to look for rhabdomyolysis should be done. Urinary myoglobin should be checked. Imaging is unhelpful initially; however, there is some evidence that a bone scan will help surgeons later determine how much limb is still viable, and whether superimposed osteomyelitis has developed.^8,^18,¹⁹

Treatment

Premedical treatment involves preventing further hypothermia and initiating resuscitation. As for hypothermia, removing the patient from the cold environment is paramount. Rubbing the limb to try to warm it should be avoided, as this increases tissue damage.^8,¹⁸

Once in emergency, the mainstay of treatment is rapid immersion rewarming.^8,¹⁸ The affected limb should be placed in a whirlpool of water about 40°C for 20–40 minutes for superficial frostbite, 1 hour for deep frostbite. This procedure will be painful, sometimes exceedingly so, hence narcotic and NSAID analgesia should be started before treatment is commenced. Rewarming is complete when the distal area of the limb is flushed, soft, and pliable. The patient should start to move the limb during rewarming to encourage blood flow in the limb. The main reason for suboptimal results is premature cessation of rewarming. After rewarming, the limb is dried and placed in a splint and elevated, and dressings applied four times a day.

Blistering of the limb will occur. The blisters are usually clear in superficial frostbite, and haemorrhagic blisters in deep frostbite. Controversy exists as to whether to aspirate these blisters. Haemorrhagic blisters should not be aspirated, as this increases trauma to the wound. The treatment of clear blisters is not as well defined.

All patients should have their tetanus status updated and, as 30% of wounds become infected, IV prophylactic antibiotics may be of use. IV penicillin G is most commonly used.¹⁸

Disposition

All patients should be admitted under a specialised (burns) unit.^8,¹⁸ Patients are observed for up to 6 weeks, which is usually the time the gangrenous parts of the limb are fully delineated so that safe amputation, if necessary, will occur. Good prognostic factors are patients with superficial injuries only, clear blisters, and sensation still present after rewarming.¹⁸

Hypothermia not due to environmental causes

There are many other causes of hypothermia,^1,³ as seen in Table 22.4.3.

Cause Details Metabolic or endocrine

Hypoglycaemia

Diabetic ketoacidosis

Toxicological

Cyclic antidepressants

CNS disorders

Subarachnoid haemorrhage

Degenerative diseases

Cerebrovascular accidents

Intracranial neoplasm

Infections

Vascular or skin

Gastrointestinal tract haemorrhage

Iatrogenic

Exposure during treatment

Prolonged extrications

Exposure during transport

Exposure post birth

Once the hypothermia is treated, then non-environmental causes should be investigated and, if found, appropriate treatment instituted. Iatrogenic causes need to be prevented. Always prevent hypothermia in trauma patients after full assessment, as hypothermia worsens the diagnosis.

Controversies

In certain countries, active rewarming is commenced prior to arrival in the emergency department.⁸ This is due to well-organised emergency medical systems catering for such emergencies, like in Canada. In Australia, this is more of a contentious issue, as we don’t see hypothermia as often.

Controversy exists regarding CPR causing arrhythmias when a patient loses spontaneous circulation.¹ However, the evidence that CPR causes ventricular fibrillation in hypothermic patients is at best circumstantial, and therefore the general consensus is that, to promote brain perfusion, CPR should be continued till the core body temperature reaches 35°C.¹³

Continuing CPR in the absence of cardiac output in a hypothermic patient has traditionally been mandatory. However, as survival occurs only in patients who have been immersed in water <5°C prior to cardiac arrest,¹ it is more likely that patients arrest in Australia before they become hypothermic. Therefore when to stop cardiac resuscitation is an issue.

The use of hypothermia in treatment, particularly in trauma and head injury, has always been of some debate.¹¹ Hypothermia causes a reduction in oxygen consumption and is theoretically cerebroprotective. This contradicts the results that trauma patients presenting with hypothermia have a worse prognosis.²