Pathophysiology of Diving Disease

Question 1

Learning objectives

Answer 1

By reading this article you should be able to:

Explain the physiological and pathophysiological
effects of working at increased ambient pressure.

Detail the effects on the human body of gases
under pressure and their toxic effects.

Identify the effects that expansion of gas may
have on the human body.

Distinguish the signs and symptoms of
decompression sickness and
arterial gas embolism secondary to pulmonary barotrauma,

which can be difficult to distinguish and,
if so, they are called
decompression illness.

Describe the principles of treatment of decompression illness.

Question 2

Key points

Answer 2

1 Divers breathe gases at high partial pressures,
which have detrimental physiological effects.

2 Knowledge of the gas laws is essential to
understand diving medicine.

3 Rapid ascent from a dive may cause barotrauma.

4 Rapid ascents can also cause decompression sickness (DCS),

but most cases of DCS follow theoretically safe dives
and are caused by paradoxical gas embolism

across a right-to-left shunt.

5 DCS has many manifestations and
can be hard to diagnose.

Question 3

Intro

Answer 3

such as nitrogen narcosis and acute oxygen toxicity.

Few people, besides divers and astronauts, deliberately
enter an environment that does not support respiration

1 The changes in ambient pressures
when diving can cause pulmonary barotrauma

At high pressure,
->
the increased tissue uptake of gases

that are usually innocuous exposes a diver to
their toxic effects,

Reduction in pressure during ascent may cause
decompression sickness (DCS).

Safe diving requires understanding the
behaviour of gases under pressure and
their effects on physiology.

Divers are also at risk of immersion pulmonary oedema.
The high thermal conductivity of water and some breathing
gases can cause hypothermia.

Question 4

Effects of descent:

gas compression and
increased gas uptake

Answer 4

1. Gases are very compressible,

but body tissues vary in their degree of compressibility.

2. Nerve tissue starts to exhibit altered
   function at a depth of approximately 150 m of
   seawater
   (16 bar, 1.62 MPa, 1.216 104 mmHg).

Bone only deforms at much higher pressures

Body cavities that contain gas are affected by pressure
according to Boyle’s law

3. Air in the lungs of a breath-holding
   diver at the surface (1 bar) compresses to half the surface
   volume at a depth of 10 m (2 bar) and to one third at a depth of
   20 m (3 bar).

The lungs typically reach residual volume at a
depth of approximately 30 m

4. Further descent causes blood to be drawn into the chest

from the limbs, spleen, and abdomen, and the diaphragm
and abdominal viscera are pushed up high
into the ribcage to compensate for
further reductions in lung volume

Thus, the record breath-hold dive to 214 m was
possible despite the amount of gas in the lungs and rigid air
spaces being reduced to <1/22nd of the surface total lung capacity.

On ascent back to the surface, the gas in the diver’s
lungs expands to occupy the original volume at the surface

Question 5

Barotrauma

Answer 5

1. If the volume of gas in a space is compressed
   by increased pressure and

further gas cannot be drawn in,

2. part of the space will be filled by body tissues
   which may cause barotrauma of descent or a ‘squeeze’

An example is pain when a diver fails to equalise

the pressure of the gas in the middle ear

with the pressure of the water outside the tympanic membrane.

When the pressure differential is great

the tympanic membrane will rupture,
which leads to entry of
cold water, vertigo, and
potentially drowning

If a diver descends with an obstructed
sinus the walls of the sinus may implode, usually by rupture of
vessels, filling the sinus with blood and causing pain

Scuba divers (and divers whose gas is supplied by an
‘umbilical’ hose) breathe gas supplied at the ambient pressure
of the surrounding water, which enables maintenance of
relatively normal lung volumes during the respiratory cycle.
Nevertheless, those divers can suffer a squeeze if there is
failure to equalise pressures in gas-containing spaces, such as
the middle ear

Question 6

Barotrauma

Answer 6

1. Barotrauma is physical damage to body tissues caused

by a difference in pressure between a gas space inside,
or in contact with, the body, and the surrounding gas or fluid.

2. If the volume of gas in a space is compressed

by increased pressure and

further gas cannot be drawn in,

part of the space will be filled by body tissues
which may cause barotrauma of descent or a ‘squeeze’

3. An example is pain when a diver fails to equalise
   the pressure of the gas in the middle ear

with the pressure of the water outside the tympanic membrane.

When the pressure differential is great

the tympanic membrane will rupture,
which leads to entry of
cold water, vertigo, and
potentially drowning

5. If a diver descends with an obstructed
   sinus the walls of the sinus may implode, usually by rupture of
   vessels, filling the sinus with blood and causing pain
6. Scuba divers
   (and divers whose gas is supplied by an
   ‘umbilical’ hose)

breathe gas supplied at the ambient pressure
of the surrounding water,

which enables maintenance of relatively normal lung volumes during the respiratory cycle.

Nevertheless, those divers can suffer a squeeze if there is
failure to equalise pressures in gas-containing spaces,
such as the middle ear

7. Also, during descent,

The supplied gas becomes denser
in proportion to the pressure

and the work of breathing becomes harder.

8. Maximum voluntary ventilation decreases in
   proportion to the square root of gas density:

at 30 m (4 bar) maximum voluntary ventilation is

half that at the surface

(1 bar) with the same breathing gas.

9. This may cause carbon dioxide retention.
10. There is free exchange of gases

between gases in the alveoli
and the dissolved gases in the bloodstream.

11. On descent, the partial pressures of the gases in the alveoli increase and, by Henry’s law, the number of molecules of gases
    dissolved in the blood and in the body tissues increases.

Question 7

Nitrogen

Answer 7

Increased PN2 leads to nitrogen narcosis,

which causes impaired cognition and predisposes to accidents

Nitrogen is poorly soluble in water and blood,
but is much more soluble in
lipids and hence cell membranes,
and importantly, neurological tissues

as diver breathing a gas with a
fixed percentage of nitrogen,
such as air,

descends and the pressure increases.

In a diver breathing air, some narcotic effects are present at 20
m and at depths >50 m,

the diver’s cognitive function is very
likely to be severely impaired

At depth, nitrogen is thought to act in a
similar manner to an anaesthetic and

may alter the equilibrium between open and

closed states of various neurotransmitter receptors,
such as the gamma-aminobutyric acid type A (GABAA) receptor.

Nitrogen narcosis is cured by ascent.
It is avoided by replacing some or
all of the nitrogen with a less narcotic gas,
usually helium.

Question 8

Oxygen

Question 9

Carbon dioxide

Answer 9

The normal partial pressure of carbon dioxide in the alveoli is
approximately 5.6 kPa (42 mmHg, 0.055 bar).

Ideally when diving,
the arterial and alveolar carbon dioxide tensions
should be maintained at approximately this level

In a diver breathing air,
the alveolar pressures of nitrogen and oxygen
increase in proportion to depth but,

because alveolar carbon dioxide is a product of metabolism and is constant at fixed workloads,
the alveolar pressure of carbon dioxide remains
virtually unchanged while its percentage decreases

However, a combination of high levels of exercise and increased work of breathing is a potent provocation for hyperventilation followed by CO2 retention secondary to perturbed respiratory
control if the CO2 concentration increases to high levels

Hypercapnia may also occur in divers using rebreather sets
(if the CO2 absorber fails)

or where there is inadequate ventilation of
a commercial diver’s helmet
because of increased dead space.

The sequential clinical features of progressively increasing
levels of hypercapnia are: increasing dyspnoea; increases in
BP and HR; mental confusion and lack of coordination; loss of
consciousness; and death.

Although CO2 is a respiratory
stimulant, most of its effects are caused by the acidosis it
produces in the CSF, which is a neurological depressant.

Adaptation to higher than normal inspired levels of carbon
dioxide can occur and is characterised by increased tidal
volume and reduced ventilatory frequency. This adaptation is
important in saturation diving, in submersibles, and during
extended submarine patrols.

Question 10

Carbon monoxide

Answer 10

By law, breathing gas must contain
<5 parts per million of carbon monoxide.

If breathing gas contains increased concentrations,

the partial pressure of carbon monoxide may
increase to lethal levels during compression.

The usual reason for carbon monoxide contamination of gas in diving cylinders is when a compressor’s air inlet is close to the exhaust of the compressor’s engine so that exhaust fumes are drawn into the gas cylinder.

Carbon monoxide has high affinity for haemoglobin
(200 times that of oxygen) and thus reduces oxygen
carriage of blood.

It is also a respiratory poison of mitochondrial
cytochrome c oxidase

Question 11

Exotic diving gas mixtures

Answer 11

Air is not used as a breathing gas for deep dives because of
the risks of CNS oxygen toxicity, nitrogen narcosis, and the
effort of breathing the dense gas

For dives deeper than 50 m,
some of the nitrogen, and depending on the depth, some of
the oxygen is replaced by helium

Helium is not narcotic
even at depths of 600 m, but has disadvantages,

1. including high thermal conductivity
   (which necessitates heating
   breathing gas and diving suits during long exposures, such
   as commercial saturation diving)
2. voice distortion,
3. High cost.
4. HPNS
   very rapid compression to depth using
   helium/oxygen mixtures (‘heliox’)
   may cause high-pressure
   nervous syndrome (HPNS).

Trimix

Originally, only divers working offshore in the oil and gas
industry used trimix and heliox.

Since the 1970s, recreational and scientific divers have increasingly used trimix to dive to greater depths.

Hydrogen has also been used in breathing mixtures by
professional divers. Hydrogen has a lower density than helium but greater narcotic potential. When present in gas mixtures containing >4% oxygen, there is a high risk of explosion.

Question 12

HPNS

Answer 12

High Pressure Nervous Syndrome

HPNS causes decreased

1. motor and intellectual performance,
2. dizziness,
3. nausea,
4. vomiting, and tremor.

The incidence of HPNS is decreased by

1. slowing the rate of compression to depth

and by

2. adding to the helium/oxygen mixture
   a small amount of an anaesthetic gas,
   usually nitrogen.

This helium/oxygen/nitrogen mixture is known as ‘trimix’.

Question 13

Liquid breathing

Answer 13

Liquid breathing

Ventilation of the lungs with an oxygenated fluid
instead of a compressible gas mixture
has been considered to avoid DCS

Liquid-filled lungs mean that the
partial pressure of respiratory gases hardly changes

with pressure and inert gas pressures in the blood
and tissues remain roughly constant during a dive.

Saline and fluorocarbons (FC-80) have been tested.
FC80 is inert in the lung, but a persistent acidosis in animal

models, possibly related to increased pulmonary vascular
resistance, and difficulty in transitions from and back to air
breathing have prevented the adoption of liquid breathing as a
diving tool in human

Question 14

Long-term effects of working under pressure

Answer 14

Long-term effects of working under pressure

Some professional divers and compressed air workers,

who have long-term exposure to pressure

or repeated decompressions,

develop dysbaric osteonecrosis,

a form of aseptic necrosis of long bones,

but a case has been reported in a sport diver

The pathogenesis is not understood.

Question 15

Effects of ascent: gas expansion and gas

Answer 15

Effects of ascent:

1. gas expansion and gas elimination

Pressure change can cause barotrauma on ascent,

as it can on the diver’s descent.

2. Therefore if a sinus has become obstructed
   whilst at depth,
   during ascent the walls of the sinus
   may explode painfully resulting in the entry of gas

and infected mucus into blood vessels
and surrounding tissues.

3. If a diver swallows air during a dive,
   he may experience abdominal pain
   or even gastric rupture during ascent,
   particularly if there is a
   history of gastro-oesophageal surgery.

The most serious forms of barotrauma of
ascent are pulmonary.

4. If the lung is obstructed on ascent

(e.g. by a scuba diver holding his/her breath),
the gas in the lung expands until
the lung reaches its bursting pressure
(roughly 70 mmHg and
at about 115% of voluntary total lung capacity)
when it ruptures.

Gas may escape from the lungs into other tissues
in three ways to cause:

(i) Arterial gas embolism
if gas invades the pulmonary
veins to cause systemic gas embolism
and typically neurological effects.

(ii) Pneumothorax,
which can become a tension pneumothorax
during continued ascent because gas in the
pleura expands as pressure is reduced.

(iii) Pneumomediastinum.

Question 16

Effects of Ascent

Answer 16

1. Arterial Gas Embolism
2. Pneumothorax
3. Pneumomediastinum

Question 17

Decompression sickness

Answer 17

Decompression sickness

1. During a dive,

the increased partial pressure of an inert gas breathed

causes tissues to take up greater
amounts of the dissolved gas than at the surface.

2. If the ambient pressure is suddenly increased
   from P1 to P2,

the gas tensions within that
tissue will increase exponentially towards P2

3. During decompression,
   the tissues contain excess numbers
   of dissolved gas molecules taken up during compression,

which means that the tissues are supersaturated
(the sum of dissolved gas pressures
in a tissue exceeds the ambient pressure).

4. The excess dissolved gas must leave
   the tissues and return to the lungs.

If a diver ascends slowly,
so that ambient pressure is reduced gradually,

the partial pressure of gases in the alveoli
and hence in arterial and
capillary blood decrease proportionately.

5. The tissues have higher partial pressures of
   dissolved inert gas (usually nitrogen)

than capillary blood and

the dissolved inert gas diffuses out of the tissues
into capillary blood down the concentration gradient

and is carried in venous blood back to the lungs to
diffuse into the alveoli

6. Gases that are largely biochemically inert in humans
   (e.g. nitrogen, helium)
   are sparingly soluble in blood.

Therefore if decompression is more rapid,
the gas that has dissolved in the tissues
will come out of solution to form
bubbles in the tissues and in venous blood.

7. Echocardiography
   shows that venous bubbles are transported to the lungs
   where, in most cases, the gas passes out of the bubbles into
   the alveoli down the concentration gradient as the bubbles
   pass through the pulmonary capillaries.
8. Usually this decompression process does not result in illness. If the rate of decompression is too rapid,
   so that the number of bubbles or
   the site where they lodge causes injury,
   the diver suffers DCS.

Answer 18

Robert Boyle in 1670 was the first to observe the effects of
decompression in animals. In the late 19th century, Paul Bert
described many of the manifestations of DCS and showed that
the more serious forms of DCS were provoked by the presence
of large volumes of free gas (mainly nitrogen), as opposed to
dissolved gas.

Early observations of DCS were on compressed air workers
during civil engineering at a time when safety regulations for
workers were poor. When they were subjected to a rapid
reduction in pressure, their blood literally frothed, to cause
cardiopulmonary DCS (dyspnoea, chest pain, and hypotension, which they called ‘the chokes’). It may be rapidly fatal
unless immediate recompression occurs. If decompression
was slower, but still rapid by current safety standards, vestibulocochlear DCS (‘the staggers’ causing ataxia, vertigo, and vomiting) or spinal DCS might occur and result in severe
neurological impairment or delayed death. The commonest
form of DCS in these workers (but not in divers) was musculoskeletal DCSd also called ‘the bends’.

The term ‘the bends’ was coined by caisson workers
building the supports under the riverbed for the bridge across
the Mississippi at St. Louis. It referred to the affected ‘stifflegged
’ gait of fashionable young ladies, which resembled the
behaviour of workmen who contracted this form of DCS
causing pain in or around a joint.

Navies realised that underwater operations would become
part of modern warfare, and became interested in preventing
DCS, because it was found that military and commercial
divers suffered clinical manifestations of DCS similar to
caisson workers but musculoskeletal DCS is less frequent and
neurological and cutaneous manifestations are much more
frequent in divers

In the early 20th century Professor J.S. Haldane was asked
to devise regulations for the safe conduct of underwater work
by divers.

He showed that if goats breathing air were exposed
to a raised pressure (P2) for a ‘prolonged period’ when it was
assumed that all the tissues were saturated
(in about 3 h) and

then the pressure was rapidly reduced to a new level (P1),

the goats would exhibit signs of DCS if the pressure reduction was >50%.

If the pressure drop was less than half, the goats did not
show signs of DCS. This ratio P1/P2 >= 0.5 was assumed to be
valid for all decompressions over a wide range of values for P1
and P2 and applicable to all tissues

It was assumed that the gas elimination curve is the
inverted image of the uptake curve in Figure 1. This elimination
curve is the rationale behind nearly all subsequent
mathematical models for treatments of dissolved gas exchange
in tissues.

Question 19

Classification of the signs and symptoms of DCS.

Answer 19

The most frequent cause for all types of DCS, other than musculoskeletal DCS, is paradoxical gas embolism across a right-to left shunt

1. Cerebral
2. Spinal
3. Vestibular
4. Cardiorespiratory
5. Cutaneous
6. Lymphatic
7. MSK
8. Constitutional

Question 20

Cerebral

Answer 20

Impairment of consciousness and higher
cerebral function, hemiplegia,
hemisensory abnormalities, visual
disturbance, isolated neurological
abnormalities

Question 21

Spinal

Answer 21

Spinal Paraplegia, sensory level, girdle
abdominal discomfort, urinary
retention, isolated neurological
abnormalities in limbs

Question 22

Vestibular

Cardiorespiratory

Answer 22

Vestibular

Ataxia, vertigo and vomiting
_________________________________

Cardiorespiratory

1. Chest discomfort,
2. dyspnoea,
3. shock

Question 23

Lymphatic

Musculoskeletal

Answer 23

Lymphatic

Lymphatic or breast swelling,
which may be tender

Musculoskeletal

Question 24

Cutaneous

Constitutional

Answer 24

Cutaneous

Rash typically on trunk, buttocks, or thighs,
which maybe pruritic,
maybe mottled or confluent,
and maybe pink,
red or purple

Constitutional

Pain usually in large joints
Severe fatigue
(this may be a variant of neurological DCS)

Question 25

Haldanes work?

Answer 25

Later, it became clear that some of Haldane’s assumptions
are not quite correct. Subsequent sets of decompression tables
have been published, most notably by the Swiss physiologist
Bu¨ hlmann.7Theyrelyondividing the bodyintomany theoretical
‘tissues’, each with its own half-time for gas elimination. Such
‘tissues’ do not correspond to any anatomical structure or
structures. Thesemathematicalmodels have been incorporated
into small computers that integrate pressure (depth) and time
and can be worn on the diver’s wrist. They allow multilevel
diving rather than restricting the diver to a single maximum
depth before return to the surface, and control ascent rates to
theoretically reduce the risk ofDCS. After a dive, a computer can
be interrogated to ascertain the dive profiles undertaken, for
example if a diver presents to a recompression chamber with
DCS

Question 26

Why did some divers get DCS when they had followed protocols

Answer 26

Analysis of the dives by divers who had DCS showed that
many had followed dive profiles that were within the limits of
conservative decompression algorithms without missed
decompression stops or rapid ascents to the surface.

The profiles would have liberated venous bubbles, but in numbers considered safe.

We now know that most of these divers have right-to left
shunts usually a large persistent foramen ovale (PFO), but
in 5-10% of cases a pulmonary shunt.

Their shunts allowed venous bubbles to bypass the
pulmonary capillaries, so that the
bubbles reached the systemic circulation and were
carried to the
tissues to cause paradoxical gas embolism.

In a person not exposed recently to high ambient pressure,
small numbers of bubble emboli do no harmda fact important
for the bubble contrast echocardiogram test for persistent foramen ovale.

Because the tissues have a lower partial pressure
of nitrogen than the bubble emboli, gas passes down the concentration
from the bubble to the tissue and the gas dissolves.

Question 27

Paradoxical Gas embolism

Answer 27

Because the tissues have a lower partial pressure
of nitrogen than the bubble emboli, gas passes down the concentration
from the bubble to the tissue and the gas dissolves.

However, soon after a dive, tissues are supersaturated with
dissolved inert gas (nitrogen if diving breathing air) andembolic
bubbles enlarge as dissolved gas passes from supersaturated
tissues into the bubbles.

The amplified bubbles cause local ischaemia
and pressure effects

The manifestations of paradoxical
gas embolism depend on which tissues are supersaturated
at the time when the bubbles traverse the shunt

The greater a tissue’s blood flow and hence the faster its nitrogen
elimination half-life, the shorter its susceptibility to paradoxical
gas embolism. However, if there are paradoxical bubble
emboli, the greater a tissue’s blood flowthe greater its chance of
being embolised

Therefore timing of venous gas nucleation is
important and there is often a delay. Another factor is the total
inert gas content of the tissue. Nitrogen is relatively lipid soluble.

Question 28

Why the brain + Spine

Answer 28

Lipid-rich tissues have the greatest ability to amplify
embolic bubbles and are at greatest risk of injury.

Of lipid-rich tissues,

the spinal cord has a slower blood flow and
hence nitrogen elimination half-life than the brain.

The spinal cord remains susceptible
to paradoxical gas embolism for longer after
surfacing than the brain.

Subcutaneous tissue also has high lipid content,
but slow blood flow,

so cutaneous DCS (Fig. 2) can
manifest later after a diver surfaces

Question 29

DCI?

What is the causes

Answer 29

It can be difficult to distinguish some types of DCS from
arterial gas embolism secondary to pulmonary barotrauma,
particularly when manifestations are neurological.

Therefore the collective clinical term
decompression illness (DCI) is used

Shunt-mediated DCS accounts for the majority of
neurological (cerebral, spinal and vestibular),

cutaneous
(Fig. 2), and cardiorespiratory DCI in amateur divers

Provocative dive profiles, when the diver had missed
decompression stops required by their decompression algorithm
(dive table or computer) or had made a rapid ascent
to the surface, cause a minority of cases

Arterial gas embolism secondary to pulmonary barotrauma also
causes a minority of cases of neurological and cardiorespiratory
DCI soon after divers surface.

Musculoskeletal
DCS is generally caused by a provocative dive profile or very
deep dives, even without obvious deviation from the
decompression algorithm

Question 30

Timing

Dx

Answer 30

About 50% of cases of DCS have signs and symptoms
within 1 h of surfacing and 90% present within 6 h.

Some 85% of neurological DCS manifests within 1 h, but cutaneous and joint DCS are often delayed

A diver with cerebral DCS may fail to notice he is unwell
and fail to seek help. Delayed diagnosis by colleagues and
doctors is common. Sensory abnormalities and painless
neurogenic urinary retention secondary to spinal DCS may
be missed. A diver (or caisson worker) with cerebral DCS
may be misdiagnosed as under the influence of alcohol or
drugs.

Question 31

Treatment of DCI

Answer 31

Rapid diagnosis of DCI is important,

because treatment is expeditious recompression
in a recompression chamber,

except for some mild forms of DCS.

Distinguishing DCS from arterial gas embolism secondary to pulmonary barotrauma does not usually affect emergency management,

but it often affects subsequent advice
about return to diving.

During transportation to a recompression chamber
the diver should breathe 100% oxygen
even if his arterial oxyhaemoglobin
saturation is normal.

The primary purpose is not to increase
oxygenation, but to eliminate nitrogen from the diver’s lungs to
increase the nitrogen elimination gradient.

Recompression within minutes of symptom onset is very
effective,
but less predictable outcomes follow longer delays.

Nevertheless, it is generally considered that recompression
should be performed as quickly as practicable,

especially in cases of serious neurological symptoms or signs.

Published algorithms show the depths, times, and treatment gases to be used depending on the manifestations of DCS.

Treatment aims to compress the bubbles of gas
that cause the problem,
create a gradient for elimination of inert gas,
and to supply oxygen to the hypoxic tissues.

Fluid is given orally or i.v.,
because dehydration is common.

Divers who have had DCI need careful assessment before
return to diving to exclude significant cardiac shunts or lung
disease that may predispose to recurrence

Transcatheter closure of a PFO is sometimes performed to permit return to diving.

The second article describes how the physiological effects
of diving interact with some medical conditions to affect
fitness to dive

Question 32

Learning objectives
By reading this article you should be able to:

Answer 32

Discuss the pathophysiology of immersion pulmonary oedema.
Explain why cardiac disease increases the risk of
immersion pulmonary oedema and decompression sickness.
Detail the risks of diving with respiratory
diseases.
Define which patients with diabetes can dive.
Describe the risks of diving with epilepsy or other
neurological and neuromuscular disorders.

Question 33

Introduction

Answer 33

In the first of our two linked articles on diving medicine we
considered the effects of changes of pressure as a diver descends and ascends, with resulting changes in partial pressures of gas breathed and risks of toxic gas effects,

Medical assessment for diving requires the exclusion of
diseases that would put a person at greatly increased risk of
diving-related illnesses or would result in an increased risk to
others who might have to conduct a rescue.

The demands of the type of diving being undertaken must
also be considered. An amateur holiday dive for an hour in
tropical waters is very different to commercial saturation
diving at depths >100 m in the North Sea. A team of saturation
divers typically lives for 4 weeks in a chamber pressurised to
11 atmospheres or more on a support shi

Question 34

Cardiovascular disorders

Answer 34

If an average-sized adult is immersed
up to the neck in warm water
(therefore without cooling) the increased hydrostatic
pressure on the legs immediately increases venous return

This increases central blood volume by about 700 ml, cardiac
filling pressures by about 15 mmHg, and stroke volume by
about 30%.

The increase in heart size reduces lung volumes
and causes release of natriuretic peptides.

The resulting natriuresis and secondary diuresis continues until the cardiac filling pressures have returned to the normal level for that person.

In cooler water, cold-induced vasoconstriction
increases preload further and also raises afterload.

Question 35

A closed-circuit rebreather,

Answer 35

A closed-circuit rebreather, used by some divers,

is analogous to ultra-low flow in an anaesthetic circle circuit.

The diver breathes via a closed circuit from a gas reservoir,
termed a counter-lung.

The carbon dioxide in the expired gas is
removed chemically and the decrease in oxygen partial
pressure is measured by oxygen sensors and replenished from
an oxygen cylinder.

The vertical distance between the counter-lung and the diver’s
lung centroid determines whether the diver is breathing with a
negative or positive airway pressure.

When a diver is using a back-mounted
counter-lung swimming horizontally in the prone position,
so that the counter-lung is above the lungs,

respiration is with continuous negative airway pressure.
When the counter-lung is mounted on the front of the chest,
there is CPAP when the diver is prone.

The work of breathing is also affected by gas density.

Density of a gas increases with depth in proportion to the
absolute pressure and

maximum voluntary ventilation decreases
in proportion to the square root of density

(and absolute pressure).

Therefore, at a depth of 30 m
(4 bar, 405.2 kPa, 3040 mmHg)

air is four times as dense as at the surface

(1 bar, 101.3 kPa, 760 mmHg)

and maximum voluntary ventilation is half that at the surface

Question 36

Immersion pulmonary oedema

How does it occur

Answer 36

Immersion pulmonary oedema

occurs in surface swimmers and divers

as a result of the increase in

pulmonary capillary pressure and

the reduction of airway pressures caused by immersion

It is exacerbated by additional increases
in pulmonary capillary pressure as a result of cold-induced
vasoconstriction with consequent centralisation of blood
volume, and by exertion

Question 37

IPO

Answer 37

Immersion pulmonary oedema is a leading cause of death
in scuba divers

When deaths from equipment failure and
diver error are excluded, IPO is probably the most common
medical cause of diving deaths

Question 38

Prevelance

Answer 38

. Immersion pulmonary
oedema is well described in fit individuals including the special forces and navy divers of many countries. The Israeli
Defence Force reported that 70 recruits (aged 18e19 yrs)
developed IPO during swimming trials in a 3-yr period (1.8% of
trials).5 When recruits drank 5 L of liquid in the 2 h before their
swim, eight of 30 developed IPO

In the 2016 Vansbro river swimming race in Sweden, 69 of
13,878 (0.5%) had symptoms varying from cough to fulminating pulmonary oedema and 46 were treated with CPAP.7 A
total of 58 (84%) of those affected were women. Unfortunately,
no breakdown is given of the numbers of women and men
participating in the race, but many reports show that IPO occurs considerably more frequently in women than men: the
reason for the difference is not known

The continuous negative airway pressure when divers
use rebreathers with back-mounted counter-lungs means
that they are at increased risk of IPO. Rebreathers are favoured by military divers because the absence of bubble
liberation reduces the probability of detection during a
combat swim, but even fit special forces and navy divers are
reported to develop IPO when using rebreathers, particularly
when they had back-mounted counter-lungs.8 Research in
French Navy divers showed that the lung comet score, a
grading of interstitial pulmonary oedema, was much
increased in prone divers when exercising whilst breathing
from a back-mounted counter-lung compared with those
exercising using a front-mounted counter-lung or at rest

However, IPO is most frequent in amateur divers older
than 50 yrs, particular those with hypertension.3 They have
higher baseline pulmonary capillary pressures before
entering the water, so that the further increases in pulmonary capillary pressure and the negative airway pressures
that occur during immersion tip them into IPO.

Immersion pulmonary oedema recurs, particularly in
people who are hypertensive, so those who have had one
episode of IPO should not dive again unless the factors
causing the IPO in that person are remov

Question 39

Other cardiovascular diseases and diving

Answer 39

As described in the first article,1 divers with a right-to-left
shunt have an increased risk of DCS after unprovocative
dives provided the dive is deep enough and long enough to
liberate venous gas bubbles

Therefore individuals who have a right-to-left shunt (e.g. cyanotic congenital heart
disease, atrial septal defect or a known pulmonary arteriovenous malformation) generally should not dive. Those who
might have a right-to-left shunt (e.g. history of cryptogenic
stroke at a young age, which is often associated with a large
persistent foramen ovale) need careful assessment and
advice if they wish to dive

Individuals should not dive if they have cardiac disease
that might result in incapacity underwater (e.g. serious arrhythmias and coronary artery disease), or may increase
the risk of IPO (e.g. cardiomyopathy, significant left heart
valve disease), or may increase the risk of DCS (e.g. atrial
septal defects, cyanotic heart disease)

Question 40

Respiratory disorders

Answer 40

The diving physician should ask ‘Does the diver have the
necessary ventilatory capacity to carry out diving and a diving
rescue safely and is there disease that would increase the risk
of pulmonary barotrauma?’

On the surface, a diver must be able to maintain a good
exercise level because when submerged, the situation will
alter radically

The effects of immersion,

increased gas density with depth,

the constraints of the diving suit and the
mechanical resistance associated
with breathing equipment

conspire to reduce the maximum voluntary ventilation
by 50% when at 30 m.

Assuming a V O2 requirement of about 2.5 L to swim against a current of 1.2 knots, then on the surface,
the minute ventilation required to maintain this
would be 75 L min

this presents little problem for most people who are reasonably fit:
at 30 m underwater, essentially normal pulmonary function is required to maintain the same level of oxygen uptake.

With abnormal pulmonary function, the work required to maintain normocapnia when breathing the more dense gas at depth may become
excessive

Question 41

What Resp condition can and cannot dive

Answer 41

Common respiratory problems such as asthma and
chronic obstructive pulmonary disease (COPD) affect the
ventilation/perfusion patterns in the lung, thereby interfering
with the efficiency of gas exchange and the possibility of gas
trapping in areas of the lung which have an increased gas
emptying time. (Note that if an area of lung is completely
closed off to gas exchange, the gas in that area will be slowly
absorbed).

Theoretical physiological considerations have meant that
most diving physicians do not allow people with asthma to
dive.

However, population surveys of divers show that
provided asthma is well-controlled with a combination of one or
more inhaled steroids, long-acting b2 agonists, or leukotriene
receptor antagonists, diving is safe.

In the UK it is recommended that a diver with asthma
should measure his or her peak flow daily
and must not go diving if peak flow is >15%
below their best value when well.

Individuals with a current chest infection should temporarily avoid diving until there is complete recovery.
A history of spontaneous pneumothorax has been
considered to be a bar to diving. Occurring mainly in fit young
men, the condition frequently recurs if left untreated. Rupture
of a bulla underwater may lead to tension pneumothorax,
especially on the ascent, or to arterial gas embolism when gas
from the bulla invades a pulmonary vein. Pleural stripping or
pleurodesis to remove the apical congenital bullae that are
usually the cause of the problem may allow the person to dive
again, but this is controversial

Conditions such as sarcoidosis or active tuberculosis will
preclude diving until treated. Clinically significant COPD and
untreated lung cancer preclude diving altogether.
At present, smokers are permitted to dive, though there is
evidence that they have an increased risk of arterial gas
embolism caused by pulmonary barotrauma on ascent, even
when their spirometry is norma

Question 42

Diving for older (aged >65 yrs) and younger
people (aged <18 yrs)

Answer 42

Some 49% of people in England aged > 65 yrs take at least five
different medications per day. Cardiovascular drugs are the
most frequent medication and may indicate diseases that
make a person unfit to dive.

b-Adrenoceptor antagonists may
limit the ability of the heart to respond maximally to exercise.

Vasodilating antihypertensive drugs, such as calcium channel
blockers and angiotensin-converting enzyme/angiotensin II
inhibitors may be acceptable in divers, because they can
reduce the risk of IPO.

Decreased fitness and reduced muscle
mass may prove problematic if the diver has to carry heavy
cylinders of breathing gas and weights.

Nonetheless, a few
people continue diving into their ninth and tenth decades
without mishap.

Young people learning to dive is an emotive issue. Occasionally parents request a medical for children as young as
7-8 yrs of age.

Physicians need to be cautious in assessing
whether a child really understands the risks and wishes to
dive, because some requests are the result of parental pressure.

Any child who expresses the wish to dive before the age
of puberty must have their mental capacity to cope with the
demands of a diving incident carefully assessed.

A few cases of decompression illness in young teenagers leading to permanent disability have been reported.16 However, most children with responsible adults as buddies will enjoy the
freedom and excitement of diving and it is good exercise

Question 43

Women and diving

Answer 43

Women scuba divers compose about 27% of UK divers.

There are some sex-related physiological differences that are
important for diving.

Women have a greater percentage of
body fat and less muscle mass than men.

Therefore female divers may have more difficulty in carrying and lifting their
diving equipment but may have some protection against hypothermia.

Women have an increased incidence of IPO, but
the reason is not known.

There is evidence that the incidence of DCS is increased in
women in the first week of the menstrual cycle and that the
oral contraceptive may be protective during this time.

A similar association has been found in US Air Force personnel
who were exposed to hypobaric conditions.

The reason is unclear, but it is probably hormonal.

Diving during pregnancy is very controversial,
because of concerns that it may adversely affect the fetus.

Many women have dived being unaware that they are pregnant
until they
later missed a period.

It is during this early stage that fetal
organogenesis and lateralisation occurs.

The observational studies on pregnant women who continued diving are subject to bias.

Therefore it is still unclear whether normal diving profiles
(which do not involve prolonged periods of decompression or rapid ascents) increase the incidence of fetal abnormalities.

Current advice is that women who are planning
to become pregnant should not dive,

but if a woman discovers that she is pregnant and has been diving, it is not an indication
for termination of pregnancy

Breast implants may absorb nitrogen during diving, but
provided rapid decompression is avoided, tissue trauma as a
result of the increased volume of the implants does not occur.

Question 44

Endocrine disorders

Answer 44

Four endocrine disorders are fairly
common in potential
divers:

diabetes mellitus (types I and II),
hypothyroidism and
hyperthyroidism.

Before 1991, no individual with diabetes was allowed to
dive, a worldwide restriction.

Since then, the restrictions have relaxed thanks to research and improved medications.

Divers with diabetes must maintain good control of their
diabetes,
have no long-term diabetic complications and have
annual medical examinations by a diving medical referee.

They must also measure their blood glucose immediately
before and after each dive if they are taking drugs with the
potential to cause hypoglycaemia and carry an emergency kit
to treat hypoglycaemia.

Hypoglycaemia underwater was a major concern for divers
with type I diabetes.

Such concerns were allayed because fit,
healthy divers who have diabetes do not get hypoglycaemia
even when strenuously exercising, provided their blood
glucose concentrations are slightly increased before diving

Some people who have type I diabetes control their blood
glucose levels using an insulin pump.

Insulin pumps should not be used when diving.
Cold and skin pressure (from a wetsuit) may lead to unreliable insulin absorption and no insulin pump has been certified for use under pressure.

People with type II diabetes have a much lower risk of
hypoglycaemia underwater.

Their main risks are from longterm complications of diabetes
(cardiac, neurological, renal).

It is estimated that the onset of type II diabetes occurs 4-6 yrs
before diagnosis, thus allowing complications to develop

People with hypothyroidism and hyperthyroidism can dive
provided their symptoms and thyroid status are well controlled.

Question 45

Neurological disorders

Answer 45

Neurological diseases that significantly increase risk when diving
are contraindications.

The risks are obvious for some diseases.

Grand mal epilepsy causes a risk of unconsciousness and
hence drowning,
particularly at depths where high partial
pressures of oxygen reduce the threshold for convulsions.

In the UK, people with epilepsy must not dive unless they have
been free of fits and not taking anticonvulsant medications for
>5 yrs,
when the risk of a convulsion during a dive
is considered to be acceptably low.

Muscle weakness, resulting from impaired central motor
control, neuropathy or muscular dystrophy, which impairs the
ability to swim or breathe on the surface or under water, is also
a contraindication to diving.

Sometimes important muscle weakness only becomes apparent when an individual starts diving.

For example, diaphragmatic paralysis secondary to
phrenic nerve palsy can result in severe breathlessness at the
surface because the hydrostatic pressure difference between
the abdomen and the mouth results in the diaphragm being
pushed up into the chest, thereby reducing lung volumes.

Impaired coordination may cause difficulty using equipment, as can impairment of touch sensation, particularly
when visibility is severely impaired, as it often is in UK waters.
A diver also needs adequate vision to read their gauges.

Question 46

Neuro Condition continued

Migraine with Aura

Answer 46

The incidence of neurological DCS is greatly increased in
people with migraine with aura.

That is because the prevalence of clinically significant right-to-left shunts (across persistent foramen ovale or pulmonary shunts)

approximately 40% in people with migraine with aura compared with
5% in those without migraine with aura.

As stated previously, right-to-left shunts facilitate DCS as a result of paradoxical gas embolism

Investigations to exclude a significant shunt
should be considered in potential divers
with a history of migraine with aura

Another consideration is whether the manifestations of
neurological disease will interfere with diagnosis and treatment if the diver develops neurological DCS after a dive. For
example, if a diver with a history of transient ischaemic attacks becomes hemiplegic soon after a dive, the differential
diagnosis is another cerebral thromboembolic event or cerebral DCS or cerebral arterial gas embolism secondary to pulmonary barotrauma

f a diver with pre-existing neurological disease develops
neurological DCS, the resulting deficit may be greater. That is
particularly so when the diver has spinal disease because the
addition of spinal DCS could result in serious disability. In
addition, a recompression chamber may continue to treat for
residual clinical signs that are not the result of DCS, but are
attributable to the prior disease.

However, there are some individuals who dive with serious
neurological disability, such as paraplegia, within disabled
diver schemes. It is recognised that these divers gain considerable freedom in underwater weightlessness. They are
carefully assessed before diving, have restrictions on the
diving they can undertake and are cared for underwater by
two or more experienced dive buddies.
Serious psychiatric diseases are a contraindication to diving, particularly when they might impair judgement or result
in panic if difficulties arise during a dive.
There are concerns that many drugs used to treat neurological and psychiatric diseases adversely potentiate the risk
of nitrogen narcosis. In many cases, the concerns are based on
theoretical considerations, but some are known to present
hazards that will limit the depth to which an individual can
div

Question 47

Summary

Answer 47

Summary
When diving, the underwater environment and particularly
the increased ambient pressure, places unique demands on
human physiology, which can cause diving-related diseases
with life-threatening consequences. Therefore, it is important
to ensure that those with medical conditions that put them at
significantly increased risk do not dive.

Question 48

UTD paragraphe

Answer 48

Decompression sickness and air embolism — Divers breathing compressed air who return to the surface too rapidly, and aviators ascending over 5500 meters are at risk for decompression sickness and arterial gas embolism.

Those with a patent foramen ovale are at increased risk [32].

Bubble formation in tissues or in blood occurs as the partial pressure of inert gas (mostly nitrogen) exceeds that of ambient air.

The obstruction of vessels and lymphatics by bubbles is accompanied by the activation of leukocytes, endothelial damage, and resultant alterations in capillary permeability

Decompression sickness manifests a range of severity from self-limited rash or joint pain to focal neurologic deficits, paralysis, seizures, hypovolemic shock, and death. Patients typically develop symptoms within several hours of ascent, with rapid onset and severe symptoms implying a more ominous course.

Arterial and venous gas embolism may arise as a consequence of pulmonary overinflation with subsequent alveolar rupture or from direct trauma. Such emboli occur during uncontrolled ascent while diving, during mechanical ventilation, or from blast injury. Alternatively, air directly introduced through a variety of means, including central venous catheter placement, cardiac, neurologic, and otolaryngological surgery, may yield venous and arterial embo

Question 48

UTD paragraphe

Answer 48

Decompression sickness and air embolism — Divers breathing compressed air who return to the surface too rapidly, and aviators ascending over 5500 meters are at risk for decompression sickness and arterial gas embolism.

Those with a patent foramen ovale are at increased risk [32].

Bubble formation in tissues or in blood occurs as the partial pressure of inert gas (mostly nitrogen) exceeds that of ambient air.

The obstruction of vessels and lymphatics by bubbles is accompanied by the activation of leukocytes, endothelial damage, and resultant alterations in capillary permeability

Decompression sickness manifests a range of severity from self-limited rash or joint pain to focal neurologic deficits, paralysis, seizures, hypovolemic shock, and death. Patients typically develop symptoms within several hours of ascent, with rapid onset and severe symptoms implying a more ominous course.

Arterial and venous gas embolism may arise as a consequence of pulmonary overinflation with subsequent alveolar rupture or from direct trauma. Such emboli occur during uncontrolled ascent while diving, during mechanical ventilation, or from blast injury. Alternatively, air directly introduced through a variety of means, including central venous catheter placement, cardiac, neurologic, and otolaryngological surgery, may yield venous and arterial embo

Question 49

Benefit of HBO - UTD

Answer 49

HBO is the primary treatment for decompression sickness and arterial gas embolism [34,35].

It is unclear whether the efficacy of HBO is due primarily

to decreased bubble size
and relief of local hypoxia,

or to modulation of the pathologic effects mediated by

bubbles in tissue and in vessels [2].

Patients should initiate HBO treatment as soon as possible
because a sharp decrease in the successful treatment
of cerebral air emboli has been noted after a four to five hour delay

Fundamentally, HBO works by providing oxygen at high atmospheres of pressure, thereby increasing the concentrations of oxygen delivered to tissues.

Question 50

Treatment consists of one

Answer 50

Treatment consists of one or more sessions at 2.5 to 3.0 atm.

Most patients respond to one treatment.

If symptoms persist, additional sessions are indicated until clinical resolution.

Some patients with neurologic symptoms suffer deterioration after seemingly successful recompression treatment.

This phenomenon may be due to the slow re-expansion of residual gas bubbles upon termination of hyperbaric therapy, post-ischemic reperfusion injury, or re-embolization from an underlying pulmonary abnormality.

In such patients with severe deficits, as many as 20 sessions may be required [35]. Adjunctive treatment with glucocorticoids, lidocaine, or a combination of prostacyclin, indomethacin, and heparin has been reported, but the efficacy of these interventions is unclear

Question 51

Complications HBO

Answer 51

HBO therapy include middle ear barotrauma (most common), sinus barotrauma, reversible myopia, pulmonary barotrauma, pulmonary oxygen toxicity, seizures (rare), and decompression sickness

Question 52

MANAGEMENT OF ARTERIAL GAS EMBOLISM AND DECOMPRESSION SICKNESS

Answer 52

The prehospital and emergency department treatment of arterial gas embolism (AGE) and significant decompression sickness (DCS) are the same [7]. Initial treatment includes administration of 100% oxygen and hydration with intravenous (IV) isotonic fluid. Definitive treatment is hyperbaric oxygen therapy.

Prehospital care — We concur with the basic prehospital interventions proposed in a 2017 expert guideline, which include the following [72]:

●Provide normobaric oxygen (ie, surface oxygen, or 1 atmosphere) administered at as close to 100% as possible, usually given by nonrebreather mask.

●Place the patient in a horizontal position.

●Keep the patient warm but avoid hyperthermia. (See “Accidental hypothermia in adults”.)

●Hydrate the patient. Oral rehydration may be used if possible (eg, mild case without hemodynamic instability or laboratory abnormalities), but IV hydration with isotonic crystalloid should be administered if necessary. This may be done initially with IV fluid boluses (500 to 1000 mL) and then an infusion, depending on the severity of illness.

Rapid transfer to a higher level of care should be arranged immediately. Ideally, the injured diver should be transported directly to a facility with a hyperbaric oxygen chamber where they can be treated with recompression therapy if necessary. If no such facility is nearby, the diver should be taken to the closest medical facility where an evaluation can be performed and transfer to a hyperbaric chamber arranged. In remote locations, there may be instances where the risk of transport outweighs the potential benefit. However, we recommend that the decision not to transfer be made in collaboration with a physician experienced in diving medicine. Resources to reach such assistance are provided. (See ‘Additional resources’ below.)

Question 53

ED Care

Answer 53

Emergency department care — The injured diver with suspected AGE or severe DCS is assessed in the emergency department (ED) to determine the extent of injury and whether hyperbaric oxygen therapy is needed. Evaluation and treatment occur concurrently. As soon as the need for hyperbaric oxygen therapy is recognized, immediate transport should be arranged as rapidly as possible. Transport should not be delayed for any study or therapy except life-saving interventions.

Treatment in the ED includes the following interventions:

●Assess and stabilize the airway, breathing, and circulation as necessary.

●Continue administering normobaric oxygen at as close to 100% as possible.

●Decompress any pneumothorax. An appropriate thoracostomy device must be in place prior to any recompression treatment to avoid further barotrauma. A pigtail catheter or comparably small device is often sufficient.

●Continue rehydration. Oral rehydration may be used for mild cases; IV hydration with isotonic crystalloid is administered for moderately or severely injured divers.

●Place a bladder (Foley) catheter if there is evidence of urinary retention.

●Obtain imaging and laboratory studies as indicated by workup. (See ‘Evaluation of the sick diver’ above.)

●Severely ill patients should be kept horizontal (Trendelenburg or reverse Trendelenburg positioning is no longer recommended); patients with mild illness may sit or otherwise assume any position of comfort.

For severely injured divers, early administration of prophylaxis against deep vein thrombosis (DVT) may be needed. No high-quality evidence is available to inform the timing, patient selection, or method of DVT prevention in divers

Question 54

Hyperbaric oxygen therapy

ethods + benefits

Answer 54

Methods, benefits, and risks — Recompression in a hyperbaric oxygen chamber is the gold standard for treatment of both DCS and AGE. Recompression therapy should begin as soon as possible once the need is recognized, but delays do not preclude treatment. There are many documented cases of marked improvement with delayed therapy [75-77], and there is no universally accepted period of delayed presentation for which treatment is considered futile

The exact protocol, duration, and number of hyperbaric oxygen treatments is determined by the hyperbaric physician and can be modified based on the patient’s response to therapy. Minor cases may resolve with a single treatment, while severe cases may require a series of treatments

Question 54

Hyperbaric oxygen therapy

ethods + benefits

Answer 54

Methods, benefits, and risks — Recompression in a hyperbaric oxygen chamber is the gold standard for treatment of both DCS and AGE. Recompression therapy should begin as soon as possible once the need is recognized, but delays do not preclude treatment. There are many documented cases of marked improvement with delayed therapy [75-77], and there is no universally accepted period of delayed presentation for which treatment is considered futile

The exact protocol, duration, and number of hyperbaric oxygen treatments is determined by the hyperbaric physician and can be modified based on the patient’s response to therapy. Minor cases may resolve with a single treatment, while severe cases may require a series of treatments

Question 55

Side effects HBO

Answer 55

Hyperbaric oxygen therapy is generally considered safe and low risk. The most common side effect is middle ear barotrauma, which occurs in approximately 2 percent of patients. The injury generally resolves with rest and time, and symptoms may be treated with decongestants. For emergency hyperbaric treatments when patients are unable to equilibrate pressures in their eustachian tubes, emergency myringotomies or tympanostomy tubes may be required.

Oxygen toxicity affecting the central nervous system may occur, with seizures being the most serious manifestation. The estimated incidence is between 1 in 5000 and 1 in 10,000 treatments. Seizures resolve after oxygen is removed and are not a permanent condition. Other, more rare side effects include transient worsening of myopia, pulmonary oxygen toxicity, and pulmonary barotrauma. Although it has not been extensively studied, no significant long-term side effects from hyperbaric oxygen treatment have been reported.

Question 56

Mechanism HBO

Answer 56

Mechanism —

The administration of pure oxygen displaces inert gases
(primarily nitrogen)
from the lungs and

increases the oxygen and nitrogen gradients
between the lungs and other tissues.

This increased gradient enhances the
removal of nitrogen from the tissues.

A gradient is created by the administration of surface oxygen

(ie, at 1 atmosphere) but is increased substantially in the hyperbaric chamber under higher pressures

____

An additional rationale for hyperbaric oxygen therapy includes the reduction of bubble size caused by higher pressures, oxygenation of ischemic tissue, reduced cerebral edema, and decreased inflammatory response (due to reduction in neutrophil adhesion to vasculature endothelium

Question 57

Prognosis

Answer 57

— The prognosis for DCS is generally good. Some studies report that 80 percent of patients had complete resolution of their symptoms [8].

At least one study of spinal cord decompression reported that divers presenting with more severe initial signs had higher likelihood of residual disease [58].

Patients with inner ear DCS have higher rates of residual symptoms [79].

The timing of recompression treatment and its effect on prognosis have not been clearly established, but it is generally accepted that early treatment is better, and recompression should be performed as soon as possible

Question 58

SUMMARY AND RECOMMENDATIONS

Answer 58

●Sickness while SCUBA diving – Decompression sickness (DCS) and barotrauma (including arterial gas embolism [AGE]) are specific to diving, but injuries such as immersion pulmonary edema, hypothermia, trauma, and submersion-related injuries can occur while diving.

Question 59

Barotrauma

Answer 59

Barotrauma is the most common form of diving-related injury

and develops when an air-filled body space
fails to equilibrate its pressure with the environment.

Barotrauma can cause lung injury
(including pneumothorax),
ear or sinus injury, or AGE.

AGE can manifest a wide range of symptoms and signs depending on its extent and the arteries affected.

AGE develops independently of the time of gas exposure and can occur during dives limited to shallow water. AGE that compromises cerebral, coronary, or pulmonary vasculature can be life threatening

Question 60

DCS –

Answer 60

DCS occurs when a diver returns to the surface
and gas tensions in the tissue

exceed the ambient pressure,
causing free gas to leave tissues in the form of bubbles.

These gas bubbles can impair organ function

by blocking blood vessels,
compressing or rupturing tissue,
or activating clotting and inflammatory cascades.

DCS is highly unlikely with dives ≤10 meters.

Symptoms usually manifest upon surfacing and can affect a wide range of organ systems.

Possible findings are myriad and can include joint pain (elbow and shoulder are common),

signs of spinal cord injury,
signs of brain injury,
characteristic rashes,
localized edema, vertigo, ataxia, tinnitus, and (less frequently)
compromised cardiac function. (See ‘Decompression sickness’ above.

Question 61

Evaluation of the sick diver

Answer 61

Evaluation of the sick diver –

Essential aspects of evaluation are the history,
including the diving profile, and the physical examination, including assessment of symptoms and signs associated with AGE and DCS.

The timing of symptom onset is critical to diagnosis. Symptoms caused by AGE typically manifest within 10 minutes of surfacing (and often immediately).

Symptoms that begin during descent or at depth are generally not due to AGE or DCS.

They may be caused by barotrauma of descent, immersion pulmonary edema, or unrelated medical problems (eg, myocardial ischemia, stroke).

Question 62

Management –

Answer 62

Basic initial treatment of AGE or DCS includes:

*Stabilization of airway, breathing, and circulation as needed

*Administration of oxygen as close to 100% as possible

*Keeping the patient warm while avoiding hyperthermia

*Hydration; sick patients can receive intravenous (IV) boluses (500 to 1000 mL) of isotonic crystalloid followed by an infusion

*Horizontal positioning