Intensive Care Med (2003) 29:2128–2136

DOI 10.1007/s00134-003-1999-1 REVIEW

Kay Tetzlaff Evaluation and management of decompression

Erik S. Shank
Claus M. Muth illness—an intensivist’s perspective

Received: 11 August 2003

Accepted: 11 August 2003
Published online: 5 November 2003
© Springer-Verlag 2003
K. Tetzlaff (✉)
1st Department of Medicine,
Christian-Albrechts-University of Kiel,
Schittenhelmstrasse 12, 24105 Kiel,
Germany
e-mail:
Kay.Tetzlaff@bc.boehringer-ingelheim.com
Tel.: +49-7351-542407
Fax: +49-7351-544735
E. S. Shank
Department of Anaesthesia
and Critical Care,
Massachusetts General Hospital,
Boston, MA 02114, USA
C. M. Muth
Department of Anaesthesiology,
Section of Pathophysiology
and Process Development,
University of Ulm,
Parkstrasse 11, 89073 Ulm, Germany
Present address:
K. Tetzlaff, Clinical Research (Respiratory),
Boehringer Ingelheim Pharma
GmbH & Co. KG,
88397 Biberach an der Riss, Germany
Abstract Decompression illness
(DCI) is becoming more prevalent as
more people engage in activities in-
volving extreme pressure environ-
ments such as recreational scuba-
diving. Rapid diagnosis and treat-
ment offer these patients the best
chance of survival with minimal se-
quelae. It is thus important that criti-
cal care physicians are able to evalu-
ate and diagnose the signs and symp-
toms of DCI. The cornerstones of
current treatment include the admin-
istration of hyperbaric oxygen and
adjunctive therapies such as hydra-
tion and medications. However,
managing patients in a hyperbaric
environment does present additional
challenges with respect to the partic-
ular demands of critical care medi-
cine in an altered pressure environ-
ment. This article reviews the under-
lying pathophysiology, clinical pre-
sentation and therapeutic options
available to treat DCI, from the
intensivist’s perspective.
Keywords Decompression illness ·
Arterial gas embolism ·
Decompression sickness ·
Hyperbaric oxygen therapy ·
Diving

Introduction induces pathology. DCI often presents with severe neu-

Aviators, astronauts, compressed air workers and divers
are all exposed to extremes in ambient pressure that may
considerably deviate from normal sea level pressure (ap-
proximately 1 bar—equivalent to 101 kPa). Though all
these occupations have unique inherent dangers, they all
have in common the risk of decompression illness (DCI).
The term DCI encompasses distinct medical disorders
that occur as a result of a decrease in ambient pressure
(i.e. decompression). They share the common character-
istic of tissue damage by excess gas during and after de-
compression, but differ with respect to the way the gas
enters the body, where it ultimately lodges, and how it
rological symptoms requiring both intensive care and hy-
perbaric oxygen [1, 2, 3]. This article reviews the mech-
anism of injury, clinical presentation and therapeutic op-
tions for DCI with special emphasis on hyperbaric inten-
sive care.
Mechanisms of decompression illness
As ambient pressure decreases, the volume of an en-
closed gas will increase in accordance with Boyle’s law.
When, during decompression, expanding intrapulmonary
gas is not exhaled through the airways, over-distension

of the alveoli and bronchi can cause pulmonary barotrau-
ma [4]. Depending on the site of tissue rupture, gas may
track along the perivascular sheaths of the pulmonary
vasculature to cause mediastinal emphysema and pneu-
mothorax. Gas may also be introduced into the pulmona-
ry vasculature with subsequent arterial gas embolism.
The position of the head in relation to the torso during
diving or flying and the buoyancy of the gas bubbles re-
sult in the passage of gas emboli into the cerebral vascu-
lature causing cerebral arterial gas embolism [5].
Henry’s law states a proportional relationship be-
tween the solubility of a gas in a liquid and the partial
pressure of that gas above the liquid. Thus, body tissues
saturate with nitrogen at ambient pressure when breath-
ing nitrogen-enriched gases such as air. During decom-
pression, the decrease in ambient pressure may exceed
the elimination rate of nitrogen, resulting in tissue super-
saturation and formation of a gas phase [6]. Decompres-
sion sickness arises when decompression-related inert
gas bubbles cause mechanical tissue compression or em-
bolisation to venous blood vessels. Normally, however,
these bubbles return to the central veins from the periph-
ery and are carried to the pulmonary circulation, where
they are filtered by the micro-vasculature of the lung [7].
Paradoxical gas embolism may occur through trans-
pulmonary passage of venous gas bubbles or via right-to-
left shunts. Small gas bubbles of less than 14–22 µm
may pass through the lungs directly into the systemic ar-
terial circulation, while larger bubbles spill over when a
certain overload threshold value has been reached [8]. Of
all extrapulmonary right-to-left shunts, a patent foramen
ovale (PFO) provides the commonest pathway for para-
doxical emboli [9]. The presence of a PFO is related to
the occurrence of decompression sickness in divers [10].
Pathology
The pathological effects of gas bubbles result from direct
obstruction of blood vessels or local tissue compression
by an expanding bubble volume, creating tissue isch-
aemia and oedema. Gas elimination impeded by in-
creased diffusion distances and reduced blood flow may
aggravate the damage. This is largely dependent on the
kinetics of the respective gas contained within the bub-
ble and the size and location of the embolus. Subsequent
interactions between the blood-gas interface and the en-
dothelium may result in further tissue damage, mediated
by a variety of secondary cellular and humoral changes
such as activation of complement, platelets and neutro-
phils [11, 12, 13]. These secondary effects promote and
maintain inflammatory cascades that eventually lead to
damage of the capillary endothelium with capillary leak-
age, fluid loss from the intravascular space, and haemo-
concentration [13].
2129
Clinical manifestations and presentation
According to the mechanisms described above, the mani-
festations of DCI largely depend on environmental and
occupational factors (e.g. gas kinetics, decompression
profiles) or individual risks (e.g. age, obesity, pre-exist-
ing pathology). The large majority of DCI occurs during
diving with self-contained underwater breathing appara-
tus (scuba), since this leisure activity has become tre-
mendously popular [14, 15]. Due to the large and rapid
pressure changes during scuba-diving ascents, arterial
gas embolism from pulmonary barotrauma is a relatively
frequent complication and accounts for more than one
third of all recreational scuba-diving fatalities [14, 16],
whereas it is rare during altitude exposures [17]. In con-
trast, acute decompression from sea level pressure to the
low pressures present at high altitudes or inside a space
suit (approximately 30 kPa) precipitate venous gas load-
ing in aviators and astronauts [18]. Although uncommon,
altitude decompression sickness is a persistent problem
during training in hypobaric chambers by military forces
familiarising their aircrews with hypoxia and rapid de-
compression [19, 20]. Severe neurological decompres-
sion sickness is most common after short, deep scuba-
dives but may occur after any decompression when there
is a significant venous gas load, especially in the pres-
ence of right-to-left shunts [21]. Exposure to altitude af-
ter diving, whether during long distance commercial
flights or by driving across mountains, imposes an addi-
tional risk of DCI [22].
The clinical presentation of DCI depends on the or-
gans involved and covers a gamut of signs and symp-
toms ranging from skin itching and vague constitutional
symptoms to shock and cardiopulmonary arrest [14]. The
particular nitrogen saturation and elimination kinetics of
the nervous tissues and its short ischaemia tolerance fa-
vour the development of neurological symptoms in the
presentation of decompression sickness. Sensory symp-
toms including numbness, tingling, paraesthesiae and ab-
normal sensation are far more common than severe neu-
rological symptoms [14]. Typically, these symptoms de-
velop progressively, beginning with mild paraesthesia,
followed by regional numbness, weakness and, occasion-
ally, paresis of the affected limbs [23]. Symptoms usual-
ly occur within hours after decompression but, in severe
cases, they may present immediately. Unlike diving-re-
lated DCI, the most common presenting feature of alti-
tude decompression sickness is musculoskeletal [19].
Distinct manifestations of decompression sickness in-
clude respiratory decompression sickness (“the chokes”),
which may occur when a high venous gas load over-
whelms the pulmonary bubble filter [3, 24], and inner
ear decompression sickness with vertigo, tinnitus and
hearing loss [25].
In contrast to decompression sickness, arterial gas
embolism typically presents as a stroke-like syndrome
2130
with unilateral neurological symptoms, depending on the
areas of the brain affected. Cognitive symptoms and un-
consciousness are most frequently observed. Seizures,
focal motor deficits, visual disturbances and sensory
changes are also common [16, 23]. Bubbles may, howev-
er, occlude any artery, including the coronary vasculature
or those perfusing skeletal muscles, causing cardiac
symptoms or rhabdomyolysis [26]. Even spinal cord le-
sions may occur, but are more likely to result from de-
compression sickness. Due to the underlying aetiology of
pulmonary barotrauma, neurological symptoms may be
accompanied by chest pain, haemoptysis and dyspnoea
[27]. A criterion to differentiate between arterial gas em-
bolism and decompression sickness is the time to onset
of symptoms, since those of arterial gas embolism devel-
op predominantly within 10 min after decompression
[16, 27]. However, symptoms of arterial gas embolism
may be indistinguishable from decompression sickness,
or even non-diving related disorders. Moreover, a com-
bined syndrome of severe neurological decompression
sickness superimposed on gas embolism may be present
[28].
Diagnostic evaluation
The term DCI allows the physician to assign a diagnosis
without needing to differentiate between arterial gas em-
bolism and decompression sickness. This is particularly
helpful in view of the fact that the clinical outcome of
severe DCI, both in scuba-diving and in aviation, largely
depends on time to treatment [29, 30]. Definitive therapy
should therefore not be delayed by excessive, time-con-
suming diagnostic tests [31].
History and physical examination, including neuro-
logical examination, are mandatory for the initial assess-
ment of DCI. The temporal relation of the patient’s com-
plaints to decompression, including information on time
to onset of symptoms, is important for diagnosis. De-
tailed history including data on decompression proce-
dure, absolute pressure attained and breathing gas com-
position are all helpful for differential diagnosis, but may
be superfluous initially. Laboratory investigations are
useful to assess haemoconcentration and dehydration.
An elevated serum creatine kinase has been reported as a
marker of the size and severity of arterial gas embolism
[32]. Imaging studies are not recommended for initial as-
sessment because they postpone the time to treatment.
However, a chest X-ray may be helpful in evaluating the
presence of a pneumothorax, which must be treated be-
fore recompression therapy [1].
Treatment of decompression illness
Depending on the amount and location of excess intracor-
poreal gas, symptoms of DCI may, at least temporarily, re-
solve spontaneously in some cases [27]. Many patients
will later deteriorate, often to a worse condition than their
initial presentation, as a result of progressive tissue dam-
age. Thus, patients affected by DCI must receive adequate
treatment promptly (Fig. 1). Effective treatment of tissue
damage caused by excess gas includes the fast elimination
of the gas phase and the correction of tissue hypoxia, this
is best achieved by hyperbaric oxygen therapy.
The assessment of effective treatment methods for
DCI must rely on empirical evidence and data from ani-
mal studies. For ethical reasons, no controlled prospec-
tive studies in humans have been published comparing
treatment with no treatment.
Initial treatment
Experimental studies in rodents revealed a significantly
faster shrinkage of air bubbles within tissues after oxy-
gen breathing, compared to air breathing [33]. Accord-
ingly, diving accident statistics indicate that early admin-
istration of supplemental oxygen with a concentration
close to 100% improves clinical outcome [27, 34]. This
prevents the patient from further inert gas uptake and in-
creases the diffusion gradient of inert gas from the bub-
ble into the tissue [35]. In order to achieve an optimal
oxygen supply, oxygen should be administered via a
tightly fitting face mask, either from a demand-valve
regulator or by a closed circuit apparatus. The adminis-
tration of fluids is useful to combat haemoconcentration
and dehydration [36].
Divers are particularly prone to dehydration because
of a loss of fluids through respiration and increased diu-
resis during the scuba dive, triggered by the immersion-
induced increase in intrathoracic blood volume. Intravas-
cular accumulation of gas bubbles with subsequent endo-
thelial damage and capillary leakage will aggravate de-
hydration [13]. Depending on the patient’s level of con-
sciousness, mild DCI may be managed by oral fluids;
otherwise, intravenous administration of 1–2 l of fluid
during the first hour post-injury is recommended, fol-
lowed by a constant infusion of 1.5 ml/kg per h [37]. In-
fusion may be guided by laboratory measurements, vital
signs and urine output. Maintenance of adequate fluid
administration will allow continued inert gas washout
from tissues via increased microvascular flow.
Positioning and transport
It was previously believed that the Trendelenburg posi-
tion would decrease the chances of additional gas emboli

Fig. 1 Flow chart for management of decompression illness
reaching the brain and possibly improve the cerebral cir-
culation [1]. However, recent animal data suggest no
benefit from adopting this position [38]. Therefore pa-
tients with DCI should be kept supine, unless a head-
down position is required for circulatory support [31].
Thermal control of the patient is necessary as hyperther-
mia worsens neurological outcome [39] while hypother-
mia impairs the out-flow of nitrogen from tissues.
For definitive therapy it may be necessary to transport
the patient from remote locations. Since exposure to alti-
tude precipitates a recurrence of symptoms by release of
further amounts of nitrogen and bubble growth under re-
duced pressure, injured patients should be transported by
specialised aeroplanes which maintain sea level cabin
pressure. However, due to expense and time delay, the
preferred option is ground transportation or by helicopter
2131
at a flight level below 300 m, with hyperbaric oxygen
therapy given at a nearby location as soon as possible.
Definitive treatment
Improvement in symptoms has historically been seen in
injured compressed air workers who returned to the
high-pressure working environment for their next shift.
Recompression will reduce excess intracorporeal gas and
increase the driving force for its return into solution.
However, since a pressure equivalent to 50 m of seawa-
ter (50 msw, equivalent to 0.6 MPa) is needed to reduce
bubble diameter by 55%, the effects of recompression
per se on mechanical bubble shrinkage are limited, espe-
cially as gas emboli do not maintain a spherical shape
when entrapped in vessels [40].
The application of hyperbaric oxygen therapy acceler-
ates the elimination of the gas phase, both by raising the
ambient pressure and by creating systemic hyperoxia.
2132
Fig. 2 Modified version of US
Navy Table 6 for treatment of
decompression illness. Three
pure oxygen breathing cycles
of 20 min duration each at
18 msw (0.28 MPa ambient
pressure) are followed by sub-
sequent oxygen cycles at
9 msw (0.19 MPa). Intermittent
5-min air breathing pauses pre-
vent oxygen toxicity. Total
treatment time is 285 min
This therapy involves placing the patient in an environ-
ment pressurised at 2–3x atmospheric pressure at sea
level while breathing 100% oxygen. This usually results
in arterial oxygen tensions in excess of 2000 mmHg
(267 kPa) and an amount of oxygen dissolved in the
blood of approximately 60 ml/l. This meets the resting
body’s oxygen requirements without any contribution
from oxygen bound to haemoglobin [41]. Physiological
effects of hyperbaric oxygen, such as an increase in the
diffusion gradient for oxygen into the gas bubble and for
nitrogen out of the bubble, an improved oxygen delivery
to tissues and hyperoxic vasoconstriction, are felt to ac-
count for the improved outcomes seen in DCI. Animal
data suggest that hyperbaric oxygen reduces brain vascu-
lar permeability and cerebral blood flow after global
ischaemia [42]. Moreover, hyperbaric oxygen inhibits
ß2-integrin-dependent adherence of human neutrophils to
injured endothelium. Therefore, it may be beneficial for
post-ischaemic reperfusion injury that develops follow-
ing cerebral arterial gas embolism [43].
There are no randomised studies in humans that have
compared recompression while breathing air with hyper-
baric oxygen therapy. In rodents air bubbles showed a
significantly faster shrinkage during recompression
breathing oxygen compared with air [44]. Clinical expe-
rience suggests that recovery from DCI both in divers
and aviators is inversely related to the time to hyperbaric
oxygen therapy [27, 29, 30, 34]. Most improvement oc-
curs when treatment is initiated within minutes of symp-
toms, however improvement has still been seen when de-
finitive treatment began hours later. Repetitive recom-
pression treatments should be considered as long as there
is an improvement in symptoms, but the more hyperbaric
treatments that are needed to relieve symptoms, the less
likely they are to be effective [14].
Several empirically derived treatment regimens for
hyperbaric oxygen therapy are in use. These differ with
respect to maximal pressure, duration of treatment and
breathing gas mixture. Fig. 2 shows the most commonly
used treatment algorithm (U.S. Navy treatment, Table 6)
that comprises cycles of oxygen breathing at 18 msw
(0.28 MPa) and 9 msw (0.19 MPa) with a total recom-
pression time of approximately 4 h 45 min [2, 31]. Re-
compression to 50 msw while breathing air has been rec-
ommended for arterial gas embolism [1, 45]. However,
studies in animal models of cerebral arterial gas embo-
lism revealed no benefits for recompression to 50 msw
compared with oxygen breathing at 18 msw, even when
additional oxygen was provided at 50 msw [46]. The use
of inert gases different from nitrogen may be advanta-
geous if the therapeutic inert gas diffuses into the gas
bubble at a slower rate than nitrogen diffuses out. Air
bubbles in aqueous tissues disappeared faster during
breathing of oxygen-helium gas mixtures (heliox) com-
pared with oxygen, or air, in rats at sea level pressure
[33] and during recompression [44]. One clinical study
compared the outcome of patients with decompression
sickness treated with oxygen or heliox during recom-
pression and revealed some benefit from the latter [47].
Nevertheless, more data in humans are needed before he-
liox may be considered preferable to the oxygen 18 msw
algorithm. Additionally, the lack of heliox facilities as
well as expense will limit its broader use.
Intensive care in the hyperbaric environment
Certain unique issues must be considered for manage-
ment of the critically ill patient in the hyperbaric cham-
ber environment. Limited patient access due to narrow
space, noise, decreased ambient lighting and altered
sound transmission all complicate clinical observation
[48, 49]. For electrocardiography and arterial blood pres-
sure monitoring, electrical pass-throughs are necessary
across the chamber wall to the outside physiological
monitor. An arterial line also permits arterial blood gas
sampling during treatment [50]. While SaO2 monitoring
with pulse oximetry is only of limited value in the hyper-

baric chamber, the use of transcutaneous PO2 sensors
may provide rough information on adequate tissue oxy-
genation. Intravenous lines should be placed prior to hy-
perbaric oxygen treatment since the hyperbaric chamber
environment complicates insertions. Central venous
catheterization is recommended in severe cases to assess
central venous pressure (CVP) properly. The CVP
should be kept at around 12 mmHg (1.6 kPa).
Because of the potential risk of occult pneumothorax,
femoral central venous lines are generally preferred to
clavicular/jugular lines. Any untreated pneumothorax
contraindicates hyperbaric exposure since it will most
likely result in an acute life-threatening tension pneumo-
thorax just by decompression and expanding gases in the
pleural space [51]. A pneumothorax must be treated by
insertion of a chest tube. Therefore, tubes and instru-
ments for chest tube placement should be readily avail-
able inside the chamber. During hyperbaric therapy chest
tubes should be removed from vacuum drainage and a
Heimlich valve inserted [48].
For fluid administration by gravity, plastic containers
should be used instead of glass bottles. Massive gas em-
bolism can result during decompression, therefore all
containers for intravenous fluids must be vented. The use
of flow-controlled automatic infusion pumps for accurate
fluid administration is possible, when the device is
equipped with a battery as a power supply for minimised
risk of fire inside the chamber. Nevertheless, there are
substantial variations in performance and accuracy of in-
fusion pumps under hyperbaric conditions [52].
Comatose or combative patients should be adequately
sedated and, if indicated, intubated before therapy starts
and the chamber is pressurised. Air has to be evacuated
from the endotracheal cuff prior to hyperbaric exposure,
and the cuff must be filled with the same amount of liq-
uid, such as distilled water or saline, to achieve an ap-
propriate seal. The endotracheal tube must be tightly se-
cured and stabilised in place with documentation of its
depth and auscultation of bilateral breath sounds. Unin-
tended displacement of the tube may cause bronchial ob-
struction and subsequent overinflation of the unventilat-
ed part of the lung with resultant barotrauma or a sudden
drop in blood pressure due to decreased venous return.
Intubated patients will need a myringotomy or, in
case of repeated hyperbaric treatments, a tympanostomy,
as they are unable actively to equilibrate their middle ear
by the Valsalva manoeuvre, especially when they are se-
dated or paralysed [53]. It should be noted that patients
with a nasal endotracheal tube can suffer from barotrau-
ma of the sinuses during compression [48].
Total intravenous anaesthesia is preferred to general
anaesthesia with volatile agents in the hyperbaric cham-
ber environment to avoid contamination of the chamber
atmosphere [54]. Although in opposition to modern respi-
ratory care strategies, ventilated patients will require deep
sedation or even muscle relaxation because of limited op-
2133
tions in terms of ventilation mode. Controlled ventilation
is mostly only possible in intermittent positive pressure
ventilation mode, similar to those simple ventilators often
used for transportation purposes [55, 56].
Cardiopulmonary resuscitation during hyperbaric
therapy imposes significant risks for the patient as well
as for the medical staff, especially when cardiac defibril-
lation is needed. Firstly, there is a significant risk of cat-
astrophic fire due to the elevated PO2 of the pressurised
chamber air atmosphere. Secondly, the medical staff
physically involved in cardiopulmonary resuscitation are
exposed to an increased nitrogen uptake into body tis-
sues. It is therefore strongly recommended to avoid elec-
tric defibrillation inside the chamber and decompress
slowly with the attendants breathing oxygen from 9 msw
until reaching surface pressure. Furthermore, only spe-
cially equipped resuscitation bags should be used to pre-
vent a contamination of the chamber with high oxygen
levels which would increase the risk of fire.
Adjunctive therapy
Anticoagulants have been advocated as a useful treat-
ment of DCI to combat haemoconcentration and coagu-
lopathy, although no randomised studies in humans have
been published. In an animal model of cerebral arterial
gas embolism, the clinical course was less severe if the
animals had been pre-treated with heparin [57]; however,
increased haemorrhage in infarcted areas of the spine
and the brain do not favour its use. Low-dose heparin or
low-molecular-weight heparin may be given in patients
with leg weakness due to DCI as a prophylaxis against
deep vein thrombosis. Aspirin inhibits platelet aggrega-
tion but may activate thromboxane and prostacyclin via
the cyclooxygenase pathway so that a beneficial effect in
vivo is questionable. Currently, anticoagulants cannot be
generally recommended for treatment of DCI.
The use of corticosteroids has been recommended for
arterial gas embolism to combat brain oedema [58].
However, cerebral arterial gas embolism is accompanied
by development of cytotoxic brain oedema with dimin-
ished extracellular spaces and enlarged intracellular ar-
eas. These, in general, do not respond to corticosteroids
[59]. Corticosteroids aggravate ischaemic injury after oc-
clusion of cerebral vessels [60]; in a canine model of ce-
rebral arterial gas embolism no beneficial effects could
be shown with dexamethasone treatment [61]. However,
in patients with spinal cord injury, a significant benefit
was demonstrated after 6 months when methylpredniso-
lone was administered within 8 h post-injury [62]. Ran-
domised studies on patients with DCI will be needed be-
fore a definitive recommendation on the use of cortico-
steroids can be made.
An attractive pharmacological agent that may im-
prove outcome in severe DCI is lidocaine. This has been
2134

shown to improve neuronal recovery in a feline model of
air embolism [63] and is effective for several conditions
associated with gas embolism [64, 65]. The mechanisms
by which lidocaine is beneficial in gas embolism are not
completely understood, but may largely be attributed to a
reduction in intracranial pressure and improved cerebral
blood flow. However, there is only one clinical trial
which showed cerebral protection during cardiac opera-
tions in patients treated with lidocaine [66]. These stud-
ies provide an argument for administration of lidocaine
in a bolus dose of 1.5 mg/kg and maintaining a therapeu-
tic concentration thereafter. Overdosing on lidocaine
should be avoided because central nervous system de-
pression, cerebral convulsions and bradyarrhythmias
may occur.
Treatment of altitude decompression illness
As many cases of altitude DCI resolve spontaneously
and completely on descent [20], administration of oxy-
gen at ground level rather than hyperbaric pressures has
been widely used in aviation medicine. According to
current guidelines and supported by literature, the treat-
ment of altitude DCI may be successfully managed by
administration of 100% oxygen for at least 2 h at ground
level pressure, if symptoms completely resolve on return
to ground level with a normal neurological examination
[20, 31]. However, should symptoms persist or occur af-
ter the return to ground level, hyperbaric oxygen therapy
is indicated and should follow the treatment algorithms
used in diving-related DCI. The same is true for severe
symptoms or symptoms that progress in intensity despite
100% oxygen administration. Should altitude DCI occur
subsequent to a pre-flight dive, altitude DCI must be
managed as a diving-related DCI.
Management after treatment
The return home of patients in commercial aircraft is
thought to be safe 3–4 days after achieving a clinical pla-
teau with treatment [67]. However, this recommendation
relies on clinical observation rather than scientific evi-
dence. Further diagnostic evaluation is recommended to
exclude the presence of risk factors for DCI in patients
who want to resume diving or flying. Imaging tech-
niques have proven helpful to detect central nervous
system lesions. As magnetic resonance imaging of the
brain is more sensitive than conventional computed to-
mography, it may be especially useful for following up
patients with DCI [68, 69]. When there is suspicion of
arterial gas embolism subsequent to pulmonary barotrau-
ma, a computed tomography scan of the lungs, prefera-
bly in the spiral mode, may rule out pulmonary cysts or
bullae that may pass undetected by pulmonary function
testing or chest X-ray [70]. The presence of such lesions
will rule out medical fitness to dive or fly [15, 71]. In
unexplained neurological DCI, i.e. DCI without evidence
of pulmonary barotrauma or procedural decompression
failure, the presence of a patent foramen ovale should be
investigated by transoesophageal echocardiography [72].
A surgical procedure to close a large flap valve foramen
ovale may prevent recurrence of neurological DCI [73].

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