Murray and Nadel's Textbook of Respiratory Medicine

78 DIVING MEDICINE
ALFRED A. BOVE, MD, PhD • TOM S. NEUMAN, MD
INTRODUCTION PRESSURE EFFECTS: BOYLE’S LAW MEDICAL QUALIFICATIONS FOR

Increased Pressure Relation of Gas Volume to Depth DIVING
Water Immersion Barotrauma Exercise Requirements
Thermal Exposure DISSOLVED INERT GAS EFFECTS: Disorders Causing Sudden
Energy Needs for Diving HENRY’S LAW Unconsciousness
EQUIPMENT Inert Gas Kinetics Pulmonary Disorders
Open-Circuit Scuba Inert Gas Supersaturation in Tissues Cardiac Disorders
Closed-Circuit Rebreather Scuba Decompression Sickness DROWNING
Surface-Supplied Equipment INERT GAS NARCOSIS Pathophysiology
DISORDERS RELATED TO DIVING: OXYGEN TOXICITY Clinical Presentation
NOMENCLATURE Treatment
Prognosis
INTRODUCTION increases transdiaphragmatic pressure, and increases

venous return.2,3 The magnitude of the increase in intra-
Diving and work in compressed air have produced occupa- thoracic blood volume during immersion with the head
tional exposure to hazardous environments for over 100 above water has been estimated to be 700 mL.2 The central
years. In the past 60 years, diving has become a recreation blood shifts result in an increase in cardiac output2 and an
for millions of individuals throughout the world. Any physi- increase in central venous pressure. The increase in intra-
cian may encounter a recreational diver for an illness thoracic blood volume causes a diuresis because of release
related to a diving exposure or for medical clearance for of natriuretic hormones and suppression of antidiuretic
diving. Occasionally a physician may be confronted with an hormone.
acute medical emergency related to diving exposure, such
as decompression sickness, arterial gas embolism, or drown- THERMAL EXPOSURE
ing. This chapter provides a basis for initiating treatment,
seeking consultation, or furthering education in this inter- Most diving takes place in water colder than skin tempera-
esting area of environmental medicine. ture, and the diver loses heat throughout the dive. Hypo-
thermia happens rapidly in the absence of protective
garments even in relatively warm water (e.g., 22° to 23° C).
INCREASED PRESSURE
Cold stress evokes thermogenic responses, reflected by a rise
Underwater exposure results in increasing pressure directly 2 ) upon exposure to cold water
in oxygen consumption ( Vo
proportional to depth (Table 78-1). There is also exposure to generate additional body heat and minimize core tem-
to pressure in hyperbaric chambers, pressurized tunnels perature change. Cold water diving also leads to peripheral
and caissons used for underwater construction, and under- vasoconstriction; the magnitude of the vasoconstriction is
water habitats. As depth increases, the diver breathes gas of dependent on body core temperature, which, in turn, is
increased density using breathing equipment that provides affected by the amount of thermal protection and the water
oxygen and allows for elimination of carbon dioxide. temperature. Heat loss is inhibited in divers doing moderate
Increased depth and pressure also lead to decreases in gas work in water above 30° C, and, in this situation, hyperther-
volume and an increased amount of gas dissolved in body mia can develop.
tissues. The terms atmosphere (ATM) and atmosphere abso-
lute (ATA) both refer to pressure; ATM, however, can be ENERGY NEEDS FOR DIVING
used as a relative term (33 feet of water depth is equivalent
to 1 ATM of water), whereas ATA is always used for abso- A scuba (self-contained underwater breathing apparatus) diver
lute pressure (33 feet of water depth is equivalent to 2 ATA). swimming underwater at a speed of 1.0 knot (about 100
ATA is the term used in this chapter and is always used for feet/min or 1.15 miles per hour or 1.85 km per mile) con-
equations, such as Boyle’s law. sumes about 25 mL of oxygen per kilogram per minute (Fig.
78-1).4,5 A diver with a maximum Vo 2 of 40 mL/kg per
minute would tolerate swimming at 1.3 knots for a few
WATER IMMERSION
minutes but would become extremely tachypneic to com-
Intrathoracic blood volume increases with water immer- pensate for lactate production. For a diver with a maximum
sion.1 Increased hydrostatic pressure during immersion 2 of 40 mL/kg per minute, sustainable swimming speed,
Vo
prevents blood from pooling in the peripheral veins, working at 50% of maximum capacity, would be about
1385
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1386 PART 3 • Clinical Respiratory Medicine
Table 78-1 Pressure Equivalents for Altitude and Depth OPEN-CIRCUIT SCUBA CLOSED-CIRCUIT REBREATHER
Feet ATA mm Hg psi Second-stage

Altitude above sea level 12,000 0.636 483 9.3 regulator
8000 0.742 564 10.9 First-stage
4000 0.863 656 12.7 regulator Breathing
bag
Sea level 0 1 760 14.7
Depth in seawater 33 2 1520 29.4
66 3 2280 44.1
99 4 3040 58.8
132 5 3800 73.5
Air CO2 O2
ATA, atmosphere absolute; psi, pounds per square inch. scrubber
40 20
O2 consumption (mL/kg/min)
35 Oxygen cons
Energy need (METS)

Figure 78-2 Two types of self-contained diving systems. The open-
30 METS 15 circuit scuba is the system commonly used for recreational diving. Air is
25 exhaled into the surrounding water. Rebreather systems allow exhaled
breathing gas to be recycled through a carbon dioxide scrubber, mixed
20 10 with additional breathing gas, and returned to the diver through a breath-
15 ing bag. Breathing gas is replenished via a demand valve. This system can
10 5 be used with 100% oxygen or oxygen-enriched air mixtures. Other forms
of rebreather systems contain separate oxygen and inert gas supplies, and
5 mixing is controlled with a small computer to maintain a constant oxygen
0 0 partial pressure.
0.4 0.6 0.8 1.0 1.2 1.4 1.6
Speed (knots)
supply would last 105 minutes at the surface but only 35
minutes at 66 feet of seawater. Open-circuit scuba is usually
Figure 78-1 Oxygen consumption and metabolic equivalents (METS)
are shown for underwater swimming. The speed is shown in knots; one
limited to depths above 200 feet because of limited air
knot is one nautical mile per hour. One knot = 100 feet per min = 1.15 miles supply, nitrogen narcosis, and oxygen toxicity.
per hr = 1.85 km per hr. (Data from Navy Department: U.S. Navy diving
manual, vol 1, rev 3: Air diving. Publication No. NAVSEA 0994-LP-001–9110.
Washington, DC, 1996, U.S. Navy Department.) CLOSED-CIRCUIT REBREATHER SCUBA
The self-contained rebreather uses a carbon dioxide absor-
bent to remove exhaled carbon dioxide and replenishes only
0.9 knots or 90 feet/min, whereas the diver with a maxi the oxygen used. Inert gas is conserved by recycling the
mum Vo 2 of 25 mL/kg per minute would be able to sustain exhaled gas through the carbon dioxide absorbent and then
a swimming speed of only approximately 0.55 knots or adding oxygen before the gas is rebreathed (see Fig. 78-2).
55 feet/min. Safety considerations suggest that the sport Little gas is released into the surrounding water, oxygen
diver should be able to tolerate a sustained workload of can be carried in volumes adequate for several hours of
about 20 mL/kg per minute (50% of maximum).4,5 Poorly exposure, and gas consumption is independent of depth.
conditioned divers can experience severe dyspnea under Although use of closed-circuit scuba in the past was con-
even mildly stressful conditions that exceed their anaerobic fined to commercial and military divers, such systems now
threshold. are becoming popular among recreational divers.
SURFACE-SUPPLIED EQUIPMENT
EQUIPMENT Commercial diving often employs this form of equipment.
The diver breathes compressed air or other gas mixtures
OPEN-CIRCUIT SCUBA
pumped from the surface to the helmet. The diving helmet
The most commonly used breathing equipment in diving is is attached at the collar to a diving suit so that air flows from
the open-circuit scuba. This equipment (Fig. 78-2) consists the helmet into the suit to maintain an air layer for thermal
of a metal cylinder containing compressed air connected to protection. Modern systems contain a demand mask built
a pressure regulator that lowers pressure to ambient pres- into the helmet.
sure. This device delivers ambient-pressure air only when
inhalation is initiated and allows flow that matches the
minute volume of the diver. Expired air is released directly
into the surrounding water. A typical scuba cylinder can DISORDERS RELATED TO DIVING:
supply approximately 2100 L of air at the surface (1 ATA). NOMENCLATURE
This volume is reduced in direct proportion to ambient pres-
sure. For example, at a depth of 66 feet of seawater or 3 Golding and coworkers6 described disorders related to
ATA pressure, the effective volume of air is decreased to supersaturation of inert gases in tissues with subsequent
700 L. With a minute ventilation of 20 L/min, this air bubble formation as decompression sickness (DCS). They
78 • Diving Medicine 1387
described a systemic form of DCS that involves the central

nervous system, the lungs, and the circulation (“serious,”
type II) and a nonsystemic (peripheral) form that involves
the skin, bones, and joints (“minor,” type I). Arterial gas
embolism is named separately based on its relationship to
pulmonary barotrauma. Francis and Smith7 suggested the
term decompression illness for these two disorders because
they can be clinically difficult to separate and require similar
therapy.
PRESSURE EFFECTS: BOYLE’S LAW

RELATION OF GAS VOLUME TO DEPTH
Boyle’s law states that, if the temperature of a fixed mass
of an ideal gas is kept constant, volume and pressure
are inversely related. Consequently, when the pressure is
doubled, the volume is reduced to one half of the original
volume. Because the gas volume is proportional to the abso-
lute pressure, the volume change from the surface to 33 feet
Figure 78-3 Chest radiograph from a diver who experienced near
of seawater (from 1 to 2 ATA) is greater than the change drowning. The diffuse pulmonary edema pattern is suggestive of water
from 33 to 66 feet (from 2 to 3 ATA). aspiration.
BAROTRAUMA
With increased pressure, volume in the lungs, middle ear, Pulmonary barotrauma can be seen in divers who would
paranasal sinuses, and gastrointestinal tract are reduced. not be considered at risk for lung overpressure. Occult lung
Displacement of tissues into the diminishing volume of disease may contribute to unexplained barotrauma and
these spaces may cause tissue injury and dysfunction of the cerebral air embolism.12 Epidemiologic studies have not
organ involved. Barotrauma can affect a paranasal sinus demonstrated a significant relationship between asthma
with an occluded orifice, a residual air pocket left between and an increased risk for pulmonary barotrauma.13
a tooth filling and the base of the tooth, or the air space
within a diving mask. Clinical Manifestations of Arterial Gas Embolism.
The brain is commonly involved. Within minutes of surfac-
Pulmonary Barotrauma and Arterial ing, the diver can experience loss of consciousness, hemi-
Gas Embolism plegia, stupor, and confusion. Seizures, vertigo, visual
The gas a diver breathes is pressurized to the ambient pres- disturbances, sensory changes, headache, and circulatory
sure so that pressure gradients from the breathing supply collapse are common. Most individuals fully recover if they
to the airways are not altered as the diver descends. Behnke8 are promptly recompressed.14
and Polak and Adams9 described lung barotrauma in When they lose consciousness in the water, victims of
ascending divers due to inadequate exhalation during arterial gas embolism frequently drown. Chest radiographs
ascent and overexpansion of the lungs. Later studies pro- (Fig.78-3) may show a diffuse lung edema pattern. About
vided further insight into mechanisms and prevention of 5% of patients immediately develop apnea, unconscious-
pulmonary barotrauma.10 After breathing compressed air, ness, and cardiac arrest. This catastrophic course results
persons who ascend to the surface from depths as shallow from filling of the heart and great vessels with air. Many of
as 4 feet can experience pulmonary barotrauma. these individuals are unresponsive to cardiopulmonary
resuscitation and advanced life support measures.15 A
Pathophysiology. Under experimental conditions, trans- report of 31 patients with cerebral air embolism from diving
pulmonary pressures (i.e., the difference between intratra- included the following findings: 25% demonstrated pneu-
cheal and intrapleural pressures) of 95 to 110 cm H2O are momediastinum; 10%, subcutaneous emphysema; 6%,
sufficient to disrupt the pulmonary parenchyma and force pneumocardium; 3%, pneumoperitoneum; and 3%, pneu-
gas into the interstitium.10 Extra-alveolar gas will migrate mothorax. Fifty-two percent had pulmonary opacities indi-
through perivascular sheaths to cause mediastinal emphy- cating associated drowning.16
sema and pneumothorax.10 Gas can also dissect into the Mediastinal emphysema is generally associated with mild
retroperitoneum and into the subcutaneous tissues of the substernal pain that may be exacerbated by inspiration,
neck. Extra-alveolar gas can pass into ruptured blood coughing, or swallowing. Unless massive, this condition is
vessels, travel to the left side of the heart, and enter the not usually associated with circulatory compromise. On
arterial circulation as gaseous emboli. The dissemination of physical examination a crunching sound synchronous
gas bubbles throughout the arterial circulation causes with cardiac action may be auscultated (the Hamman sign).
injury to other organ systems and to skeletal muscle, which The chest radiograph confirms the diagnosis. No treatment
is evident by a rise in serum creatine kinase level.11 is usually necessary.
Subcutaneous emphysema causes swelling and crepitus gradient between the inner ear perilymph and the middle
in the base of the neck and supraclavicular fossa, sore ear. The round or oval window can rupture, and perilymph
throat, hoarseness, and dysphagia. Radiographs may be can then leak from the inner ear to the middle ear.
helpful in detecting subtle cases, but computed tomography Symptoms include vertigo, nausea, vomiting, tinnitus,
(CT) scans are more sensitive and can be useful to confirm and loss of hearing on the affected side. Severity may vary,
the diagnosis of barotrauma in doubtful cases. Extra- and some divers complain of hearing loss, tinnitus, or
alveolar gas that ruptures into the pleural space will cause vertigo only after diving.
a pneumothorax. Laboratory evaluation may show an ele- Treatment varies from conservative therapy to surgical
vated hematocrit level and elevation of several serum repair of the round or oval window. Vertigo and nausea can
enzyme levels.17 Treatment for arterial gas embolism be treated with benzodiazepine medications. Tinnitus and
requires recompression in a hyperbaric chamber (see later). reduced hearing may become chronic, particularly if no
treatment is provided. Divers who exhibit clinical evidence
Middle Ear Barotrauma of inner ear barotrauma with intact round and oval
Middle ear barotrauma is the most common diving-related windows may have a pressure injury to the organ of Corti
disorder encountered in divers.18 The middle ear undergoes and the vestibular system.21
barotrauma when the eustachian tube is blocked during Inner ear DCS may be seen within 2 hours of surfacing
descent and the middle ear space cannot equilibrate with and may include vertigo and hearing loss.22 The mecha-
the increasing ambient pressure. The tympanic membrane nism is poorly understood but may involve formation of
is displaced inward and may rupture. The middle ear may bubbles in the inner ear or embolism of systemic bubbles.
fill with blood from engorged mucous membranes. Infection Divers with inner ear DCS have been reported to have a
and hearing loss are complications. Symptoms during higher prevalence of patent foramen ovale (PFO), a condition
descent include pain in the affected ear that increases with that increases risk for right to left shunts of air bubbles
depth. Relief of pain without proper equalization of the and thus of decompression events; such an association sug-
middle ear pressure usually indicates that the tympanic gests that the inner ear DCS may also result from air
membrane has ruptured. Cold water entering the middle emboli.23,24 The proper therapy for inner ear DCS is hyper-
ear when the tympanic membrane ruptures may cause baric recompression.
vertigo because of unilateral vestibular stimulation. Late
complications include bacterial otitis media, serous otitis Sinus Barotrauma
media, and chronic tympanic membrane perforation.18 In When a sinus orifice is occluded, pressure within the sinus
rare cases of middle ear barotrauma, the facial nerve is becomes negative with respect to ambient pressure, and
injured by the increased pressure and a temporary facial mucosal blood vessels become engorged and eventually
paralysis results.19 A modified Valsalva maneuver is com- rupture. Pain over the affected sinus during descent and
monly used to equilibrate middle ear pressure. Because epistaxis on ascent are usual symptoms. Headache follow-
middle ear barotrauma causes edema and hemorrhage in ing a dive may indicate sphenoid sinus barotrauma. Treat-
the middle ear, equalization is usually impossible to achieve ment includes decongestants and maneuvers to drain the
until healing is complete. The presence of middle ear baro- affected sinus. Persistence of blood in the sinus may result
trauma usually prohibits diving until it is resolved. in bacterial sinusitis. Prevention is accomplished by avoid-
ing diving with congestion of the nasopharynx and prudent
Alternobaric Vertigo. Vertigo may develop on ascent use of decongestants. If a maxillary sinus orifice is occluded,
when the reduction of middle ear pressure is not uniform the maxillary branch of the trigeminal nerve may be com-
in both ears. The pressure imbalance causes differential pressed during ascent and result in infraorbital paresthesias
stimulation of the labyrinths, resulting in what is called that usually resolve in 2 to 3 hours.25
alternobaric vertigo. The sensation of vertigo may persist for
1 to 2 hours after diving and gradually disappears without Less Common Forms of Barotrauma
therapy. Symptoms are similar to labyrinthitis and can Facial barotrauma (mask squeeze) happens in the area of
include nausea, vomiting, and generalized malaise. Some distribution of the diving mask. Facial edema, ecchymoses,
subjects may be particularly susceptible to alternobaric and conjunctival hemorrhages can be noted after diving.
vertigo if they have had previous injury or infection of the Retro-orbital hematoma and diplopia have been described
labyrinths. In susceptible individuals, use of moderate doses as complications.26,27 The disorder is self-limiting; no treat-
of antihistamines or decongestants may prevent symptoms. ment is needed.
The disorder must be differentiated from vestibular DCS, Tooth barotrauma leading to severe toothache results
which is usually associated with deeper, prolonged diving. when air pockets under fillings or in areas of decay become
compressed on descent. Careful dental work prevents this
Inner Ear Barotrauma disorder.28
Inner ear barotrauma may develop on descent in divers Gastrointestinal barotrauma results when air enters
who perform a forceful Valsalva maneuver to equalize the stomach during diving due to faulty breathing appara-
middle ear pressure. When the eustachian tube is blocked, tus or by air swallowing. On ascent the expanding air will
middle ear pressure becomes progressively more negative distend the stomach or intestine. Gastric distention can
relative to ambient pressure.18,20 When a Valsalva maneu- occlude the esophageal-gastric junction and prevent eruc-
ver is then performed, intrathoracic pressure, central tation. Distention of the stomach may cause stomach
venous pressure, spinal fluid pressure, and inner ear pres- rupture and pneumoperitoneum.29 The diver experiences
sure rise above ambient pressure, thereby increasing the abdominal pain, which increases during ascent. Treatment
Table 78-2 Characteristics of Inert Gases* of supersaturation becomes excessive, dissolved gas will
leave solution and form free gas. Recent studies suggest that
Molecular Lipid Water Narcotic blood microparticles may act as a nidus for bubble forma-
Gas Weight Solubility† Solubility Potential‡
tion in blood.33
Helium 4 0.015 0.009 0.23
Neon 20 0.019 0.009 0.28
DECOMPRESSION SICKNESS
Hydrogen 2 0.036 0.018 0.55
Nitrogen 28 0.067 0.013 1.00 Excess supersaturation causes dissolved gases to change
Argon 40 0.140 0.026 2.32 phase to the gaseous form.34 Expansion of gases in blood
and tissues on ascent results in damage and dysfunction of
*Solubility of the various gases in lipid is related to their narcotic potential. tissues and organs and venous gas embolism to the lungs.
Helium is the least, and argon the most, narcotic gas in the list. DCS is the disorder caused by damage to organs and tissues
†
Expressed as gas volume/solute volume at 1 bar.
‡
Values relative to nitrogen. as a result of free gas production.
Adapted from Bennett PB: Inert gas narcosis and HPNS. In Bove AA, editor: Bert35 first described the pathophysiology of DCS. Subse-
Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004, WB Saunders, pp quent investigators in the early twentieth century con-
225–240. cluded from autopsies on divers and caisson workers that
DCS is caused by free gas in blood and tissues.36 Based on
free gas volume and location, they were able to explain the
requires surgical repair of the ruptured viscus. Divers variety and severity of the symptoms. Paralysis resulted
with previous gastric surgery may be prone to gastric air from free gas in the spinal cord, cerebral dysfunction was
trapping.30 thought to result from free gas in the brain, and dyspnea
was associated with free gas in the pulmonary circulation.
Muscle and joint pain may be due to free gas in ligaments,
fascia, periosteum, marrow, or nerve sheaths.
DISSOLVED INERT GAS EFFECTS: Hallenbeck and colleagues37 described effects of free gas
in blood and tissues that were not caused by mechanical
HENRY’S LAW obstruction. Subsequent studies identified clotting and
platelet activation, intravascular coagulation, plasma
INERT GAS KINETICS leakage from the intravascular space, hemoconcentration,
Gases dissolve in tissues, fats, and water according to and hypovolemia as manifestations of surface effects of the
Henry’s law: Q = c • P, where c, a solubility coefficient, and bubbles.38 Venous gas emboli are commonly present before
P, the partial pressure of the gas, determine the quantity (Q) overt symptoms of DCS appear.39 Free gas and tissue injury
of dissolved inert gas. Increased ambient pressure increases result in activation of the inflammatory cascade.40 The
dissolved gas concentration in the tissues. The partial pres- inflammatory response causes fluid to leak into the intersti-
sure of the gas and the solubility of the gas in the specific tial tissues of the systemic and pulmonary vascular beds.41
tissue (Table 78-2) determine dissolved gas content.
Although Henry’s law determines the amount of gas in the Factors Affecting Risk for
tissue, there is a finite time required for equilibrium to be Decompression Sickness
achieved. Factors that affect the rate of entry include blood The use of ultrasonography for intravascular bubble detec-
flow and the rate of diffusion of gases into the tissue. Tissue tion has provided insight into the presence of bubbles fol-
gas concentration follows an asymptotic curve in which the lowing diving.42 Many divers demonstrate venous gas emboli
tissue gas concentration approaches the maximum concen- but no manifestations of DCS. The concept of a threshold
tration for the given pressure after time has elapsed. Similar or dose-response effect has been postulated, wherein a
kinetics control the washout of inert gas from tissues when certain volume of free gas is needed to produce the clinical
ambient pressure is reduced. Different body compartments disorder and lesser amounts are asymptomatic.43 Venous
have different gas exchange characteristics.31 bubbles in asymptomatic divers and aviators are associated
Because most diving is of short duration (i.e., minutes to with increased risk for developing DCS after diving or alti-
hours) and shallow (i.e., in depths shallower than 200 feet), tude exposure.44,45 Exercise and temperature during decom-
only a few tissue compartments reach equilibrium based on pression are considered to be risk factors for DCS. Breath-hold
Henry’s law. Divers can return to the surface from these divers can develop DCS from frequent repetitive dives.45a
short-duration dives by following a schedule of ascent based Symptoms can be prevented by keeping the degree of
on depth and time.31 When diving exposure is long enough, supersaturation below a certain level.46 The concept of a
all tissues reach equilibrium at the new ambient pressure critical pressure ratio is the basis for most decompression
and are fully saturated with inert gas. Divers can spend tables used to prevent DCS. The body can be considered as
prolonged periods (weeks) under pressure, with all tissues a set of tissue compartments with different rates of gas
saturated at the increased pressure, without serious physi- uptake and elimination.46 Although these tissues do not
ologic changes.32 represent discrete anatomic structures, they provide a con-
venient means for understanding the kinetics of inert gas
exchange. In most decompression schedules, stops during
INERT GAS SUPERSATURATION IN TISSUES
ascent are selected to avoid excess supersaturation in tissues
When the diver ascends after breathing pressurized gas, with specific gas-exchange rates (Fig. 78-4). Decompression
tissues become supersaturated with gas. When the degree procedures are well defined for air and other mixtures of
75 Table 78-3 Frequency of Decompression Sickness (DCS)

Symptoms in 100 Cases
60 Symptom Percentage of All DCS Symptoms
Skin itch 4
Pressure (psi)
45 Headache 11
Fatigue/malaise 13
Bone/joint pain 54
30 Spinal/back pain 11
Spinal/neurologic 22
15 Respiratory 21
Adapted from Navy Department: U.S. Navy diving manual, Vol 5, Rev 6:
Diving medicine and recompression chamber operations (NAVSEA
0910-LP-106-0957), Washington DC, 2011. http://www.supsalv.org/
10 20 30 40 00c3_publications.asp.
Time (minutes)
Figure 78-4 Theoretical nitrogen gas concentrations are expressed in
units of pressure for an exposure of 75 psi (5.1 ATA) following the Age. A 10-year study by the U.S. Air Force on flight expo-
depth-time profile indicated by the heavy line. Curves are shown for five
theoretical tissue compartments with different rates of gas exchange. Gas sures ranging from 1500 to 30,000 feet shows a threefold
concentrations increase to different levels in the different tissue compart- increase in susceptibility to altitude DCS in aviators 42
ments during exposure to pressure. When pressure is reduced, gas con- years of age and older compared with those 18 to 21 years
centrations in the different tissue compartments fall at different rates. of age.55 Carturan and colleagues56 found a correlation
Stops during return to baseline allow tissue concentration to fall to a safe
level of supersaturation before reducing pressure further. (Data from
between bubble formation, increased age, and decreased
Boycott AE, Damant GCC, Haldane J: The prevention of compressed air illness. physical condition in sport divers. Klingmann and cowork-
J Hyg [Cambridge] 8:342–443, 1908.) ers57 reported an increased incidence of DCS in novice
divers compared to more experienced divers. Blatteau and
associates58 reported that age and depth of dive exposure
increased DCS risk.
nitrogen and oxygen; helium and oxygen; nitrogen, helium,
and oxygen (trimix); hydrogen and oxygen; and a few rare Relation to Altitude. Exposure to altitudes above 18,000
earth gases such as argon and neon. feet (0.5 ATA) may result in free gas formation in tissues
because of supersaturation of inert gases dissolved at atmo-
Patent Foramen Ovale. Moon and coworkers47 reported spheric pressure.59 Divers can develop free gas in tissues
30 patients with a history of DCS who were studied with when going to higher altitude after diving even though they
echocardiography for identification of a PFO. Sixty-one follow established protocols for ascent from depth to the
percent of 18 patients with serious DCS had shunting, surface. It is common for sport divers to fly in commercial
whereas a 25% prevalence was seen in normal volunteers. aircraft (about 8000 feet equivalent altitude) shortly after
Wilmshurst and associates48 identified a single patient with diving.
paradoxical gas embolism through an atrial septal defect
and suggested that the atrial septal defect augmented Clinical Manifestations
symptoms of DCS. Moon and coworkers49 evaluated 90 Compared to sport and military divers, commercial divers
divers with previous DCS who were studied using echocar- have the highest incidence of DCS. Musculoskeletal DCS
diography to detect right-to-left shunting through a PFO. (type I) is the most common form. The incidence of DCS is
Fifty-nine of 90 had experienced serious decompression about 1 in 5000 dives for the sport diver. 60,61
symptoms, whereas 31 had experienced pain only or mild DCS can mimic a variety of other disorders (Table 78-3).
symptoms. Free gas entering the venous system will cause varying
In the presence of a PFO, cerebral gas embolism can be degrees of pulmonary vascular obstruction. A classic syn-
caused by venous bubbles transiting a PFO.50 Germonpré drome (“chokes”) manifested by chest pain, dyspnea, and
and associates51 found that divers with cerebral DCS have a cough is described.62 DCS is often associated with free gas
high incidence of large PFO compared to control subjects. in the blood and tissue injury that activates an inflamma-
Billinger and colleagues52 demonstrated an increase in tory process, with damage to vascular endothelium, micro-
magnetic resonance imaging–detected brain objects in vascular occlusion, and focal regions of tissue ischemia.63
divers with a PFO. Honek and colleagues52a demonstrated A common manifestation of DCS in divers is spinal cord
that a large PFO could increase risk of DCS in divers with dysfunction, usually at levels below the diaphragm.64
exposures that resulted in significant venous gas emboli. Symptoms include paresthesias, muscle weakness, paraly-
The presence of a PFO may be associated with a twofold to sis of the lower extremities, bowel or bladder incontinence,
fourfold increase in the risk for DCS.53 The high prevalence urinary retention, and sexual impotence.65 A sudden ascent
of PFO in the population and the very low incidence of DCS from deep depth (blowup) can cause a massive DCS syn-
suggest that a PFO can play only a minor role in the patho- drome with both cerebral and spinal neurologic symptoms,
physiology of DCS. There is no current need to close a PFO unconsciousness, hypovolemic shock, pulmonary edema,
as a prophylactic measure.54 and a high mortality rate. A rare but important symptom
of serious (type II) DCS is sudden acute neurologic hearing assessment, should be obtained before treatment when pos-
loss and vestibular dysfunction. DCS of this type usually sible. Therapy is provided in a hyperbaric chamber by a
follows deep, prolonged diving exposures and, if untreated, trained medical team. The usual practice is to follow the
can result in permanent deafness.66 standard protocols for pressure treatment outlined in the
The musculoskeletal form of DCS is manifested by pain U.S. Navy Diving Manual,5 which involves a pressure expo-
in the extremities and joints.67,68 Symptoms of local joint sure equivalent to a 60-foot depth in seawater (60 fsw)
pain are often confused with pain from injuries, and the using intermittent oxygen therapy.
diagnosis of DCS may be missed. In some populations a high Most practitioners use a hyperbaric treatment protocol
incidence of osteonecrosis is found in divers who have expe- lasting about 6 hours (see Table 6 in U.S. Navy Diving
rienced musculoskeletal DCS in the distant past or who have Manual5) for treatment of types I and II DCS. Recompression
experienced deep, prolonged exposures in caisson work,68 as therapy for cutis marmorata resulting from DCS
well as in diving instructors69 and workers in commercial has been recommended by some, but most cases resolve
diving operations. An erythematous or purpuric skin rash spontaneously. Itching and erythema of the skin may also
(cutis marmorata) may also be a manifestation of DCS. A be noted following hyperbaric chamber exposures, but
systematic method for diagnosing DCS is described by these skin findings alone do not require recompression
Grover and coworkers.70 therapy.
When a diver ascends from extreme depths with signifi-
Diagnostic Testing cant missed decompression, the practitioner may choose to
Chest radiography can be used to diagnose pneumothorax, use recompression tables that pressurize the diver to a
pneumomediastinum associated with pulmonary overpres- “depth of relief,” to use alternate gas mixtures (i.e., helium
sure accidents, and the pulmonary abnormalities associ- and oxygen), or to hold the diver for over 24 hours at a
ated with aspiration or capillary leakage associated with single depth to stabilize the medical status (saturation treat-
chokes. Chest or abdomen CT can be used to diagnose pneu- ment).74 For surface-supplied air and scuba divers, the prin-
mothorax, pneumomediastinum, or pneumoperitoneum. cipal treatment gases are oxygen and air. For treatment
In most cases it is not necessary to postpone recompression depths greater than 60 fsw, enriched nitrogen-oxygen
treatment in order to obtain radiographic studies. If pneu- (nitrox) or helium-oxygen (heliox) may also be used.
mothorax is suspected, a chest radiograph can be helpful in Repeated hyperbaric oxygen treatments can be given,
making the decision to insert a chest tube. Neurologic and although end points for repetitive therapy are not well
psychological testing may be useful in determining response defined. Treatments can be administered until no further
to treatment when brain injury is present. Electronystag- change of symptoms is found or for a fixed number of expo-
mography and audiography may be useful in distinguishing sures (e.g., five). Controlled trials to determine efficacy of
inner ear DCS from inner ear barotrauma. Inner ear DCS repetitive treatments are not available. Treatment of arte-
requires recompression, whereas inner ear barotrauma is rial gas embolism follows similar protocols. Recompression
managed with bed rest, avoidance of straining, and possibly to 60 fsw and oxygen therapy are usually successful.76
surgical intervention. The circumstances causing the two Recompression to 165 fsw depth equivalent (6 ATA) is rec-
syndromes are distinct (see earlier) and are helpful in the ommended if symptoms persist after recompression to
differential diagnosis. Central nervous system injury can be 60 fsw.5
diagnosed by magnetic resonance imaging and correlated
with clinical findings.71,72 Magnetic resonance images of Supplemental Oxygen and Fluids. Early administration
the brain in divers with no history of decompression-related of 100% oxygen on the surface is thought to be beneficial
disorders are also found to be abnormal in some studies.73 for treating both DCS and arterial gas embolism.77 Intrave-
nous fluid administration also may be a useful initial treat-
Treatment ment. Central nervous system injury may be exacerbated
The clinical manifestations of arterial gas embolism and by hyperglycemia, and glucose-containing intravenous
DCS often overlap. The initial treatment of DCS and arterial solutions should be administered cautiously. Measurements
gas embolism should always be a return to pressure by of hematocrit and urine specific gravity are useful to guide
recompression in a hyperbaric chamber and administration fluid replacement therapy.
of oxygen at increased ambient pressure.74,75 Fluid replace-
ment and antiplatelet agents are also a part of the initial Emergency Treatment
treatment. Once stabilized with pressure and oxygen, the Because divers may be injured in areas remote from medical
patient must be decompressed slowly to permit the inert gas care, treatment measures should be instituted during transit
to be carried away from tissues by the circulatory system to a hyperbaric chamber facility. Emergency treatment
and then to be exhaled by the lungs. With early treatment, should include 100% oxygen by mask, aspirin 325 to
DCS and air embolism generally have an excellent prognosis 975 mg by mouth, and Ringer lactate (or normal saline)
for recovery. When treatment is delayed or when the injury intravenously. One study of oxygen, aspirin, intravenous
is severe, there may be permanent injury to the brain or fluids, and hydrocortisone 1 to 2 g intravenously during
spinal cord. transit to a hyperbaric chamber found that two thirds of the
cases had a favorable outcome78; however, it remains
Hyperbaric Therapy. Treatment of DCS and arterial gas unproven whether emergency treatment alters long-term
embolism should be instituted with recompression as soon outcome. A favorable response to urgent care should not
as possible after the injury.75a A history and physical evalu- prolong transfer to the closest facility capable of providing
ation, including a neurologic examination and cognitive recompression therapy.
risk for drowning and may compromise the safety of others

INERT GAS NARCOSIS who attempt a rescue. A diving candidate with a history of
a seizure disorder should be seizure-free without antiseizure
Inert gas narcosis (nitrogen narcosis) results from breath- medications for 4 years before being considered for diving.82
ing air at depths greater than 100 fsw.79 Symptoms include Insulin-dependent diabetes mellitus is considered a contra-
loss of fine motor control and high-order mental skills, indication to commercial and military diving because of the
inappropriate response to emotional stress, hostility, and risk for hypoglycemia. Special training has allowed safe
unconsciousness. Symptoms increase with increasing diving for insulin-dependent sport divers.83
depth below 100 feet. At 300 to 400 fsw, unconsciousness
may result from the anesthetic effect of nitrogen at this PULMONARY DISORDERS
pressure. Fatigue, heavy work, and hypothermia can
augment the narcotic effect of nitrogen. Symptoms disap- Asthma has been a subject of controversy in diving because
pear immediately on ascending to a shallow depth. Often of possible air trapping and pulmonary overinflation during
there is amnesia for the events.79 Narcotic potential varies ascent. Increased risk for pulmonary barotrauma has not
among the inert gases (see Table 78-2). been supported by clinical observation.84 Criteria for safe
diving by patients with a history of asthma include evi-
dence that midexpiratory flow is not reduced after exercise
OXYGEN TOXICITY by greater than 50%. A more detailed discussion of issues
related to asthma and diving has been published.85 Clinical
Oxygen toxicity in divers primarily affects the central and operational experience suggests that patients with a
nervous system.80 Pulmonary oxygen toxicity is rare in history of spontaneous pneumothorax or those with bullae
diving but may be of some concern in prolonged hyperbaric or cysts may be at risk for a tension pneumothorax during
oxygen treatments. Acute toxicity to the brain usually diving. Treatment requires immediate decompression of the
results when oxygen partial pressure exceeds 1.4 ATA. pleural space through an intercostal needle or chest tube
Higher partial pressures can be tolerated for brief periods. and may be difficult at remote diving sites.
The affected diver may experience auditory or visual hal-
lucinations and commonly suffers a grand mal seizure. CARDIAC DISORDERS
When underwater, a seizure can lead to drowning. For
example, a 32% oxygen mixture will expose a diver to 1.4 Patients with coronary disease may develop angina pecto-
ATA of oxygen partial pressure at 111 fsw. Divers have been ris, myocardial infarction, or sudden death while diving.
known to develop seizures when using this breathing gas at The highest incidence of diving-related death from cardio-
depths greater than this. vascular disease in divers is in the age range from 60 to
70 years.86 Of 33 cases of sudden death while diving
reported by the Divers Alert Network, 31 were attributed to
MEDICAL QUALIFICATIONS coronary disease, 1 was related to a stroke, and 1 was
FOR DIVING related to aortic stenosis.87 Screening of diving candidates
for coronary disease is particularly important in the sport
Military divers have the most stringent requirements, diving community, where candidates at increased risk for
whereas recreational divers have the most relaxed require- coronary disease due to age and chronic illness may present
ments. Commercial divers, caisson and tunnel workers, and for training.
hyperbaric chamber workers all have unique standards. Diving candidates with atrial septal defects risk paradoxi-
Disorders that limit cardiovascular or pulmonary function cal embolism of gas bubbles that form in the venous circula-
during exercise, physical deconditioning, metabolic disor- tion during decompression.75 The presence of an atrial
ders that limit exercise capacity, and certain physical handi- septal defect is considered to be a contraindication to diving.
caps can compromise diving safety. Compared to an atrial septal defect, a PFO appears to have a
minor role in DCS, and prophylactic closure is not advised.
A ventricular septal defect does not appear to produce a risk
EXERCISE REQUIREMENTS
for paradoxical embolization of bubbles. Patients with a
Workloads in diving vary based on the type of diving (see right-to-left shunt and arterial hypoxemia will normally
previous). A diver swimming underwater at a speed of 1.0 have severely limited exercise capacity and should not dive.
knot consumes about 25 mL of oxygen per kilogram per A detailed treatment of this topic can be found elsewhere.81
minute.81 Safety considerations suggest that divers should
tolerate a sustained workload of about 25 mL/kg/min to Diving-Induced Arrhythmias
ensure safety under adverse diving conditions. Divers who Reflex bradycardia from diving has been described by a
do not achieve this level of fitness should avoid exposures number of investigators88 and may be related to the response
that may require high levels of physical exertion. to facial immersion and cooling found in diving mammals89
as well as in humans. The autonomic adjustments to apneic
DISORDERS CAUSING SUDDEN diving in marine mammals appear to be an oxygen-
conserving reflex, but this effect does not appear to be sig-
UNCONSCIOUSNESS
nificant in humans. Drowning has been associated with the
Seizure disorders are considered to be a contraindication to familial-inherited long QT syndrome in swimmers,90 and
diving because a diver sustaining a seizure underwater is at the same risk is likely to apply to divers.
hyperosmotic fluid causes transudation of fluid into alveoli,

DROWNING and the aspiration of debris (sand, diatoms, algae, etc.)
causes a reactive exudate. As a result, alveoli become filled
Drowning is reported as the leading cause of death in the and are not ventilated. In freshwater aspiration, it is believed
approximately 100 to 150 scuba fatalities in the United surfactant is washed out of the lungs, causing areas of focal
States each year91,92; however, sudden cardiac death or arte- alveolar collapse, leading to areas of low ventilation-
rial gas embolism may be the precipitating factor or even perfusion ratio, and hypoxemia. These abnormalities persist
the cause of death in many of these accidents.93,94 Histori- until the lung damage resolves or until surfactant can be
cally the terms drowning and near drowning have been used regenerated.
to describe victims who either died or survived, respectively. Victims often swallow large amounts of fluid during the
It is simpler and preferable to use the term drowning for all drowning episode, so further decreases in ventilatory func-
individuals who suffer from submersion incidents.95 tion may result from gastric distention. Vomiting and aspi-
Intentional hyperventilation before breath-hold diving is ration of gastric contents may further complicate the
associated with drowning episodes. Hyperventilation drowning episode. Hypoxemia and decreased alveolar ven-
reduces the arterial PCO2, so the breath-hold breakpoint is tilation produce a number of consequences. Arterial PCO2
prolonged sufficiently for hypoxemia to develop before the quickly rises, and pH quickly falls. Metabolic acidosis can be
individual is forced to breathe. The hypoxemia in turn severe because the victim often struggles during the drown-
causes the individual to lose consciousness, and then ing episode. Finally, there may be cardiovascular collapse,
drown.96 This is termed “shallow water blackout.” Atrial resulting in cardiac arrest. If hypoxemia and decreased
and ventricular arrhythmias are known to happen during cardiac output persist long enough, anoxic cerebral damage
prolonged breath-holding experiments, but whether these can ensue.103,104 Although electrolyte disturbances are
arrhythmias play an important role in drowning incidents usually not a significant problem in drowning, the excep-
needs further study.97 tion to this situation appears to be drowning victims in the
Hypothermia leading to drowning has been reported fre- Dead Sea, where electrolyte concentrations are greater
quently; however, in diving fatalities this is unusual due to than those in normal seawater.103 The remaining specific
the almost universal use of thermal protection by divers. consequence of drowning is aspiration pneumonia. The
Hypothermia reduces a person’s ability to function until the pathogens and the clinical picture of pneumonia associated
point of unconsciousness or helplessness is reached.98 At with drowning have been reviewed extensively.104
that time, for someone at the surface, the head falls into the Because, in drowning, cardiac arrest is secondary to
water, resulting in drowning. Maximum breath-hold times hypoxemia, it may be delayed by a significant amount of
can drop dramatically in cold water, further compromising time. If the water in which the victim is immersed is cold
the ability to survive in rough water when intermittently enough, if the surface area–to-mass ratio of the victim is
submerged. In rare circumstances, hypothermia can have large enough, and if the victim swallows enough water,
a protective effect on the drowning victim (see later). Hypo- core temperature may decrease significantly; at low core
thermia is only one of many conditions that can precipitate temperatures the oxygen demands may be low enough
drowning by causing unconsciousness. In the case of scuba that victims can occasionally survive even prolonged
diving incidents, contamination of the diver’s air supply submersion.105
with carbon monoxide produces rapid unconsciousness,
and oxygen-induced seizures (see earlier) have been impli-
CLINICAL PRESENTATION
cated as the cause of death in divers using oxygen-enriched
air as a breathing mixture. The clinical presentation of drowning victims is highly vari-
able. The patient who is unconscious and reported to be
without vital signs at the site of the accident may be hemo-
PATHOPHYSIOLOGY
dynamically stable and neurologically intact in the emer-
Approximately 10% to 15% of drowning victims may not gency department, whereas the victim initially thought to
aspirate fluid during immersion.99 To account for the lack be hemodynamically stable at the scene might deteriorate
of aspiration in these individuals, it has been hypothesized significantly before arrival at the hospital.
that reflex laryngospasm persists until reflex ventilatory
activity ceases. However, review of early “dry” animal Cardiovascular System
studies does not support the dry drowning hypothesis for Victims of significant drowning may suffer cardiac arrest
fatal cases.100 It is much more likely that these cases actually and respond to on-scene resuscitative measures. Whether
represent arrhythmic deaths. In these cases, if ventilation this represents premature cardiopulmonary resuscitation
can be reestablished before injury secondary to hypoxemia or a response to therapy is not certain. However, it is also
happens, recovery is typically rapid and uneventful. not uncommon for a victim to be brought to the emergency
Unlike the victim without aspiration, the individual who department still requiring cardiopulmonary resuscitation.
aspirates remains hypoxemic, even after being removed If the patient “responds” to cardiopulmonary resuscitation
from the fluid medium and after ventilation is reestablished. at the scene of the rescue with a stable rhythm or if the
As a result, the period of hypoxemia is longer, and second- patient never suffers a cardiac arrest, supraventricular
ary damage to other organ systems is more likely.101,102 The tachycardias are commonly seen. If the patient presents
continuing hypoxemia is due to direct lung injury from the with a viable rhythm, it will most likely be supraventricular
aspirated fluid, which creates areas of low ventilation- tachycardia secondary to hypoxemia and acidosis.106
perfusion ratio. With saltwater aspiration, it is believed that Patients with underlying cardiac disease may have a
Table 78-4 Average Blood Gas Measurements in Hospitalized goal must be to establish a reliable airway and to supply as
Near Drowning Victims Breathing Room Air upon Admission high an inspired oxygen concentration as possible. Until the
results of arterial blood gas determinations are available,
PaCO2 PaO2 Base Excess
pH (mm Hg) (mm Hg) (mEq)
100% oxygen should be provided. Endotracheal intubation
is the preferred method for establishing an airway. This
Freshwater 7.26 38 66 −9 approach needs to take into account the possibility of a
Seawater 7.37 36 56 −5 concomitant unstable neck injury if there is associated
All 7.30 37 62 −7 trauma117 as well as the risk for the aspiration of gastric
contents. However, without signs or a history of trauma,
Adapted from Modell JH, Davis JH, Giammona ST, et al: Blood gas and
electrolyte changes in human near-drowning victims. JAMA 203:337–343,
the risk for an unstable cervical spine injury is low.118
1968. Patients with cardiac arrest due to drowning can have a
profound metabolic acidosis. The doses of bicarbonate
required to reverse such acidosis may be far larger than the
doses recommended for patients suffering cardiac arrest
primary cardiac arrest that may mimic a drowning from primary heart disease.119 If bicarbonate is to be given,
episode.93 The spectrum and frequency of cardiac channel arterial blood gas determinations are necessary to guide
defects in swimming-triggered arrhythmia syndromes may dosing. Concurrently a nasogastric tube should be inserted
be greater than previously suspected.106,107 Pathologic diag- to decompress the stomach, and body temperature readings
noses may be further complicated by terminal aspiration should be obtained to rule out hypothermia. In the presence
secondary to agonal breathing after cardiac arrest, and of a significantly lowered body temperature, rewarming
thus postmortem analyses that depend upon aspiration measures should be instituted. Once an adequate airway
may be misleading.108,109 has been obtained and spontaneous cardiac activity
achieved, an adequate arterial PO2 must be established to
Pulmonary System ensure adequate oxygen delivery to the tissues. Occasional
Patients with water aspiration may present with few or no patients will have marked decreases in blood pressure
respiratory complaints or with severe pulmonary edema and cardiac output. The initial therapy for hypotension of
due to direct lung injury.110 Patients who have aspirated any most causes is a trial of fluids, but, for a drowning victim
significant quantity of water will likely have a widened with pulmonary edema, this may not be appropriate. As
alveolar-arterial oxygen gradient and anything from mild a result, this group of patients may require invasive hemo-
to severe hypoxemia. Arterial PCO2 can be low or elevated dynamic monitoring. With knowledge of pulmonary artery
depending on alveolar ventilation (Table 78-4). Chest radio- wedge pressure and cardiac output, more rational decisions
graphs can show patchy opacities, which are most common concerning the need for fluids or pressors can then be made.
in the periphery or in the medial basal regions, or frank Isolated measurement of the central venous pressure is
(noncardiac) pulmonary edema (see Fig. 78-3). The clinical generally not an accurate method of judging intravas-
course cannot be predicted with certainty by the radio- cular volume status in the presence of noncardiac pulmo-
graphic picture of lung injury. Victims with clear-cut pul- nary edema. In the case of immersion pulmonary edema
monary difficulties may show minimal radiographic in a diver, the cause of hypoxemia is not water aspiration,
abnormalities, and those with minimal clinical injury may and therapy should include diuretics to reduce lung
have severely abnormal radiographic pictures. congestion.112
An interesting form of pulmonary edema found in divers Positive end-expiratory pressure is extremely effective in
was described by Wilmshurst and colleagues111 and by reversing the abnormal ventilation-perfusion relationships
Hampson and Dunford.112 This is manifest as severe dyspnea leading to hypoxemia. Usually only modest amounts of
while diving, associated with arterial hypoxemia, lung con- pressure are necessary to achieve adequate oxygenation.
gestion, and a normal cardiovascular system. The syn- Positive end-expiratory pressure apparently does not alter
drome may be related to negative-pressure pulmonary the course of the underlying pulmonary injury but rather
edema, a phenomenon well described in the anesthesia lit- allows for adequate oxygenation while the lung is recover-
erature113; however, there is also evidence that there are ing. It also allows this recovery to take place at a level of
multiple cardiovascular effects that may precipitate this inspired oxygen that is not in itself toxic to the lung.120,121
syndrome.114,115 Usually the pulmonary injury resolves over a period of 48
to 72 hours, and ventilatory support in most circumstances
Neurologic Status is relatively brief, unless infection develops. Consequently,
The neurologic status of patients can also be quite vari- in patients who are able to tolerate it, nasal continuous or
able. Severe permanent neurologic injury is the most bilevel positive airway pressure may be a reasonable method
devastating long-term consequence of the victim of a for short-term ventilatory support. At present there are
drowning episode. insufficient data to warrant the use of inverse-ratio ventila-
tion in cases of drowning.122 It may be prudent to manage
some drowning victims with high-flow oxygen delivery
TREATMENT
systems for relatively brief periods before resorting to more
Restoration of normal neurologic function, although invasive methods of providing adequate oxygenation. Opti-
unusual, has been described even after prolonged drowning- mization of oxygen and carbon dioxide levels (as well as
induced cardiac arrest.116 Because cardiac arrest in this serum glucose level) is likely important to help manage con-
setting is invariably due to hypoxemia and acidosis, the first comitant neurologic injury as well.
The use of antibiotics in the drowning victim who aspi- Key Points
rates ocean water or swimming pool water is generally nec-
essary only for those individuals who become febrile, ■ Middle ear barotrauma is the most prevalent diving
develop new pulmonary opacities, or develop purulent injury, whereas pulmonary barotrauma, although
secretions.123 Prophylactic antibiotics do not improve mor- uncommon, is the most severe form of barotrauma
tality or decrease morbidity.103 Because most pulmonary injury due to the risk for accompanying cerebral arte-
infections in the near drowning victim appear to be hospital rial gas embolism.
■ Decompression sickness results when inert gas dis-
acquired, prophylactic antibiotics seem only to select for
more resistant organisms.124 If the victim aspirates heavily solved in the body at increased pressure forms free gas
contaminated water with a known or suspected organism in blood and tissues upon decompression.
■ Clinical manifestations of acute decompression sick-
(as in the case of aspiration in a hot tub), the use of
prophylactic antibiotics may be appropriate. A rare compli- ness include disorders of the brain and spinal cord,
cation of drowning is the aspiration of sand or gravel.125 musculoskeletal pain, chest pain, dyspnea, and skin
Although bronchoscopy for the routine management of the rash seen up to 24 hours following an exposure to
drowning victim is probably not warranted, consideration increased pressure.
■ Treatment of decompression sickness and arterial gas
of this procedure should be made when unexpected difficul-
ties with mechanical ventilation arise. embolism should be instituted with recompression in
Routine use of adrenocorticosteroids to treat the lung a hyperbaric chamber as soon as possible after the
injury associated with near drowning is unwarranted. injury.
■ Assessment for fitness for diving includes consider-
Experimental evidence with this form of aspiration, as well
as others, strongly suggests that steroids do not improve the ation of the type of diving (recreational, commercial,
long-term outcome or short-term morbidity.126 Artificial military) and a number of chronic disorders that can
and animal-derived surfactants,127 extracorporeal mem- be aggravated by the diving environment. Because of
brane oxygenation,124 cardiopulmonary bypass,128 and the increased risk of arterial gas embolism, the pres-
hypothermia129 have also been used to treat the pulmonary ence of an atrial septal defect is considered to be a
injury associated with drowning. Any victim who has more contraindication to diving.
■ Although drowning without aspiration is theoretically
than minimal respiratory symptoms, an abnormal chest
radiograph, or abnormal arterial blood gas measurements possible, the majority of drownings are associated
should be observed, because pulmonary damage may not with aspiration of water into the lungs and an accom-
be clinically manifest for several hours after the incident.130 panying hypoxemia.
■ Goals of therapy for a drowning victim include revers-
Nearly all patients who will demonstrate significant prob-
lems of gas exchange will do so by 4 to 8 hours after the ing hypoxemia with positive-pressure ventilation and
incident; therefore consideration for discharge from the oxygen, treating metabolic acidosis, managing accom-
emergency department may be appropriate in people who panying cardiac arrhythmias, and administering anti-
can be observed in this fashion.131 Indeed, current evidence biotics when indicated.
suggests many victims can safely be sent home by lifeguards
after a water rescue.104 Complete reference list available at ExpertConsult.
PROGNOSIS Key Readings

Ackerman MJ, Tester DJ, Porter CJ: Swimming, a gene-specific arrhythmo-
The prognosis for the drowning victim depends mainly on genic trigger for inherited long QT syndrome. Mayo Clin Proc 74:1088–
the duration of immersion, the length of the anoxic period, 1094, 1999.
and the degree of damage secondary to the anoxic episode. Bierens JJLM, editor: Handbook on drowning: prevention, rescue, and treat-
Patients who arrive at the hospital neurologically intact ment, Berlin, 2006, Springer-Verlag.
have an excellent prognosis and should survive neurologi- Bove AA: Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004,
Elsevier.
cally unimpaired. An apparent (i.e., undocumented) cardiac Bove AA: The cardiovascular system and diving risk. Undersea Hyperb Med
arrest does not in itself suggest a poor outcome; however, 38:261–269, 2011.
cardiac arrest that persists through the period of initial first Hampson NB, Dunford RG: Pulmonary edema of scuba divers. Undersea
aid and transport to the hospital is a poor prognostic sign. Hyperb Med 24:29–33, 1997.
Lynch JH, Bove AA: Diving medicine: a review of current evidence. J Am
The presence of spontaneous respirations on presentation Board Fam Med 22:399–407, 2009.
to the emergency department following cardiac arrest in Navy Department: U.S. Navy diving manual, Rev 6 (Publication No. NAVSEA
the field is a good prognostic sign.132 The duration of immer- 0910-LP-106–0957), Washington, DC, 2008, U.S. Navy Department.
sion correlates with the degree of damage secondary to the Slade JB Jr, Hattori T, Ray CS, et al: Pulmonary edema associated with
anoxic episode and therefore with the outcome. No prog- scuba diving: case reports and review. Chest 120:1686–1694, 2001.
Szpilman D, Bierens JJLM, Handley AJ, et al: Drowning. N Engl J Med
nostic test has proven to be a reliable basis for treatment 366:2102–2110, 2012.
decisions, and predictions concerning outcome cannot be Vann RD, Butler FK, Mitchell SJ, et al: Decompression illness. Lancet
made in the presence of severe hypothermia. 377:153–164, 2011.
78 • Diving Medicine 1395.e1
References 30. Hayden JD, Davies JB, Martin IG: Diaphragmatic rupture resulting
from gastrointestinal barotrauma in a scuba diver. Br J Sports Med
1. Hong SK, Cerretelli P, Cruz JC, et al: Mechanics of respiration during 32:75–76, 1998.
submersion in water. J Appl Physiol 27:537–538, 1969. 31. Vann RD: Mechanisms and risk of decompression sickness. In Bove
2. Arborelius M, Balldin UI, Lidja B, et al: Hemodynamic changes in AA, editor: Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004,
man during immersion with the head above water. Aerosp Med WB Saunders, pp 127–164.
43:592–598, 1972. 32. Bond G: New developments in high pressure living. Arch Environ
3. Craig AB Jr: Causes of loss of consciousness during underwater Health 9:310–314, 1964.
swimming. J Appl Physiol 16:583–586, 1961. 33. Thom SR, Milovanova TN, Bogush M, et al: Microparticle produc-
4. Pendergast DR, Tedesco M, Nawrocki DM, et al: Energetics of under- tion, neutrophil activation, and intravascular bubbles following
water swimming with SCUBA. Med Sci Sports Exerc 28:573–580, open-water SCUBA diving. J Appl Physiol 112:1268–1278, 2012.
1996. 34. Harvey EN, Barnes DK, McElroy WD, et al: Bubble formation in
5. Navy Department: U.S. Navy diving manual, Vol 5, Rev 6: Diving animals. I. Physical factors. J Cell Comp Physiol 24:1–22, 1944.
medicine and recompression chamber operations (NAVSEA 0910- 35. Bert P: Barometric pressure: researches in experimental physiology,
LP-106-0957), Washington DC, 2011. http://www.supsalv.org/ (Hitchcock MA, Hitchcock FA, transl), 1943, Columbus Book Co.
00c3_publications.asp. Reprinted by the Undersea Medical Society, Bethesda, Md, 1878.
6. Golding FC, Griffiths P, Hempleman HV, et al: Decompression sick- 36. Erdman S: Aeropathy of compressed air illness among tunnel
ness during construction of the Dartford Tunnel. Br J Ind Med workers. JAMA 49:1665–1670, 1907.
17:167–180, 1960. 37. Hallenbeck JM, Bove AA, Moquin R, et al: Accelerated coagulation
7. Francis TJR, Smith DH: Describing decompression illness (42nd UHMS of whole blood and cell free plasma by bubbling in vitro. Aerosp Med
workshop), Kensington, Md, 1991, Undersea and Hyperbaric Medical 44:712–714, 1973.
Society. 38. Bove AA, Hallenbeck JM: Changes in blood and plasma volumes in
8. Behnke AR: Analysis of accidents occurring in training with the dogs during decompression sickness. Aerosp Med 45:49–55, 1974.
submarine “lung.” US Naval Med Bull 30:177–184, 1932. 39. Eftedal OS, Lydersen S, Brubakk AO: The relationship between
9. Polak B, Adams H: Traumatic air embolism in submarine escape venous gas bubbles and adverse effects of decompression after air
training. US Naval Med Bull 30:165–177, 1932. dives. Undersea Hyperb Med 34:99–105, 2007.
10. Schaefer KE, Nulty WP, Carey C, et al: Mechanisms in development 40. Bove AA: Basis for drug therapy in decompression sickness. Undersea
of interstitial emphysema and air embolism on decompression from Biomed Res 9:91–112, 1982.
depth. J Appl Physiol 13:15–29, 1958. 41. Levin LL, Stewart GJ, Lynch PR, et al: Blood and blood vessel wall
11. Smith R, Neuman T: Elevation of serum creatine kinase in divers changes induced by decompression sickness in dogs. J Appl Physiol
with arterial gas embolism. N Engl J Med 330:19–24, 1994. 50:944–949, 1981.
12. Tetzlaff K, Reuter M, Leplow B, et al: Risk factors for pulmonary 42. Spencer MP: Decompression limits for compressed air determined by
barotrauma in divers. Chest 112:654–659, 1997. ultrasonically detected blood bubbles. J Appl Physiol 40:227–235,
13. Neuman TS, Clausen JL: Recommend caution in defining risk factors 1976.
for barotrauma. Chest 114:1791–1792, 1998. 43. Butler BD, Robinson R, Fife C, et al: Doppler detection of decompres-
14. Elliott DH, Harrison JAB, Barnard EEP: Clinical and radiographic sion bubbles with computer assisted digitization of ultrasonic
features of 88 cases of decompression barotrauma. In Shilling CW, signals. Aviat Space Environ Med 62:997–1004, 1991.
Beckett MW, editors: Proceedings of the sixth symposium on underwater 44. Conkin J, Waligora JM, Foster PP, et al: Information about venous gas
physiology, Bethesda, Md, 1978, Federation of American Societies emboli improves prediction of hypobaric decompression sickness.
for Experimental Biology, pp 527–535. Aviat Space Environ Med 69:8–16, 1998.
15. Neuman TS, Jacoby I, Bove AA: Fatal pulmonary barotrauma due to 45. Kumar VK, Waligora JM: Billica RD: utility of Doppler-detectable
obstruction of the central circulation with air. J Emerg Med 16:413– microbubbles in the diagnosis and treatment of decompression sick-
417, 1998. ness. Aviat Space Environ Med 68:151–158, 1997.
16. Harker CP, Neuman TS, Olson LK, et al: The roentgenographic find- 45a. Lemaitre F, Kohshi K, Tamaki H, et al: Doppler detection in ama
ings associated with air embolism in sport scuba divers. J Emerg Med divers of Japan. Wilderness Environ Med 25(3):258–262, 2014.
11:443–449, 1993. 46. Boycott AE, Damant GCC, Haldane J: The prevention of compressed
17. Smith RM, Van Hoesen KB, Neuman TS: Arterial gas embolism and air illness. J Hyg (Cambridge) 8:342–443, 1908.
hemoconcentration. J Emerg Med 12:147–153, 1994. 47. Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and
18. Hunter SE, Farmer JC: Ear and sinus problems in diving. In Bove AA, decompression sickness in divers. Lancet 1:513–514, 1989.
editor: Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004, WB 48. Wilmshurst PT, Byrne JC, Webb-Peploe MM: Relation between
Saunders, pp 431–460. intraatrial shunts and decompression sickness in divers. Lancet
19. Whelan TR: Facial nerve palsy associated with underwater baro- 2:1302–1305, 1989.
trauma. Postgrad Med J 66:465–466, 1990. 49. Moon RE, Kisslo JA, Massey EW, et al: Patent foramen ovale (PFO)
20. Freeman P, Edmonds C: Inner ear barotrauma. Arch Otolaryngol and decompression illness. Undersea Biomed Res 13(Suppl):15,
95:556–563, 1972. 1991.
21. Sheridan MF, Hetherington HH, Hull JJ: Inner ear barotrauma from 50. Wilmshurst PT, Treacher DF, Crowther A, et al: Effects of a patent
scuba diving. Ear Nose Throat J 181(184):186–187, 1999. foramen ovale on arterial saturation during exercise and on cardio-
22. Klingmann C: Inner ear decompression sickness in compressed-air vascular responses to deep breathing, Valsalva manoeuvre, and
diving. Undersea Hyperb Med 39(1):589–594, 2012. passive tilt: relation to history of decompression illness in divers. Br
23. Klingmann C, Praetorius M, Baumann I, et al: Barotrauma and Heart J 71:229–231, 1994.
decompression illness of the inner ear: 46 cases during treatment 51. Germonpré P, Dendale P, Unger P, et al: Patent foramen ovale and
and follow-up. Otol Neurotol 28:447–454, 2007. decompression sickness in sports divers. J Appl Physiol 84:1622–
24. Ignatescu M, Bryson P, Klingmann C: Susceptibility of the inner ear 1626, 1998.
structure to shunt-related decompression sickness. Aviat Space 52. Billinger M, Zbinden R, Mordasini R, et al: Patent foramen ovale
Environ Med 83(12):1145–1151, 2012. closure in recreational divers: effect on decompression illness and
25. Butler FK, Bove AA: Infraorbital hypesthesia after maxillary sinus ischaemic brain lesions during long-term follow-up. Heart 97:1932–
barotrauma. Undersea Hyperb Med 26:257–260, 1999. 1937, 2011.
26. Butler F: Orbital hemorrhage following facemask barotrauma. 52a. Honek J, Sramek M, Sefc L, et al: Effect of catheter-based patent
Undersea Hyperb Med 28:31–34, 2001. foramen ovale closure on the occurrence of arterial bubbles in scuba
27. Latham E, van Hoesen K, Grover I: Diplopia due to mask barotrauma. divers. JACC Cardiovasc Interv 7(4):403–408, 2014.
J Emerg Med 41:486–488, 2011. 53. Torti SR, Billinger M, Schwerzmann M, et al: Risk of decompression
28. Kieser J, Holborow D: The prevention and management of oral baro- illness among 230 divers in relation to the presence and size of
trauma. N Z Dent J 93:114–116, 1997. patent foramen ovale. Eur Heart J 25:1014–1020, 2004.
29. Cramer FS, Heimbach RD: Stomach rupture as a result of gas- 54. Moon RE, Bove AA: Transcatheter occlusion of patent foramen
trointestinal barotrauma in a SCUBA diver. J Trauma 22:238–240, ovale:A prevention for decompression illness? Undersea Hyperb Med
1982. 31:271–274, 2004.
1395.e2 PART 3 • Clinical Respiratory Medicine
55. Sulaiman ZM, Pilmanis AA, O’Conner RB: Relationship between age 81. Bove AA: Cardiovascular disorders and diving. In Bove AA, editor:
and susceptibility to altitude decompression sickness. Aviat Space Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004, WB Saun-
Environ Med 68:695–698, 1997. ders, pp 485–506.
56. Carturan D, Boussuges A, Vanuxem P, et al: Ascent rate, age, 82. Massey EW, Greer HD: Neurologic consequences of diving. In Bove
maximal oxygen uptake, adiposity, and circulating venous bubbles AA, editor: Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004,
after diving. J Appl Physiol 93:1349–1356, 2002. WB Saunders, pp 461–474.
57. Klingmann C, Gonnermann A, Dreyhaupt J, et al: Decompression 83. Scott DH, Marks AD: Diabetes and diving. In Bove AA, editor:
illness reported in a survey of 429 recreational divers. Aviat Space Bove and Davis’ diving medicine, Philadelphia, 2004, WB Saunders,
Environ Med 79:123–128, 2008. pp 507–518.
58. Blatteau JE, Gempp E, Simon O, et al: Prognostic factors of spinal 84. Neuman TS, Bove AA, O’Connor RD, et al: Asthma and diving. Ann
cord decompression sickness in recreational diving: retrospective Allergy 73:344–350, 1994.
and multicentric analysis of 279 cases. Neurocrit Care 15:120–127, 85. Elliott DE: Are asthmatics fit to dive?, Kensington, Md, 1996, Undersea
2011. and Hyperbaric Medical Society.
59. Ryles MT: Pilmanis AA: the initial signs and symptoms of altitude 86. Denoble PJ, Caruso JL, Dear Gde L, et al: Common causes of open-
decompression sickness. Aviat Space Environ Med 67:983–989, circuit recreational diving fatalities. Undersea Hyperb Med 35(6):393–
1996. 406, 2008.
60. Hart AJ, White SAS, Conboy PJ, et al: Open water scuba diving acci- 87. Mebane GY, Low N, Dovenbarger J: A review of autopsies on recre-
dents in Leicester: five years’ experience. J Accid Emerg Med 16:198– ational scuba divers: 1989–1992. Undersea Hyperb Med 20(Suppl):
200, 1999. 70, 1993.
61. Bove AA: Risk of decompression sickness with patent foramen ovale. 88. Irving L: Bradycardia in human divers. J Appl Physiol 18:489–491,
Undersea Hyperb Med 25:175–178, 1998. 1963.
62. Neuman TS, Spragg RG, Wagner PD, et al: Cardiopulmonary conse- 89. Irving L, Solandt OM, Solandt DY, et al: The respiratory metabolism
quences of decompression sickness. Respir Physiol 41:143–155, of the seal and its adjustment to diving. J Cell Comp Physiol 7:137–
1980. 151, 1935.
63. Hallenbeck JM, Bove AA, Elliott DH: Mechanisms underlying spinal 90. Ackerman MJ, Tester DJ, Porter CJ: Swimming, a gene-specific
cord damage in decompression sickness. Neurology 25:308–316, arrhythmogenic trigger for inherited long QT syndrome. Mayo Clin
1975. Proc 74:1088–1094, 1999.
64. Vann RD, Butler FK, Mitchell SJ, et al: Decompression illness. Lancet 91. McAniff JJ: United States underwater fatality statistics, 1970–82,
377:153–164, 2011. including a preliminary assessment of 1983 fatalities (Report No. URI-
65. Hawes J, Massey EW: Neurologic injuries from scuba diving. Neurol SSR-84–17), Providence, 1984, National Underwater Accident
Clin 26:297–308, xii, 2008. Data Center, University of Rhode Island.
66. Farmer JC, Thomas WG, Youngblood DG, et al: Inner ear decompres- 92. Powers AT, Bass B, Stewart J, et al: A six year review of SCUBA diving
sion sickness. Laryngoscope 86:1315–1326, 1976. fatalities in San Diego County. Undersea Biomed Res 19(Suppl):20,
67. Gempp E, Blatteau JE, Simon O, et al: Musculoskeletal decompression 1992.
sickness and risk of dysbaric osteonecrosis in recreational divers. 93. Sadler C, Nelson C, Neuman T, et al: Dilemma of natural death while
Diving Hyperb Med 39:200–204, 2009. scuba diving. Acad Forensic Pathol 3:202–212, 2013.
68. McCallum RI, Walder DN: Bone lesions in compressed air workers. 94. van Beeck EF, Branche CM, Szpilman D, et al: A new definition
J Bone Joint Surg 48:207–235, 1966. of drowning: towards documentation and prevention of a global
69. Cimsit M, Ilgezdi S, Cimsit C, et al: Dysbaric osteonecrosis in public health problem. Bull World Health Organ 83:853–856,
experienced dive masters and instructors. Aviat Space Environ Med 2005.
78:1150–1154, 2007. 95. Idris AH, Berg RA, Bierens J, et al: ILCOR Advisory Statement. Rec-
70. Grover I, Reed W, Neuman T: The SANDHOG criteria and its valida- ommended guidelines for uniform reporting of data from drowning:
tion for the diagnosis of DCS arising from bounce diving. Undersea the “Ulstein style.” Resuscitation 59:45–57, 2003.
Hyperb Med 34:199–210, 2007. 96. Lindholm P, Lundgren C: The physiology and pathophysiology of
71. Hennedige T, Chow W, Ng YY, et  al: MRI in spinal cord decom- human breath-hold diving. J Appl Physiol 106:284–292, 2009.
pression sickness. J Med Imaging Radiat Oncol 56:282–288, 2012. 97. Hansel J, Solleder I, Gfroerer W, et al: Hypoxia and cardiac arrhyth-
72. Gempp E, Blatteau JE, Stephant E, et al: MRI findings and clinical mias in breath-hold divers during voluntary immersed breath-holds.
outcome in 45 divers with spinal cord decompression sickness. Aviat Eur J Appl Physiol 105:673–678, 2009.
Space Environ Med 79:1112–1116, 2008. 98. Wester TE, Cherry AD, Pollock NW, et al: Effects of head and body
73. Yoshiyama M, Asamoto S, Kobayashi N, et al: Spinal cord decom- cooling on hemodynamics during immersed prone exercise at 1
pression sickness associated with scuba diving: correlation of imme- ATA. J Appl Physiol 106:691–700, 2009.
diate and delayed magnetic resonance imaging findings with severity 99. Modell JH, Bellefleur M, Davis JH: Drowning without aspiration: is
of neurologic impairment—a report on 3 cases. Surg Neurol 67:283– this an appropriate diagnosis? J Forensic Sci 44:1119–1123, 1999.
287, 2007. 100. Gu MN, Xiao JF, Huang YR, et al: Study of Direct Lung Injury by sea
74. Moon RE: Treatment of decompression illness. In Bove AA, editor: water in canine models. Di Yi Jun Yi Da Xue Xue Bao 23:201–205,
Bove and Davis’ diving medicine, ed 4, Philadelphia, 2004, WB Saun- 2003.
ders, pp 195–224. 101. Giammona ST, Modell JH: Drowning by total immersion: effects on
75. Bennett MH, Lehm JP, Mitchell SJ, et al: Recompression and adjunc- pulmonary surfactant of distilled water, isotonic saline and sea
tive therapy for decompression illness. Cochrane Database Syst Rev water. Am J Dis Child 114:612–616, 1967.
(5):CD005277, 2012. 102. Yagil Y, Stalnikowicz R, Michaeli J, et al: Near drowning in the Dead
75a. Moon RE: Hyperbaric oxygen treatment for air or gas embolism. Sea: electrolyte imbalances and therapeutic implications. Arch Intern
Undersea Hyperb Med 41(2):159–166, 2014. Med 145:50–53, 1985.
76. Bove AA, Clark JM, Simon AJ, et al: Successful therapy of cerebral 103. Seidel-Ode LR, Almog Y: Near drowning in the dead sea: a retrospec-
air embolism with hyperbaric oxygen at 2.8 ATA. Undersea Biomed tive observational analysis of 69 patients. Israeli Med Jour 5:856–
Res 9:76–80, 1982. 858, 2003.
77. Longphre JM, Denoble PJ, Moon RE, et al: First aid normobaric 104. Szpilman D: Near-drowning and drowning classification: a proposal
oxygen for the treatment of recreational diving injuries. Undersea to stratify mortality based on the analysis of 1,831 cases. Chest
Hyperb Med 34:43–49, 2007. 112:660–665, 1997.
78. Saumarez RC, Bolt JF, Gregory RJ: Neurologic decompression sick- 105. Young RSK, Zaineraitis ED, Dooling EO: Neurologic outcome in cold-
ness treated without recompression. Br Med J 1:151–152, 1973. water drowning. JAMA 244:1233–1235, 1980.
79. Bennett PB: Inert gas narcosis and HPNS. In Bove AA, editor: Bove 106. Choi G, Kopplin LJ, Tester DJ, et al: Spectrum and frequency of
and Davis’ diving medicine, ed 4, Philadelphia, 2004, WB Saunders, cardiac channel defects in swimming-triggered arrhythmia syn-
pp 225–240. dromes. Circulation 110:2119–2124, 2004.
80. Clark JM, Thom SR: Toxicity of oxygen, carbon dioxide, and carbon 107. Efremidis M, Loukas K, Pappas LK, et al: Swimming-triggered
monoxide. In Bove AA, editor: Bove and Davis’ diving medicine, ed 4, aborted sudden cardiac death in a patient with Andersen-Tawil syn-
Philadelphia, 2004, WB Saunders, pp 241–260. drome. Int J Cardiol 112:e45–e47, 2006.
78 • Diving Medicine 1395.e3
108. He F, Huang D, Liu L, et al: A novel PCR-DGGE-based method for 121. Lapinsky SE, Mount DB, Mackey D, et al: Management of acute
identifying plankton 16S rDNA for the diagnosis of drowning. Foren- respiratory failure due to pulmonary edema with nasal positive pres-
sic Sci Int 176:152–156, 2008. sure support. Chest 105:229–231, 1994.
109. Kakizaki E, Takahama K, Seo Y, et al: Marine bacteria comprise a 122. Shanholtz C, Brower R: Should inverse ratio ventilation be used in
possible indicator of drowning in seawater. Forensic Sci Int 176:236– the adult respiratory distress syndrome? Am Rev Respir Dis 149:
247, 2008. 1354–1358, 1994.
110. Fine NL, Myerson DA, Myerson PJ, et al: Near drowning presenting 123. Hughes JA: Drowning—an overview. J Am Coll Emerg Physicians
as the adult respiratory distress syndrome. Chest 65:347–349, 6:172, 1977.
1974. 124. Thalmann M, Trampitsch E, Haberfellner N, et al: Resuscitation in
111. Wilmshurst PT, Nuri M, Crowther A, et al: Cold-induced pulmonary near drowning with extracorporeal membrane oxygenation. Ann
oedema in scuba divers and swimmers and subsequent development Thorac Surg 72:607–608, 2001.
of hypertension. Lancet 1:62–65, 1989. 125. Dunagan DP, Cox JE, Chang MC, et al: Sand aspiration with near
112. Hampson NB, Dunford RG: Pulmonary edema of scuba divers. drowning: radiographic and bronchoscopic findings. Am J Respir Crit
Undersea Hyperb Med 24:29–33, 1997. Care Med 156:292–295, 1997.
113. Deepika K, Kenaan CA, Barrocas AM, et al: Negative pressure pul- 126. Calderwood HW, Modell JH, Ruiz BC: The ineffectiveness of steroid
monary edema after acute upper airway obstruction. J Clin Anesth therapy for treatment of fresh-water near drowning. Anesthesiology
9:403–408, 1997. 43:642–650, 1975.
114. Preacher DF, Pecorella SRH, Freiberger JJ, et al: Effects of hyperoxia 127. Onarheim H, Vik V: Porcine surfactant (Curosurf) for acute respira-
on ventilation and pulmonary hemodynamics during immersed tory failure after near-drowning in 12 year old. Acta Anaesthesiol
prone exercise at 4.7 ATA: possible implications for immersion pul- Scand 48:778–781, 2004.
monary edema. J Appl Physiol 109:68–78, 2010. 128. Eich C, Bräuer A, Timmermann A, et al: Outcome of 12 drowned
115. Fraser JAV, Preacher DF, Freiberger JJ, et al: Risk factors for immer- children with attempted resuscitation on cardiopulmonary bypass:
sion pulmonary edema: hyperoxia does not attenuate pulmonary an analysis of variables based on the “Utstein Style for drowning.”
hypertension associated with cold water-immersed prone exercise at Resuscitation 75:42–52, 2007.
4.7 ATA. J Appl Physiol 110:610–618, 2011. 129. Varon J, Marik PE: Complete neurological recovery following delayed
116. Sekar TS, McDonnell KF, Namsirikul P, et al: Survival after prolonged initiation of hypothermia in a victim of warm water near-drowning.
immersion in cold water without neurologic sequelae. Arch Intern Resuscitation 68:421–423, 2006.
Med 140:775–779, 1980. 130. Putman CE: Drowning: another plunge. Am J Roentgenol Radium Ther
117. Hwang V, Shofer FS, Durbin DR, et al: Prevalence of traumatic inju- Nucl Med 125:543–549, 1975.
ries in drowning and near drowning in children and adolescents. 131. Causey AL, Tilelli JA, Swanson ME: Predicting discharge in uncom-
Arch Pediatr Adolesc Med 175:50–53, 2003. plicated near-drowning. Am J Emerg Med 18:9–11, 2000.
118. Watson RS, MD, MPH, Cummins P, MD, MPH, Quan L, MD, et al: 132. Jacobsen WK, Mason LJ, Briggs BA, et al: Correlation of spontaneous
Cervical spine injuries among submersion victims. Journal of Trauma respiration and neurologic damage in near drowning. Crit Care Med
51:658–662, 2001. 11:487–489, 1983.
119. Guidelines for cardiopulmonary resuscitation (CPR) and emergency
cardiac care (ECC). JAMA 268:2171–2302, 1992.
120. Rutledge RR, Flor RJ: The use of mechanical ventilation with positive
end expiratory pressure in the treatment of near drowning. Anesthe-
siology 38:194–196, 1973.

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What are some of the main equipment used in diving?

What are some disorders related to diving pressure effects?

78 DIVING MEDICINE

ALFRED A. BOVE, MD, PhD • TOM S. NEUMAN, MD

INTRODUCTION PRESSURE EFFECTS: BOYLE’S LAW MEDICAL QUALIFICATIONS FOR

INTRODUCTION increases transdiaphragmatic pressure, and increases

Feet ATA mm Hg psi Second-stage

Energy need (METS)

described a systemic form of DCS that involves the central

PRESSURE EFFECTS: BOYLE’S LAW

75 Table 78-3 Frequency of Decompression Sickness (DCS)

risk for drowning and may compromise the safety of others

hyperosmotic fluid causes transudation of fluid into alveoli,

PROGNOSIS Key Readings

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