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Extremes of t emper ature 255
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with increased incidence seen at the extremes of age, due to suboptimal homeostatic thermoregulation. Peaks of incidence are common during heatwaves, exemplied by the 70 000 heat-related deaths
reported during the 2003 European heatwave. Conversely, exertional
heat illness predominantly affects young, physically t individuals (such
as soldiers and athletes), reecting a failure to dissipate intrinsic heat
production from physical activity.
Risk factors for the development of heat illness are well established
(Box 12.6).
Pathophysiology of heat stroke
The pathophysiology of heat stroke can be summarised as organ dysfunction from the high temperature itself, and end-organ ischaemia from
diminished blood ow. Increased sweating results in dehydration and
blood pools in vasodilated peripheral vasculature resulting in a decreased
effective blood volume. The blood viscosity increases resulting in heart
strain. Enzymes denature at 40 °C and at 41 °C mitochondrial activity
stops; the subsequent loss of oxidative phosphorylation results in organ
ischaemia. The muscles and gastrointestinal tract are affected rst, followed by the central nervous system, circulatory and clotting systems.
The pathophysiology is similar to sepsis, severe trauma and extensive
burns (Box 12.7).
Management
Mortality of heat illness is around 30% and is directly proportional to the
duration and magnitude of hyperthermia, therefore immediate cooling
should begin at the scene, before transfer to hospital. The aim should be
to reduce core temperature to approximately 39°C.
A patient should be removed from the heat source and put into shade
to reduce radiant heat gain. Resting in an air-conditioned room has cooling rates of 0.03–0.06°C/min. Clothes should be removed, high-ow
oxygen administered, intravenous access established and a rectal temperature taken. If temperature measurement is unavailable but the history
and clinical ndings are consistent with heat illness, initiation of treatment
with cooling techniques should not be delayed.
A number of cooling strategies exist ( Box 12.8), and their implementation will depend on what is feasible within each particular environment.
Two meta-analyses have concluded that ice water immersion is the most
effective treatment strategy with cooling rates of 0.20–0.35°C/min for
iced water and 0.11°C/min for wet towels. Immersion is unlikely to be
feasible in the wilderness environment and many hospitals, with further consideration of the potential dangers of immersing a patient with
a reduced conscious level. Immersing the hands and forearms in cold
water results in reduction of heat stress in normal subjects, but has not
been evaluated in the treatment of heat stroke patients.
The placement of ice/cold packs in the axillae, groin and neck has
been recommended as an easy method to use in the eld, but when
compared with evaporative cooling in healthy subjects, cooling times
were longest when the ice packs were used alone and shortest when
both methods were used simultaneously. Evaporative cooling involves
the removal of clothing, spraying tepid or cool water over the patient, and
facilitating evaporation and convection with the use of a fan.
The role of invasive cooling methods such as gastric, bladder or peritoneal lavage has not been fully established. Neither hyperhydration
nor dantrolene (used in the treatment of malignant hyperthermia) have
12
12.6 Risk factors for the development of heat-related illness
Risk factor Mechanism
High ambient temperatures Increased radiant heat gain
High humidity Ineffective evaporative heat loss at
humidities > 75%
Little shade Increased radiant heat gain
Intercurrent illness Raised core temperature
Extremes of age Suboptimal homeostatic thermoregulation
Overweight/unt The main identiable risk factor for heat
Effects of alcohol and medication
(diuretics, ACE inhibitors,
β-adrenoceptor antagonists,
vasodilators, antidepressants,
illness during military training was a body
mass index (BMI) ≥ 30 kg/m
Either through dehydration, decreased
cardiovascular and peripheral response
to dissipate heat, reduced sweating or
increased metabolic rate
2
anticholinergics, antihistamines
and stimulants)
Inappropriate clothing Reduced heat loss through combination
of radiation, convection and evaporation
Dehydration Regardless of body habitus or tness
level, uid losses that result in a 2%–3%
decrease in body weight correlate with
decreased aerobic performance, increased
perception of fatigue, and greater core
temperatures at a given workload
Previous heat-related illness Impaired homeostatic thermoregulation
No acclimatisation Body uid decits are reduced by around
30% in acclimatised individuals, despite
increased sweat rates of up to 18%, as a
result of a more accurate thirst
response
Intense work/duration Increased heat generation
12.7 Pathophysiology of heat stroke
Increased heart rate and an increase in cardiac
output by 3 L/min for each 1°C rise in core
temperature. Increased peripheral blood ow from
0.2 L/min up to 8 L/min. Dehydration with sweat
rates increasing from 0.5 L/day up to 15 L/day. Risk
of heart failure if pre-existing cardiac disease
Ischaemia and cerebral oedema due to the high
temperature itself and vascular endothelial damage
Intestinal mucosal impairment results in toxins
entering the portal vein and circulating systemically
resulting in sepsis
Tachypnoea and pulmonary vasodilatation result
in acute respiratory distress syndrome (ARDS)
(p. 201)
Acute renal failure due to ischaemia, dehydration
and rhabdomyolysis (p. 198)
Acute liver injury from ischaemia and high levels of
circulating inammatory cytokines (p. 879)
Microthrombus formation causing further
ischaemia and disseminated intravascular
coagulation (p. 988)
2+
K
Mg
H
H
K
K
2+
Mg
Mg
Multiple electrolyte abnormalities including
H
hypokalaemia, hypomagnesaemia, hypoglycaemia
and metabolic acidosis
2+
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12.8 Summary of cooling rates
Cooling technique (target < 39°C)
Cooling rate
Ice water immersion 0.20–0.35°C/min
Wet towels 0.11°C/min
Evaporative and convective
0.034–0.31°C/min
combined
Air-conditioned room 0.03–0.06°C/min
Intravenous cold saline 0.03°C/min
Intravenous room-temperature saline 0.015°C/min
12.9 Wet Bulb Globe Temperature (WBGT)
Meteorological conditions affect environmental temperatures and a widely used
index to calculate this is the WBGT, originally developed by the US Marines.
WBGT is an apparent temperature measurement taking into account temperature,
humidity, wind speed and solar radiation. This gives a much more accurate
representation of the degree of heat stress experienced. WBGT is used to
formulate a set of guidelines that guide activity levels, hydration and rest periods.
For example, a ‘do not start’ WBGT of 21°C has been suggested for American
marathons based on an unsuccessful attempt of 160 per 1000 nishers above this
level, although the incidence of heat-related illness is not well described.
evidence of benet. Cold intravenous uids may supplement cooling. In a
study of healthy volunteers, infusion of 4°C saline over 30 minutes cooled
the body by 1°C, compared to 0.5°C with room-temperature saline.
Highest
Pressurised
aircraft cabin
(< 2400 m)
22
20
18
16
14
12
10
Partial pressure of oxygen (kPa)
Partial
pressure of
inspired oxygen
8
6
4
0 2000 4000 6000 8000
Altitude above sea level (m)
permanent
habitation
(< 5200 m)
Arterial
oxygen
saturation
Summit
of Everest
(8848 m)
100
90
80
70
60
50
40
Arterial oxygen saturation (%)
Fig. 12.4 Change in inspired oxygen tension and blood oxygen saturation at
altitude. The blue curve shows changes in oxygen availability at altitude and the red
curve shows the typical resultant changes in arterial oxygen saturation in a healthy
person. Oxygen saturation varies between individuals according to the shape of the
oxygen–haemoglobin dissociation curve and the ventilatory response to hypoxaemia.
(To convert kPa to mmHg, multiply by 7.5.)
period of acclimatisation, the body is able to adapt and overcome even
profound hypoxaemia with arterial partial pressures of oxygen ( PaO
2.55 kPa recorded at 8400 m in a healthy climber (normally > 10.6 kPa
at sea level).
) of
2
Prevention
Cooling in a wilderness setting may be incredibly challenging, with likely
no access to ice or cold uids. Prevention of heat illness is therefore
paramount. Strategies include:
1. Ensuring adequate hydration. The 2019 Wilderness Medical Society
heat illness guidelines identify hydration as the ‘most readily modiable physiologic risk factor’. Fluid ingestion is also identied as the
most effective approach to mitigate the rise in core temperature
amongst athletes. Military guidelines recommend a 0.25–1.25 L/hr
hydration strategy that varies for work rates (low/medium/high/very
high) at a given Wet Bulb Globe Temperature (WBGT) (Box 12.9).
2. Consider accepted WBGT cut-offs for activities (Box 12.9).
3. Expedition participants should receive high-level education predeparture on the dangers of heat-related illness with evidencebased advice on risk reduction. Increased hydration and cooling
strategies have been documented following educational material
targeting older people prior to heatwaves.
4. If possible, implementing a period of acclimatisation with at least
1–2 hours of mild exertion in a hot environment for at least 8 days.
Body uid decits are reduced by around 30% in acclimatised
individuals as a result of a more accurate thirst response.
Acute high altitude illness
Illness due to high altitudes represents over a quarter of all serious medical incidents from reviews of expeditions in a range of environments.
High altitude is generally considered to be over 2500 m and extreme
altitude over 5500 m. The summit of Mount Everest stands at 8848 m,
where the barometric pressure and atmospheric partial pressure of oxygen (PO
gen remains the same at 20.9%.
utes if the body is exposed to an altitude over 8000 m. However, with a
) is around one-third of that at sea level; the percentage of oxy-
2
Unconsciousness secondary to hypoxia normally occurs within 3 min-
Physiological effects of high altitude
There are a number of physiological systems affected by altitude.
Respiratory
Reduction in oxygen tension results in a fall in arterial oxygen saturation (Fig. 12.4). This varies widely between individuals, depending on
the shape of the sigmoid oxygen–haemoglobin dissociation curve (see
Fig. 25.5) and the ventilatory response. Alveolar ventilation increases
with altitude, lowering carbon dioxide and resulting in a respiratory
alkalosis, with metabolic compensation via renal bicarbonate loss. At
high altitude, individuals are at the steep section of the oxygen dissociation curve whereby a small fall in PaO
decrease in oxygen saturation. The initial respiratory alkalosis shifts the
curve to the left but with a period of acclimatisation, increased production of 2,3-diphosphoglycerate moves the curve rightwards towards a
sea-level position.
can result in a substantial
2
Haematological
Measured haemoglobin concentration increases with acclimatisation –
a 20% fall in plasma volume causes haemoconcentration and erythropoietin release (stimulated by hypoxia) leads to increased production of
haemoglobin.
Cardiovascular
There is an initial increase in cardiac output due to increased sympathetic
activity and heart rate. The reduction in plasma volume causes a fall in
preload and stroke volume. Cardiac output returns to baseline over several weeks but the stroke volume remains lowered.
Illness at high altitude
Neurological and respiratory complications from high altitude occur in
individuals who ascend rapidly and are not acclimatised. Acute mountain
sickness (AMS) is seen in over a third of people who ascend to 3000 m.
Serious illness includes high altitude pulmonary oedema (HAPE) and
Suba qu atic medic ine 257
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high altitude cerebral oedema (HACE), occurring in 0.1–4% of people
climbing over 4000 m. Prevention is essential and achievable through
controlled ascents.
Acute mountain sickness
AMS is a syndrome comprised principally of non-specic symptoms
including headache, fatigue, anorexia, nausea and vomiting, insomnia
and dizziness. The pathophysiology of AMS is not fully understood but
it is thought that hypoxia results in vasodilation and increased capillary hydrostatic pressure causing a uid leak and a raised intracranial
venous volume with risk of raised intracranial pressure. There is believed
to be an increase in CSF production with a reduced buffering capacity.
Non-acclimatised individuals show impaired gas exchange and a lower
degree of hyperventilation, alongside uid retention and a heightened
sympathetic activation. Symptoms can occur within 4 hours, with the
diagnostic denition specifying an ascent to > 2500 m within the prior
4 days. The symptoms can vary in severity, from trivial to completely
incapacitating.
Management
Treatment of mild cases consists of rest and symptomatic control with
simple analgesia; symptoms usually resolve after 1–3 days at a stable
altitude, but may recur with further ascent. Occasionally there is progression to cerebral oedema (HACE). Persistent symptoms indicate the need
to descend, which is considered the denitive treatment.
Medication options include acetazolamide and dexamethasone.
Acetazolamide is used in both the prophylaxis of AMS and as a treatment option. It works as a carbonic anhydrase inhibitor in the kidneys,
increasing bicarbonate excretion and inducing a metabolic acidosis,
thereby offsetting the hyperventilation-induced alkalosis seen at altitude.
It also decreases CSF production, reducing intracranial pressure and risk
of progression to HACE. Ideal dosing strategies are debated, however
125 mg twice daily may be used as prophylaxis and 250 mg three times
daily for treatment. Higher doses (750 mg) have greater efcacy but also
increased side-effects. Dexamethasone (8 mg) moderates capillary leak
and reduces the inammatory response, improving symptoms to allow
for a safe descent.
High altitude cerebral oedema
HACE is considered a severe sequela of AMS, presenting as ataxia or
cognitive impairment in addition to the symptoms described above. It
very rarely occurs without being preceded by milder AMS symptoms,
making early recognition and treatment of AMS essential. Untreated
HACE can progress to coma within 24 hours.
Management
Management is directed at improving oxygenation. Descent is essential and dexamethasone (8 mg immediately, followed by 4 mg four times
daily) should be given. If descent is impossible, descent can be simulated
with the use of portable hyperbaric chambers, such as a Gamow bag.
Use of these devices, however, can be difcult in patients with vomiting
or a reduced level of consciousness.
High altitude pulmonary oedema
HAPE is a life-threatening condition that usually occurs in the rst 4 days
after ascent above 2500 m and is the leading cause of mortality from high
altitude illness. It is dened as an imbalance of hydrostatic pressure within
the alveoli with no evidence of inammatory changes. Hypoxic pulmonary vasoconstriction causes alveolar capillary stress failure and subsequent pulmonary hypertension. This results in capillary uid leak which is
exacerbated by exercise and compounded by impaired epithelial sodium
transport, normally essential for uid reabsorption. Initial symptoms
include a dry cough, exertional dyspnoea and extreme fatigue. Later,
the cough becomes wet with haemoptysis and orthopnoea. Tachycardia
and tachypnoea occur at rest and crepitations may often be heard in
both lung elds. Fever may also be present. There may be profound
hypoxaemia and radiological evidence of diffuse alveolar oedema. HAPE
may occur without the preceding signs of AMS, although around 50% of
patients with HAPE have concurrent AMS and 14% have HACE.
Management
Treatment is directed at reversal of hypoxia, with immediate descent
(by a minimum of 1000 m) and oxygen administration targeting saturations > 90%. A portable hyperbaric chamber should be used if descent
is delayed. Nifedipine (60 mg modied release divided into 2–3 doses)
is recommended prophylactically, starting 1 day before attempting
ascent above 2500 m and continued for a further 5 days at altitude or
until descent below 2500 m. For treatment of HAPE there is no evidence
of benet for any pharmacological therapy compared to descent and
oxygen.
Subaquatic medicine
Drowning
Drowning remains a leading cause of death globally and is dened as
‘the process of experiencing respiratory impairment from submersion/
immersion in liquid’. Immersion refers to the upper airway being above
the water surface and submersion below it. The drowning process
involves initial breath holding, followed by a period of laryngospasm.
Gas exchange is prevented resulting in hypoxia, hypercarbia and acidosis. Respiratory movements are stimulated by the respiratory centre
due to hypercarbia, however the laryngospasm results in obstruction of
the airway. The laryngospasm eventually falters with continued hypoxia
resulting in the aspiration of liquid of a variable amount, usually < 4mL/kg.
Aspiration of either saltwater or freshwater results in changes to the
alveolar surfactant and the alveolar capillary barrier causing atelectasis,
ventilation–perfusion mismatch and hypoxia. Saltwater is hypertonic
resulting in bronchoconstriction, inammation and pulmonary oedema;
aspiration of 2.5 mL/kg of seawater results in a 75% increase in rightto-left shunting of deoxygenated blood. Fresh water is hypotonic and is
generally absorbed through the pulmonary circulation, entering the systemic circulation and damaging the alveolar capillary membrane. This
can also generate foam which further decreases ventilation efciency.
The clinical signicance of swallowing water into the stomach during the
drowning process remains unclear. Clinically signicant electrolyte abnormalities from aspiration and swallowing of both hypotonic and hypertonic
uids are uncommon requiring > 22 mL/kg of uid, although both hyperand hyponatraemia have been described.
The majority of drownings occur in cold water that results in body
cooling, water being considered thermoneutral at around 35°C. Skin
cooling (cold shock) and tissue cooling (hypothermia) are important factors in drowning. The historical term ‘dry-drowning’ refers to the 10%
of drowning cases that are documented to have ‘macroscopically dry
lungs’ on examination, attributed to laryngospasm from water irritation
on contact. This remains controversial but is no longer felt to be true, with
newer evidence demonstrating the presence of microscopic liquid in the
lungs of all drowned patients. ‘Secondary drowning’, referring to patients
who develop acute respiratory distress syndrome (ARDS), is now also
considered a misnomer as there is no second submersion and ARDS is
a recognised complication of the drowning process.
Cold shock
The cold shock response is believed to be responsible for the majority of drowning deaths. Sudden cold-water immersion results in an
uncontrolled reex inspiratory gasping, hyperventilation with profound
hypocapnia and tachycardia from activation of peripheral sub-epidermal cold receptors. There is a 75% reduction in breath hold time, which
can therefore result in the aspiration of water. The response is maximal
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at water temperatures of 10–15 °C and peaks within the rst 30 seconds of immersion, waning over 2–3 minutes. Continued immersion
then results in physical incapacitation from neuromuscular cooling, with
peripheral paralysis occurring at regional limb temperatures of 5–15 °C.
Hypothermia develops after around 30 minutes in cold water.
Autonomic conict
Simultaneous positive and negative chronotropic triggers are considered
arrhythmogenic. Bradycardia from vagal stimulation (initiated when face
down in water – dive reex) coupled with a tachycardia from sympathetic
activation (cold, stress or exercise) can generate arrhythmias in previously healthy individuals and can be fatal in those with structural cardiac
abnormalities.
Pre-hospital management
In-water CPR and rescue breaths are no longer recommended. In-water
rescue is not recommended for untrained individuals – remember ‘Reach,
Throw, Row, Don’t Go’. If extracting someone from the water following
prolonged immersion, the patient should be kept horizontal to prevent
post-immersion hypotension; the loss of hydrostatic pressure that the
water was applying can result in venous pooling and a sudden circulatory
collapse. The patient should be kept warm, with life support commenced
at the earliest opportunity. Cervical spine precautions should be considered as there may be a traumatic precursor to the drowning incident (e.g.
tombstoning), although these injuries are uncommon (0.5% of cases).
Postural drainage techniques to try to clear uid from the lungs have no
proven benet.
In-hospital management
Treatment is often focused on re-warming and organ support including
non-invasive ventilation (CPAP) and protective lung ventilation strategies
for acute lung injury/ARDS. Prolonged immersion can result in hypovolaemia due to the hydrostatic pressure effect of water and the patient
may require IV uid. Prophylactic antibiotics are not recommended
unless submersion was in grossly contaminated water. Asymptomatic
patients, with no respiratory compromise, a normal chest X-ray and
normal arterial blood gas can be discharged home after 6–8 hours’
observation.
A brief review of the physics and physiology of diving is essential in
understanding the medical issues encountered. The two most important
gas laws are Boyle’s law and Henry’s law (Fig. 12.5).
Decompression sickness
Nitrogen bubble formation on ascent can cause direct mechanical
damage to the vascular endothelium and an inammatory response.
The bubbles occur almost anywhere in the body; therefore, the clinical
presentation is broad ranging from malaise and headache to paraesthesiae, lymphoedema, rash, joint pain and neurological manifestations
including ataxia, paralysis and altered mentation. The overall incidence
is low (0.03%) for recreational divers. Decompression sickness is very
uncommon for diving depths less than 10 m and is normally seen following multiple dives.
A
Boyle’s law
Depth in
metres
0
10
20
30
40
Henry’s lawB
Pressure in
atmospheres
1
2
3
4
5
Volume of a
sealed container
1
1/2
1/3
1/4
1/5
6L
3L
2L
1.5L
1.2L
Lung
volume
CPR modications
Five initial rescue ventilations are recommended given the hypoxic
nature of a cardiac arrest in drowning. The patient’s chest should be
dried before application of debrillation pads; however less than 5% of
drowned patients are in a shockable rhythm. The common progression
of cardiac rhythm is from bradycardia, to pulseless electrical activity,
to asystole. Submersion in ice-cold water (less than 6°C) may confer improved survival due to neuroprotection from rapid brain cooling
before the onset of severe hypoxia; children in particular appear to have
greater protection, believed in part to be due to a greater surface area
to mass ratio allowing quicker cooling. For submersion times greater
than 30 minutes in water warmer than 6°C, resuscitation is likely to
be futile. If water temperature is below 6°C resuscitation is likely to be
futile following a submersion over 90 minutes long. Submersion within a
vehicle may prolong these times due to the potential presence of an air
bubble. International guidelines do vary on the futility associated with
submersion duration. The overall mortality of drowned patients who
present in cardiac arrest is 93%.
Decompression illness
Changes in environmental pressure (as seen in diving) can result in
decompression illness due to intravascular or extravascular bubbles, the
clinical manifestations of which include both arterial gas embolism and
decompression sickness. Diagnosis of decompression illness is based
on the history and clinical features in patients following a dive; 90% of
cases are symptomatic within 6 hours, however, delays up to 72 hours
are described.
Surface
Compression
Decompression
Isopression
= Nitrogen
Fig. 12.5 Boyle’s law and Henry’s law.
inversely proportional to the pressure. Atmospheric pressure increases with depth,
increasing by 1 atmosphere for each 10 m of depth in water. During diving this
increasing pressure compresses the gas within the human body, including the lungs,
ears, sinuses and bowels. During ascent this gas expands and can cause barotrauma
liquid is proportional to the partial pressure of the gas. Nitrogen is not metabolised
by the body and increasingly dissolves into the blood on descent. The reverse occurs
on ascent, which if ascending too quickly can cause bubbles to form, resulting in
decompression sickness.
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Arterial gas embolism
Expanding gases during ascent from diving, from depths as little as
1 metre, can rupture the alveolar capillary membrane (barotrauma), introducing alveolar gas into the arterial circulation. The brain is the most
commonly affected organ. Small venous gas emboli are common with
diving and usually are of no clinical consequence due to pulmonary capillary ltering. A patent foramen ovale is seen in around a quarter of the
population which can result in these emboli transferring to the arterial
circulation, causing neurological sequelae. Overall, the risk of arterial gas
embolism is rare, representing only around 4% of documented decompression illnesses. Risks include rapid ascents, breath holding and
pre-existing pulmonary disease. If there is rapid onset of neurological
signs, including seizures or a reduced consciousness following ascent,
arterial gas embolism should be suspected.
Management
Any obtunded patient should have appropriate rst aid. Denitive treatment for decompression illness is providing 100% oxygen to wash out
gas from the tissues to the lungs and remove bubbles. This should be
instigated for all patients regardless of their oxygen saturations.
Chamber recompression is the gold standard therapy and should be
performed as soon as possible causing a theoretical crushing of bubbles
(as per Boyle’s law) and providing improved oxygenation to damaged tissues. Extraction to a recompression chamber may require aeromedical
retrieval and helicopters at low altitude (less than 300 m) or those with
cabins pressurised to 1 atmosphere are recommended. In-water recompression is controversial and is recommended only for divers, including
the patient, with specic training in decompression procedures underwater. Previous recommendations of a head-down position to stop cranial
spread of bubbles is no longer recommended due to the increased risk
of cerebral oedema; patients should be kept horizontal. One litre of intravenous uid should be given to correct the intravascular uid loss from
endothelial bubble injury and dehydration associated with immersion.
Analgesia should be avoided; non-steroidal anti-inammatory drugs can
result in haemorrhage whilst opiates raise the risk of oxygen toxicity.
The Divers Alert Network can be contacted for international advice and
support.
Immersion pulmonary oedema
Immersion pulmonary oedema can affect surface swimmers as well as
divers and is believed to be a leading cause of death during the swim
stage of triathlons, previously felt to be due to drowning. Immersion
results in exposure to hydrostatic pressure which collapses veins and
redistributes blood to the thorax, causing increased preload, cardiac
contractility and stroke volume. Rising pulmonary alveolar capillary
pressure results in a uid shift into the lung interstitium initially, followed
by the alveoli. This is normally balanced by the release of natriuretic
peptides (ANP and BNP) causing a natriuresis and diuresis, however
in immersion pulmonary oedema this compensation is overwhelmed.
Risk factors include overhydration, overexertion, heart disease, hypertension and cold water, all resulting in raised ventricular lling pressures.
Breathing into a snorkel or scuba equipment can result in higher negative pressures in the alveoli with a subsequent greater uid transudation into them (the opposite of positive pressure ventilation used to
treat pulmonary oedema). Symptoms range from shortness of breath
to haemoptysis and frothy sputum, generally occurring within 10 minutes of starting swimming, and of variable onset with diving. Treatment
involves extraction from the water to remove the hydrostatic pressure,
which in turn decreases ventricular lling pressures. Patients should
be kept warm to prevent vasocontriction, sat upright and given 100%
oxygen. In-hospital management involves a combination of vasodilators
(nitrates), diuretics and positive-pressure ventilation (CPAP). Recurrence
rates are around 30%.
Shallow-water blackout
This condition refers to the loss of consciousness underwater when
hyperventilation is followed by breath holding. It generally occurs in
water less than 5 m in depth and can affect even experienced swimmers. Hyperventilation (as rapid shallow breaths before diving) preceding
a breath hold lowers the arterial CO2 and delays the hypercarbic stimulus to breathe, which may not occur before hypoxaemia and unconsciousness develop. Unconsciousness usually occurs on ascent as the
hydrostatic pressure decreases, reducing the thoracic shunting of blood
and gas exchange, coupled with a decreasing partial pressure of oxygen
(Boyle’s law) and resulting in a signicant hypoxaemia.
Further information
Books
Edmonds C, Bennett M, Lippmann J, Mitchell S. Diving and subaquatic medicine,
5th edn. Boca Raton: CRC Press; 2016. An excellent review of subaquatic
medicine.
Websites
rgs.org Royal Geographical Society. Multiple downloadable expedition guidance
documents for a range of environments.
christopherimray.co.uk/highaltitudemedicine Extensive publications on high
altitude medicine and cold injury by Professor Chris Imray.
altitude.org A website written by doctors with expertise and experience of
expedition and altitude medicine.
scholar.google.co.uk/citations?user=ZJRl2HEAAAAJ&hl=en Lists publications
by Professor Mike Tipton of the Extreme Environments Laboratory, University
of Portsmouth, on cold water immersion, thermoregulation and environmental
physiology.
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Multiple Choice Questions
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12.1 You are part of a search and rescue team looking for a trapped
skier, following an avalanche 20 minutes prior. On nding the
patient you are instructed by the team leader to move them very
carefully, to not induce a cardiac arrhythmia. Below what core
temperature can ventricular brillation be induced from excessive
movement?
A. 36°C
B. 32°C
C. 35°C
D. 30°C
E. 33°C
Answer: D.
Answer: D.
There are a number of adaptations to resuscitation algorithms for
hypothermic patients in cardiac arrest. Assessment for signs of life
should be extended to 1 minute. Ventricular brillation and ventricular
tachycardia can be debrillated, however if after three shocks there is
no response, additional shocks should be delayed until core temperature is greater than 30°C. Stacked shocks are not recommended.
Withhold adjunctive medications (adrenaline, amiodarone, etc.) if the
patient is below 30°C, and double the interval time between doses
between 30°C and 35°C.
Markers of futility 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.
12.4 With regards to freezing cold injury (frostbite), which of the
following statements around management is correct?
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%. Initial conduction abnormalities include a sinus bradycardia, progressing to slow atrial brillation (AF) and then to ventricular
brillation (VF). VF may be induced below 30°C with excessive stimulation/movement, which is why handling of hypothermic patients needs to
be performed with great care.
12.2 You are working as a medic for a 100-mile ultramarathon,
environmental conditions are wet (moderate rain), with a
temperature of 8°C. You are asked to see a competitor who
has come into the medical tent after 12 hours of running. The
competitor is drowsy, confused and is not shivering. Blood sugar
is normal. You do not have access to a rectal thermometer.
Using the Swiss Staging System, quantify the possible degree of
hypothermia for this patient.
A. < 24°C
B. 28–31°C
C. 24–27°C
D. 32–35°C
E. 35–36°C
Answer: B.
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 (see Fig. 12.3). This
has been shown to overestimate the degree of hypothermia in around
20% of cases but remains a helpful classication when an accurate core
temperature cannot be obtained.
12.3 Which of the following statements is true for adaptations to
resuscitation algorithms for hypothermic patients in cardiac
arrest?
A. The affected area should always be rewarmed immediately in
the pre-hospital environment
B. Early amputation is the gold standard therapy
C. Rubbing of the area with direct application of heat pads to
thaw the affected region is recommended
D. Analgesia is not required, freezing injuries are not painful
E. Aspirin 75–300 mg and ibuprofen 800 mg are recommended
Answer: E.
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.
Denitive 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 uid replacement with warmed uids (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 should
be given following local protocols; frostbite wounds are not considered
tetanus-prone.
12.5 The most readily modiable physiological risk factor for the
development of heat illness is:
A. Withhold all shocks – chance of shockable rhythm < 5%
B. Signs of life should be checked for 30 seconds rather than 10
seconds
C. Do not warm hypothermic patients in cardiac arrest – the
hypothermia is neuroprotective
D. Withhold medications (adrenaline, amiodarone etc.) until core
temperature > 30°C and double the interval time between
doses between core temperatures of 30°C and 35°C
E. A potassium level of 7 mmol/L is diagnostic of resuscitation
futility
A. Obesity
B. Hydration
C. Acclimatisation
D. Use of beta-blockers
E. Aerobic tness
Answer: B.
The 2019 Wilderness Medical Society heat illness guidelines identify
hydration as the ‘most readily modiable physiologic risk factor’. Fluid
ingestion is also identied as the most effective approach to mitigate the
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rise in core temperature amongst athletes. Military guidelines recommend
a 0.25 L/hr – 1.25 L/hr hydration strategy that varies for work rates (low/
medium/high/very high) at a given Wet Bulb Globe Temperature (WBGT).
12.6 The denition of heat stroke is:
A. Mild swelling to the limbs during the rst few days of heat
exposure due to increased plasma volume
B. Neurological impairment with core body temperature ≥ 40°C
C. A transient loss of consciousness in the context of heat expo-
sure with a relatively rapid return to normal function and baseline
D. It is an inability to continue an activity due to heat stress
E. Body spasms related to sodium loss
Answer: B.
Heat-related illness denes a spectrum of pathology from benign heat
oedema to lethal heat stroke. The denition of heat stroke is: neurological
impairment with core body temperature ≥ 40°C (rectal temperature is
gold standard in a pre-hospital environment). Symptoms can involve a
coarse muscle tremor, confusion, aggression and loss of consciousness.
Sweating may be absent due to dehydration and failure of thermoregulatory mechanisms.
12.7 You are working on an expedition in the Costa Rican jungle. The
expedition leader asks you theoretically what the best cooling
strategy is for patients with heat stroke. In your current location
you only have access to cold water. You suggest:
A. Removing the patient into the shade
B. Calling for a helicopter to use the downwash from the blades
C. Forcing the patient to drink cold water
D. Spraying the patient with cool water and using a combination
of evaporative and convective heat loss
E. Ice water immersion.
Answer: D.
A number of cooling strategies exist and their implementation will
depend on what is feasible within each particular environment. Two
meta-analyses have concluded that ice water immersion is the most
effective treatment strategy, with cooling rates of 0.20°C–-0.35°C/min
for iced water and 0.11°C/min for wet towels. Immersion is unlikely to be
feasible in the wilderness environment and in many hospitals, with further
consideration for the dangers of potentially immersing a patient with a
reduced conscious level.
The placement of ice/cold packs in the axillae, groin and neck has
been recommended as an easy method to use in the eld, but when
compared with evaporative cooling in ve healthy subjects, cooling times
were longest when the ice packs were used alone and shortest when
both methods were used simultaneously. Evaporative cooling involves
the removal of clothing, spraying tepid or cool water over the patient, and
facilitating evaporation and convection with the use of a fan.
12.8 You are working on an expedition on Mont Blanc and are
asked to see a patient who at 3500 m has developed a wet
cough with frothy sputum. The patient is tachycardic with
a high respiratory rate and you hear bibasal crepitations in
both lungs. The patient insists they have mild acute mountain
sickness, which they have had previously, and wants to
continue to summit. They have taken no prophylactic
medications. What is the most appropriate plan?
A. The patient likely has high altitude pulmonary oedema and
should immediately descend by at least 1000 m alongside
giving high-ow oxygen
B. The patient is most likely correct and has mild acute mountain
sickness and should be allowed to summit
C. The patient has high altitude cerebral oedema and should
be given 8 mg of dexamethasone and then start to
descend
D. The patient has no evidence of high altitude illness, and the
ndings are consistent with normal physiological changes at
altitude. No action is required
E. The patient has severe acute mountain sickness and should
remain at their current altitude for 2–3 days
Answer: A.
HAPE is a life-threatening condition that usually occurs in the rst 4 days
after ascent above 2500 m and is the leading cause of mortality from high
altitude illness. Hypoxic pulmonary vasoconstriction causes alveolar capillary stress failure and subsequent pulmonary hypertension. This results in
capillary uid leak which is exacerbated by exercise and compounded by
impaired epithelial sodium transport, normally essential for uid reabsorption. Initial symptoms include a dry cough, exertional dyspnoea and extreme
fatigue. Later, the cough becomes wet with haemoptysis and orthopnoea.
Tachycardia and tachypnoea occur at rest and crepitations may often be
heard in both lung elds. Fever may also be present. There may be profound
hypoxaemia and radiological evidence of diffuse alveolar oedema. HAPE
may occur without the preceding signs of AMS, although around 50% of
patients with HAPE have concurrent AMS and 14% have HACE.
Treatment is directed at reversal of hypoxia, with immediate descent
(by a minimum of 1000 m) and oxygen administration targeting saturations > 90%. A portable hyperbaric chamber should be used if descent
is delayed. Prophylactically, nifedipine (60 mg modied release divided
into 2–3 doses) should be given to reduce pulmonary arterial pressure,
ideally 1 day preceding ascent and continued for a further 5 days.
12.9 You are working in an Emergency Department and are asked
to review a 17-year-old male patient who 1-hour prior aspirated
some water whilst swimming in the sea and was rescued by
members of the public who described initial panicking and
respiratory impairment. The patient appears well, with normal
observations. The most appropriate plan is:
A. The patient is suitable for discharge with no evidence of
ongoing respiratory distress
B. The patient is suitable for discharge following a normal chest X-ray
C. The patient is suitable for discharge following 6–8 hours’
observation if his observations remain normal, with a normal
chest X-ray ± normal arterial blood gas
D. The patient should be admitted for 72 hours to observe for
delayed acute respiratory distress syndrome (ARDS)
E. The patient does not need to be seen in an Emergency
Department and should be discharged home without review
Answer: C.
Drowning is dened as ‘the process of experiencing respiratory impairment from submersion/immersion in liquid’. Asymptomatic patients, with
no respiratory compromise, a normal chest X-ray and normal arterial
blood gas can be discharged home after 6–8 hours’ observation.
12.10 You are on holiday on a beach and see a 50-year-old female
swimmer in difculty. She is dragged from the water by a rst
aider on scene and is currently lying on her back in the shallow
water with small waves breaking over her. She is alert but is
coughing frequently, with a fast respiratory rate. The rst aider
does not wish to move the patient due to the risk of a cervical
spine injury. The most appropriate plan is:
A. Assist the rst aider by applying cervical spine immobilisa-
tion and wait for an ambulance to arrive with a scoop
B. Drag the patient up the beach out of the water to prevent
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further aspiration or development of hypothermia
C. Acknowledge the rst aider’s concern, but reassure that
the risks are low (0.5%) for a cervical injury and it would be
safest to ask the patient to move with help up the beach
D. Do nothing, the patient is clearly alert and breathing and no
further intervention is required
E. Administer 5 rescue breaths, followed by raising the patient’s
body above their head to allow for postural drainage of
water from the lungs
Answer: C.
The safest option is to remove the patient from the water due to the
ongoing risk of further aspiration and ongoing cooling with subsequent
hypothermia. Risk of cervical spine injury is low (0.5%). Asking the
patient if they are able to move up the beach with support is the most
appropriate initial step. Postural drainage techniques are not recom-
mended, with no evidence of benet.
DH Dockrell
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S Sundar
BJ Angus
13
Infectious disease
Clinical examination of patients with infectious disease 262
Presenting problems in infectious diseases 264
Fever 264
Positive blood culture 270
Sepsis 271
Acute diarrhoea and vomiting 272
Infections acquired in the tropics 274
Infections in adolescence 278
Infections in pregnancy 279
Viral infections 279
Systemic viral infections with exanthem 279
Systemic viral infections without exanthem 283
Viral infections of the skin 290
Gastrointestinal viral infections 292
Respiratory viral infections 292
Viral infections with neurological involvement 298
Viral infections with rheumatological involvement 299
Prion diseases 299
Bacterial infections 299
Bacterial infections of the skin, soft tissues and bones 299
Systemic bacterial infections 303
Gastrointestinal bacterial infections 309
Respiratory bacterial infections 312
Bacterial infections with neurological involvement 314
Mycobacterial infections 314
Rickettsial and related intracellular bacterial infections 316
Chlamydial infections 319
Protozoal infections 319
Systemic protozoal infections 319
Leishmaniasis 326
Gastrointestinal protozoal infections 330
Infections caused by helminths 332
Intestinal human nematodes 332
Tissue-dwelling human nematodes 335
Zoonotic nematodes 337
Trematodes (ukes) 338
Cestodes (tapeworms) 340
Ectoparasites 342
Fungal infections 342
Supercial mycoses 343
Subcutaneous mycoses 344
Systemic mycoses 344
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