Thermoregulation:
Body heat is generated by basal metabolic activity and muscle move-
ment, and lost by four main mechanisms: conduction, convection,
evaporation and radiation . Body temperature is controlled
in the hypothalamus, which is directly sensitive to changes in core
temperature and indirectly responds to temperature-sensitive neu-
rons in the skin. The normal ‘set-point’ of core temperature is tightly
regulated within the range 37 ±0.5°C, which is necessary to preserve
the normal function of many enzymes and metabolic processes.
Thermoregulation in old age:
1. Age-associated changes: impairments in vasomotor function, skeletal muscle
response and sweating mean that older people react more slowly to changes in
temperature.
2. Increased comorbidity: thermoregulatory problems are more likely in the
presence of pathology such as atherosclerosis and hypothyroidism, and
medication such as sedatives and hypnotics.
3. Hypothermia: this may arise as a primary event, but more commonly
complicates other acute illness, e.g. pneumonia, stroke or fracture.
4. Ambient temperature: financial pressures and older equipment may result in
inadequate heating during cold weather.
The cold environment:
Protective mechanisms in a cold environment include activation of the
sympathetic nervous system with cutaneous vasoconstriction, shivering
and increases in both heart rate and cardiac contractility. Shivering, an
involuntary contraction and relaxation of muscles, is an early adaptive
cold response that results in a two- to fivefold increase in heat generation. As core temperature drops these protective mechanisms fail; shivering stops between 29°C and 31°C.
Physiological effects:
The cold environment has six main effects on physiological systems:
1. Metabolism:
Regional organ blood flow is reduced in the cold environment with
marked variation; the kidneys demonstrate the most significant change,
similar in response to that seen with haemorrhage or sepsis. The stress
response results in glycogenolysis and gluconeogenesis with a relatively
defective insulin efficacy resulting in hyperglycaemia.
2. Fluid and electrolytes:
As the body cools there is a relative decrease in plasma volume as fluid
moves intracellularly with subsequent inadequate tissue perfusion. There
is a decrease in intracellular potassium below a core temperature of
25°C, which is linked to the risk of arrhythmias.
3. Respiratory
For every 1°C reduction in core temperature there is a 6% drop in oxygen
consumption. The initial increased respiratory rate declines with ongoing
cooling, with animal studies suggesting a cessation of breathing at a core
temperature of 24°C. There is direct respiratory centre depression from a
reduction in both oxygen expenditure and production of carbon dioxide.
4. Cardiovascular
As the core temperature falls there is a reduction in cardiac output with
initial maintenance of stroke volume. At around 28°C the heart rate is
reduced by 50% with a subsequent increased risk of arrythmias . Initial
conduction abnormalities include a sinus bradycardia, progressing to
slow atrial fibrillation (AF) and then to ventricular fibrillation (VF). VF may be
induced below 30°C with excessive stimulation/movement, which is why
handling of a hypothermic patient needs to be performed with great care.
5. Haematological:
There is an increased plasma viscosity, with a 150% rise in haematocrit
documented at a core temperature of 25°C. Enzymatic reactions within
the coagulation cascade are prolonged, alongside platelet trapping
within the liver and spleen, resulting in an increased bleeding risk
6. Neurological:
There is a decline in cognitive function in the cold environment with
unconsciousness occurring at a core temperature around 28–30°C.
Slurred speech, ataxia and paradoxical undressing are all described
with lowering core temperatures. Absence of brain electrical activity is
seen below 20°C; this is generally considered to be neuroprotective. It is
believed that the cold stabilises the blood–brain barrier and cerebral cell
membranes that would otherwise be disrupted by hypoxia.
Hypothermia:
Hypothermia is defined as a core temperature below 35°C and can be subcategorised into primary hypothermia due to environmental exposure and
secondary hypothermia due to abnormal thermoregulatory mechanisms
as a result of an underlying altered physiological state. Measurement of
core temperature can be challenging, with tympanic measurements often
considered inaccurate; monitors are often not calibrated below 35.5°C.
Alternatives such as oesophageal temperature can be difficult to achieve
in practice, and rectal measurements (considered the gold standard
measurement) can lag behind the true core temperature.
Traditionally, hypothermia is categorised as mild (32–35°C), moderate
(28–32°C) and severe (<28°C), however, newer staging systems, such
as the Swiss Staging System, adopted by some ambulance services,
dene the level of hypothermia based on symptoms . This has
been shown to overestimate the degree of hypothermia in around 20%
of cases but remains a helpful classification when an accurate core temperature cannot be obtained.
Management:
Following resuscitation, the objectives of management are to rewarm the
patient in a controlled manner whilst treating associated hypoxia (by oxygenation and ventilation if necessary), fluid and electrolyte disturbance,
and cardiovascular abnormalities. Careful handling is essential to avoid
precipitating arrhythmias. The Swiss Staging System can be used to
guide treatment at various levels of hypothermia .
Mild hypothermia:
Continued heat loss can be prevented by sheltering the patient from the
cold, replacing wet clothing, covering the head and insulating the patient
from the ground. Hibler’s method is the best available technique for
packaging a patient, which involves wrapping the patient in an insulating
layer, followed by an outer vapour-tight layer. Warm drinks and active
movement can raise the core temperature by 2°C per hour. Forced-air
re-warming blankets and heat packs can increase core temperature by
0.1–3.4°C per hour. Warmed intravenous fluids have been shown to pro-
vide no active warming but they do prevent further cooling.
Severe hypothermia:
For severe hypothermia a number of invasive warming methods can
be instigated in hospital. This includes bladder lavage, which involves
flushing the bladder with 300 mL of warm saline resulting in a 1–2°C
rise in core temperature per hour. Thoracic lavage through two uni-
lateral chest drains (anterior and lateral) can result in a 2–3°C rise per
hour. A single chest drain approach can be used by clamping a 32–36
French tube for 2–3 minutes after flushing in 300 mL of warm saline,
then allowing it to drain.
Extracorporeal membrane oxygenation (ECMO) and cardiopulmonary
bypass (CPB) are performed in specialist hospitals and represent the best
warming strategies, with increases in core temperature of 6–10°C per hour.
Swiss Staging System and the treatment of hypothermia.| Stage / Core temperature | Symptoms | Treatment |
|---|
| Stage 1(32-35) |
Alert and shivering
|
Pragmatic support: place in a warm environment and provide clean warm clothes. Offer hot sugary drinks if the patient is conscious and can swallow. Encourage active movement (if safe) — muscle activity can increase heat production (note: active movement may increase temperature generation substantially compared with basal metabolic rate).
|
| Stage 2(28-32) |
Drowsy and not shivering
|
Same general measures as Stage 1 plus airway support as necessary. Monitor closely; may require escalation to more invasive warming methods depending on response and core temperature (see Stage 3 options).
|
| Stage 3(24-28) |
Unconscious with vital signs present, no shivering
|
Escalate care: continue supportive measures and manage airway, breathing and circulation. Consider invasive active internal rewarming techniques when available (for example extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass (CPB)) in severe or refractory cases.
|
| Stage 4(<24) |
Unconscious with no vital signs (cardiac arrest)
|
Manage as cardiac arrest with simultaneous rewarming strategies. Use the same principles as Stage 3 but institute advanced resuscitation and rewarming — external and internal rewarming and advanced life support measures as indicated.
|
Additional pragmatic measures (use clinical judgement):
- Insulate whole body; use wind and vapour barriers.
- External rewarming tools: warming blankets, chemical heat packs around axilla/groin (avoid direct skin burns).
- Warm IV fluids: help prevent further cooling but do not actively rewarm the core by themselves.
- Reduce unnecessary movement and keep patient horizontal to reduce risk of arrhythmia; avoid rough handling in severe hypothermia.
There are a number of adaptations to resuscitation algorithms for hypo-
thermic patients in cardiac arrest . There is an old adage that
'you’re not dead until you’re warm and dead’ with documented cases of
full recovery following extended periods of ECMO obvious .
There are, however, some markers of futility. These include: obvious lethal injury, prolonged asphyxia (mouthful of snow etc.), incompressible
thorax (distinct from a stiff chest which is common), frozen abdomen, or
potassium >12 mmol/L.
Management of cardiac arrest in hypothermic patients
Assessment for signs of life should be extended to 1 minute
Ventricular fibrillation and ventricular tachycardia can be defibrillated, however if after
three shocks there is no response, additional shocks should be delayed until core
temperature is >30°C (3-shock ‘stacked’ sequences are not recommended)
Withhold adjunctive medications (adrenaline, amiodarone etc.) if the
temperature is below 30°C; or double the interval between doses when
temperature is 30–35°C
Cases of full recovery following extended periods of ECMO
and CPB
*** In 1999 a 29-year-old Norwegian radiology registrar fell whilst skiing into an
ice waterfall gully. She was cut out after 1 hour and 20 minutes with a core
temperature of 13.7°C. Following 9 hours of CPR and CPB she survived with no
neurological impairment.
In 2011 a 7-year-old Swedish girl fell from a cliff into the sea and was found in
the water after 3–4 hours with a core temperature of 13.2°C. Following CPR
and warming she survived with no neurological impairment.
(CPB = cardiopulmonary bypass; CPR = cardiopulmonary resuscitation;
ECMO = extracorporeal membrane oxygenation)
Cold injury:
Freezing cold injury (‘frostbite’):
Hypothermia-induced vasoconstriction results in tissue cooling and
frostbite refers to ice formation and freezing within the tissue, most commonly affecting the hands and feet (around 90% of cases). Risk factors
include alcohol consumption (which impairs decision-making and results n peripheral vasodilatation), previous frostbite, drug use, inappropriate
clothing, fatigue and dehydration. There are two distinct phases to cold
injury: a ‘cooling–supercooling–freezing’ stage during exposure; and
a vascular stage during re-warming. When skin tissues cool to below
0°C ice crystal formation causes microvascular and cell damage. During
warming, this results in a degree of circulatory failure and fluid loss. The
release of inflammatory mediators causes ischaemia and clot production. Re-freezing following warming is particularly destructive, resulting in
massive cell inflammatory changes, therefore re-warming should only be
initiated if there is no risk of further refreezing.
Patients often describe an initial numbness and woody sensation
followed by a severe pain during warming with a persistent throbbing
sensation. Pain can endure for months alongside potentially perma-
nent sensory changes. The skin can look waxy, discoloured or blistered
( however prognostication using initial skin changes can be
very challenging.
Early amputations have a higher morbidity and surgery should be delayed
unless there is evidence of sepsis. There is also a potential role for hyperbaric oxygen treatment and this is an area of current research.
Non-freezing cold injury:
This results from prolonged exposure to cold, damp conditions and is
often seen in individuals who become wet but are unable to dry out.
The important distinction from frostbite is that the tissues do not freeze.
It is almost exclusively seen in the lower limb and feet, however concomitant injury to the hands is sometimes seen. It is often described
as a patch of numbness, which when rewarmed, changes in colour
from pale to red, with associated swelling and pain. These symptoms
can last for months or indefinitely; often far longer than an equivalent
freezing injury. The pathology remains uncertain but probably involves
endothelial injury. Gradual re-warming is associated with less pain than
rapid re-warming. The pain and associated paraesthesia are difficult
to control with conventional analgesia and may benet from early use
of amitriptyline. The patient is at risk of further damage on subsequent
exposure to the cold.
If concerned about the possibility of cold injury, immediate pre-hospital treatment is to try to shelter from the environment, consume warm
drinks, remove shoes, wet clothing and jewellery and re-dress in warm,
dry clothing. If there is absolutely no risk of re-freezing then warming the
area can be achieved by placing the area into a companion’s armpit or
groin. Aspirin 75–300 mg and ibuprofen 800 mg are recommended. Do
not rub the area and do not place heat sources directly onto the area.
Evacuation for formal medical review should be obtained. Warmed areas
need to be made non-load-bearing and therefore prior thought about
extraction needs to be considered. Aloe vera gel has anti-prostaglandin
effects and can be applied before application of a non-adherent dressing, splinting and elevation of the affected region.
Definitive warming involves placing the affected area into circulating water between 37°C and 42°C with small amounts of antiseptic
for around an hour, avoiding contact with the sides of the container.
Additional treatment involves fluid replacement with warmed fluids (due
to cold diuresis), strong analgesia and blister care. Blisters may present
as clear, cloudy or haemorrhagic. Blister management remains controversial, with current evidence recommending débridement of all blisters
in hospital (likely under a general anaesthetic) to improve wound healing.
There is no evidence for prophylactic antibiotics and tetanus prophylaxis
should be given according to local protocols; frostbite wounds are not
considered tetanus-prone.
In-hospital management includes specialist imaging (e.g. angiography
and technetium bone scanning) to inform prognosis. A combination of
thrombolysis and vasodilators (such as nitroglycerin), given within
24 hours, has evidence of good outcomes. Iloprost, a prostacyclin
analogue that causes vasodilation and reduces the requirement for
amputation, can be given intravenously after 24 hours of injury.
