Internal Medicine


Cover image: Cold incapacitation is the most common cause of death from immersion in cold water, not hypothermia. | Photo courtesy of the USCG


Drop in core body temperature below 95°F/35°C


Pediatric definitions:

  • Normal body temperature: 36.5°C to 37.5°C
  • Hypothermia: Axillary temperature < 36.5°C
    • Cold stress: 36.0-36.4°C
    • Moderate hypothermia: 32-35.9°C
    • Severe hypothermia: <32°C




ATP turnover of cells as a function of time exposed to anoxia or hypothermia. The main figure shows the debilitating cascade of events leading to necrotic cell death. When cellular ATP demand exceeds ATP supply, this cascade is the same (in general if not in specific detail) whether the cells are ‘anoxia- or cold-sensitive’ or ‘anoxia- or cold-tolerant’. The inset shows that a regulated suppression of ATP turnover (i.e. a regulated hypometabolism in which ATP demand balances ATP supply) extends the time to the onset of the debilitating cascade in ‘anoxia- and cold-tolerant cells’. In contrast, an early mismatch between ATP supply and demand in ‘anoxia- and cold-sensitive cells’ leads to a forced hypometabolism which is, in effect, early metabolic failure. Mito, mitochondria; ER, endoplasmic reticulum. | Boutilier, R. G. (2001). Mechanisms of cell survival in hypoxia and hypothermia. Journal of Experimental Biology, 204(18), 3171 LP-3181. Retrieved from
A generalised model of cell membrane ‘channel arrest’ and mitochondrial membrane ‘H+-ATPase activation’ in response to anoxia. In this model, anoxia-induced decreases in Na+ and K+ channel densities (and associated ion-channel activities) lead to a net reduction in Na+/K+-ATPase activity, thereby lowering the ATP demand for maintaining transmembrane ion concentration gradients. At the level of the mitochondria, oxidative phosphorylation during normoxia occurs when protons are transferred across the inner mitochondrial membrane (at complexes I, III and IV), thereby generating a proton-motive force that provides the driving force for proton influx through the F1Fo-ATPase (also known as ATP synthase). Proton influx apparently drives the ATP synthase to phosphorylate ADP to ATP. At standard metabolic rate (SMR) during normoxia, a significant fraction of the protons pumped out of the respiratory chain leak back into the mitochondrial matrix without synthesizing ATP (i.e. effectively uncoupling mitochondrial oxygen consumption from ATP synthesis). This futile cycle of mitochondrial proton pumping and proton leak across the inner mitochondrial membrane is estimated to make up approximately 20% of the SMR of mammals (Rolfe and Brown, 1997; Brand et al., 2000). In the absence of oxygen, proton transfer no longer occurs at complexes I, III and IV, but the inverse operation of the F1Fo-ATPase attempts to maintain the mitochondrial membrane potential by using ATP to translocate protons into the intermembrane space. | Boutilier, R. G. (2001). Mechanisms of cell survival in hypoxia and hypothermia. Journal of Experimental Biology, 204(18), 3171 LP-3181. Retrieved from
Model of the hypothermia response seen in rat brain glial cells. Hypothermia inhibits the Na+/K+-ATPase and also upsets the normal balance between Na+ influx and K+ efflux in favour of Na+ influx. This leads to a net accumulation of Na+ that is exacerbated by hypothermia-induced activation of the Na+/H+ exchanger, leading to cell swelling | Plesnila et al., 2000, Cambridge University Press
The effect of hypothermia on rate of metabolism and oxygen consumption | Hypothermia. (2016). Deranged Physiology. Retrieved 18 May 2018, from

Clinical features

Other cold-related injuries that can be present either alone or in combination with hypothermia include:

  • Chilblains
    • Superficial ulcers of the skin that occur when a predisposed individual is repeatedly exposed to cold
  • Frostbite
    • Freezing and destruction of tissue
  • Frostnip
    • Superficial cooling of tissues without cellular destruction
  • Trench foot or immersion foot
    • Condition caused by repetitive exposure to water at non-freezing temperature

Pediatric age-group:

Peripheral vasoconstriction:

  • Acrocyanosis
  • Cool extremities
  • ↑ capillary refill time (CRT)

Cardiovascular manifestations:

  • Bradycardia
  • Hypotension
  • ↑ pulmonary artery pressure with resultant hypoxemiatachypnea and distress

Neurological depression:

  • Lethargy
  • Poor reflexes
  • Decreased oral acceptance
  • Apnea

Enteric disturbance:

  • Abdomen distension
  • Vomiting
  • Feeding intolerance 
  • Chronic or recurrent episodes of hypothermia:
    • Poor weight gain


  • Acidosis
  • Hypoglycemia
  • Oliguria
  • Azotemia
  • Generalized bleeding


Atrial fibrillation and Osborn J waves in a person with hypothermia. | WikiSysop – CC BY 3.0,



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