Neurologic Complications of Scuba Diving
© American Family Physician written by Herbert B. Newton
Recreational scuba diving has become a popular sport in the United
States, with almost 9 million certified divers. When severe diving injury
occurs, the nervous system is frequently involved. In dive-related
barotrauma, compressed or expanding gas within the ears, sinuses and lungs
causes various forms of neurologic injury. Otic barotrauma often induces
pain, vertigo and hearing loss. In pulmonary barotrauma of ascent, lung
damage can precipitate arterial gas embolism, causing blockage of cerebral
blood vessels and alterations of consciousness, seizures and focal
neurologic deficits. In patients with decompression sickness, the vestibular
system, spinal cord and brain are affected by the formation of nitrogen
bubbles. Common signs and symptoms include vertigo, thoracic myelopathy with
leg weakness, confusion, headache and hemiparesis. Other diving-related
neurologic complications include headache and oxygen toxicity. (Am Fam
Physician 2001;63:2211-8,2225-6.)
Recreational scuba diving, which is defined as pleasure diving without
mandatory decompression to a maximum depth of 130 ft, has become a popular
activity in the past 20 years. In the United States alone, there are almost
9 million certified divers.(1) Although divers are concentrated along
coastal regions, many others dive in inland lakes, streams, quarries and
reservoirs, or fly to distant dive sites. Physicians practicing almost
anywhere in the United States may see a patient with a dive-related injury
or complaint.
In general, severe injury and death are uncommon in recreational diving
accidents.(1-5) The Divers Alert Network(1) reports an average rate of 90
fatalities per year since 1980. Each year, between 900 and 1,000 divers are
treated with recompression therapy for severe dive-related complications. In
many of these patients, one or more of the major symptoms are neurologic in
origin. The nervous system is frequently involved in dive-related
complications and fatalities.(5) Physicians need to be aware of the broad
spectrum of neurologic injuries that can occur during dive accidents to
ensure early recognition, accurate diagnosis and appropriate therapy.
Dive-Related Barotrauma
During descent and ascent in the water, the diver is constantly exposed to
alterations of ambient pressure. Barotrauma refers to tissue damage that
occurs when a gas-filled body space (e.g., lungs, middle ear) fails to
equalize its internal pressure to accommodate changes in ambient
pressure.(2-4) The behavior of gasses at depth is governed by Boyle's law:
the volume of a gas varies inversely with pressure.(6) During descent, as
ambient pressure increases, the volume of gas-filled spaces decreases unless
internal pressure is equalized. If the pressure is not equalized by a larger
volume of gas, the space will be filled by tissue engorged with fluid and
blood. This process underlies the common "squeezes" of descent that affect
the middle ear, external auditory canal, mask, sinuses and teeth.
OTIC AND SINUS BAROTRAUMA
Barotrauma to the middle or inner ear can occur during the descent or ascent
phases of the dive and may cause vertigo and other neurologic
symptoms.(2-5,7) Middle ear barotrauma of descent is the most common type of
diving injury and may involve hemorrhage and rupture of the tympanic
membrane. Symptoms include the acute onset of pain, vertigo and conductive
hearing loss that lateralizes to the affected side during the Weber's test.
In severe cases (usually during ascent), increased pressure in the middle
ear can cause reversible weakness of the facial nerve and Bell's palsy
(facial baroparesis).(8)
Vertigo can also be induced if barotrauma differentially affects the two
vestibular organs (alternobaric vertigo). The vertigo resolves after
pressure equalization occurs. Treatment of middle ear barotrauma involves
decongestants (e.g., intranasal oxymetazoline, oral pseudoephedrine),
antihistamines, analgesics and antibiotics (amoxicillin-clavulanate [Augmentin]
in a dosage of 500/125 mg three times per day or clindamycin [Cleocin] in a
dosage of 300 mg three times per day for 10 to 14 days) in patients with
otorrhea and perforation.(2,4,7)
Inner ear barotrauma also can develop in patients with middle ear barotrauma.(2-5,7)
A pressure gradient between the perilymph of the inner ear and the middle
ear cavity can occur, causing rupture of the labyrinthine windows (round and
oval) and leakage of perilymph into the middle ear (i.e., fistula). Symptoms
include the acute onset of vertigo, sensorineural hearing loss, tinnitus,
nausea and emesis. The Weber's test will lateralize to the unaffected side
in this group of patients. Reducing intracranial and perilymphatic pressures
through bed rest, head elevation and with stool softeners can help. Surgical
exploration may be necessary for repair of the fistula if conservative
treatment is ineffective within five to 10 days (i.e., the symptoms persist
or worsen).
PULMONARY BAROTRAUMA
Pulmonary barotrauma is the most severe form of barotrauma and occurs during
ascent.(2-4,9) In accordance with Boyle's law, as the ambient pressure is
reduced during ascent, gas inside the lungs will expand in volume.(6) If the
expanding gas is not allowed to escape by exhalation, the alveoli and
surrounding tissues will tear. The most common cause of pulmonary barotrauma
among recreational divers is breath holding. Other causes are related to
pulmonary obstructive diseases, such as asthma or bronchitis, which can lead
to the trapping of gas. Several forms of pulmonary barotrauma can develop,
including mediastinal emphysema, subcutaneous emphysema, pneumothorax and
arterial gas embolism. Arterial gas embolism is the most dangerous form of
pulmonary barotrauma and accounts for nearly one fourth of fatalities per
year among recreational divers.(3) In addition, it is the only form in which
neurologic symptoms predominate over pulmonary symptoms.(9)
Arterial gas embolism develops when free air enters the pulmonary
vasculature and is carried to the heart and arterial circulation.(9,10) A
large proportion of air bubbles can reach the brain, occlude blood vessels
and cause stroke-like events. The most common signs and symptoms of arterial
gas embolism are neurologic (Table 1(2,4,6,7)), although pulmonary symptoms
may also be present. In more than 80 percent of patients, symptoms develop
within five minutes of reaching the surface, but they also can occur during
ascent or after a longer surface interval.
TABLE 1
Presenting Signs and Symptoms
in Patients with Arterial Gas Embolism
Sign or symptom Percentage
Stupor or confusion 24
Coma without seizures 22
Coma with seizures 18
Unilateral motor deficits 14
Visual disturbances 9
Vertigo 8
Unilateral sensory deficits 8
Bilateral motor deficits 8
Collapse 4
Information from references 2,4,6 and 7.
Almost two thirds of patients with arterial gas embolism have alterations of
consciousness (i.e., coma or obtundation). Seizures, focal motor deficits,
visual disturbances, vertigo and sensory changes are also common. Spinal
cord lesions occur less frequently. Many patients show initial improvement
within minutes to hours, secondary to partial clearance of air emboli.
Magnetic resonance imaging (MRI) may demonstrate focal lesions in the brain
after arterial gas embolism.(10) Arterial gas embolism can mimic
decompression sickness, and the presentation of the two syndromes may be
clinically indistinguishable (Table 2(1-5,7-10).2,4,6) Arterial gas embolism
and decompression sickness can develop simultaneously in some patients. In
fact, the air emboli of arterial gas embolism may act as a nidus, or "seed,"
to precipitate decompression sickness. Therefore, the two syndromes are
often described and treated together using the more global term,
decompression illness.(4)
TABLE 2
Clinical Features, Dive Profile and Treatment of the Neurologic
Complications of Scuba Diving
Disorder Clinical features
Middle ear Acute pain, vertigo, hearing
barotrauma loss, rupture or hemorrhage
of descent of tympanic membrane
Facial baroparesis Ipsilateral facial paralysis,
resolves within hours
Inner ear Acute vertigo, nausea, emesis,
barotrauma tinnitus, sensorineural hearing
loss; often associated with
middle ear barotrauma
Arterial gas Stupor, confusion, coma,
embolism seizures, focal weakness,
visual loss
Inner ear DCS Acute vertigo, nausea, emesis,
nystagmus, tinnitus,
sensorineural hearing loss
Cerebral DCS Confusion, focal weakness,
fatigue, visual loss, diplopia,
speech dysfunction, gait
abnormality, headache
Spinal cord DCS Paresthesias/sensory loss in trunk
and/or extremities, leg weakness,
loss of bowel/bladder function
Headache (arterial Severe generalized headache
gas embolism associated with alteration of
or DCS) consciousness and other signs
Headache Pounding, throbbing pain;
(migraine) nausea, emesis, photophobia
Oxygen toxicity Focal seizures, visual constriction,
nausea, emesis, vertigo,
paresthesias, rare generalized
seizures
Disorder Dive profile
Middle ear During descent usually,
barotrauma possible during ascent
of descent
Facial baroparesis During ascent
Inner ear During descent usually,
barotrauma possible during ascent
Arterial gas Within five minutes of surfacing
embolism ([greater than] 80 percent) or during ascent;
significant time-depth exposure
not required
Inner ear DCS Within 30 to 60 minutes of
surfacing ([greater than] 50 percent),
90 percent by six hours; significant
time-depth exposure required
Cerebral DCS Same as above
Spinal cord DCS Same as above
Headache (arterial Usually develops within minutes
gas embolism of ascent, may persist without
or DCS) recompression treatment
Headache Usually precipitated during
(migraine) pre-dive activities or at depth
Oxygen toxicity Occurs at depth
Disorder Treatment
Middle ear Improved equalization techniques,
barotrauma oral and nasal decongestants;
of descent with otorrhea use antibiotics
Facial baroparesis No treatment
Inner ear ENT evaluation, bed rest, head
barotrauma elevation, stool softeners;
consider surgical exploration
if symptoms persist
Arterial gas 100 percent oxygen, United
embolism States Navy Table 6 algorithm
recompression, supportive care
Inner ear DCS Same as above
Cerebral DCS Same as above
Spinal cord DCS Same as above
Headache (arterial Same as above; analgesics
gas embolism
or DCS)
Headache Avoid precipitating stimuli,
(migraine) dive conservatively, consider
prophylactic therapy
Oxygen toxicity Reduce depth and oxygen
exposure, supportive care, seizure
management; see arterial gas
embolism treatment
ENT = ear, nose and throat; DCS = decompression sickness.
Information from references 1 through 5 and 7 through 10.
Treatment of arterial gas embolism consists of basic or advanced cardiac
life support, 100 percent oxygen, rehydration and transport to a
recompression facility.(2,4,9,10) Oxygen reduces ischemia in affected
tissues and accelerates the dissolution of air emboli. Seizures,
arrhythmias, shock, hyperglycemia and pulmonary dysfunction should be
treated, if present. Recompression therapy should be initiated immediately,
using the United States Navy (USN) Table 6 algorithm.(2-5,10,11)
Recompression therapy reduces the size of air bubbles by increasing ambient
pressure, expedites passage of emboli through the vasculature and
re-establishes blood flow to ischemic tissues.
Decompression Sickness
Decompression sickness is caused by the release of inert gas bubbles
(usually nitrogen) into the bloodstream and tissues after ambient pressure
is reduced.(2-5,10) At depth, the partial pressures of gasses in the
breathing mixture increase in proportion to the ambient pressure, according
to Dalton's law.(6) Although oxygen is actively metabolized, nitrogen is
inert and becomes dissolved in body tissues until saturation, proportional
to the ambient pressure as defined by Henry's law.(6) The propensity for the
formation of nitrogen bubbles depends on the depth of the dive, the length
of time at depth and the rate of ascent. If ambient pressure is released too
quickly, the dissolved nitrogen gas that cannot remain in solution will form
air bubbles within the blood, interstitial fluids and organs (Figure 1).
Decompression sickness is traditionally classified into type I and type II.
In type I decompression sickness, symptoms are usually mild and may manifest
as fatigue or malaise (i.e., constitutional decompression sickness) or may
be more specific, involving the muscles, joints and skin.(10) Type II
decompression sickness is more severe and can affect the lungs, vestibular
apparatus and the nervous system.
In inner ear and neurologic decompression sickness, the formation of bubbles
affects the brain, spinal cord, cranial and peripheral nerves, and the
neural vasculature. Nitrogen bubbles can injure neural tissues by mechanical
disruption, compression, vascular stenosis or obstruction, and activation of
inflammatory pathways (e.g., cytokines, complement).(4,10) Cerebral
decompression sickness (30 to 40 percent of cases) usually involves arterial
circulation, while spinal cord decompression sickness (50 to 60 percent of
cases) involves obstruction of venous drainage and the formation of bubbles
within the cord parenchyma.(12)
The incidence of decompression sickness among recreational scuba divers is
estimated to be one case per 5,000 to 10,000 dives.(1) Diving within the
limits of dive tables is no guarantee against decompression sickness,
because more than 50 percent of cases of decompression sickness occur after
no-decompression dives. In addition to the dive profile and rate of ascent,
other factors may influence the risk of decompression sickness, including
hypothermia, fatigue, increased age, dehydration, alcohol intake, female
gender, obesity and patent foramen ovale.(2-5,13)
In type II neurologic decompression sickness, more than 50 percent of
patients develop symptoms within one hour of ascent; within six hours, 90
percent of divers are symptomatic.(1,4,14) Inner ear decompression sickness
presents with acute vertigo, nausea, emesis, nystagmus and tinnitus. The
pathophysiology remains unclear; one mechanism is bubble rupture of the
intraosseous membranes in the semicircular canals. In many cases, inner ear
decompression sickness is clinically indistinguishable from otic barotrauma,
although the dive profile and timing of symptoms may help to clarify the
diagnosis (Table 2).(2-5,7,10)
Neurologic decompression sickness can present with a wide spectrum of
symptoms (Table 3). The most severe presentation is partial myelopathy
referable to the thoracic spinal cord.(10,15) Patients complain of
paresthesias and sensory loss in the trunk and extremities, a tingling or
constricting sensation around the thorax, ascending leg weakness ranging
from mild to severe, pain in the lower back or pelvis and loss of bowel
and/or bladder control. The neurologic examination will often reveal
monoparesis or paraparesis, a sensory level and sphincter disturbances.
However, neurologic examination also may be normal.
TABLE 3
Presenting Signs and Symptoms
in Patients with Decompression Sickness
Sign or symptom Percentage
Numbness 59
Pain 55
Dizziness 27
Extreme fatigue 25
Headache 24
Weakness 23
Nausea 14
Gait abnormality 12
Hypoesthesia 10
Visual disturbance 8
Itching 5
Information from references 1,2,4,5 and 9.
Pathologic features within the spinal cord include hemorrhagic
infarctions, edema, bubble defects, axonal degeneration and demyelination
(Figure 2).(12,15) Cerebral decompression sickness can occur alone or in
combination with spinal decompression sickness and manifests as an
alteration of mentation or confusion, weakness, headache, gait disturbance,
fatigue, diplopia or visual loss. The neurologic examination may show
hemiparesis, dysphasia, gait ataxia, hemianopsia and other focal signs.
Behavioral and cognitive aspects of cerebral decompression sickness may be
persistent or slow to improve.(10,16) The pathologic features are similar to
those of spinal decompression sickness, although not as pronounced.(10,17)
The diagnosis of neurologic decompression sickness is clinical and should be
suspected in any patient with a recent history of diving who has a
consistent presentation. Neuroimaging studies may further clarify the
diagnosis but should not delay treatment. MRI demonstrates high-signal
lesions of the brain and spinal cord in 30 to 55 percent of cases (Figure
3), which suggests ischemia, edema and swelling. The lesions do not enhance
with contrast. However, images on MRI are often normal.(5,10,16)
The initial management of neurologic decompression sickness is similar to
that of arterial gas embolism and decompression illness, and requires
transport to a recompression facility.(2-5,10,16) If transport by helicopter
is necessary, the patient should be flown at an altitude of less than 1,000
ft to minimize exacerbation of symptoms. The definitive treatment is
recompression therapy using the USN Table 6 algorithm.(11) USN Table 6
consists of initial recompression to 60 ft of salt water with 100 percent
oxygen for 60 minutes. The patient is then decompressed to 30 ft of salt
water for two additional periods each of breathing pure oxygen and air.
Recompression therapy reduces the size of bubbles, allowing easier
reabsorption and dissipation, and increases the nitrogen gradient to
expedite off-gassing. The majority of recreational divers with neurologic
decompression sickness have an excellent recovery after prompt recompression
therapy.
The Divers Alert Network (DAN) at Duke University Medical Center, Durham,
N.C., is available 24 hours a day to discuss arterial gas embolism or
decompression sickness and provide divers a referral to the nearest
recompression facility, if necessary. The emergency hotline number is
919-684-8111. For nonemergency medical questions, call DAN at 919-684-2948.
Headache
Headache is a common symptom in divers. There are numerous benign causes,
including exacerbation of tension or migraine headaches, exposure to cold,
mask or sinus barotrauma, sinusitis and a tight face mask. Migraines are not
often precipitated by diving, but can be severe when they occur. If a
migraine develops, the dive should be terminated because of the potential
for nausea, emesis and alteration of consciousness. Dangerous causes of
headache include cerebral decompression sickness, contamination of the
breathing gas with carbon monoxide, arterial gas embolism, severe otic or
sinus barotrauma with rupture, and oxygen toxicity.(2-5,10) If headache
occurs in a patient with potential arterial gas embolism or decompression
sickness, it should be considered an emergency, because it suggests the
presence of intracerebral bubbles. This type of headache usually develops
within minutes of ascent. Immediate use of 100 percent oxygen and of
recompression therapy is indicated.
Oxygen Toxicity
In the recreational diver, the most likely cause of oxygen toxicity is
diving with oxygen enriched air (i.e., Nitrox). Nitrox is a breathing
mixture that contains more than 21 percent oxygen (usually 32 to 36
percent), and allows extended bottom time. When diving with Nitrox, the
diver is at risk of oxygen toxicity if the maximum oxygen depth limit and/or
the oxygen time limit is exceeded. In general, the higher the oxygen content
in the Nitrox mixture, the shallower the dive to minimize the potential for
oxygen toxicity. Symptoms develop at depth without warning and consist of
focal seizures (e.g., facial or lip twitching occurs in 50 to 60 percent of
patients), vertigo, nausea and emesis, paresthesias, visual constriction and
respiratory changes.(18) Generalized seizures or syncope can also occur in 5
to 10 percent of patients. Although uncommon, generalized seizures at depth
are often fatal, because divers may drown or arterial gas embolism may be
precipitated during rescue to the surface.(4) The cause of oxygen toxicity
to the nervous system mainly involves oxygen-free radical formation, as well
as reduction of the inhibitory neurotransmitter, gamma-aminobutyric acid.
Treatment consists of reducing oxygen exposure and dive depth and, if
necessary, managing seizures.
Figures 1 and 2 used with permission from James PB. Bubbles, brain damage
and hyperbaric oxygenation. World Neurology 1998;13:6.
Figure 3 used with permission from Elliott DH, Moon RE. Manifestations of
the decompression disorders. In: Bennett PB, Elliott DH, eds. The physiology
and medicine of diving. 4th ed. London: Saunders, 1993;17:481-505.
Dr. Newton received support in part from a National Cancer Institute grant,
CA 16058.
The author thanks Harrison Weed, M.D., for critical review of the manuscript
and David Carpenter for his editorial expertise.
© American Family Physician written by Herbert B. Newton