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Sickness
Richard E. Moon, MD,
FACP, FCCP, FRCPC, and
Des F. Gorman, MBChB, MD, PhD
Cardiorespiratory Decompression
CHAPTER OUTLINE
Sickness
WHAT IS DECOMPRESSION SICKNESS?
Radiography
PATHOGENESIS
Neuropsychology
Bubbles
Neurophysiology
Direct Bubble Effects
Diagnostic Criteria
Cellular and Tissue Effects
Scoring Systems of Severity and
Endothelial Disruption Recovery
Heat Shock Protein Expression Summary
Complement Activation TREATMENT
Platelet Activation Natural History if Untreated
Nitric Oxide Production First-Aid Treatment
Leukocyte Activation Recompression Therapy
Organ Effects Choice of Pressure
Joints and Long Bones Oxygen
Spinal Cord Inert Gas
Brain Therapeutic Protocols
Peripheral Nerve Standard U.S. Navy Oxygen Tables
Lung Oxygen Tables Designed for
Inner Ear Monoplace Use
Skin and Soft Tissue Short Oxygen Treatment Tables with
CLINICAL MANIFESTATIONS Excursion to Pressure Greater Than
EVALUATION OF THE PATIENT 2.8 Atmospheres Absolute
History Deep Tables
Physical Examination Saturation Treatment after Shallow Dives
Pain-Only Bend In-water Recompression
Skin Bends Choice of Treatment Algorithms
Neurologic Decompression Illness Surface-Oriented Diving
283
Incidence obs
Timing, Duration of Treatment, and 30%
Follow-up Treatment
ADJUNCTIVE MEASURES TO RECOMPRESSION
20%
Fluid Administration
Corticosteroids
10%
Anticoagulants and Nonsteroidal
Anti-inflammatory Drugs
Lidocaine 0%
sites of stable gas micronuclei.13,14 Such mi- in certain types of DCS, particularly those
cronuclei could be stabilized against the forms that involve the skin, inner ear, and cen-
forces of surface tension by a coating of sur- tral nervous system.
factant.15 Alternatively, if the gas micronucleus Under certain circumstances, VGEs can tra-
exists in the crevice of a hydrophobic mole- verse the pulmonary circulation. Arteriovenous
cule, surface tension would intrinsically tend shunt vessels have been demonstrated in nor-
to stabilize the bubble. mal human lungs,36 through which 25- and
Bubbles can form in the absence of a de- 50-m diameter microspheres can pass. High
crease in ambient pressure when local tissue exercise cardiac output and pulmonary artery
supersaturation occurs because of a change pressure, such as during exercise, may facilitate
in breathing gas.This was originally described right-to-left shunting through the lung.37,38 High
in a series of divers in a heliox-filled hyper- bubble rates can also facilitate right-to-left shunt-
baric chamber at 7 ATA at Duke University ing through the lung (Fig. 14.2).
when the breathing gas was switched from
heliox to nitrox16 (see Skin Bends section
later in this chapter and also Fig. 14.10). This Direct Bubble Effects
observation was subsequently observed at
the University of Pennsylvania,17 after which Bubbles may cause tissue damage because of
a series of studies led to its understanding. direct mechanical effects. Bubble-induced
When the ingress into a tissue of a new gas distraction of connective tissue is believed
exceeds the egress of a resident gas, the sum to be the cause of DCS-related pain. Bubbles
of partial pressures can exceed ambient pres- within and proximal to spinal cord neurons
sure. Isobaric bubble formation has been have been described as a possible cause of
demonstrated at 1 ATA in experimental ani- neuronal dysfunction39 (Fig. 14.3). Increased
mals surrounded by helium while breathing intraosseous pressure within the marrow
nitrous oxide/oxygen.18,19 cavity of long bones has been hypothesized
The presence of bubbles in tissues per se as the cause of the pain of limb bends and
does not imply DCS. Tissue bubbles have osteonecrosis that can occur.40 Increased
been observed radiographically in the ab-
sence of symptoms, but only during altitude
Percent of Animals with Arterial Bubbles
100
exposure.20,21 Bubbles in absence of symp- Pigs
toms in the veins or right heart (venous gas
80
emboli [VGEs]) can be observed commonly
using ultrasound after dives.22,23 The blood- Dogs
60
stream is relatively resistant to de novo
bubble formation.24 VGEs are believed to
originate in extravascular tissue, possibly 40
ED
IJ
N
L
Figure 14.4 ENDOTHELIAL EFFECTS OF BUBBLES. Left,
Scanning electron microscopy (EM) of luminal surface
of jugular vein from control dog. Individual endothelial
cells can be seen, outlined by intercellular junctions (IJ)
and their nuclei (N). There are no adhering blood cells.
Right, Scanning EM of an area of jugular vein in an ani-
mal with severe decompression sickness. There are
numerous adhering leukocytes (L) and platelets (P).
ED, endothelial damage. (From Levin LL, Stewart GJ,
Lynch PR, et al: Blood and blood vessel wall changes
induced by decompression sickness in dogs. J Appl
Physiol 50:944–949, 1981, by permission.)
Brain
In situ gas bubble formation is believed to
be unlikely because of high tissue blood
flow and rapid inert gas washout. Hydrogen
washout has been measured in the cerebral
cortex and has a half-time on the order of
45 seconds.80 The half-time even in white A
matter would be only approximately 3 min-
utes. In addition, cerebral manifestations
are usually focal. Therefore, most cerebral
manifestations are believed to be caused
by bubble emboli, either from pulmonary
barotrauma (PBT) or arterialization of VGEs
(see later).
Peripheral Nerve
Isolated peripheral nerve manifestations in
DCS have rarely been described. This is usu- B
ally in locations where increased pressure Figure 14.8 PULMONARY EDEMA IN A SHEEP WITH
and entrapment could occur,81,82 although “CHOKES” AFTER A 42 FEET SEA WATER (FSW) DIVE
one case report exists of a mononeuropathy FOR 22 HOURS, FOLLOWED BY A SIMULATED ALTITUDE
involving the medial branch of the deep pe- EXPOSURE TO 8000 FEET (0.75 ATMOSPHERE
ABSOLUTE [ATA]). A, Before dive. B, After dive and altitude
roneal nerve.83 exposure. Patchy pulmonary infiltrates are consistent with pulmonary
edema. (From Atkins CE, Lehner CE, Beck KA, et al: Experi-
mental respiratory decompression sickness in sheep.
Lung J Appl Physiol 65:1163–1171, 1988, by permission.)
High levels of VGEs after decompression cause
“chokes,” which is associated with radio-
graphic pulmonary edema (Fig. 14.8).84 Intra-
Inner Ear
venous (IV) bubble infusion also causes pul- Inner ear DCS can involve the vestibular appa-
monary edema (Fig. 14.9). The mechanism ratus, the cochlea, or both. It was initially be-
appears to involve leukocytes, which adhere lieved to occur only in heliox divers, and usu-
to bubbles70 (see Fig. 14.9) and accumulate in ally after a gas switch during decompression.
the lung after VGE.49 However, it does occur in air divers, typically
PA Pressure
PA air bubble in a small pulmonary artery.
(mm Hg)
40 B, Intravenous bubble infusion, causing
20
pulmonary hypertension and increased
lymph flow due to pulmonary edema.
0 AE, air embolism; PA, pulmonary artery.
AE (From Albertine KH, Wiener-Kronish JP,
6 Koike K, et al: Quantification of
Lymph Flow
(g/15 min)
4 damage by air emboli to lung
microvessels in anesthetized sheep.
2
J Appl Physiol 57:1360–1368, 1984,
0 by permission.)
0 2 4 6
A Time (hours)
B
Paresthesia
Pain
Dizziness
Muscular Weakness
Fatigue
Nausea
Headache
Coordination
Skin
Pulmonary
Muscular Problems Prevalence as an Initial Symptom
Mental Total Prevalence
Consciousnesss
Barotrauma
Lymphatic
Vision
Vertigo
Bladder Bowel
Nystagmus
Hearing
0 25 50 75 100
Percent of All Divers
Figure 14.10 SYMPTOMS OF DECOMPRESSION SICKNESS IN RECREATIONAL DIVERS. White
bars represent prevalence as an initial symptom; black bars represent total prevalence. (From the Divers
Alert Network Report on Decompression Illness, Diving Fatalities and Project Dive Exploration. Dur-
ham, NC, Divers Alert Network, 2005.)
urinary retention, ataxia, and impaired con- ticularly the one immediately before symptom
sciousness. Dyspnea and cough are character- onset. One way to do this is to compare the
istic of high levels of VGEs, referred to as car- diver’s depth–time profile with a standard
diorespiratory DCS (“chokes”). decompression table, such as the U.S. Navy Air
Decompression Table (from the U.S. Navy
Diving Manual,92 available via the Internet at:
EVALUATION OF THE PATIENT http://www.supsalv.org). However, adherence
to a standard decompression procedure (table
DCS is a clinical diagnosis based on history or computer) does not exclude either DCS or
and physical examination. AGE. Breath-holding during ascent or a rapid
ascent can suggest PBT and intravascular gas,
which can occur from depths as shallow as
History 1 m (3 feet).93
Muscle strains and bruises can be mistaken
The patient evaluation should include the fol- for DCS. Conditions other than DCS that can
lowing information: mimic the disease after a dive include myocar-
dial infarction, subarachnoid hemorrhage, acute
• Time of onset and progression of
disc herniation, complicated migraine, trans-
symptoms
verse myelitis, vasculitis,94 multiple sclerosis,
• Index of gas burden (e.g., depth–time
carotid dissection,95 maple syrup urine dis-
exposure).
ease,96 or neurologic symptoms from fish
• Evidence of barotrauma, such as rapid
toxin.97 Psychiatric disease such as somato-
or panic ascent, breath-holding during
form disorders, factitious disorders, and malin-
ascent, chest pain, or dyspnea
gering have been mistaken for DCS.98–101
Severe cases tend to present early after sur-
facing, whereas minor symptoms can occur
after delay. In a published series of 1070 cases Physical Examination
of central nervous system (CNS) DCS, symp-
toms occurred within 10 minutes of surfacing Pain-Only Bend
in half of cases and within 3 hours in 90% of Physical examination is usually negative in
cases.86 Unless there has been an altitude ex- true pain-only DCS. Signs of joint inflamma-
posure, almost all symptoms occur within tion are absent, and joint movement rarely
24 hours of surfacing. Pain-only bends tend to alters the pain. Sometimes increasing the local
have a longer latency; however, around 90% of tissue pressure in the affected area may dimin-
cases become symptomatic within 6 hours or ish the pain, for example, by having the
more of surfacing.11,87–89 Causes for a diver’s patient stand up (as in the case of involve-
symptoms other than DCS should be enter- ment of the legs or hips) or by inflation of a
tained if the latency between dive and onset blood pressure cuff placed around the af-
of symptoms is prolonged beyond 24 hours. If fected area102; however, absence of a change
there has been intervening altitude exposure, in pain does not exclude the diagnosis.
onset can be longer, especially after saturation
dives.90,91 Symptoms that occur during com-
pression or at maximum depth cannot be due
Skin Bends
to DCS. In such cases, one should consider si- There are several types of skin bends. The
nus or otic barotrauma, gas narcosis, poison- most common type is a nonspecific, erythem-
ing from gas contamination (e.g., carbon mon- atous macular eruption, often on the trunk
oxide), immersion pulmonary edema, or (Fig. 14.11A). A rash that is almost specific
causes unrelated to diving. for DCS is reticulated and known as cutis
An estimate of inert gas uptake can be ob- marmorata, or more correctly, livedo reticu-
tained from the profiles of recent dives, par- laris (see Fig. 14.11B). This rash is sometimes
A
associated with neurologic DCS and a PFO.32
Other types of skin bends include urticaria
(see Fig. 14.11C ), usually associated with a
gas switch (see Fig. 14.11C ). Generalized pru-
ritus without visible rash tends to occur in
divers wearing dry suits or after dives in a dry
chamber. It is believed to be due to supersatu-
ration of inert gas taken up directly through
the skin. Lymphatic bends typically occurs in
the trunk and consists of painful swelling
(see Fig. 14.11D).
B
Neurologic Decompression Illness
Because AGE and neurologic DCS can be dif-
ficult to distinguish, and because the treat-
ment is mostly the same, the term DCI rather
than DCS is used in this section and in the
treatment section (see page 294).
Standard evaluation of patients with sus-
pected DCI includes a complete neurologic
examination. The time required to obtain a
complete neurologic assessment is usually
worth a small delay in recompression treat-
ment. It provides a baseline with which to
assess evolving manifestations and measure
the efficacy of treatment. In the event the
diver is deteriorating rapidly, the examination
can be abbreviated to the minimum neces-
sary to establish a diagnosis. Sensory abnor-
malities are often patchy and may not follow
C the cortical distributions usually seen in pa-
tients with hemispheric stroke or standard
dermatomal distributions seen in patients
with other types of spinal cord injury. Find-
ings are often multifocal, with combinations
of cortical, brainstem, spinal cord, and periph-
D eral nerve damage. Abnormalities of gait
or tandem gait often predominate, out of
proportion to the degree of weakness or sen- rate,108 although it may be useful if the clinical
sory abnormality. Two tests of balance with evaluation suggests alternative diagnoses such
the patient standing barefoot on a hard floor as cerebral hemorrhage or thromboembolic
are particularly useful. For the sharpened stroke. Emission tomography (single-photon
Romberg test, the patient stands with one emission computed tomography and positron
foot in front of the other, arms crossed across emission tomography) is less sensitive than
the chest.The score is the number of seconds clinical evaluation109 or shows nonspecific
balance can be maintained (maximum score, findings.110 Limb radiographs can occasionally
60). A score of 30 has been proposed as the show soft-tissue gas,20 but this is neither sensi-
lower limit of normal.103 Tandem gait requires tive nor specific for the diagnosis of DCS.
the patient to walk heel-to-toe without falling.
This can be performed in increasing order of
difficulty as follows: with eyes open, walking Neuropsychology
forward then backward; with eyes closed,
forward then backward. Formal neuropsychological testing can be ab-
normal in DCS111,112 and may be more sensitive
for the detection of cortical DCI than standard
Cardiorespiratory Decompression
neurologic examination.113 However, a base-
Sickness line test is rarely available, a wide variation
Hypotension, tachycardia, dyspnea, and cough exists in the normal performance range, and
are usually due to massive pulmonary AGE test results are strongly influenced by mood,
(cardiorespiratory DCS, “chokes”), which may especially if depressed; education level; the
present as a worsening shock state. language of the test; alcohol and other drug
use; head injuries; and practice.114 Follow-up
studies of divers with DCI, which have cited
Radiography neuropsychometric abnormalities as the basis
of recovery, have overestimated morbidity and
A chest radiograph is not essential, but it can be confused brain injury in many patients with a
useful in patients with DCI104 to demonstrate post-traumatic stress disorder.113,115,116
barotrauma that may not be detectable on
physical examination, such as mediastinal em-
physema or small amounts of subcutaneous air. Neurophysiology
The presence of a pneumothorax may require
a chest tube, which is essential if treatment is Abnormalities in the electroencephalogram
to be administered in a monoplace chamber. can be found in acute DCI,113 although it is not
Aspiration of vomitus or salt water, or pulmo- a practical test in this setting and an abnormal
nary overdistension, can cause focal air-space finding is nonspecific and not useful to follow
opacities.105 Severe VGE, which can result in treatment. Because severe spinal cord DCS
cardiopulmonary DCS (“chokes”), causes often involves the posterior columns, somato-
increased pulmonary capillary permeability, sensory-evoked potentials may be abnormal.
which can manifest as pulmonary edema.106 Somatosensory-evoked potentials are a com-
Radiographs of the skull and sinuses may monly used end point in animal studies of
occasionally reveal fluid in the paranasal severe spinal cord DCS.117–127 However, expe-
sinuses suggestive of sinus barotrauma. Sinus rience in human DCS reveals that it is not
barotrauma of ascent may also produce tissue sensitive enough to detect mild abnormalities
gas, which has been observed in the subdural that can be observed clinically.108,116,128
space107 or in the subcutaneous tissue. Head In contrast, both audiometry and vestibular
scanning by both computerized tomography testing are useful to investigate patients with
and magnetic resonance imaging is generally inner ear DCS. Clinical testing of hearing dur-
not useful in making the diagnosis of neuro- ing a physical examination is neither sensitive
logic DCI because of a high false-negative nor quantitative. For patients with vertigo or
ataxia, physical examination is usually inade- against a clinical series and appears to be rela-
quate to differentiate vestibular from brain- tively specific, though not sensitive. Given the
stem or cerebellar pathology. In particular, utility of point systems in other areas of medi-
nystagmus caused by vestibular lesions is typ- cine, a validated diagnostic tool would be
ically detectable only with the eyes closed. In welcome in undersea medicine.
inner ear DCS, neurophysiologic testing in the
form of electronystagmography with caloric
Scoring Systems of Severity
stimulation and air/bone audiography is more
sensitive and specific than clinical evaluation.
and Recovery
Brainstem auditory-evoked responses interro- One of the most commonly used classifica-
gate the patient’s acoustic pathways from the tions of DCS was published by Golding and
cochlea to the brainstem and may be useful in colleagues,132 who proposed two types: type I,
the assessment of an uncooperative patient. pain only; and type II, patients with symptoms
Inner ear DCS is the only form of DCI in other than pain or with abnormal physical
which neurophysiologic testing is more sensi- signs. Over the years this classification has
tive than clinical examination.129 been modified in various ways. Instead of clas-
sifying the type of DCS, the current U.S. Navy
Diving Manual classifies symptoms.92 Type I
Diagnostic Criteria symptoms include joint pain (musculoskeletal
or pain-only symptoms) and symptoms that
In the absence of an unequivocal diagnostic test involve the skin (cutaneous symptoms) or
for DCI, empirical clinical criteria have been swelling and pain in lymph nodes. Type II
used. These have typically included for DCS a symptoms include neurologic, inner ear (stag-
minimum depth–time exposure, typical clinical gers), and cardiopulmonary (chokes) symp-
manifestations, and a response to recompression toms. In this scheme, type I and II symptoms
treatment (recognizing that incomplete response may be present in the same patient.
to treatment may occur with severe cases or The term type III DCS was introduced to
long delays). For AGE, criteria have included describe patients who suffered AGE after tak-
evidence of rapid ascent or breath-holding dur- ing up a significant inert gas load during the
ing ascent, short onset time (usually minutes), earlier part of a dive and who experienced
cerebral manifestations, evidence of PBT, and re- manifestations characteristic of both AGE and
sponse to recompression. Insight was gained neurologic DCS.133 Previously, these classifica-
into the diagnostic criteria actually used by tions were used to decide treatment; however,
asking undersea medicine experts to diagnose a this is no longer the case.92
series of false clinical vignettes.130 Using this Although the traditional classification is of-
scheme, for the diagnosis of DCS, the most im- ten adequate for simple descriptive purposes,
portant factors in order of importance were: the term type II encompasses a huge range of
(1) a neurologic symptom as the primary pre- severity. For epidemiologic research, a classifi-
senting symptom, (2) onset time of symptoms, cation or scoring scheme with more grada-
(3) joint pain as a presenting symptom, (4) any tions is required. Several such scoring systems
relief after recompression, and (5) the maxi- have been published.131,134–141
mum depth of the last dive. For the diagnosis of
AGE, the top five factors were: (1) onset time of
symptoms, (2) altered consciousness, (3) any Summary
neurologic presenting symptom, (4) motor
weakness, and (5) seizure as the primary pre- Before treating a patient with suspected DCI,
senting symptom. the only required components are a medical
A point system for the diagnosis of DCS has history and physical examination. Ancillary
been proposed, based on specific clinical diagnostic tests such as a blood hemoglobin
markers of DCS, time of onset, and depth–time and chest radiograph may be helpful but
exposure.131 It has been tested retrospectively are not absolutely required. Although further
testing may be indicated (e.g., vestibular or can occur because of aspiration of water or
auditory), it can be postponed until after ini- vomitus, pneumothorax, or cardiorespiratory
tial recompression treatment. DCS.The use of supplemental oxygen has two
benefits: the treatment of arterial hypoxemia
and an enhanced rate of resolution of inert
TREATMENT gas bubbles. The fact that O2 administration
can reduce bubble load in DCI was first dem-
Natural History if Untreated onstrated by Bert in the 19th century using
experimental animals.9 The mechanism is be-
The natural history of untreated DCS was pro- lieved to be a decrease in tissue inert gas par-
vided by authors in the 19th and early 20th tial pressure and, therefore, a higher diffusion
centuries. A compressed air environment with- gradient for inert gas from bubble to tissue.
out recompression facilities was used during Supplemental oxygen, therefore, is routinely
construction of the Eads Bridge over the recommended. As high an inspired concentra-
Mississippi River in St. Louis from 1867 to 1874. tion of O2 as is possible should be adminis-
Of about 600 men employed, there were 91 re- tered, preferably using a tightly fitting face
ported cases of bends, of which 30 were classi- mask. Other appropriate interventions may
fied as serious; 2 were crippled for life; and there include endotracheal intubation and chest
were 13 deaths. Some of the severe cases im- tube insertion to treat pneumothorax.
proved spontaneously,142 including Dr. Alphonse Systemic capillary leak, coronary artery em-
Jaminet, the physician hired to provide medical bolism, or peripheral vasodilation caused by
support for the men. After spending 2¾ hours spinal cord injury (“spinal shock”) may cause
at a pressure of 45 pounds per square inch hypotension and tissue hypoperfusion. Fluid
gauge (psig; approximately 31 meters sea water administration should be routine, except in
[msw]) and decompressing over 3½ minutes, he isolated cerebral AGE occurring after a short
experienced epigastric pain, leg weakness, and time in shallow water (see later). In cases of
speech difficulty. Twelve hours later, he began cardiorespiratory DCS (chokes) occurring in
moving his legs and recovered completely.43,142 the field, the benefits of aggressive fluid resus-
Even after introduction of therapeutic recom- citation should be weighed against a possible
pression, many cases of pain-only bends were risk for worsening pulmonary edema. In an
untreated and resolved spontaneously.11 animal model of chokes, diuretics appear to
In pearl divers working around Broome, improve short-term outcome.
Australia, 60 of 200 divers with DCS experi- For DCS or AGE, recommendations have
enced rapid death, and 11 died later (8 of sep- traditionally included placement of the pa-
ticemia caused by cystitis and decubitus tient in head-down or left lateral decubitus
ulcers, and 3 of meningitis). The majority of position. The rationale is based on one study
the remaining divers recovered spontaneously, in which dogs were more tolerant of intrave-
with only approximately 10% permanently nously injected bubbles when placed on their
affected by slight paresis, generally of the ante- left sides,144 possibly because in that position
rior muscles of the legs.6 Spontaneous recov- the right ventricular outflow tract is inferior
ery in 8 of 187 cases of serious DCS was to the right ventricular cavity, allowing air to
reported in a series collected by the Royal migrate superiorly and prevent obstruction to
Navy between 1965 and 1984.143 blood flow. Furthermore, left-sided air injec-
tion was more likely to cause death when
dogs were embolized in the head-up position
First-Aid Treatment compared with supine or head-down posi-
tion.145 In another study, head-down position
Initial treatment of the injured diver should reduced the volume of intra-arterial bubbles
be similar to the treatment of any patient with in the cerebral vessels because of the hydro-
a major injury. Attention to airway, breathing, static effect on intravascular pressure.146
and circulation are paramount. Hypoxemia A case report describes unconsciousness and
hypotension after injection of air into the aor- 15 psi higher were sometimes used.158 After
tic root, which resolved within 1 minute after reaching the pressure of relief, the consensus
placing the 63-year-old woman in the vertical at the time favored waiting 20 to 30 minutes
head-down position.147 However, increased before starting decompression.
brain swelling has been observed when the Oxygen administration was not routinely
head-down position is used.146,148 Moreover, used until much later, although its scientific
buoyancy appears to have little effect on the rationale had been available since the latter
distribution or hemodynamic consequences part of the 19th century. In the 1870s, in Paris,
of either arterial149,150 or venous151,152 air. For Paul Bert first noted that when 100% oxygen
mild cases (e.g., pain-only bends), there is no was administered to animals after decompres-
known reason for body position to be impor- sion, some of the signs would resolve.9 He
tant. For severe cases, the patient should be observed that oxygen administration caused
placed in the best position possible for deliv- resolution of intravascular gas, but that recom-
ery of care and maintenance of blood pres- pression (with air) was necessary to resolve
sure, usually supine. Lateral decubitus position bubbles that had migrated into the central ner-
may be indicated if the patient is unconscious vous system. Zuntz159 first suggested using
and does not have a protected airway. both pressure and oxygen, although he did not
have the opportunity to administer it. When it
was tried, the initial results, in fact, were some-
Recompression Therapy what disappointing, probably because it was
not administered for long enough.11
Recompression therapy for caisson disease
was first proposed in 1854 by Pol and Wattelle
in Europe10 and then by Andrew Smith, the Choice of Pressure
physician for the Brooklyn Bridge construc-
tion in the 1870s3,153; however, it was not Compression reduces bubble volume by
implemented until 1889 during the Hudson physical means, such that bubble volume re-
River tunnel construction when Ernest Moir duces in inverse proportion to ambient pres-
effectively used recompression to reduce the sure. Although the volume may be consider-
caisson disease death rate.154 Improved out- ably reduced in this manner, the reduction in
come with recompression was then reported the various bubble dimensions will depend
in 1896 in England during excavation of the on the shape. For example, compression of a
Blackwall Tunnel under the Thames River.155 spherical bubble to 6 ATA (606 kPa) will
Statistical evidence for the benefit of recom- reduce bubble volume to just under 17% of
pression was shown in New York City by the original, but will reduce the diameter by
Keays,11 who reported a failure rate of 13.7% only 43%. Cylindrical bubbles, such as might
in caisson workers with pain treated without occur inside a blood vessel, will experience a
recompression versus a 0.5% failure rate with relatively greater reduction in dimensions,
recompression treatment. but predominantly in bubble length.
Initiation of recompression therapy for div- Although a reduction in bubble volume
ers took much longer. It was not until the will continue to occur as ambient pressure is
1924 edition of the U.S. Navy Diving Manual156 increased, several factors limit the maximum
that air recompression was recommended. In compression. Bubble size reduction is asymp-
different settings treatment pressure was totic rather than linear. Progressive recom-
based either on the depth of the dive (or a pression will also result in a further uptake of
fraction or multiple thereof) or on the depth inert gas, unless 100% oxygen is breathed. As
of relief.157 During construction of the a result of this inert gas uptake, symptoms
New York-Queens Midtown Tunnel in 1938, may become even more pronounced during
the recommended treatment pressure was the subsequent decompression.160 In addi-
equal to that to which the worker was origi- tion, nitrogen narcosis impairs the perfor-
nally exposed, although pressures 5, 10, or mance of chamber tenders at pressures
greater than 4 to 6 ATA. Therefore, except 60 fsw (compared with the current standard
under unusual circumstances, conventional of 60 minutes). In the 20 years after World
(air/oxygen-nitrogen) recompression therapy War II, the failure rate for the tables used
is limited to 6 ATA (606 kPa). (mostly air) was nearly 30%.164
Canine models have been used to investi- A PO2 of 3 ATA is the greatest ambient pres-
gate different pressures systematically.161 After sure at which 100% O2 administration is practi-
AGE, the investigators tested different pres- cal: central nervous system oxygen toxicity is
sures varying from 2.8 to 10 ATA breathing air limiting at higher PO2. A study of the treatment
and at 2.8 ATA breathing 100% oxygen. No of spinal cord DCS with different PO2 (from
significant differences were observable in the 1–3 ATA) at a constant ambient pressure
different rates of recovery, and none of the (5 ATA) revealed the optimum inspired PO2 was
treatments was better than oxygen administra- 2 to 2.5 ATA.121 In a follow-up study to com-
tion at 2.8 ATA (60 fsw). In a series of experi- pare PO2 of 2.0 ATA with 2.8 ATA, no significant
ments in anesthetized dogs with spinal cord difference in outcome was observed.123
DCS, ambient treatment pressures of 3, 5, and
7 (inspired PO2 2 ATA) and 2.8 ATA (inspired
PO2 2.8 ATA) were tested; results showed no Inert Gas
measurable advantage of any pressure.122
During a therapeutic compression, the use
of a different inert gas from the one that
Oxygen was breathed during the dive may facilitate
bubble resolution. If the properties of the
The effect of 100% O2 breathing to “wash out” “therapeutic” inert gas are appropriately
inert gas results in an increased partial pressure chosen such that its rate of transport through
gradient for inert gas from inside to outside a tissue is lower than the first, then bubble
bubble. This increases the rate of resolution of shrinkage will be accelerated. Helium is
tissue gas. Use of O2 also prevents any addi- approximately 40% less soluble than nitro-
tional uptake of inert gas during recompres- gen in blood and could therefore facilitate
sion therapy of decompression illness. HBOT bubble resolution in this way. Anecdotal
currently represents the standard of care for reports have suggested an advantage of he-
treatment of DCI. liox treatment of DCI after nitrogen-oxygen
The initial rationale for hyperbaric oxygen (or air) dives.165 Although some animal stud-
provided by Zuntz159 was accelerated washout ies of cardiopulmonary decompression ill-
of inert gas and bubble resolution. There are ness have failed to demonstrate an advan-
probably additional, possibly more important, tage of heliox,166,167 compared with air or
mechanisms by which hyperbaric oxygen oxygen breathing, its administration causes
treats DCI. These include increased oxygen more rapid shrinkage of air bubbles in adi-
delivery and pharmacologic effects of hyper- pose tissue,168 spinal cord white matter,169
baric oxygen such as edema resolution and tendon, muscle, and aqueous humor.170 After
inhibition of 2-integrin–mediated neutrophil heliox diving, bubbles tend to grow when
adhesion to injured endothelium.162 air is breathed; shrinkage is fastest with
In 1939,Yarbrough and Behnke163 reported 100% oxygen.171
the superiority of hyperbaric oxygen in treat- In humans, almost all cases of DCI can be
ing DCS, but it was not immediately adopted. treated at 2.8 ATA (60 fsw), where 100% oxy-
It became officially available to the U.S. Navy gen is both safe and effective. Choice of an
in 1944157 but was rarely used. In the Navy inert gas is important only at greater pres-
oxygen table, 100% O2 was administered sures. Experience with the use of deeper
at depths of 60 fsw and shallower, but only tables in which either nitrogen or helium can
for a total of 95 minutes, of which only be used as the inert gas have not consistently
30 minutes were spent breathing O2 at demonstrated an advantage of helium.172
Neurologic DCI, AGE, or pain-only or skin bends that fail to resolve within 10 minutes on the
table above:
2.8 ATA (18 m, 60 feet, 26 psig) for 30 minutes
30-minute decompression to 1.9 ATA
1.9 ATA for 60 minutes
30-minute decompression to 1 ATA
The monoplace table that Hart177,178 de- propriate because of the likelihood of greater
signed specifies 100% oxygen administration gas volume. An experimental study in anesthe-
at 3 ATA for 30 minutes followed by 2.5 ATA tized dogs using intracarotid air injection and a
for 60 minutes. skull window technique revealed that all visible
bubbles disappeared at a compression depth
of 100 fsw,183 suggesting that this would be an
Short Oxygen Treatment Tables
appropriate compression depth for AGE in div-
with Excursion to Pressure Greater ers. However, on the basis that fleet diving
Than 2.8 Atmospheres Absolute medical officers would demand a 165 fsw table,
U.S. Navy Tables 5A (later abandoned) and 6A
Different tables were developed in the U.S. (Fig. 14.15), incorporating a 30-minute period
Navy for the treatment of AGE, in which it was of air breathing at 165 fsw (50 msw), were in-
believed that a higher pressure would be ap- troduced. Many practitioners use 40% to 50%
Air
Oxygen
Descent rate 8 msw/min (25 fsw)
Total elapsed time 4 h 45 min
18 (not including descent time)
15 Ascent rate 0.3 msw/min (1 fsw)
Depth (msw)
12
9
6
3
0
2.4 20 5 20 5 20 5 30 15 60 15 60 30
Time (min)
Figure 14.13 U.S. NAVY TREATMENT TABLE 6. Table 6 is used for treatment of neurologic decompression
illness and pain-only or mild cutaneous symptoms that are not relieved within 10 minutes of reaching 60 feet (18 m)
breathing oxygen. Table 6 can be extended at 60 feet (18 m) and at 30 feet (9 m) if symptoms have not been
relieved within the first three oxygen cycles. A modified U.S. Navy Table 6 has been designed at the Catalina Marine
Science Center, allowing for up to 5 extensions at 60 fsw (18 msw; see Fig. 14.11). White areas denote air; gray
areas denote oxygen. fsw, feet sea water; msw, meters sea water. (From Moon RE, Gorman DF: Treatment
of the decompression disorders. In: Neuman TS, Brubakk AO (eds): The Physiology and Medicine of
Diving. New York, Elsevier Science, 2003, pp 600–650, by permission.)
oxygen (rather than air, as originally intended) pressure (up to 8.6 ATA, 868 kPa; 76 m,
during the 30-minute period at 6 ATA. Comex 250 feet), Leitch and Green160 concluded that
Table 30 (Fig. 14.16) uses an excursion to 30 m additional recompression rarely either al-
(98 feet), with 50/50 oxygen/helium or oxy- tered the clinical course or produced clini-
gen/nitrogen as the breathing gas by mask cally significant improvements. A published
while the ambient pressure is greater than series of the routine use of deep initial re-
2.8 ATA (282 kPa). When this table is used, compression (up to 8.5 ATA) indicated excel-
European practice tends to favor the use of lent outcomes but no advantage over stan-
heliox, whereas American experience suggests dard U.S. Navy Tables.185 However, anecdotal
that nitrogen/oxygen is as efficacious. reports suggest that a small number of divers
Although compression deeper than 2.82 ATA with DCI who do not respond to treatment
remains in the armamentarium of most na- at 2.8 ATA (282 kPa) may respond at a higher
vies and offshore commercial diving opera- pressure,186 particularly if 50/50 or 40/60
tors, and many practitioners have observed oxygen/nitrogen mixtures are used in prefer-
good clinical results, published evidence for ence to air at 6 ATA.187–190
its efficacy is lacking. Animal experiments
have thus far failed to find an advantage of
Table 6A over Table 6 in models of AGE.184 In Deep Tables
a retrospective review of 14 divers with DCI
who had not responded satisfactorily to ini- Decompression illness during or after short-
tial compression to 2.8 ATA (282 kPa) and duration deep dives (usually deeper than 50 m
who were then recompressed to a greater or 165 feet) may benefit from recompression
0
20 20 20 20 20 20 20 20 30 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 30
5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5
Time (min)
Figure 14.14 CATALINA TREATMENT TABLE. The “Catalina” Table is a modified version of U.S. Navy Treatment Table 6. All oxygen
breathing cycles are of 20 minutes in duration followed by 5 minutes breathing air. In its current implementation, shorter versions of this table
may be used as follows. After 3 oxygen cycles at 60 feet (18 m), a minimum of 6 cycles are required at 30 feet (9 m; equivalent to U.S. Navy
Table 6); after 4 cycles at 60 feet, 9 cycles are required at 30 feet; after 5 to 8 cycles at 60 feet, a minimum of 12 cycles are required at
30 feet. Up to 18 cycles at 30 feet (as shown above) can be used. Tenders must breathe oxygen for 60 minutes at 30 feet and during the
decompression to the surface (total, 90 minutes). If there have been fewer than 4 oxygen cycles at 60 feet and fewer than 9 cycles at 30 feet,
then only 30 minutes of oxygen breathing is required for the tender at 30 feet in addition to the decompression time (total, 60 minutes),
although some practitioners prefer the longer recommendation above. Further treatments can be started only after 12 hours of air breathing at
the surface. For further detail on this table, see Pilmanis.175 White areas denote air; gray areas denote oxygen. fsw, feet sea water;
msw, meters sea water. (From Moon RE, Gorman DF: Treatment of the decompression disorders. In: Neuman TS, Brubakk AO
(eds): The Physiology and Medicine of Diving. New York, Elsevier Science, 2003, pp 600–650, by permission.)
30
Total elapsed time 5 h 19 min
24
18
Ascent rate 0.3 msw/min (1 fsw/min)
12
6
0
30 4 20 5 20 5 20 5 30 15 60 15 60 30
Time (min)
Figure 14.15 U.S. NAVY TABLE 6A. U.S. Navy Table 6A consists of a 30-minute excursion to 6 atmospheres absolute (ATA;
606 kPa; 165 feet, 50 m) while the patient breathes air, followed by an oxygen breathing portion identical to U.S. Navy Table 6. The original
rationale of this table was to provide for maximum Boyle’s Law compression of gas during the 6 ATA (606 kPa) excursion, followed by bub-
ble resolution augmented by oxygen breathing. It was initially recommended for treatment of arterial gas embolism. Although the U.S. Navy
still recommends air as the appropriate breathing gas at 6 ATA, others have used nitrogen-oxygen mixtures (usually 60/40 or 50/50). The
advantage of U.S. Navy Table 6A compared with U.S. Navy Table 6 has been called into question by some controlled animal studies in sug-
gesting that compression beyond 2.82 ATA (282 kPa) provides no additional benefit. Nevertheless, clinical experience has suggested that a
small percentage of patients may respond to treatment at 6 ATA but fail to do so at 2.8 ATA. The major use of U.S. Navy Table 6A, compared
with U.S. Navy Table 6, is likely to be for patients with large volumes of gas treated with short delay. White areas denote air; light gray
areas denote oxygen; dark gray areas denote air or optional 50/50 nitrogen/oxygen. fsw, feet sea water; msw, meters sea water.
(From Moon RE, Gorman DF: Treatment of the decompression disorders. In: Neuman TS, Brubakk AO (eds): The Physiol-
ogy and Medicine of Diving. New York, Elsevier Science, 2003, pp 600–650, by permission.)
CX 3086
BREATHING MIX
DEPTH DURATION ELAPSED
PATIENT ATTENDANT TIME
HELIOX 50/50 AMBIENT
30 m 60 min 60 min ON BIBS 01h.00
HELIOX 50/50: 1 BIBS session AMBIENT
30–24 m 30 min 01h.30
25 min ON + 5 min OFF
HELIOX 50/50: 1 BIBS session AMBIENT
24 m 30 min 02h.00
25 min ON + 5 min OFF
HELIOX 50/50: 1 BIBS session AMBIENT
24–18 m 30 min 02h.30
25 min ON + 5 min OFF
OXYGEN: 2 BIBS sessions AMBIENT
18 m 60 min 03h.30
25 min ON + 5 min OFF
OXYGEN: 1 BIBS session AMBIENT
18–12 m 30 min 04h.00
25 min ON + 5 min OFF
OXYGEN: 6 BIBS sessions OXYGEN: 6 BIBS sessions
12 m 180 min 07h.00
25 min ON + 5 min OFF 25 min ON + 5 min OFF
OXYGEN OXYGEN 07h.30
12–0 m 30 min 30 min ON BIBS 30 min ON BIBS
DEPTH
Ascent rate
30 m 5 min/m HELIOX 50/50
OXYGEN
Ascent rate
24 m
5 min/m AMBIENT
Ascent rate
18 m 5 min/m
Ascent rate
2 min 30/m
12 m
60 25 25 25 25 25 25 25 25 25 25 25 25 30
0
5 5 5 5 5 5 5 5 5 5 5 5 TIME
Figure 14.16 COMEX TABLE 30. This 30-m (100-feet) table is frequently used with 50/50 heliox in European
diving practice for the initial treatment of decompression illness (Kol S, Adir Y, Gordon CR, et al: Oxy-helium treatment
of severe spinal decompression sickness after air diving. Undersea Hyperb Med 20:147–154, 1993). It is also used
with 50/50 oxygen/nitrogen. (From James PB, Imbert J-P, Arnoux G, et al: Comex Medical Book, Revised
ed. Marseille, France, Comex SA, 1986.)
to depths greater than those specified by the col, based on the recommendations of the
standard tables, particularly if there has been European Undersea Biomedical Society and
significant missed decompression.191 Exam- the U.K. Association of Diving Contractors,
ples are the Lambertsen/Solus Ocean Systems consists of compression to 18 m (60 feet)
Table 7A (Fig. 14.17) and U.S. Navy Treatment or depth of relief breathing helium/oxygen.
Table 8 (Fig. 14.18). Table 8 was designed for The decompression schedule is shown in
treating deep, uncontrolled ascents (“blow- Table 14.2. Guidelines for the use of this table
ups”) when more than 60 minutes of decom- are discussed later in the “Closed-Bell and
pression has been missed.192 Another proto- Saturation Diving” section.
50
46
Depth (msw)
30 Air or helium–oxygen
Oxygen
21
18
12
9
6
3
0
30 1 h 5h 5h 21/2 h 21/2 h 5h 1h
min 30 min intervals 30 min intervals 30 min intervals
Figure 14.17 LAMBERTSEN/SOLUS OCEAN SYSTEMS TABLE 7A. This table is most commonly used
in commercial diving for symptoms that develop at pressure, for recompression deeper than 165 feet (50 m), or
when extended decompression is necessary. The patient is held at the treatment depth for 30 minutes. If he or she
is breathing air, the depth limit should be 200 feet (61 m). After the 30-minute compression, the patient is de-
compressed to 165 feet (50 m) in 1 minute, and then the table followed as shown. If the patient is breathing he-
lium/oxygen, he or she should be compressed to depth of relief plus 33 feet (10 m), but not deeper than the bot-
tom depth of the dive. After a 30-minute period at that depth, the chamber should be decompressed to 165 feet
at 15 ft/hr (50 m at 4.5 m/hr), and the remainder of the table followed as shown. White areas denote air of he-
lium/oxygen; gray areas denote oxygen. fsw, feet sea water; msw, meters sea water. (Reproduced from Moon
RE, Gorman DF: Treatment of the decompression disorders. In: Neuman TS, Brubakk AO (eds): The
Physiology and Medicine of Diving. New York, Elsevier Science, 2003, pp 600–650, by permission.)
Saturation Treatment after Shallow be used for the chamber atmosphere without
Dives causing pulmonary oxygen toxicity (for de-
tails, see U.S. Navy Diving Manual92; Fig. 14.19).
In the event that a patient with significant In this table, the patient is maintained at pres-
neurologic symptoms, especially weakness, sure for a minimum of 12 hours.
has incomplete relief of symptoms after a Saturation treatments are labor intensive and
period at 2.8 ATA (282 kPa) during U.S. Navy expensive and require capabilities not available
Table 6, or if there is evidence of deterioration at most chamber facilities, including chamber
during decompression from that treatment atmosphere monitoring and maintenance, as
table, then saturation recompression may be well as two inside tenders and two chamber
an option.This technique consists of maintain- operators constantly on duty. Saturation treat-
ing the patient in the hyperbaric chamber at a ment, therefore, should not be used unless the
fixed ambient pressure while administering patient has significant neurologic injury and
intermittent enriched O2 treatment.188,193 The adequate facilities exist for its implementation.
most straightforward saturation treatment ta- Saturation treatment has not been shown to be
ble is U.S. Navy Table 7 because it is designed more effective than repetitive oxygen tables.
for a depth (2.8 ATA, 60 fsw) at which air can Proposed guidelines for saturation treatment
76
69 msw: 0.5 h
61
50 msw: 3 h
46
Depth (msw)
43 msw: 5 h
37 msw: 8 h
30 30 msw: 11 h
24 msw: 15 h
18 msw: Unlimited
15
12 msw: Unlimited
6 msw: Unlimited
0
0 10 20 30 40 50 60
Time (h)
Figure 14.18 U.S. NAVY TREATMENT TABLE 8. Designed for treatment of deep “blowups,” in which there
has been more than 60 minutes of missed decompression stop time. It can be used in other situations, for exam-
ple, to compress to a depth greater than 165 feet sea water (fsw; 50 meters sea water [msw]), or to stop decom-
pression between 165 and 60 fsw. Maximum times at each depth are shown; times at 60, 40, and 20 fsw are un-
limited; decompression occurs in increments of 2 fsw. When deeper than 165 fsw (50 msw), to reduce narcosis, a
16% to 21% O2 in helium can be administered. Four treatment cycles, each consisting of 25 minutes of “treatment
gas” followed by 5 minutes of chamber air, can be administered deeper than 60 fsw. Treatment gas used deeper
than 60 fsw is 40% O2 in either He or N2; at 60 fsw (18 msw) or shallower, treatment gas is 100% O2. For O2
administration at 60 fsw or shallower, U.S. Navy Treatment Table 7 guidelines are used. Further details can be found
in the U.S. Navy Diving Manual.92 (From Moon RE, de Lisle Dear G, Stolp BW: Treatment of decompres-
sion illness and iatrogenic gas embolism. Respir Care Clin N Am 5:93–135, 1999, by permission.)
12
0.6 msw/h (2 fsw/h)
6
0.3 msw/h (1 fsw/h)
4 h stop
0 25 252525 2h 25 252525
555 555 0 6 12 16 18 24 30 32 36
12 h Minimum Time (min)
No maximum limit
Figure 14.19 U.S. NAVY TREATMENT TABLE 7. This table allows for a prolonged (saturation) stay at 60 feet
(18 m). It is used for serious cases of decompression illness that resolve incompletely during one of the standard
oxygen tables, or for deterioration during decompression from one of those tables. U.S. Navy guidelines specify that a
minimum of 12 hours must be spent at 60 feet, but the maximum duration is not specified. To simplify timekeeping,
oxygen breathing periods of 25 minutes are followed by 5 minutes of breathing chamber atmosphere (air). Four oxygen
breathing periods are alternated with 2 hours of continuous air breathing; if the patient is conscious, this cycle should
be continued until a minimum of eight oxygen breathing periods have been administered. Oxygen breathing periods
made before the decision to saturate at 60 feet may be counted. Oxygen breathing periods may be continued to
maximize the benefit, but symptoms of pulmonary oxygen toxicity (e.g., pain on inspiration) may require a modification
of the above schedule. If the patient is unconscious, oxygen breathing should generally be stopped after a maximum of
24 oxygen breathing periods. White areas denote air; light gray areas denote oxygen; dark gray areas denote
oxygen breathing periods of 25 minutes are followed by 5 minutes of breathing chamber atmosphere. *See
U.S. Navy Diving Manual92 for details. (From Moon RE, Gorman DF: Treatment of the decompression
disorders. In: Neuman TS, Brubakk AO (eds): The Physiology and Medicine of Diving. New York,
Elsevier Science, 2003, pp 600–650, by permission.)
locations where chamber recompression is should be given 100% oxygen for 1-hour peri-
not available.194,197–200 ods, interspersed with similar periods breath-
Australian guidelines198,200,201 include the ing air.
following mandates: (1) oxygen administration
(and adequate oxygen supply) via a full face
mask, which protects the airway of a semicon- Choice of Treatment Algorithms
scious diver; (2) adequate thermal protection
(e.g., wet suit); (3) a rope 10 meters long Surface-Oriented Diving
(a seat or harness may be rigged for support of Mild Bends or Limb Pain Only
the diver); (4) an attendant to accompany the
diver; and (5) some form of communication According to U.S. Navy guidelines and com-
among patient, attendant, and surface. Oxygen mon practice, divers with pain-only or skin
should be delivered to the diver from a tank bends can be treated using U.S. Navy treat-
on the surface with a nonreturn valve between ment Table 5, provided there are no neuro-
the supply line and the mask. The initial com- logic abnormalities by history or on examina-
pression depth is 9 m (30 feet). Time at depth tion and if complete relief of symptoms occurs
is usually 30 minutes, although this can be ex- within 10 minutes of compression to 2.8 ATA
tended for 30 or 60 minutes for severe cases. (282 kPa). Green and colleagues202 have
Ascent is at a rate of 12 min/m (4 min/ft). If the reviewed a series of cases treated by the U.S.
symptoms recur, the patient should remain at Navy and found that Table 5 is as effective
depth an additional 30 minutes before surfac- as Table 6 when used according to these
ing. For 12 hours after surfacing the diver guidelines.
From Mitchell SJ, Doolette DJ, Wachholz CJ, et al. (eds): Management of Mild or Marginal Decompression Illness in Remote Locations. Durham, NC, Divers Alert
Network, 2005.
Table 14.4 Undersea and Hyperbaric Medical Society Summary Guidelines for Adjunctive
Therapy
AGE (NO SIG- DCS: PAIN DCS: NEU- DCS: CHOKES DCS WITH LEG
NIFICANT INERT ONLY, ROLOGICAL IMMOBILITY
GAS LOAD) MILD (DVT PROPHY-
LAXIS)
Aspirin 2B(C) 2B(C) 2B(C) 2B(C)
NSAIDs 2B(C) 2B(B) 2B(B) 2B(C)
Surface O2 1(C) 1(C) 1(C) 1(C)
Anticoagulants, 2B(C) 3(C) 2B(C) 2B(C) 1(A)
thrombolytics,
IIB/IIIA agents
Corticosteroids 3(C) 3(C) 3(C) 3(C)
Lidocaine 2A(B) 3(C) 2B(C) 3(C)
Fluid
D5W 3(C) 3(C) 3(C) 3(C)
LR/crystalloid 2B(C) 1(C) 1(C) 2B(C)
Colloid 2B(C) 1(C) 1(C) 2B(C)
be more likely to suffer recurrences caused by 5. Bassett-Smith PW: Diver’s paralysis. Lancet 1:309–
habitual use of provocative depth–time expo- 310, 1892.
6. Blick G: Notes on diver’s paralysis. Br Med J 2:1796–
sures and conditions or by individual physio-
1799, 1909.
logic predisposing factors. Speculation also 7. Bendrick GA, Ainscough MJ, Pilmanis AA, et al: Prevalence
exists that DCS is more likely to occur in tis- of decompression sickness among U-2 pilots.Aviat Space
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supporting evidence is anecdotal.
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times, shallower depths, or both).298 Few iden- Bethesda, MD, Undersea Medical Society, 1978.
10. Pol B, Wattelle TJJ: Mémoire sur les effets de la com-
tifiable individual predisposing factors have
pression de l’air appliquée au creusement des puits à
been described.Testing for a PFO is not gener- houille. Ann Hyg Pub Med Leg 2:241–279, 1854.
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present: (1) the preceding depth–time profiles 3,692 cases. Dept Med Publ Cornell Univ Med Coll
2:1–55, 1909.
are likely to have been associated with
12. Gillis MF, Karagianes MT, Peterson PO: Detection of gas
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severe (i.e., include motor weakness, vertigo, pler flowmeter. J Occup Med 11:245–247, 1969.
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222:251–252, 1969.
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