Download Pulmonary Edema Associated With Scuba Diving

Pulmonary Edema Associated With
Scuba Diving*
Case Reports and Review
John B. Slade, Jr, MD; Takashi Hattori, MD; Carolyn S. Ray, MD;
Alfred A. Bove, MD, PhD; Paul Cianci, MD
Acute pulmonary edema has been associated with cold-water immersion in swimmers and divers.
We report on eight divers using a self-contained underwater breathing apparatus (scuba) who
developed acute pulmonary edema manifested by dyspnea, hypoxemia, and characteristic chest
radiographic findings. All cases occurred in cold water. All scuba divers were treated with
complete resolution, and three have returned to diving without further episodes. Mechanisms
that would contribute to a raised capillary transmural pressure or to a reduced blood-gas barrier
function or integrity are discussed. Pulmonary edema in scuba divers is multifactorial, and
constitutional factors may play a role. Physicians should be aware of this potential, likely
underreported, problem in scuba divers.
(CHEST 2001; 120:1686 –1694)
Key words: altitude sickness; diving; hypoxia; immersion; pulmonary edema; respiratory distress syndrome; swimming
Abbreviations: ECM ⫽ extracellular matrix; fsw ⫽ feet of sea water; HAPE ⫽ high-altitude pulmonary edema;
msw ⫽ meters of sea water; scuba ⫽ self-contained underwater breathing apparatus
pulmonary edema has been described preA cute
viously in swimmers and divers using a selfcontained underwater breathing apparatus (scuba).1– 6 The prevalence of pulmonary edema during
scuba diving and surface swimming is unknown but
is probably underreported. In a survey4 of 1,250
divers, of the 460 responders, 5 (1.1%) had a history
suggestive of pulmonary edema. With ⬎ 3 million
scuba divers currently in the United States alone,
literally thousands of divers could be at risk for
developing pulmonary edema.
Acute pulmonary edema occurs when the pulmonary
capillary permeability is increased (noncardiogenic),
when the pulmonary capillary hydrostatic pressure
exceeds the plasma oncotic pressure (cardiogenic), or
both. In swimmers and divers, an increased transalveolar pressure gradient due to a combination of factors
has been implicated in the pathogenesis of the condition. The final common pathway appears to be stress
failure of pulmonary capillaries manifested by leaks in
the capillary endothelial layer and the alveolar epithe*From Doctors Medical Center (Drs. Slade, Ray, and Cianci),
San Pablo, CA; Community Hospital of the Monterey Peninsula
(Dr. Hattori), Monterey, CA; and Temple University Medical
Center (Dr. Bove), Philadelphia, PA.
Manuscript received August 24, 1999; revision accepted March
27, 2001.
Correspondence to: John B. Slade, Jr, MD, Doctors Medical Center,
San Pablo, San Pablo, CA 94806; e-mail: [email protected]
lial layer, and sometimes the breakdown of the full
thickness of the alveolar wall leading to highpermeability pulmonary edema or even frank hemorrhage.7 The exact nature of the stress in scuba divers
and immersion victims is not clear but may be due to
raised pulmonary capillary pressure from systemic sympathetic discharge, the development of high negative
intrathoracic pressure due to multiple factors, or as-yet
undefined biochemical or adrenergic responses to conditions encountered during swimming and diving.
As in high-altitude pulmonary edema (HAPE),
constitutional factors may predispose a subgroup of
individuals to the development of pulmonary edema
with scuba diving or water immersion. The occurrence of hypoxemia or severe acid-base abnormalities make prompt recognition and treatment important.8
Materials and Methods
Information was collected on scuba divers from 1986 to 1999,
who were referred to the Pacific Grove Hyperbaric Facility in
Monterey, CA, the John Muir Medical Center in Walnut Creek,
CA, or Doctors Medical Center in San Pablo, CA, for the
evaluation of pulmonary edema that developed during diving.
Data regarding patient diving history, details of incident dives,
medications, medical history including prior episodes, laboratory
and radiograph evaluations, treatments, and outcomes were
reviewed and are summarized in Table 1.
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Discussion
The pathophysiologic mechanisms for the development
of acute pulmonary edema in apparently otherwise
healthy scuba divers are not clear. In most divers, the
pulmonary edema occurs without an obvious precipitating
cause, can occur in shallow or deep dives and in cold or
warm water, and has been reported in swimmers.2–4
Patients may have arterial blood gas findings of acidosis
and hypoxemia, chest radiographic abnormalities, rarely
have evidence of heart failure, and survivors respond
completely to conventional therapy for pulmonary edema.
Water aspiration may be a contributing or causative factor
and should be considered.
In our series of eight patients, the only obvious
factor common to all was the history of scuba diving.
Other possible contributing factors included but
were not limited to, poor physical conditioning, cold
water exposure, immersion effects, strenuous exer-
Table 1—Case Summaries*
Variables
Case 1
Case 2
Case 3
Case 4
Case 5
Case 6
Case 7
Case 8
Age, yr/sex
52/M
61/M
46/F
53/F
58/F
55/F
49/F
45/M
Scuba history
20 yr
Experienced
First dive
Prior experience
⬎ 140 dives
New diver
2 yr
Not documented
Maximum depth
85 fsw
20 fsw
15 fsw
110 fsw
110 fsw
45 fsw
Unknown
40–60 fsw
(26 msw)
(6 msw)
(4.6 msw)
(33.8 msw)
(33.8 msw)
(13.8 msw)
Water temperature
55°F
55°F
55°F
50–55°F
80s°F
50–55°F
Cold
50–55°F
Symptom onset
Prior to ascent
Prior to ascent At depth
At 20 fsw
During ascent
At depth
On surfacing
At 15 fsw
Symptoms and signs on
Dyspnea and
Dyspnea,
N2 narcosis (?),
Cough (frothy, pink Severe dyspnea
Copious,
Cough (clear,
surfacing
hemoptysis
Dyspnea,
hemoptysis
hemoptysis
aspirated at
(fatigue with
(cyanosis on
surface,
dive prior
surfacing)
hemoptysis
sputum)
(12–18 msw)
frothy
copious yellow
hemoptysis
fluid)
day)
History of symptoms and
1 wk prior
No
No
HTN
HTN, arthritis HTN, asthma
Yes
No
Yes
No
Unknown
Unremarkable
Allergies, no
Asthma, depression
Childhood
Chronic atrial
signs
Medical history
asthma
Family history
CAD, HTN
CAD, DM
Medications
Metoprolol
Thyroid, 1 g/d; Atenolol
D/C 5 mo prior
Not listed
asthma
fibrillation (1 yr)
Unremarkable
CHF, CVA, cancer
Unremarkable
Unremarkable Not listed
None
ND
Fluoxetine, nortryptyline
None
indomethacin
medroxyprogesterone
prn
acetate, estrogens
Digoxin, warfarin,
Sotalol
Cigarettes
No
No
No
No
No
No
No (prior)
No
Alcohol consumption
No
Rare
No
Occasional
Moderate
Moderate
Unknown
Occasional
Physical examination
BP, 160/100; P,
BP, 154/100;
BP, 204/P; P,
BP, 80/60, P, 100
BP, 172/72; 2/6
BP, 120/80; trace lower
BP, 110/70;
Bibasilar rales; heart:
84 beats/min;
P, 96 beats/
80 beats/min;
beats/min;
R, 18 breaths/
min; R, 22
R, 22
diffuse bilateral
no rub or
min; bilateral
breaths/min;
breaths/min;
rales
murmur
rales
bibasilar
bilateral rales;
rales
Chest radiograph
Bilateral perihilar Retic-nodular
Bilateral diffuse
Bilateral pulmonary Anterior, patchy
infiltrates; heart
bilateral
pulmonary
patchy perihilar
vascular
normal.
infiltrates;
edema
alveolar
congestion
Room air:
heart: click,
RRR, no murmur
pulmonary edema
None
obtained
Bibasilar infiltrates L
⬎ R and mild
cardiomegaly
densities. Heart
normal.
Room air: 7.31/
extremity edema
obesity
Diffuse
heart
Blood gas measurements at
systolic murmur
normal.
ED-100% O2:
Room air: 7.33/37/ ND
ND
ND
Sao2 (room air) 91–
presentation, pH/Pao2/
52/42; 5 L O2:
7.13/44/41;
7.27/192/46;
31; 100% O2:
94%; ECG: afib,
Paco2
7.33/97/46
40% O2:
ICU-4 L O2:
7.3/105/34
ventricular rate
7.4/73/42
7.34/57/43
110 beats/min;
CPK 124 (NL)
Diagnostic studies
V̇/Q̇ scan (⫺) for
ND
ECG (⫺)
PE; ETT (⫺);
Lactic acid, 3.7
(0.5–2.2 nmol/L)
CKMB (⫺)
CPK (⫺); cardiolyte PFTs (⫺); ETT (⫺);
scan (⫺); ETT
ND
stress echo (⫺)
rate 110 beats/
(⫺); ECG:
min; echo normal;
LBBB
Treatment
Furosemide, O2
NTG,
40% O2 by
Venti-mask
Furosemide, O2 Furosemide, O2 by Furosemide, O2
albuterol, K⫹
ECG: afibrillation
CPK (⫺)
ND
ND
mask
Furosemide, O2,
ciprofloxacin
diltiazem
Resumed scuba
Yes
Unknown
Unknown
Unknown
Yes
Yes
Unknown
Unknown
*M ⫽ male; F ⫽ female; CAD ⫽ coronary artery disease; HTN ⫽ hypertension; DM ⫽ diabetes mellitus; CVA ⫽ cerebrovascular accident; CHF ⫽ congestive heart failure; P ⫽ pulse;
R ⫽ respiration; Sao2 ⫽ arterial oxygen saturation; ED ⫽ emergency department; RRR ⫽ regular rate and rhythm; CPK ⫽ creatinine phosphokinase; PE ⫽ pulmonary embolism;
ETT ⫽ exercise tolerance test; CKMB ⫽ creatine kinase MB; (⫺) ⫽ negative; NTG ⫽ nitroglycerin; echo ⫽ echocardiogram; PFT ⫽ pulmonary function test; LBBB ⫽ left bundle-branch
block; V̇/Q̇ ⫽ ventilation/perfusion; afib ⫽ afibrillation; D/C ⫽ discontinued; NL ⫽ normal; ND ⫽ not documented; ? ⫽ condition suspected.
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tion, tight-fitting wet suit, anxiety, malfunctioning
regulators or other equipment, aspiration, and hypertension.
All the patients in this report were middle-aged
(age range, 46 to 61 years) people of average fitness.
The water temperature was 50 to 55°F for six of the
divers, in the low 80s for one, and was recorded as
“cold” for one. None of the patients reported having
strenuous exertion during the dive. One diver (case
5) had a wet suit that was too tight and was considerably apprehensive during her dive. There were no
reports of equipment malfunction, but one diver
(case 2) ran out of air on the day prior to his incident
dive, had to “buddy-breathe” with his diving instructor, and complained of significant postdive fatigue
that evening. The fatigue had resolved by the next
morning when he developed pulmonary edema during his first scuba dive that day. Aspiration is included in the differential diagnosis of one diver (case
4) but is unlikely because she became symptomatic
during ascent at about 20 feet of seawater (fsw),
which was clearly before the apparent surface aspiration. Three of the eight patients had histories of
hypertension, and four reported histories suggestive
of asthma, which points to a possible role for these
conditions. Six of the eight divers had prior diving
experience, one was a new diver, and for one
experience was not documented. Interestingly, three
of the patients reported histories of similar episodes
on previous scuba dives. One diver (case 1) had 20
years of diving experience, had suffered a similar
episode 1 week prior, and subsequently resumed
diving. One diver (case 4) also had prior diving
experience. One diver (case 6) was a relatively new
diver and resumed scuba following this episode. The
onset of symptoms occurred while at depth, during
ascent, or shortly after surfacing. Pulmonary edema
occurred in water as shallow as 15 fsw (4.6 m of sea
water [msw]), and as deep as 110 fsw (34 msw), with
an average of 54 fsw (17 msw). Depth was not
reported for one diver. There was a variable time of
onset as well. In five of the divers, the onset of
symptoms occurred during the first dive of the day.
None of the divers were current cigarette smokers,
although two had a history of tobacco use.
The results of each patient’s initial physical examination were consistent with the clinical presentation
of pulmonary edema; only one diver (case 4) presented initially with hypotension. Chest radiographic
findings ranged from interstitial edema to diffuse,
bilateral alveolar densities, which are characteristic
of the radiographic findings of early and late pulmonary edema, respectively. One diver (case 8) had
chest radiographic findings that were consistent with
cardiogenic pulmonary edema, including heart size
at the upper limits of normal (Fig 1) and cough
Figure 1. Chest radiograph showing acute pulmonary edema in
one diver (case 8). A mild perivascular infiltrate is suspected at
the lung bases. Upper lobe vessels are prominent.
productive of copious, clear yellow sputum. He had
a (known) 1-year history of treated chronic atrial
fibrillation. Six of the eight patients had hemoptysis,
suggesting the presence of permeability pulmonary
edema caused by disruption of the entire blood-gas
barrier. One diver (case 6) was physically fit and was
severely dyspneic following her dive. The results of
her cardiac workup were negative. Her chest radiographic findings (Fig 2) demonstrated an unusual
and “patchy” distribution (which is consistent with
the known anatomic distribution of vascular smooth
muscle in the lungs) that also can occur in patients with
HAPE. Echocardiograms were performed or were
available in only two patients. Neither patient showed
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Pulmonary Edema
Figure 2. Chest radiograph showing acute pulmonary edema in
one diver (case 6). Primarily, upper lobe distribution involves at
least the left upper lobe, and probably bilateral upper lobes. This
focal, patchy distribution is unusual. These finding suggest a
permeability pulmonary edema. These findings, a normal heart
size and infrequent interstitial edema or pleural effusion, suggest
a microvascular permeability pulmonary edema.
any ventricular or valvular abnormalities. In the four
patients with documented initial room air arterial blood
gas measurements, the results for each patient indicated metabolic acidosis (pH range, 7.13 to 7.33) with
eucapnia (Paco2 range, 31 to 46 mm Hg).
The development of pulmonary edema represents
a pathophysiologic spectrum. On one end of this
spectrum is the pure cardiogenic origin of pulmonary
edema (as in congestive heart failure) due to increased pulmonary capillary hydrostatic pressure
that produces edema fluid with a relatively low
protein content. At the other end is a more severe,
noncardiogenic form caused by increased capillary
permeability, as in patients with ARDS. In patients
with ARDS, the edema arises from lung cell injury
rather than from increased hydrostatic filtration
pressures and, thus, is considered to be noncardiogenic, at least during the initial clinical phase. Inflammation is a principal contributing factor in acute
lung injury in patients with ARDS and is associated
with inflammatory mediators such as tumor necrosis
factor and interleukins.9
It has been well documented that chemicals and a
variety of other factors can cause the alveolar-capillary leak syndrome that, potentially, can lead to acute
pulmonary edema.10 Stimulant-associated pulmonary edema can result either from direct local cellular toxic reactions or microvascular pulmonary effects.11 Overdoses from diphenhydramine and
cocaine abuse may have common mechanisms that
are different from heroin-related pulmonary edema.12 Mechanisms have been proposed to explain
the patterns of lung reaction and lung leakage that
result from exposure to cigarette smoke and other
particles.13 None of the eight patients in this study
were current smokers.
Stress failure of the pulmonary capillaries occurs
in several pathologic conditions and likely plays a
major role in the development of pulmonary edema
in scuba divers and swimmers. The blood-gas barrier
must be extremely thin to allow for the diffusion of
oxygen and carbon dioxide but must maintain structural integrity under the most challenging physiologic conditions. The thin portion of this barrier is
formed by the capillary endothelium, alveolar epithelium, and the extracellular matrix (ECM). The
ECM consists of the fused basement membranes of
the two cellular layers and confers most of the
barrier strength.7,14 As capillary pressure increases,
“pore stretching” of the capillary endothelial cell may
occur, leading to larger tracer molecules such as
hemoglobin moving into the interstitium of the
alveolar wall.7 Finally, at even higher pressures,
stress failure of the blood-gas barrier occurs, resulting in a high-permeability type of edema. The
resultant edema fluid is characterized by a protein
content approaching that of blood, due to the loss of
the sieving properties of the microvascular barrier.15
Scanning electron microscopy16 and transmission
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electron microscopy17 studies have demonstrated
alveolar epithelial breaks as capillary transmural
pressure is raised (Fig 3). Alveolar epithelial cell
active sodium transport is the primary mechanism
regulating the removal of excess alveolar fluid from
the distal airspaces.18 The impairment of this function (as seen in cold conditions) could contribute to
the development of pulmonary edema.19 Rapid
changes in gene expression for ECM proteins and
growth factors occur in response to increases in
capillary wall stress.20 The patchy nature of stress
failure is consistent with anatomic findings of the
patchy distribution of smooth muscle in small pulmonary arteries in the healthy adult lung21 and the
observation of uneven vasoconstriction that occurs
when the pulmonary arterial pressure rises in patients with HAPE.22 In patients with ARDS, the
concept that alveolar damage is always a diffuse
bilateral process is not consistent with clinical or
morphologic data. Even in patients who die of
respiratory failure secondary to ARDS, although the
lung is (usually) extensively involved, focal areas may
be inexplicably spared.23 The chest radiographic
findings shown in Figure 2 indicate an unusual
distribution of pulmonary edema that is consistent
with focal lung involvement.
Immersion Effects
Immersion causes the central pooling of blood by
facilitation of the venous return, which increases the
preload. This physical shift of blood centrally during
immersion is further aided by the high density of
water, which diminishes or eliminates the usual
pooling of blood in the peripheral veins that occurs
in air (in this respect, immersion is analogous to a
gravity-free state).24 Blood redistribution during immersion in thermoneutral water (ie, 91.4 to 95°F)
and in cool water corresponds to a reduction in vital
Figure 3. Scanning electron micrographs showing disruptions of the blood-gas barrier in rabbit lungs
perfused in situ to high capillary transmural pressures of 52.5 cm H2O (top left, a, top right, b, and
bottom left, c) and 72.5 cm H2O (bottom right, d). Top left, a: a circular disruption of the epithelial layer
(open arrow) and complete ruptures of the blood-gas barrier (closed arrows) are shown. Top right, b:
a break involving the whole blood-gas barrier (closed arrow) at about 2.1 ␮m from an intercellular
junction (white arrow) is shown. Bottom left, c: complete ruptures of the blood-gas barrier (closed
arrows) with a flap of endothelium (open arrow) partly covering one break are shown. Bottom right, d:
a slit of the blood-gas barrier (closed arrow) very close (about 0.4 ␮m) to an intercellular junction (white
arrow) is shown. Almost no breaks occurred at intercellular junctions, although many were seen within
1 ␮m of the junctions. This suggests a considerable mechanical strength of the junctions, but one that
is so rigid that the cell in the vicinity of the junction is more vulnerable to mechanical failure. Scale
bars ⫽ 2 ␮m (top right, b, and bottom left, c) and 3 ␮m (top left, a, and bottom right, d). Reprinted by
permission of West et al.17
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capacity of 5% and 10%, respectively.25 The smaller
change in vital capacity that occurred in warm water
indicates a significant amount of peripheral pooling
persisted. For scuba divers, water is generally considered to be cold at temperatures ⬍ 77°F, and
much of the surface water in the United States is
below 70°F.26 In our patients, the recorded water
temperatures ranged from 50°F to the mid-80s°F. At
these temperatures, peripheral vasoconstriction in
the water would be expected, bringing about a
further increase in the central blood volume at the
expense of the peripheral volume.26
Pulmonary edema associated with immersion previously has been described in 11 divers and swimmers exposed to cold water.2 Cardiac preload and
afterload augmentation due to cold-induced vasoconstriction combined with immersion effects was
thought to cause the pulmonary edema.2,14
Several case reports5,27–29 have associated cold
exposure during swimming, scuba diving, or immersion with the onset of pulmonary edema. Rapid
rewarming after prolonged hypothermia may cause
vasomotor collapse, leading to acute pulmonary edema.30 Significant increases in pulmonary artery pressures due to short-term cold exposure in rats also
have been demonstrated.31 In divers and swimmers,
the physiologic response to cold water, combined
with the centralization of blood due to immersion
effects, may promote the development of pulmonary
edema.
Negative-Pressure Effects
Clinically silent negative-pressure pulmonary
edema as a consequence of acute airway obstruction
or vigorous attempts to breathe against a high resistance to flow has been described.32,33 Factors that
could contribute to pulmonary edema in scuba divers
include scuba valve failure (rare), low tank air pressure with certain types of regulators, a tank not
turned completely on, the use of a breathing apparatus with a high inspiratory resistance, and panic
associated with an increased effort of breathing so
that inspiratory pressure was slightly negative with
respect to water pressure.34 Filling compressed air
scuba tanks in locales such as the island of Hawaii
with air containing volcanic dust has resulted in
regulator malfunction.
Relatively negative intrathoracic pressures can result from decreased lung volumes due to chest
constriction as when the diver wears a tight wet suit.
Central bronchial diameter varies with lung volume
(M. Knafels; personal communication; July 1998),
leading to increased resistance to breathing as the
total lung volume decreases during a dive exposure.
Resistance to breathing also is increased due to
greater gas density leading to turbulent flow and an
increase in the breathing apparatus internal impedance has been postulated.35 In swimmers, there is a
potential to increase pulmonary capillary pressures
due to negative-pressure breathing as alveolar pressure decreases below mouth pressure. Direct measurements during head-out immersion have shown a
65% increase in respiratory work associated with
immersion to the xiphoid when compared with immersion to the neck under resting conditions.36 This
could contribute to pulmonary edema in swimmers.
Neurogenic Pulmonary Edema
Pulmonary edema develops in several clinical conditions that have both cardiogenic and noncardiogenic (permeability) components. Although the
pathogenesis of nervous system-induced pulmonary
edema remains incompletely understood, the two
major mechanisms are elevated intravascular pressure and pulmonary capillary leak. Intracranial hypertension causes a massive centrally mediated sympathetic discharge, which increases systemic and
pulmonary vascular resistance and leads to high
transmural pressures. The hemodynamic component
is relatively brief and may unmask a pure noncardiogenic pulmonary edema.37 A report38 of pulmonary
edema in association with surgical resection of a
brain tumor suggests the medulla oblongata as an
important anatomic site of origin for neurogenic
pulmonary edema in humans. The importance of
these mechanisms in our divers is unknown.
HAPE
Although not directly relevant to divers and swimmers, a discussion of HAPE may help to clarify the
pathophysiology of pulmonary edema. HAPE is associated with high pulmonary arterial pressures,
normal wedge pressures, and reduced barrier function of the pulmonary vascular wall. HAPE-prone
mountaineers had significant (p ⬍ 0.01) elevations of
plasma endothelin-1 levels compared to HAPEresistant control subjects. This potent pulmonary
vasoconstrictor peptide causes an exaggerated pulmonary hypertension at high altitude and also augments microvascular permeability.39 Primary intracranial events elevate peripheral sympathetic activity
that acts neurogenically in the lung to cause pulmonary edema and in the kidney to promote salt and
water retention. Striking increases of aldosterone,
vasopressin, and atrial natriuretic peptide40 likely
modulate the adrenergic responses. The edema fluid
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that is produced in HAPE patients is the highpermeability type, with large concentrations of primarily alveolar macrophages and high-molecularweight proteins.41 In HAPE-prone individuals,
urinary leukotriene E4 levels are elevated,42 and
levels of BAL fluid cytokines (including interleukin-6
and tumor necrosis factor-␣) are markedly elevated,43 suggesting that inflammatory mechanisms play
a major role in HAPE. HAPE has been associated
with the major histocompatibility complex, which
suggests immunogenetic mediation.44 The responses
of HAPE-susceptible individuals to exercise include
lower diffusing capacities of the lung for carbon
monoxide, smaller functional residual capacities, and
smaller increases in stroke volumes compared to
HAPE-resistant subjects.45 Since HAPE tends to
occur subacutely, the mechanisms involved may be
more complex than for scuba divers and swimmers.
Peak Exercise and Pulmonary Edema
There have been several published case reports46 –50 of pulmonary edema in athletes during
peak exercise and during bicycle ergometry,51 and it
is well-known to occur in racehorses.52,53 Increased
cardiac output during exercise rarely would be expected to raise pulmonary capillary pressure to the
point of microvascular rupture in humans. However,
combined with the pulmonary mechanics of effort
associated with extreme exertion, capillary tolerance
could be exceeded. A role for the activation of
proinflammatory pathways associated with the development of pulmonary edema in patients under conditions of peak exertion has been proposed.50
An Israeli group reported3 on the development of
dyspnea and pulmonary hemorrhages in 8 of 30
healthy young men engaged in an elite military
fitness training program involving a 2.4-km open-sea
swimming time trial. All eight young men developed
shortness of breath within 45 min and prematurely
terminated their swim. The conditions of all eight
men resolved with treatment. Two men had recurrent episodes of pulmonary edema, hemoptysis, or
both during subsequent swimming.3
Pulmonary Barotrauma
Breath-hold diving has been reported to result in
intra-alveolar hemorrhaging54 and death from diffuse bilateral pulmonary vascular injury.6 Pulmonary
barotrauma due to lung overinflation usually is associated with a rapid or uncontrolled ascent while
breathing from a compressed air source and can lead
to air embolism.55 This serious condition may be
second only to drowning as a cause of death among
recreational scuba divers. Neither condition seems to
play a role in our cases.
Conclusion
There are ⬎ 3 million scuba divers in the United
States alone. Physicians will increasingly be asked to
evaluate and treat scuba diving-related problems and
to assess individuals for fitness to dive. Factors
potentially contributing to the development of pulmonary edema in the diver or swimmer include poor
physical condition, underlying cardiovascular dysfunction, hypertension, asthma, anxiety, and strenuous exertion before, during, or after diving. External
factors contributing to the development of pulmonary edema include thermal exposure, the effects of
tight wet suit wear, exposure to respiratory irritants
in the compressed air source, increased work of (or
resistance to) breathing due to low air pressure in the
scuba tank, aspiration, particulates in the air supply,
and malfunction or poor state of repair of the
regulator.
The quantity of pulmonary edema fluid formed in
divers is presumably augmented by the centralization of blood flow from immersion and cold-exposure effects. Massive pulmonary edema significantly
decreases pulmonary compliance, leading rapidly to
hypoxemia and acidosis. This mechanical pulmonary
failure is of sufficient scope to diminish the victim’s
ability to compensate with hyperventilation, leading
to the uncharacteristic arterial blood gas picture of
acidosis and hypoxemia with eucapnia or hypercapnia. The onset of pulmonary edema in divers is a
rapid, acute process that is usually due to patchy,
focal disruption of portions or the entire thickness of
the blood-gas barrier in discrete areas of the lungs,
which is similar to the edema found in patients
experiencing cocaine overdoses.
Rapid clearing of the pulmonary edema and metabolic acidosis is expected in these patients. Bloodgas barrier disruptions are known to quickly resolve
in experimental conditions after the reduction of the
elevated pulmonary venous pressure. Rapid improvement is similarly seen in patients experiencing
HAPE when they are taken to a lower altitude
(higher oxygen partial pressure). During the healing
phases, pulmonary blood flow is preferentially
shunted to functional alveoli. This flow redistribution
allows for rapid clinical recovery while healing of the
injured focal areas occurs. All patients in this report
had complete resolutions of the signs and symptoms
of pulmonary edema with treatment.
For divers or swimmers who experience pulmonary edema, a generic recommendation to avoid
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future exposures seems unwarranted. Many of these
swimmers and divers have not suffered any recurrences on subsequent diving or swimming activities.
Of the three patients in this report who were questioned (two of whom had previously experienced
pulmonary edema while scuba diving), all have returned to diving with no further problems. However,
all of those patients adopted more conservative
diving habits. Unfortunately, there is currently no
accurate way to predict whether or not a scuba diver
is at risk to develop acute pulmonary edema. In those
divers who have experienced a prior episode, a
complete history should be obtained in an attempt to
identify potential triggers that might be eliminated.
Extreme conditions in future scuba dives or swimming exposures should be avoided. Health-care providers involved in the management of these patients
should ask specifically about possible contributing
factors. Certainly, divers with pulmonary complaints
prior to entering the water should refrain from
diving and should receive medical evaluations or
advice before attempting to dive. Although impractical for the vast majority of divers, tests that may be
of value in evaluating problems during scuba diving
would include high-resolution, thin-section CT scanning, measurement of the diffusing capacity of the
lung for carbon monoxide, and serial pulmonary
function tests. There is still much to be learned
about this rare, but potentially fatal (autopsy results
from the Divers Alert Network case files of an
experienced female diver were consistent with pulmonary edema and showed no significant cardiac
abnormalities), complication of scuba diving.
ACKNOWLEDGMENTS: We acknowledge the assistance of
John B. West, MD, PhD, Claude A. Piantadosi, MD, and
Anthony Woolf, MD, for their thorough reviews of the manuscript and invaluable suggestions. We also thank James L. Caruso,
MD, for his assistance in providing case information from the
Divers Alert Network files.
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