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Hypothermia: a medical emergency

In this article, Drs Lohith Bachegowda, Jeremy Williams and Abhaya Gupta discuss the pathophysiology, clinical features and management of hypothermia in the accident and emergency setting.

Hypothermia is defined as a dangerously low body temperature below 35ºC. Risk factors for the condition include extremes of age (young and old), malnourishment, intoxication (alcohol, drugs), exhaustion and chronic illness. There are also various environmental/social factors (such as poor domestic heating1 and self-neglect) that contribute to hypothermia. Although the condition can affect any age group, it has been shown to have a greater impact on older patients2. In particular, hypothermia affects more elderly woman than men3.


The hypothalamus is the main regulator of body temperature. Falling body temperatures leads to a decreased blood flow in the skin due to an increased sympathetic outflow. This in turns leads to increased muscle tone and shivering.

These released inhibitory mechanisms of the hypothalamus can only increase the resting heat production to 500 watts and, unlike new born infants and some mammals, adult humans fail to generate non-shivering heat production. Shivering increases the metabolic rate (by two to five times) but can only act as long as the glycogen stores last. Vasoconstriction also fails below 24ºC.

Clinical features of hypothermia

Hypothermia presents in several ways – varying from simple illness to death. Falling temperature leads to progressive decline in function. With a body temperature between 34 and 36ºC, an individual will need extra clothing and protection. If their temperature falls further (33-34ºC), their coordination is affected. Also, their mental process will start to slow down, they will develop amnesia4 and make judgement errors.

Near such temperatures, ‘paradoxical undressing’ may occur. Rhythm abnormalities are also commonly noted; this consists of tachycardia followed by bradycardia and asystole – which could ultimately lead to cardiac caused death. There is also respiratory stimulation, followed by depression. This will manifest as the body metabolism slows and causes carbon dioxide to accumulate, which leads to acidosis. As the renal blood flow drops, the patient develops oliguria –  preceded by an initial transient increased diuresis. The most commonly used classifications for the different stages of hypothermia (and their physiological effects) are shown in Table 2.

Table 1. Causes of Hypothermia


  • Extreme age (young/old)
  • Systemic illness
  • Sepsis
  • Malnutrition


  • Cold, wet, windy conditions
  • Immersion, exhaustion


  • Multiple trauma
  • Minor trauma and immobility (e.g. neck of femur)
  • Burns, shock


  • Ethanol
  • Sedatives (e.g. benzodiazepines, tricyclic antidepressants, opioids) in overdose
  • Phenothiazines (impaired shivering)


  • Cerebrovascular accident
  • Paraplegia
  • Parkinson’s disease


  • Hypoglycaemia and diabetes
  • Hypothyroidism
  • Hypoadrenalism


Diagnosis is based on assessing the core body temperature, which is traditionally measured via the rectum, and reviewing external factors. After an initial quick assessment of airways, breathing and circulation, routine blood tests should be performed. At this stage, accompanying major injuries and co-morbidities should be ruled out.

In the hypothermic patient, hypo/ hyperkalaemia, raised urea and creatinine are usually noted; and occasionally, rhabdomyolysis is seen. Rewarming the patient can bring about unstable flux changes (they may give false electrolyte values) across the membranes; therefore, analysing biochemical parameters must be done with caution from cold peripheral samples.

Hypothermic patients will also present with raised heamatocrit due to volume depletion. Thrombocytopenia associated with disseminated intravascular coagulation is also commonly seen. In addition, blood gases will show initial respiratory alkalosis followed by respiratory and metabolic acidosis.

An electrocardiogram (ECG) will show J waves along with arrhythmias, and the size of the wave is proportional to a degree of hypothermia. However, sinus bradycardia, atrial fibrillation with slow ventricular response and other atrial arrhythmias should be considered to be physiological €“ they usually settle with rewarming.

Ventricular Fibrillation (VF) also occurs – usually at temperatures less than 29ºC – and is often because the patient has been mishandled in some way – such as an inappropriate transfer or movement. In addition, a patient with a cold heart is susceptible to arrhythmias, and they could become more susceptible if they are given incorrect first aid. If they are massaged, made to stand erect or given alcohol, blood could be diverted from the critical organs to peripheries and worsen the metabolic rate.

Table 2. Classification of hypothermia5

Temperature Level Physiologic effects
35€“32°C Mild
  • Increased basal metabolic rate
  • Maximum shivering thermogenesis, pale, cold skin
  • Amnesia, dysarthria, ataxia, apathy
  • Maximum respiratory stimulation, tachycardia
  • Normal blood pressure
  • Stupor, shivering stops, muscular rigidity
  • Atrial fibrillation and other dysrhythmias,
  • Pulse and cardiac output 2/3 of normal = low blood pressure
  • Insulin ineffective
32€“29°C Moderate
  • Progressive loss of consciousness, pulse and respiration, pupils dilated at temperature
  • Susceptible to VF
  • Oxygen requirements 50 per cent of normothermics at temperature 28°C
  • Clinical signs of life may become almost undetectable
  • Pupils fixed and dilated
<29°C Severe
  • Loss of reflexes and voluntary motion (knee jerk the last reflex to be lost and first to return)
  • Major acid-base disturbance
  • Cerebral blood flow 1/3 normal and cardiac output 45 per cent normal at 25°C
  • Risk of pulmonary oedema
  • Significant hypotension
  • Absent corneal and oculocephalic reflexes at 23°C
  • Maximum risk of VF at 22°C Flat EEG at 19°C Asystole at 18°C
  • Lowest successful survival from accidental hypothermia is 16°C.


After stabilising the airway, breathing and circulation, early recognition and measurement of the core body temperature is necessary. In general if there is a prolonged history of cooling, rewarming must be undertaken with caution and with full resuscitation equipment available.

Wet clothing should be removed and the patient should be insulated to prevent further heat loss.

The primary cause of the hypothermia should be identified and then followed by specific symptomatic treatment. Dehydration will often be present because of cold induced diuresis, which is followed by a decreased ability of kidneys to retain salts. Dextrose infusions will help provide calorie substrate along with fluid balance.

For mild hypothermia, cosmetic care with warm clothing, hot drinks, and warm environment should suffice with careful observation. In immersion casualties (immersed in water, but not necessarily completely submerged), the recumbent posture during rewarming helps minimise the risk of postural hypotension. External exogenous warming is used for moderate hypothermia; this aims to achieve a temperature rise of two degrees per hour.

However in hospital-based studies, aggressive and fast rather than slow rewarming has been shown to improve outcome6. Warm intravenous fluids, peritoneal warmed fluids, heated humidified air or cardiac bypass7 are all methods (under specialist supervision) for increasing core body temperature. It is thought that there is a need in cases of severe hypothermia to rapidly raise core temperatures using these options.

The active core rewarming method is the therapeutic choice in hypothermic individuals with cardiac arrest and unconscious individuals with a slow heart rate. Transient ventricular arrhythmias should be ignored. Magnesium is found to have some beneficial effect in treating VF. Whereas lignocaine appears to be less effective. Special caution should be given for safe use of defibrillation on wet surfaces.

Cardiopulmonary resuscitation

Remember the old adage: ‘Hypothermic casualties are not dead until they are warm and dead.’ During defibrillation if there is no response to initial three shocks, then subsequent shocks should be delayed till temperature rises above 30ºC. Cardiac drugs and defibrillation are often not effective in moderate and severe hypothermia. Repeated doses of drugs can be dangerous due to the effect of the accumulated drug while rewarming. Therefore, specialist help must be sought when giving repeated doses.


The prognosis depends on the severity and nature of the cause. Mild hypothermia is tolerated by most without significant mortality. However, there is around a 20 per cent mortality in cases of moderate hypothermia8. There is no clear definite evidence, but less favourable outcome are observed with:

  • Potassium >10mmol/l
  • Core temperatures <6€“7ºC
  • Severe coagulopathy
  • Failure to obtain venous return during cardiopulmonary bypass
  • Venous PH Core temperature <15ºC if there has been no circulation for more than two hours.


Effects of cold on the human body have a spectrum of manifestations, and treatment of hypothermia is a medical emergency. The implementation of strategies to treat various biochemical and electrophysiological abnormalities of hypothermia is complex. It requires specialist advice to understand the effects of treatment on thermoregulatory adaptations of the human body. Further research should be carried out on how to manage arrhythmia in moderate to severe hypothermia.


  1. Hwang SW, Lebow JM, Bierrer MF, et al. Risk factors for death in homeless adults in Boston. Arch Intern Med Arch Intern Med 1998; 158:1454-60
  2. Vassilieff N, Rosencher N, Sessler DI, Conseiller C. Shivering threshold during spinal anesthesia is reduced in elderly patients. Anesthesiology 1995; 83: 1162-6
  3. Hospital Episode Statistics, Department of Health, England 2002-03
  4. Castellani JW, Young AJ, Sawka MN, et al. Amnesia during cold water immersion: a case report. Wilderness Environ Med Wilderness Environ Med 1998; 9: 153-55
  5. The British Association of Accident and Emergency. http:// BAEM/ (Date last accessed: 10/05/06)
  6. Gentilello LM, Cobean RA, Offner PJ, et al. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. J Trauma 1992; 32(3): 316€“25; discussion 325-7
  7. Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood warming. N Engl J Med 1997; 337(21): 1500-5
  8. Patient Plus. http://www.patient. (Date last accessed: 10/05/06)

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