Section I – Drowning

Epidemiology

Water sports are favorite recreational pursuits of many Australians and it is therefore unfortunate that so many,
particularly the young suffer injury through misadventure.

Drowning accidents are largely preventable and generally affect previously healthy individuals. Between 1992 and
1996 accidental drowning claimed the lives of some 1643 Australians and was the fifth most common ‘external cause
of death’ behind suicide, motor traffic accidents, accidental falls and homicide (RLSSA 1997). The Royal Life Saving
Society Australia estimates there are approximately 90,000 ‘near misses’ annually in Australia. The peak incidence of
drowning is seen in the 0-4 age group followed by males in the 20 - 45 year age group. A combination of alcohol and
risk taking activity (boating, jet skis, surfing) occurs frequently. Hyperventilation prior to entering the water is known to
increase breathold time and prolong the time one may spend submerged. Hyperventilation lowers the arterial carbon
dioxide level and hence removes the most potent respiratory stimulant. Hypoxia alone is a less powerful stimulant
and loss of consciousness and drowning may occur before the impulse to breath becomes apparent. Drowning may
occur as the primary event or be secondary to e.g. a sudden cardiac event, epileptic seizure or in scuba divers
cerebral arterial gas embolism.

Key points

• Drowning accidents are largely preventable and generally affect previously healthy individuals

Mechanism of injury

Whatever the cause, a drowning victim will initially hold their breath (voluntary apnea) until they reach ‘breaking
point’. The level of hypercarbia and hypoxia govern this breaking point and once reached inspiration of water occurs
and this is usually followed by involuntary gasping. Significant volumes of water may also be swallowed. Progressive
respiratory failure, metabolic acidosis, cardiac arrhythmias and finally brain death ensue.

Key points

• A drowning victim will initially hold their breath (voluntary apnea) until they reach ‘breaking point’

Classification

The litreature classifies the drowning syndromes in many ways. Drowning is defined as suffocation by submersion,
especially in water (Modell 1993) whilst near drowning is defined as survival, at least temporarily, after aspiration of
fluid into the lungs (Golden et al. 1997). Classically the litreature refers to ‘wet’ and ‘dry’ drowning and then further
subdivides drowning according to whether fresh or salt water was involved.
Wet drowning with aspiration of fluid into the lungs is said to occur in 80 – 93 % cases. At least 85% of patients who
survive near drowning are thought to aspirate 22 ml of water per kilogram or less (Modell 1993). The physiologic
basis of the hypoxia will depend on the nature and the volume of the aspirated fluid. Most authors (Pearn 1985,
Modell 1993, Mitchell and Gorman 1994, Weinstein and Krieger 1996, Golden et al. 1997, Reed 1998, Thanel 1998)
refer to the theory of ‘dry drowning’ and state that between 7-20% of individuals who drown aspirate no fluid as a
consequence of laryngeal spasm. It is stated a small volume of water enters the larynx or trachea and initiates
laryngeal spasm, a vagally mediated reflex. In this case the progressive hypoxia occurs on a background of apnea.
Edmonds (1998) questions the concept of dry drownings and states ‘dry drowning could well be an artifact of fluid
absorption from the lungs or death from other causes’.

Key points

• Drowning is suffocation by submersion, especially in water whilst-

• Near drowning is survival, at least temporarily, after aspiration of fluid into the lungs

Pathophysiology

Fresh water is hypotonic and rapidly absorbed into the pulmonary circulation so the presence of the aspirate within
the alveoli is not a problem. Although the fresh water is absorbed into the circulation and theoretically could cause
hypervolemia, electrolyte abnormalities and red blood cell hemolysis, this is rarely seen in survivors. However, the
fresh water denatures the alveolar surfactant, rendering the alveoli unstable and promoting alveolar collapse and
ventilation perfusion mismatching. Denaturization of the surfactant may continue even after rescue of the victim from
the water and damage to the alveolar epithelium results in a transudate into the alveoli and resulting pulmonary
oedema. This transudate may be of such volume to render the survivor hypovolemic on arrival at hospital.

Salt water is hypertonic and draws fluid from the intravascular space into the already fluid filled alveoli. Ventilation
perfusion mismatching occurs and is compounded by the washing out of surfactant from the alveoli. This fluid shift
again theoretically may result in haemoconcentration, hypovolemia and electrolyte abnormalities, however this is
rarely seen clinically.

No matter whether the fluid is salt or fresh water the end result is pulmonary oedema, ventilation perfusion
mismatching with progressive respiratory distress and the clinical management is identical for both groups.
Consciousness is always lost within three minutes of involuntary submersion (Pearn 1985) and is almost always due
to cerebral hypoxia.

Initial management

The victim should be removed from the water without delay. Effective CPR in water is not possible and although it is
possible to perform mouth to mouth in water, this must not delay retrieval to land. The focus of initial management is
on restoring effective oxygenation and alleviating hypoxia. CPR should be instituted for the apnoeic and pulseless
patient. The Heimlich manoeuvre (previously advocated to aid drainage of fluid from the lungs) should not be used
unless obstruction of the airway from foreign body is strongly suspected (Weinstein 1996). The patient should be
transported to a medical facility promptly.

Key points

• Remove from water (effective CPR in water is not possible)

• Start CPR

• Heimlich only for obstruction

• Move to medical facility

Definitive management

On arrival at the emergency department medical staff should evaluate the airway and perform endotracheal
intubation if indicated. Circulatory support with intravenous fluids should be initiated. For patients presenting
pulseless and apnoeic advanced clinical life support procedures should be continued until all hopes of achieving a
salvageable patient are exhausted. Hypothermic patients must be rewarmed to a core temperature of 340 C before
death is pronounced. A high index of suspicion should exist for cervical spine injury particularly if there is any history
of a diving or boating accident and cervical spine X-rays arranged.

Key points

• CPR

• Where pulseless and apnoeic CONTINUE advanced clinical life support procedures until all hope gone.

• Warm hypothermic patients to a core temperature of 340 C

• Check for cervical spine injury

Patients with mild symptoms/no symptoms on arrival

All victims with a history of near drowning who arrive with minimal or no symptoms must be observed as secondary
deterioration with the onset of pulmonary oedema may develop precipitously. As a minimum all patients should have
a CXR, arterial blood gases (ABGs), serum electrolytes and ECG. Mild hypoxemia should be managed with
supplemental oxygen and ABGs on room air should have returned to normal before the patient is discharged.

Aspiration of water, particularly if contaminated may result in pulmonary infection, however routine prophylactic use of
antibiotics is not indicated. Antibiotics are indicated only if there is clinical signs of infection and microbiological
studies should be used to guide the choice.

Pulmonary oedema, if it occurs, will usually develop within several hours of aspiration and may be rapidly
progressive. For this reason most authors suggest a minimum period of observation of 24 hours however, for the
subset of patients who at presentation are asymptomatic both clinically and biochemically and remain so, discharge
after 6 hours may be possible.

Key points

• Observe near drowning (with minimal or no symptoms) for at least 24 hours and do CXR, arterial blood
gases (ABGs), serum electrolytes and ECG

• May need antibiotics

Patients with evidence of respiratory compromise

Patients with evidence of respiratory embarrassment require urgent intervention to correct the hypoxemia. The single
treatment most effective in reversing hypoxemia, regardless of whether it is caused by aspiration of fresh water or
seawater, is the application of continuous positive airway pressure (CPAP) (Modell 1993). CPAP may be used in both
spontaneously breathing and mechanically ventilated patients and should be withdrawn gradually as the patient’s
ABGs and ventilation perfusion ratio normalizes. These patients require cardiac monitoring, serial ABGs, serum
electrolytes and CXRs. ABGs may vary between mild to severe hypoxemia with a widened alveolar-arterial gradient
whilst the pCO2 may be low or high dependent on the level of alveolar ventilation. CXR may reveal patchy infiltrates
suggestive of aspiration or frank pulmonary oedema. These patients may be significantly hypovolemic as a
consequence of pulmonary oedema (irrespective of the type of immersion) and a Swan-Ganz catheter may prove
useful in monitoring their cardiovascular status. Consideration should be given to the insertion of a nasogastric tube
to decompress the stomach.

Some centers in the past have recommended aggressive cerebral resuscitative techniques in near drowning victims
in an attempt to maximize neurological salvage. The HYPER regime (Modell 1993) involved fluid restriction,
hyperventilation, hypothermia, barbiturate coma and invasive intracranial pressure monitoring however these
techniques have largely been abandoned due to lack of data supporting its use. Steroids have also been advocated
in the past to in an attempt to reduce the lung injury, but again lack of supporting evidence for their benefit has seen a
decline in use.

Animal studies (Waugh 1993) have suggested warm butyl alcohol vapor inspired in 100% oxygen may improve the
hypoxemia associated with aspiration of salt water. The entry of salt water into the lungs is associated with the
production of foam bubbles that remain relatively stable due to the inclusion of surfactant from the alveolar lining.
Waugh postulates the warm butyl alcohol vapor has a defoaming action within the small airways and may also act as
a free radical scavenger to reduce the risk of oxygen toxicity. No human data is available at this time.

Key points

• Apply CPAP

Outcome predictors
Newspaper reports of ‘success’ stories of drowning victims whom have survived neurologically intact after prolonged
periods of immersion particularly in cold water are frequent however the reported rates of survival with full
neurological recovery vary. For patients presenting awake and alert full neurological recovery is reported to be 100%
(Modell 1993) and more than 90% of victims who arrive at the emergency department with a pulse survive
neurologically intact (Reed 1998). Pediatric data reveals for near drowning victims who required admission to ICU
56% survived neurologically intact, 32% survived in a persistent vegetative state and the remaining 32% died (Lavelle
and Shaw 1993). Factors which are said to adversely affect survival are prolonged submersion, delay in effective
cardiopulmonary resuscitation, severe metabolic acidosis (pH< 7.1), asystole on arrival at a medical facility, fixed
dilated pupils, and a low Glasgow coma score (<5) (Modell 1993). However survivors with intact neurological function
have been reported after presenting with each of these factors. Hypothermia appears to be protective, but only if it
occurs at the time of near drowning (Modell 1993); the basis of this appears to be the reduced cerebral oxygen
requirements.

Key points

• Hypothermia appears to be protective, but only if it occurs at the time of near drowning

Section II -Diving accidents

Introduction

Recreational SCUBA (self-contained underwater breathing apparatus) diving is a growth industry in Australia. It is
estimated approximately 1.29 million SCUBA dives occur in Queensland waters each year and the total value of the
diving industry to Queensland in direct expenditure annually is approximately $100 million (Windsor 1996). In recent
years there has also been a growing interest in the recreational community in mixed gas diving (diving on gas
mixtures other than air, for example mixtures of nitrogen and oxygen: nitrox and mixtures of helium and oxygen:
heliox) and on closed circuit equipment, previously the realm of the military alone. Figures from Australian and New
Zealand hyperbaric medicine units for the 1997/1998 financial year (HTNA 1998) reveal some 398 divers required
recompression therapy for a diving related illness during this period. The most common injury in divers is middle ear
barotrauma of descent, resulting from the non equalization of the middle ear cavity with the ambient pressure,
however the most serious injuries are those of decompression illness and pulmonary barotrauma with cerebral
arterial gas embolism. It is these serious injuries which will be dealt with in this chapter and readers are referred to
standard diving medicine texts for further information on the less serious forms of dysbaric illness.

Key points

• The most common injury in divers is middle ear barotrauma of descent

Pulmonary barotrauma

Barotrauma is defined as the tissue damage resulting from the expansion or contraction of closed gas spaces, and is
a direct effect of gas volume changes causing tissue damage (Edmonds et al. 1992). Pulmonary barotrauma of
ascent or pulmonary overinflation syndrome is the tissue damage resulting from pressure changes acting on the lung
when a diver ascends to the surface. Every time a diver descends beneath the surface of the water they subject their
body to an increase in environmental pressure. This pressure relationship is illustrated in Table 24.1. Pascal’s
principle dictates that this pressure is distributed equally across all body tissues. Boyle’s Law states that if the
temperature of a fixed mass of gas is kept constant, the relationship between the volume and the pressure will vary in
such a way that the product of the pressure and the volume will remain constant i.e. P1V1 = P2V2 . It is important to
recognize the greatest pressure changes and therefore the greatest danger to a diver occurs between 0-10 msw
negating the popular myth that you cannot get into trouble if you only dive to shallow depths. Put simply this means if
a diver fills his lungs with (5 litres) gas at a depth of 20 meters of sea water (msw) or 3 atmospheres absolute (ATA)
and holds his breath until he reaches the surface, in accordance with Boyle’s Law the gas within his lungs will have
expanded to 15 litres. As the lungs cannot expand to accommodate this volume pulmonary tissue damage is likely to
occur. Pulmonary barotrauma occurs most commonly in novice and inexperienced divers and submarine escape
training candidates who perform rapid ascents. Classically divers who suffer pulmonary barotrauma are seen to have
an ‘incident’ at depth causing them to panic and they then make a rapid uncontrolled ascent to the surface. A high
pitched scream may be heard as the diver breaks the surface of the water. This is said to be due to the exhalation of
the expanding gas from the lungs.

Historically, individuals with a history of asthma or bullous lung disease, and therefore increased likelihood of gas
trapping, have been excluded from diving due to their theoretical increased risk of pulmonary barotrauma.

A transpulmonary pressure difference of as little as 70 mmHg water near the surface (Edmonds et al. 1992) is
enough to cause alveolar rupture and can result in pulmonary tissue damage, pneumothorax, pneumomediastinum/
subcutaneous emphysema and cerebral arterial gas embolism (CAGE). Although all four manifestations can occur
simultaneously this is uncommon and less than 10% of CAGE victims will have a detectable pneumothorax.

Key points

• Barotrauma is defined as the tissue damage resulting from the expansion or contraction of closed gas
spaces, and is a direct effect of gas volume changes causing tissue damage

Pulmonary tissue damage

Pulmonary tissue damage resulting in widespread alveolar rupture is rarely seen and is usually associated with a
history explosive decompression back to the surface. If the patient survives first aid management includes ventilatory
support with 100% oxygen.

Pneumothorax

Pneumothorax presents in the same way as a pneumothorax from non-diving causes. Clinically the diver may
complain of sharp chest pain associated with shortness of breath with increased percussion note and decreased
breath sounds. Resolution of the pneumothorax may be hastened by the breathing of 100% oxygen, needle
aspiration or the insertion of an intercostal drain.

Key points
 • Clinically the diver may complain of sharp chest pain and SOB

Pneumomediastinum/subcutaneous emphysema

Alveolar gas may also track through the interstitial pulmonary tissues and into the mediastinum
(pneumomediastinum) and up into the subcutaneous tissues of the neck (subcutaneous or surgical emphysema, Fig
24.1). The symptoms may occur immediately on exiting the water or take several hours to develop. The diver may
complain of retrosternal chest pain, shortness of breath, a feeling of fullness in the throat, and changes in the
character of the voice. On palpation of the neck region the ‘crunching’ sensation of subcutaneous emphysema may
be felt. Radiologically, air may be seen tracking along the border of the heart and other mediastinal structures and
along the major vessels in the neck region. Symptomatic relief will occur with the administration of 100% oxygen.
Recompression is usually not indicated although will also provide symptomatic relief.

Key points

• The diver may complain of retrosternal chest pain, SOB, a fullness in the throat and voice changes

Cerebral Arterial Gas Embolism (CAGE)

CAGE occurs when alveolar gas ruptures into the pulmonary veins and is then carried via the heart into the cerebral
circulation. Typically the site of the alveolar rupture is not demonstrable even by sophisticated radiological techniques
as rapid closure of the perforation site occurs. Bubbles reaching the arterial circulation distribute according to
buoyancy in large blood vessels and according to flow in small blood vessels (Gorman et al. 1987) explaining why
cerebral involvement is so common. Bubbles traveling to the brain can do one of three things:

• lodge permanently in the cerebral vasculature, typically in successive branching arterioles of 100um or less
diameter resulting in an ischaemic infarct,

• lodge temporarily in the cerebral vasculature, and then redistribute, traveling back through the venous
circulation to the lungs. This redistribution is a consequence of a reflex rise in arterial blood pressure,
increased cerebral blood flow and increased intracranial pressure resulting in the driving arterial pressure
overcoming the surface tension of the bubble. Whilst the temporary arresting of blood flow secondary to
lodgment of the bubble may cause clinical symptoms and signs, bubbles also cause damage to the vascular
endothelium as they pass through the cerebral vasculature stripping the endothelium and activating
inflammatory pathways. This process can result in progressive cerebral dysfunction via alterations in the
blood brain barrier and local cerebral blood flow even though the bubbles have long since passed.

• most bubbles are not trapped within the cerebral vasculature and pass through into the venous system and
back to the lungs. The bubbles again cause damage to vascular endothelium as they pass through.
Accumulation of platelets and polymorphonuclear leukocytes at the site of injury and activation of
inflammatory proteins such as kinins and complement pathways occurs. It is this inflammatory response
which is believed to underlie many of the symptoms experienced by divers with decompression illness. The
lungs are usually an effective bubble filter and the majority of bubbles will trap in the lungs (due to the low
pulmonary pressures compared with the arterial circulation), the inert gas will then diffuse into the alveoli
and be expired. This bubble filter may be overwhelmed in the presence of large numbers of bubbles with
 bubbles again passing through into the arterial circulation and redistributing once more to the brain. This
explains the presentation sometimes seen in divers who have collapse unconscious, recover, sit up (bubbles
distributing with buoyancy) and then collapse once more. Bubbles may also reach the brain via abnormal
arteriovenous channels within the lungs or through heart defects e.g. a patent foramen ovale (PFO). Some
30% of the general population are said to have a probe patent PFO (Langton 1996) and reversal of flow
across the defect can be seen in many with a Valsalva manoeuvre.

A diver presenting with acute neurological symptoms or signs either on surfacing or soon after a dive must be
considered to have had a CAGE. CAGE may present as sudden death (typically with embolization of the brain stem),
loss of consciousness or with focal neurological abnormalities such as confusion, paralysis, convulsions, and variable
sensory abnormalities. The first aid and definitive management of victims with CAGE is the same as for DCI and will
be discussed below.

Key points

• A diver presenting with acute neurological symptoms or signs either on surfacing or soon after a dive must
be considered to have had a CAGE

DECOMPRESSION ILLNESS

DCI refers to the spectrum of diseases that result from decompression and the consequent lowering of pressure
(Gorman 1993). When a diver descends below the surface of the water the physics laws of Dalton and Henry explain
why the diver’s body absorbs an increased amount of inert gas (in most cases this gas being nitrogen). Put simply,
the partial pressure of nitrogen in the breathing mixture rises with the increase in ambient pressure resulting in
increased diffusion of nitrogen into the body tissues. While the diver remains at depth this increased nitrogen load is
of no significance, however, as the diver returns to the surface the inert gas must once more obey the laws of physics
and one of two things may happen:

• the diver ascends at a rate which allows the dissolved inert gas to be carried back in solution to the lungs
where it is expired, or

• if the diver ascends at a rate that exceeds this capacity, bubbles will form in the tissues and venous blood.

These bubbles may then travel back to the lungs, which acts as a filter to trap the bubbles, and the bubbles may
resolve through gas diffusion into the alveoli. Excessively large numbers of bubbles may overwhelm this filter
resulting in the passage of the bubbles into the arterial circulation. Bubbles formed in the tissues may also reach the
arterial circulation via a patent foramen ovale or through pulmonary arteriovenous malformations.

Most divers will plan their dives using decompression tables or computers. These tables advise the diver as to how
long they should stay at a particular depth and how to control their ascent. Unfortunately many of these
decompression schedules have a failure rate varying between 0.5 -5 % so the belief that staying within the tables
excludes the possibility of developing DCI is wrong. Other factors which are said to increase the risk of DCI are
dehydration, obesity, high levels of exertion during the dive, physical injury, multiple ascents, repetitive and multiday
diving exposures.
Key points

DCI refers to the spectrum of diseases that result from decompression and the consequent lowering of pressure

• Decompression tables or computers: advise the diver as to how long they should stay at a particular depth
and how to control their ascent

• However staying within the tables does NOT exlude the possibility of developing DCI.

• Other factors which are said to increase the risk of DCI are: dehydration, obesity, high levels of exertion
during the dive, physical injury, multiple ascents, repetitive and multiday diving exposures

Effects of bubbles

Bubbles in the tissues cause direct mechanical damage e.g. disrupting myelin sheaths in the spinal cord, cell rupture
and indirect damage through the activation of inflammatory pathways. Bubbles in the venous system damage the
vascular endothelium also activating inflammatory pathways. If bubbles trap in sufficient quantity in the lungs the
resultant back pressure on the venous drainage system can result in haemorrhagic infarction, particularly in the spinal
cord. Bubbles in the arterial circulation will travel largely to the brain where they may lodge causing infarction or they
may pass through into the venous circulation damaging the vascular endothelium as they pass. It is this damage with
the subsequent activation of the inflammatory cascade, which is thought to underlie many of the systemic symptoms
of cerebral DCI.

Key points

• Bubbles in the tissues cause direct mechanical damage

Clinical presentation of DCI

DCI may affect all organ systems of the body. Most commonly divers present with constitutional symptoms which are
believed to be secondary to activation of the inflammatory pathways. Patients complain of generalized malaise,
fatigue and headache. They often complain of profound tiredness despite a full night’s sleep. Bubbles in and around a
joint produce pain that can be severe and typically involves the knees, shoulders, elbows and wrists. The pain is
described as dull, throbbing, gradual in onset and is unaccompanied by effusion. The nervous system is almost
always involved and cerebral involvement may present as difficulty in concentration or mentation, changes in
personality, mild confusion and impaired judgment to frank confusional states and loss of consciousness. Spinal cord
involvement occurs frequently and presents with bladder, motor and sensory disturbance. The presence of girdle pain
should be taken seriously as it often progresses into serious spinal disease. Cutaneous involvement is often transient
and varies from allergic type rashes, pruritus to purpura. Respiratory symptoms (breathlessness, increased
respiratory rate and chest pain) due to the overwhelming of the pulmonary bubble filter are uncommon however
indicates serious disease.

Classification
Conventionally serious diving accidents were classified as either decompression sickness (DCS) Type 1 and 2 and
cerebral arterial gas embolism (CAGE). Type 1 DCS was considered minor and involved the skin and joints whilst
Type 2 DCS was considered serious and involved typically the neurological or respiratory systems. It has become
apparent however, that most divers presenting with DCS have neurological involvement, which can be detected with
careful neurological examination. In the past poor history taking and examination skills may have resulted in the over
diagnosis of Type 1 disease. It is also difficult at times to differentiate between disease caused by pulmonary
barotrauma with resultant CAGE and disease due to the arterialization of bubbles generated in the tissues. For this
reason a new descriptive classification system encompassing all decompression illnesses has been introduced.
(Table 24.2)

Management of DCI

The definitive treatment for a diver with DCI is recompression (Fig 24.2), however not all patients will experience
100% resolution of their symptoms. Reported treatment failures vary from 32% - 54% (Drewry and Gorman 1992),
some evidence suggests the earlier a patient is treated the better the prognosis. Early consultation with a diving
medicine specialist is encouraged.

Important history that should be obtained from the diver includes depths/times of all recent dives, the nature of the
symptoms, are the symptoms/ signs stable, progressive or resolving and were there any uncontrolled or multiple
ascents during the dive.

A full examination including a detailed neurological evaluation with an assessment of mental state is essential and
should be repeated as necessary to document any progression of the disease. The diagnosis of DCI is made on
clinical findings and there are no specific laboratory investigations which will aid this decision process and which may
in fact delay the time to definitive recompression. Specifically, a CXR should not delay recompression if pulmonary
barotrauma and CAGE is suspected.

First aid management includes the administration of 100% oxygen, intravenous fluids and keeping the patient supine.
In recent years divers were positioned in the head down position in an attempt to prevent further embolization of the
cerebral vasculature (bubbles distribute with buoyancy in large vessels), however, this resulted in increasing cerebral
oedema and is no longer recommended. A compromise is reached with lying the patient flat. Under no circumstances
should a patient suspected of having a CAGE be allowed to stand. Fluid replacement using crystalloid (1 litre stat
followed by 1 litre over 4 hours, titrating to urinary output and hemodynamic status) is recommended avoiding
glucose solutions as they may contribute to cerebral oedema. Although pulmonary oxygen toxicity is possible with
prolonged use of 100% oxygen it is usual to apply it continuously unless advised differently by the consulting
hyperbaric physician. A Hudson mask cannot deliver 100% oxygen and more appropriately a circuit using an
anesthetic mask, rebreather bag and high flow oxygen should be used (Fig 24.3). Alternatively a closed circuit
rebreather system will conserve oxygen.

If aerial transfer to a recompression facility is required consultation with the receiving unit is vital. Any ascent to
altitude will result in an expansion of bubbles both in the tissue and the circulation and may result in a further
deterioration in their clinical state. Aerial transfer can be achieved safely in an aircraft capable of pressurizing the
cabin to 1 ATA or with rotary wing aircraft flying at an altitude less than 300 meters. Similarly, if the patient is intubated
the air in the endotracheal tube cuff will also expand with altitude and contract with recompression. For this reason it
is advised ventilated patients requiring recompression have the air in the tube cuff replaced with water.

Key points

• The definitive treatment for a diver with DCI is recompression