(Chest. 2001;120:1686-1694.)
© 2001
American College of Chest Physicians
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 and
Paul Cianci, MD
*
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.
Correspondence to: John B. Slade, Jr, MD, Doctors Medical Center, San Pablo, San Pablo, CA 94806; e-mail: jslade1515{at}aol.com
 |
Abstract
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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.
Key Words: altitude sickness • diving • hypoxia • immersion • pulmonary edema • respiratory distress syndrome • swimming
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Introduction
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Acute
pulmonary edema has been described previously in swimmers and divers
using a self-contained underwater breathing apparatus
(scuba).1
2
3
4
5
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
epithelial layer, and sometimes the breakdown of the full
thickness of the alveolar wall leading to high-permeability 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
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Materials and Methods
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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
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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
3
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 exertion, 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 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 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).
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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.
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Pulmonary Edema
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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 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.
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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 µm
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 µm) to an intercellular junction (white arrow) is
shown. Almost no breaks occurred at intercellular junctions, although
many were seen within 1 µm 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 µm (top right,
b, and bottom left, c) and
3 µm (top left, a, and bottom
right, d). Reprinted by permission of West et
al.17
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Immersion Effects
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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 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
28
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.
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Negative-Pressure Effects
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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.
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Neurogenic Pulmonary Edema
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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.
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HAPE
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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 HAPE-resistant
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 that is produced in
HAPE patients is the high-permeability type, with large concentrations
of primarily alveolar macrophages and high-molecular-weight
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.
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Peak Exercise and Pulmonary Edema
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There have been several published case reports46
47
48
49
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
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Pulmonary Barotrauma
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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.
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Conclusion
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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. Blood-gas 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 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.
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Acknowledgements
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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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Footnotes
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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
Received for publication August 24, 1999.
Accepted for publication March 27, 2001.
|
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Abstract
Introduction
