Barotrauma of the ears and sinuses after scuba diving

Eur Arch Otorhinolaryngol (2001) 258:159-163
O Springer-Verlag 2001
Gary D. Becker' G. Joseph Parell
Barotrauma of the ears and sinuses after scuba diving
Received: 7 February 2001 / Accepted: 15 February 2001
Abstract The pathophysiology, differential diagnosis, and
curently available management of barotrauma affecting
Pathophysiology of barotrauma
the ears and sinuses after scuba diving are reviewed, along
with medical standards for resuming scuba diving after
barotrauma has resolved.
Keywords Athletic injuries . Barotrauma .
Decompression sickness . Diving . Ear diseases
lntroduction
Underlying principles
Barotrauma in scuba divers results from the interplay between internal physiologic pressure levels and pressure
levels in the water surounding the diver. Explanation of
barotrauma therefore requires discussion of these physical
principles.
Water is non-compressible, and pressure increases linearly at a rate of I atm (14.7 1b1in2,160 mmHg, 10 m of sea-
The self-contained underwater breathing apparatus (scuba)
currently in use was developed in 1943 by Jacques Cousteau
water, and 101.3 kPa) every 33 ft (- 10 m). In contrast, air is
compressible and is therefore denser near the surface of the
and Emile Gagnon in France. Since then, we have seen
explosive growth in the popularity of recreational diving.
The United States alone has more than 3 million active
divers, and more than 250,000 divers are trained and certified each year. However, this growth has been accompanied by a concomitant increase in diving-related injuries,
the most common of which involve the ears and sinuses
[12]. Of these, middle-ear barotrauma is generally the most
common but usually resolves spontaneously and without
sequelae. Inner-ear barotrauma is seen less frequently but
is potentially more serious and can be permanent and disabling. Although sinus barotrauma is usually self-limiting,
the condition may have neurologic sequelae.
earth. Most air is concentrated within 6 miles (9654 m)
G. D. Becker (8)
Department of Otolaryngology-Head and Neck Surgery,
Kaiser Permanente Medical Center, 13652 Cantara Street,
Parrorama City, Califomia 91402-5497 ,
USA
G. J. Parell
Department of Otolaryngology-Head and Neck Surgery,
University of Florida, Gainesville, Florida, USA
above the surface of the earth. Whereas a 1 atm change in
pressure requires an ascent into the stratosphere, a 0.5 atm
change occurs at an elevation of 18,000 ft (5486 m). This
significant pressure disparity between water and air explains why barotraumatic injury occurs more frequently after diving than after flying.
Boyle's law relates to all forrns of barotrauma. The rule
states, in essence, that the volume of a gas varies inversely
with pressure if temperature is held constant. Given the
1 atm change in pressure occurring in seawater for every
33 ft of depth, the volume of gas in seawater decreases by
half during descent to (or doubles during ascent from) a
depth of 33 ft (10 m). For example, a balloon inflated to
volume of 1 liter at a depth of 33 ft below the surface will
expand to 2 liters at the surface but must rise to 18,000 ft
(5486 m) above sea level to expand another 1 liter in volume.
Barotrauma is defined as tissue damage resulting from
the direct effects of pressure. For a diver to avoid barotrauma, the pressure in air-filled spaces must be equalized
to ambient pressure; otherwise, as the diver descends, the
surrounding hyperbaric pressure forces blood and tissue
fluids into the air-filled spaces until ambient pressure is
realized. Similarly, expansion of trapped air causes barotrauma ("barotrauma of ascent") as the diver surfaces. In
typical recreational diving, a hose connects a tank of com-
160
pressed air to a pressure regulator placed in the mouth and
the diver breathes through the regulator. This regulator
senses change in depth and delivers air at ambient pressure. Most sport dives take place at a depth of 60 to 130 ft
(' 18--40 m), where the pressure level is equivalent to
about 3 to 5 atm of absolute pressure. As the diver surfaces, the volume of trapped air expands three to five times
and can develop a very destructive force if not vented.
Equalizing pressure early and often is an important pre-
is equalized through the perforated eardrum. A scuba diving mask (such as the ProEar 2000) which maintains dryness of the ear while diving has recently become commercially available. We have patients who dive after ossicular reconstruction and stapedectomy without problems. A
recant retrospective study [15] concluded that patients with
stapedectomy have no increased incidence of inner ear
barotrauma. However, we are aware of at least two divers
with stapedectomy who became deaf after diving (Joseph
ventive safety measure.
C. Farmer, Jr., MD, Duke University Medical
Henry's law explains decompression sickness (also
known as caisson disease or "the bends"). This law states
that the amount of gas dissolved in a liquid at a given temperature is a function of the partial pressure of that gas in
contact with the liquid. As the diver descends in water, the
Durham, North Carolina, personal communication, 2000).
Faulty pressure equalization during descent is common
to both middle-ear and inner-ear barotrauma. Methods for
equalizing pressure in the ear include Valsalva, Frenzel,
Toynbee, Lowry, Edmonds, and BTV (b6ance tubaire voluntaire) maneuvers. A forceful Valsalva maneuver is especially injurious to the inner ear, whereas BTV is the most
physiologic (but is difficult to leam). The jaw thrust involves forcefully exhaling through the nose into the mask
and is often successful in equalizing middle-ear pressure.
Individuals who admit to difficulty in clearing the ear when
scuba regulator in the mouth senses and delivers air at am-
bient pressure; the air is then distributed throughout the
body and saturates the tissues. Oxygen is metabolized, but
nitrogen is inert and thus remains in the body. During the
diver's ascant and as ambient pressure decreases, tissues
become desaturated of nitrogen, and the bloodstream
transports excess nitrogen to the lungs for exhalation. If,
during the diver's ascent, gas bubbles form either in tissues
or in blood vessels, decompression sickness can result.
Once formed, these bubbles grow during ascent according
to Boyle's law and not only cause vascular obstruction but
also initiate a cascade of biochemical events in various tissues. The most common such condition is joint pain; the
most devastating is spinal decompression sickness, which
can result in paralysis; and the most deadly is pulmonary
decompression sickness (chokes), a medical emergency.
These conditions require recompression in a hyperbaric
chamber while a temporizing first aid measure (1007o
oxygen) is delivered by mask.
Ear barotrauma
Many unanswered questions exist regarding patients who
dive with tympanostomy tubes or ear perforation and who
have a history of ossicular reconstruction, stapedectomy,
or mastoidectomy. We are not aware of any prospective
clinical trials or studies in this regard. Our comments are
anecdotal and are based on personal diving experience,
observation, and discussion with divers and pundits. Concerns about diving with ear perforation, tympanostomy
tubes, or mastoidectomy relate to infection and to dizziness (which can result from cold-water stimulation of the
inner ear). Dizziness may lead to disorientation. vomiting
underwater (with possible aspiration and pneumonia), and
If dizziness begins, the dive must be aborted
promptly and safely. Ear infection with marine organisms
even drowning.
can occur after a dive. Use of one-way valve (Caste11i-type)
tympanostomy tubes has proved successful in a small co-
hort of divers (David Beal, MD, Anchorage, Alaska, personal communication, 1998). We have also seen divers with
tympanic membrane perforation or open mastoid cavities
use earplugs or molds without problems; in these divers,
pressure in the space between the earplug and middle ear
Center,
traveling in airplanes, driving at high elevations (e.g. in
mountains), or diving when swimming, should be counseled
to avoid scuba diving. In addition, successful autoinflation of the ear (as observed by otoscopy in the office) does
not necessarily predict success during descent [14].
In divers who have difficulty in equalizing pressure,
barotrauma can be minimized by gently equalizing pressure in the ears at the water's surface, descending slowly
and feet-first along a line to control the rate of descent,
equalizing the ears at every breath (preferably using the
jaw thrust-nose exhalation technique), and descending
head-down after reaching a depth of about 20 ro 25 ft
(- 6-1.6
m).
People who have difficulty equalizing the ear when
flying have used a silicone earplug with a ceramic insert
(EarPlanes). The ceramic insert delays air movement into
the external ear canal and thus allows more time for pressure to become equalized in the middle ear via the eustachian tube. Similarly, an earplug with a small fenestrum
(Doc's ProPlugs) has been used by divers and functions
in the same way as EarPlanes. Although we admonish
divers never to dive with nasal congestion, judicious use
of an oral decongestant (e.g. pseudoephedrine) or nasal
decongestant (e.g. oxymetazoline) may be considered before the dive if these remedies are not otherwise contraindicated.
External auditory canal barotrauma
The outer ear is affected by barotrauma if the ear canal is
not equalized to ambient pressure. This barotrauma is most
commonly due to occlusion with an earplug, earwax, exostoses, or a tight-fitting wetsuit hood. In these situations,
blood is forced from the surounding soft tissue into the
relative vacuum ofthe ear canal. Otoscopy then can show
vascular congestion, hemorrhagic vesiculation of the external auditory canal, or tympanic membrane rupture.
161
Treatment
Treatment of auditory canal barotrauma is symptomatic
and can include topical analgesic drops or drops with a
topical steroid (e.g. diluted acetic acid with hydrocortisone). Diving can be resumed after tissue damage resolves.
Middle-ear barotrauma
Middle-ear barotrauma is by far the most common barotraumatic otologic injury and has been experienced by all
divers to some extent. It occurs almost exclusively during
descent and results from failure to actively open the normally closed eustachian tube. In contrast, expanding air in
the middle ear during ascent passively opens the eustachian
tube. To avoid separation from other divers, many inexperienced divers continue to descend despite ear pressure
and pain. Attempts to equalize pressure in the ears at this
time are often ineffective because the eustachian tubes irreversibly block with a pressure differential of approximately 90 mmHg, equivalent to the pressure at a depth of
4.5 ft (1.37 m). Avoiding barotrauma by diving ar a shallow depth (advocated by some non-diving otologists) is
not helpful, because the greatest change in volume - and
therefore the most difficult time to equalize pressures occurs near the water's surface. Indeed, the eardrum may
rupture in as little as 4 ft (I.22 m) of water if pressure is
not equalized. Injury to the middle ear may be as mild as
minimal edema of the middle ear mucosa (manifested as
"stuffy ears" after the dive) or hemorrhagic streaking along
the manubrium of the malleus. At the other extreme, the
middle ear may fill with blood or the tympanic membrane
may rupture.
Treatment
round and oval window. The round window is most commonly affected because it is covered by a thin membrane,
whereas the oval window is protected by the stapes footplate and ligament. Inner-ear barotrauma results from
injudicious equalization of middle-ear pressure. A forceful Valsalva maneuver during descent may suddenly open
the eustachian tube and result in high-pressure air (up to
250 mmHg) in the middle ear, thus causing violenr outward movement of the stapes footplate and inward movement of the round-window membrane. This pressure
wave traveling between the oval and round windows may
rupture blood vessels or tear Reissner's membrane or the
basilar membrane. In addition, the stapes footplate may become dislocated or a tear may develop in the round-window membrane, resulting in a perilymphatic fistula.
When relating a medical history, a patient may admit to
difficulty equalizing the ears when descending during a
dive. Hearing loss is usually perceived at the time of surfacing or within several hours after leaving the water. Tinnitus and a sense of fullness in the ear are usual accompaniments. Vertigo or dizziness commonly occurs but is usually transient and mild, and is rarely the only symptom.
Nausea may be present but is rarely severe enough to induce vomiting. Persistent or episodic vertigo over a period
of several days is highly suggestive of a perilymph fistula.
Otoscopic examination may reveal middle-ear barotrauma
and thus lead the examiner to attribute the patient's symptoms to middle-ear barotrauma. To differentiate between
middle-ear barotrauma and inner-ear barotrauma and to
determine the site of injury, serial audiometry studies of
bone and air are mandatory for patients after a dive. Initial
sensorineural hearing loss is often severe no matter where
the site of injury, because hemorrhage and mixing of endolymph and perilymph dissipate the inner-ear action potential. Mild to moderate sensorineural hearing loss at the
onset of inner-ear barotrauma often results in excellent
lnner-ear barotrauma
hearing recovery and suggests inner-ear hemorrhage alone.
Severe sensorineural hearing loss often improves substantially within 4 to 6 weeks after the inner-ear membranes
heal and the action potential retums. Persistent frequencyspecific hearing loss suggests a tear in the cochlear membrane. Hearing loss associated with a perilymph fistula is
variable and occasionally is accompanied by no hearing
loss but only dizziness caused by injury to the labyrinth.
In such cases, neurologic examination may show unsteadiness of the patient, especially with eyes closed. The DixHallpike maneuver may show rotatory nystagmus. However, electronystagmography has not proved helpful in differential diagnosis or in determining the site of a lesion.
Although inner-ear barotrauma occurs infrequently, it may
lead to persistent hearing loss, tinnitus , and dizzrness. We
Treatment
Treatment of middle-ear barotrauma is generally symptomatic. In our experience, routine use of antibiotic agents
and oral or topical nasal decongestants has not proved use-
ful. Most ear perforations heal spontaneously. Diving may
be resumed after the middle-ear contusion or tympanic
membrane perforation has healed and after any predisposing condition (e.g. septal deviation or nasal allergy) is con-
trolled.
hypothesized that there are three mechanisms of injury to
the inner ear: hemorrhage, labyrinthine membrane tear,
and perilymph fistula through the round or oval window
Treatment of inner-ear barotrauma consists of bed rest (with
sedation, ifnecessary) for 7 to 10 days. Strenuous activity
[7]. Recent temporal bone histopathology and audiometric
evidence of each of these types of injury corroborate this
hypothesis [2]. Injury is produced by transmission of pressure changes within the middle ear to the cochlea by the
is avoided for 6 weeks. Noseblowing is proscribed, and
sneezing is done through an open mouth. To minimize a
Valsalva effect on the inner ear during bowel movements,
use of a laxative is recommended. Although we cannot
162
substantiate any modification of the natural history, we often ffeat our patients with oral corticosteroids, starting
prednisone therapy at a dosage of 60 mg/day and tapering
ihis therapy to 0 mg within 2 weeks. Use of carbogen inhalation or sublingual histamine has not proved useful. If
the patient is asymptomatic and has normal hearing in the
speech frequencies after treatment, we recommend that
diving can be resumed after 6 months'
not show further deterioration in hearing from many years
of diving after these divers were
Surgical exploration
Decompression sickness
-
reinstructed in the various methods of equalizing pressure within the middle ear;
admonished to never dive if nasal congestion is present;
-
cautioned to abort the dive ifequalizing pressure in the
-
and
ears is difficult.
In patients who have either continued deterioration of With regard
heaiing or newly acquired vertigo, or both, the diagnosis
of perilymph fistula must be considered' Immediate middle-ear exploration may be advisable if hearing is non-serviceable; the rationale for this suggestion is that the patient's hearing cannot become worse [11]. We prefer an
initial observation period, however, because clinically significant spontaneous improvement may occur within several weeks in about 5O7o of patients with profound sensorineural hearing loss [7]. In addition, intraoperative
identification of anatomic landmarks is made difficult by
the presence of the hemotympanum and mucosal edema
caused by middle-ear barotrauma.
If surgery is to be done, we use a post-auricular approach for best exposure. A high-speed drill is used to
open the posterior-superior canal wall and round-window
niche. A false membrane lateral to the round-window membrane requires removal for proper placement of a graft if a
perilymph fistula is found. Gentle palpation of the stapes
capitulum will elicit a round-window reflux if the structure
seen is truly the round-window membrane. After the roundwindow membrane is identified, the patient is placed in
the reverse Trendelenberg position and the anesthesiologist inflates the lungs for 30 s. The round and oval windows
are then carefully inspected for leaking perilymph. Findings suggesting a fistula include delicate tent-like adhesions
draping the stapes superstructure or round window or the
presence of reaccumulating fluid. To make a definitive diignosis of perilymph fistula, we require identification of a
displaced stapes or a hole in the round-window membrane'
Any adhesions are then removed, and the mucosa around
the round- and oval-window membranes are scored circumferentially. Several small plugs of fibroadipose tissue are
used to fill the round- and oval-window niches whether or
not a fistula is found. Several pledgets ofgelfoam are placed
over these areas and the tympanic membrane is replaced.
During the past 25 years, we have explored approximately
25 ears for suspected perilymph fistulas. In only two ears
was the definitive diagnosis of fistula made [7].
to differential diagnosis, the symptoms of inner-ear decompression sickness and inner-ear barotrauma
are similar. Patients with both conditions have rarely been
described [1]. In recreational divers breathing air, innerear symptoms are rarely the sole manifestation of decompression'sickness, especially if the dive profile was within
recreational dive-table limits [131.
Treatment
If
decompression sickness is a consideration, recompression in a chamber is required.
Paranasal sinus barotrauma
The sinus ostia must remain patent throughout a dive to
equalize ambient pressure through the nose- Failure to
equalize pressure during descent results in a relative vacuum in the sinus cavity and thus elicits mucosal congestion, edema, hemorrhagic bullas, and free blood.
During ascent, expanding air blocked by non-patent
ostia may cause fracture of the sinus walls and thus cause
subcutaneous or orbital emphysema. Although this result
is unusual, various neurologic sequelae have been reported,
including blindness [3], pneumocephalus [5], meningitis
[4], and trigeminal nerve dysfunction [6].
During descent, patients often note sharp, intense pain
which is relieved as the sinus cavity fills with edema and
blood. During ascent to the surface, epistaxis may occur.
Although most patients complain of frontal pain, radiography most commonly shows involvement of the maxillary,
ethmoid, or frontal sinuses, in that order. Obtaining a complete medical history is very important because what initially
appears to be sinus barotrauma may actually be referred pain
from the ear, teeth, or temporomandibular joint. A complete
head and neck examination, including endoscopic examination of the nasal cavities, may show the presence of blood,
mucosal congestion, obstruction due to septal deviation,
nasal polyps, pus, or a combination of these.
Recommendations
We believe that published recommendations suggesting no
further diving after inner-ear barotrauma are based on theoretical assumptions and are unnecessarily restrictive. Our
study of U.S. Navy, commercial, and sport divers [8] did
Treatment
We treat sinus barotrauma symptomatically. Antibiotic
agents or oral or nasal decongestants are not routinely
163
used. Depending on the extent of barotrauma, the diver
may usually return to diving within 6 weeks if X-ray films
show that the sinuses have cleared (if radiography was
initially done) and if any underlying predisposing conditions have been remedied (i.e. by treatment of coexistent
infection, allergy, septal deviation, or polyps). We advise
divers that nasal congestion from any cause (e.g. upper respiratory infection, sinus infection, allergy, or smoking) will
predispose them to barotrauma.
Patients with recurrent sinus barotrauma have no clinical or radiologic evidence of sinusitis between episodes.
Initiating causes of ostial insufficiency include upper respiratory infection, allergic and non-allergic rhinitis, and intranasal pathology (e.g. polyps or septal deviation causing
impaction). In some divers, small ostia may hinder effective sinus equalization even in the absence of obvious intranasal damage. Successful surgical endoscopic enlargement of the natural osteum is reported in aviators with recuffent sinus barotrauma [10]. Divers who have had sinus
surgery should be particularly wamed of the risks to the
central nervous system. We suggest the following guidelines [9] when examining a patient with recurrent sinus
barotrauma:
-
-
-
Investigate for and eliminate any inciting disorder. This
investigation should include examining the nasal cavities
with an endoscope and may include obtaining a sinus
computed tomography scan;
Diving should not be done if nasal congestion is present, e.g. during an upper respiratory infection or flareup of allergic or non-allergic rhinitis. Intranasal pathology, e.g. nasal polyps or septal deviation compromising
the osteomeatal complex, may require coffection;
Divers with persistent difficulty in equalizing the sinuses
should be taught the various methods of equalizing pressure and should be advised to equalize at the water's
surface and descend slowly, feet first, equalizing continuously for at least 20 fl (- 6 m). Persons in whom difficulty in clearing their sinuses persists should not dive;
A test ofpressure should be done when no clinical or radiologic evidence of ostial insufficiency persists. This
testing can be accomplished in a hyperbaric chamber or,
more practically, in a swimming pool. If pain does not
develop, diving may be resumed.
Ghronic sinusitis
Recurrent sinus barotrauma must be differentiated from
chronic sinusitis. Patients with evidence of chronic sinusitis should be treated with appropriate medical management.
Sinus surgery is recommended if radiologic evidence of
disease persists. In our personal experience, divers with
chronic sinus disease have had clinically significant improvement in their ability to clear their ears and sinuses
after resolution of the sinus disease with medical treatment, surgery, or both. However, these patients are warned
that they may still have difficulty in clearing the ears and
sinuses and that this difficulty could result in significant
morbidity or disabling injury. In addition, because of ostial
insufficiency, patients with clinical and radiologic evidence
of sinusitis are always at risk for barotrauma when scuba
diving. Our experience with several hundred professional
divers has taught us that these divers continue to dive no
matter how sternly they are warned. Under such circumstances, the best course is to instruct them in optimal control of their sinus disease and in non-forceful methods of
sinus ventilation.
Acknowledgement The Medical Editing Department, Kaiser Foundation Research Institute, provided editorial assistance.
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