Cold incapacitation is the most common cause of death from immersion in cold water, not hypothermia. | Photo courtesy of the USCG
Contents
Cover image: Cold incapacitation is the most common cause of death from immersion in cold water, not hypothermia. | Photo courtesy of the USCG
Introduction
Drop in core body temperature below 95°F/35°C
MEDICAL EMERGENCY
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
Classification
Swiss system
Symptoms
By degree
Temperature
HT1
Awake and shivering
Mild
32–35 °C (89.6–95.0 °F)
HT2
Drowsy and not shivering
Moderate
28–32 °C (82.4–89.6 °F)
HT3
Unconscious, not shivering
Severe
20–28 °C (68.0–82.4 °F)
HT4
No vital signs
Profound
< 20 °C (68.0 °F)
Pathophysiology
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 http://jeb.biologists.org/content/204/18/3171.abstractA 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 http://jeb.biologists.org/content/204/18/3171.abstractModel 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 PressThe effect of hypothermia on rate of metabolism and oxygen consumption | Hypothermia. (2016). Deranged Physiology. Retrieved 18 May 2018, from http://www.derangedphysiology.com/main/required-reading/trauma-burns-and-drowning/Chapter%204.0.6/hypothermia
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
Toes inflamed by chilblains | Sapp – Public Domain, https://commons.wikimedia.org/w/index.php?curid=3297622
Frostbitten toes two to three days after mountain climbing | Dr. S. Falz – CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20223066
Frostbite 12 days later | Dr. S. Falz – CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20284634
Trench foot as seen on an unidentified soldier during World War I LAC/BAC – Public Domain, https://commons.wikimedia.org/w/index.php?curid=11023168
Pediatric age-group:
Peripheral vasoconstriction:
Acrocyanosis
Cool extremities
↑ capillary refill time (CRT)
Cardiovascular manifestations:
Bradycardia
Hypotension
↑ pulmonary artery pressure with resultant hypoxemia, tachypnea 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
Complications
Acidosis
Hypoglycemia
Oliguria
Azotemia
Generalized bleeding
Diagnosis
Atrial fibrillation and Osborn J waves in a person with hypothermia. | WikiSysop – CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=9460540
