Hypothermia

Hypothermia, whilst an infrequently encountered issue during foundation, is a high-risk condition with a need for investigation and often rapid intervention.

It is defined as a core body temperature less than 35°C and can be divided into mild, moderate and severe (by the extent of hypothermia and associated signs/symptoms) or into the duration of onset (acute, subacute and chronic). Measure temperature centrally to ensure accuracy (rectal, oesophageal or endovascular are commonest).

Modified Swiss Hypothermia staging (& additional considerations)

Stage Temperature
(degrees Celsius)
Swiss staging criteria Additions
Mild (HT I) 32-35°C Normal mentation, shivering Raised RR, HR, BP
Moderate (HT II) 28-32°C Altered mentation, absent shivering Low RR, HR, BP, dilated pupils, hyporeflexia
Severe (HT III) 24-28°C Unconsciousness Low RR, HR, BP, fixed dilated pupils, hyporeflexia, pulmonary oedema
Severe (HT IV) 13.7-24°C Apparent death (resus possible) Apnoea, loss of cardiac output, fixed dilated pupils, oliguria
Death (HT V) <13.7°C Death

Risk Factors

  • Elderly/frail patients
  • Cognitive impairment
  • Homelessness
  • Drug/alcohol intoxication
  • Malnourishment
  • Exhaustion
  • Chronic disease

Common Causes
Usually, this is recognised due to the regular monitoring of vital signs in hospital, but it can also present with confusion, cardiac arrest and shock.

As an inpatient, common causes of hypothermia include hypothyroidism, sepsis and perioperative hypothermia (often due to administration of cool fluids, exposure and drugs administered such as neuroleptic agents).

Common causes can be divided into the following categories:

Category Potential causes
Loss of central regulation Hypothalamic dysfunction possibly secondary to head injury, haemorrhage, infarction, tumour, centrally acting toxins
Endocrine dysfunction Hypothyroidism, hypopituitarism, hypoadrenalism, hypoglycaemia
Increased peripheral losses Exposure (incl. drowning), burns, erythroderma, sepsis, toxins (from vasodilation)
Iatrogenic (may fit into the categories above) Toxins, trauma hypothermia, fluid administration
It is key to remember there are risks of rebound fluid status, cardiac and metabolic alterations on rewarding so ECG, BM and clinical monitoring are important.

Key investigations

  • ECG
    • Often shows sinus bradycardia, J (Osborn) waves
    • Non-specific ST changes (elevation, depression, T wave inversion etc)
    • Slowed conduction (prolonged PR, QRS, QTc intervals)

HypothermiaECG 1

  • Chest Xray
    • May reveal underlying pneumonia, aspiration, pulmonary oedema (secondary to an increased central circulating volume from peripheral vasoconstriction)
  • ABG
    • Resp alkalosis from tachypnoea (mild)
    • Resp acidosis from bradypnoea (mod-severe)
    • Metabolic acidosis from hypoperfusion and reduced hepatic activity
  • FBC
    • Hb often increased due to haemoconcentration, WCC and Plt often fall due to splenic sequestration (even in the event of infection as the precipitation cause)
  • U&Es
    • Oliguria and AKI due to renal hypoperfusion, hypokalaemia due to reduced reabsorption with hyperkalaemia in rhabdomyolysis and reperfusion injury
  • Blood glucose
    • Hyperglycaemia due to increased cortisol from the stress response and reduced insulin activity
    • Hypoglycaemia both due to and a result of hypothermia (and it’s inhibition of insulin activity)
  • Coagulation
    • Often PT is prolonged to reduced enzymatic activity
  • Investigation of cause
    • Toxins (urine tox & blood alcohol)
    • Endocrine (TFTs & cortisol)
    • Cranial (CT head)
    • Infection (FBC, CRP [may be falsely low], blood cultures)
    • Complications (amylase, CK)

Management

  • Consideration for the cause and treating in parallel (antibiotics in sepsis, reversal of toxins, covering of burns etc)
  • ABCDE approach
  • Prevention of further heat loss
  • Rewarming (passive if mild-mod vs active if mod-severe [external vs invasive])
    • Passive – removal of wet clothing, warm blankets, warm room (works if shivering intact)
    • Active – external: immersion warming, heated blankets, thermal lamps, warmed circulated air (bair hugger) *senior advice*
    • Active – invasive: warmed IV dex/saline, bladder/gastric lavage, pleural/peritoneal/surgical lavage
    • Extracorporeal (haemodialysis, cardiac bypass, ECMO)
  • Identification of complications requiring monitoring (ECG, BM, bloods, temperature)
    • Rebound hypoglycaemia
    • Rebound hypovolaemia (secondary to peripheral vasodilation – give fluids)
    • Triggering of arrhythmias (be gentle when examining, minimise movement)
  • As an FY1 you’re only expected to initially assess and manage, senior review is warranted in all but very mild hypothermia
  • If severe or moderate refractory to normal treatment get HDU/ITU input early
  • Identification of other complications (aspiration, thrombosis, hyperkalaemia, repercussion injury, AKI, pancreatitis, frostbite etc)

Hypothermia and cardiac arrest

  • Whilst you will not be alone in an arrest, it is helpful to know some of the modifications to ALS algorithms. I have included formal guidelines in the references which you should review.
  • Whilst hypothermia is the likely cause and active rewarming measures should be taken, ensure all reversible causes of arrest are considered
  • If the temperature is less than 30°C and shockable up to 3 shocks can be given, no drugs should be administered
  • Once the temperature is above 30°C, shocks should be delivered in line with the standard ALS algorithm, drugs should be given however the frequency should be halved (1mg adrenaline IV every 6-10 minutes)
  • Once the temperature is above 35°C conduct the ALS algorithm as normal
  • It can be a long process, CPR should not be ceased until a temperature of at least 32°C is achieved, preferably normothermia, as such mechanical compression devices will often play a role

References

Written by Dr Adam Foster (FY1)

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