569
OTOLARYNGOLOGIC ASPECTS OF SCUBA DIVING GARY
D. BECKER, MD
LOS ANGELES, CALIFORNIA G. JOSEPH PARElL, MD PANAMA CITY, flORIDA
Among the most common injuries encountered by the 700,000 active sport scuba divers in the United States are sinus and otitic barotrauma. The management of these injuries and the identification of high-risk patients during their required pretraining physical examination are discussed.
INTRODUCTION OF the 2.5 million scuba divers in the United States, 700,000 are actively diving, and 200,000 more are trained and certified each year. The authors, both certified and experienced divers, have observed that the most common injuries to the diver are sinus and otitic barotrauma. Since the otolaryngologist is likely to be consulted regarding these injuries, he (she) should not only familiarize himself (herself) with their diagnosis and treatment, but also be able to identify those persons "at risk" for these injuries. The purpose of this paper is (1) to identify the high-risk divers during the required pretraining physical examination and (2) to briefly discuss the management of these injuries.
Submitted for publication Nov 27,1978. From the Section of Head and Neck Surgery, Veterans Administration, Wadsworth Hospital Center, Los Angeles, and the Department of Surgery, University of California, Los Angeles, School of Medicine. Presented as a Scientific Poster Presentation at the 1978 Annual Meeting of the American Academy of Otolaryngology, Las Vegas, Sept 10-13. Reprint requests to 6200 Wilshire Blvd, Suite 1710, los Angeles, CA 90048 (Dr Becker).
BAROTRAUMA (SQUEEZE) Barotrauma, commonly called "squeeze" by the diver, is an injury resulting from a pressure difference between the environment and an air-containing space within the body. While pressure changes encountered during the ascent in air are relatively minimal (18,000-ft elevation is one half atmosphere), pressure changes on descent in water are great (16.5-ft depth is one half atmosphere). Changes in volume of a gas vary inversely with pressure (Boyle's law). As the diver descends, the increased (water) pressure is transmitted throughout the body, and compressed air at ambient pressure is breathed from a pressure-sensitive regulator. As long as the diver is able to equalize the pressure of the various noncollapsible spaces within the body to ambient pressure, barotrauma does not occur.
EXTERNAL EAR SQUEEZE Occlusion of the external auditory canal (EAC) by cerumen, exostoses, or ear plugs prevents effective equalization during descent. This may cause vertigo, owing to unilateral caloric stimulation of the unaffected ear, or a squeeze, resulting in injection or hemorrhagic vesiculation of the EAC. No treatment of the injury is necessary. Insuring a patent EAC before diving will avoid this type of injury.
MIDDLE EAR SQUEEZE As the diver descends, increased water pressure results in an inward movement of the tympanic membrane (TM). Rupture of the normal TM occurs at a depth
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct> 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
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of between 4 and 17 ft unless there is equalization of pressure via the eustachian tube (ET). This is usually accomplished by the Valsalva maneuver, even though many divers have voluntary control over opening their ETs. While continuous equalization from the surface throughout the descent is ideal, equalization every 2 to 3 ft is usually sufficient to prevent a locked ET and possible TM rupture. Depending on the pressure difference between the water and the middle ear space owing to inability to equalize, varying degrees of injury (barotitis) take place. These may be graded from I through V according to Edmonds' classification.' Injection of the TM is the mildest injury (grade I), followed by contusion (grades II and 111), bleeding into the middle ear space (grade IV), and rupture of the TM (grade V). Management of all grades of barotitis is expectant. Ear drops, oral antibiotics, and nasal decongestants are not necessary unless subsequent infection occurs.' Depending on the severity of the injury, at least one month is necessary for satisfactory resolution before diving again. Divers at risk for barotitis include those with abnormal nasal (especially ET) physiology. All divers should be able to autoinflate their ears without difficulty before diving. Conditions such as allergic rhinitis, nasal polyposis, chronic sinusitis, or a deviated septum may need correction if autoinflation is not easily accomplished. Correction of a deviated nasal septum restores the ability to autoinflate the ears in most persons.! Patients with a perforated TM should not dive, since water in the middle ear space will cause vertigo and, probably, infection. Also, patients with a perforation healed by an atrophic membrane should not dive, because minimal pressure changes are likely to cause perforation.
INNER EAR SQUEEZE (WINDOW RUPTURE)
Perilymph fistula resulting from rupture of the oval or round window results in a variety of cochleovestibular symptoms, singly or in combination. Forceful autoinflation of the ears during descent is a common denominator of most fistulas. It is speculated that increased CSF pressure or violent movement of the stapes during a forceful Valsalva maneuver is causative. The result is an immediate but variable combination of hearing loss, tinnitus, and dizziness. Audiometry may reveal a sensorineural hearing loss, and electronystagmography (ENG), while often normal, may demonstrate a positional nystagmus or a hypoactive caloric response. Results of the fistula test are not specific. If other causes of vertigo are excluded, management should consist of bed rest with the head of the bed elevated and avoidance of increased CSF and middle ear pressure. If the cochleovestibular symptoms persist for several days, exploratory tympanotomy and repair of the fistula are indicated. Patients who are unable to easily autoinflate their ears are at risk for window ruptures. Although no documentation to this effect was found, patients with a stapes prosthesis should not dive for two reasons. First, many patients have a hypoactive caloric response after stapes surgery that may result in unequal caloric vestibular stimulation in the water, causing vertigo. Second, even if a predive caloric examination is normal, large movements of the TM owing to pressure changes in the water and autoinflation are likely to tear the oval window membrane (two patients with perilymph fistulas owing to scuba diving after stapes surgery were mentioned at a recent meeting).3 VERTIGO
Unequal caloric stimulation during diving may be the result of a preexisting
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
SCUBA DIVING peripheral vestibular deficit or of unequal douching of cold water in the EAC owing to a unilateral EAC obstruction, eg, cerumen, exostoses, ear plugs, or a tightfitting hood. This problem may be avoided by insuring that the diver has a patent EAC and a properly fitting hood, which may include cutting holes in the areas of the EAC. If the history or physical examination suggests the possibility of peripheral vestibular pathology, symmetric nystagmus responses to caloric testing should be demonstrated before diving is permitted. Alternobaric vertigo is a transient vestibular dysfunction occurring, by definition," on ascent, and is probably due to unequal equilibration of middle ear pressure.! Hearing loss and tinnitus are not components of this disorder, which has been noted to cause vertigo in 26% of sport divers.s Patients who cannot easily autoinflate their ears are at risk for alternobaric vertigo. Decompression sickness (bends) is the result of nitrogen coming out of solution in the blood and tissues in the form of bubbles after ascent to the surface. On descent, the increased (water) pressure causes a high partial pressure of gas (according to Dalton's law) that, depending on the time spent at depths greater than one atmosphere of gauge pressure (33 ft sea water), will come out of solution as bubbles on ascent. While the most common manifestation is pain (usually in the joints), otologic dysfunction as an isolated manifestation may occur. Any patient with cochleovestibular symptoms, isolated or not, occurring shortly after a dive in which the "no decompression limits" were exceeded and in which window rupture is unlikely, should be considered as having otologic decompression sickness and be recompressed in a hyperbaric chamber," Air embolism is the result of rapidly expanding air against a closed glottis
571
(during ascent) causing "alveolar rupture and escape of air into the intra-arterial system. This is usually a catastrophic event, and any otologic symptoms are overshadowed by life-threatening cardiac, pulmonary, and CNS disorders. Patients with roentgenographic evidence of pulmonary blebs or air trapping should not be allowed to dive, as these conditions may lead to overinflation and rupture on ascent. Breath holding on ascent must be avoided by any diver, as this may lead to pulmonary overinflation and possible air embolism. Treatment is immediate recompression in a hyperbaric chamber. Many authorities advocate transporting the patient in the head-down, left lateral position to prevent systemic embolism.
BAROSINUSITIS Injury to the mucoperiosteum of the sinuses may result from unequalization of the sinus air space to ambient water pressure. Pain is experienced on descent and disappears when the sinus fills with blood. Roentgenograms are nonspecific and reveal mucoperiosteal thickening, an air-fluid level, or an opaque sinus." The maxillary sinus is most frequently involved. Treatment is symptomatic. Prophylactic antibiotics and nasal decongestants are unnecessary, and sinus lavage may contaminate the contents of the sinus cavity. Any patient with abnormal nasal physiology is at risk for barosinusitis. Baseline roentgenograms of the sinus may be useful in detecting persons with abnormal roentgenograms as a normal varlant.s
SUMMARY The potential diver with a high risk of the described otolaryngologic injuries may be detected during the required physical examination if the following standards are observed:
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
BECKER AND PARELL
572
1. Normal nasal and ET function (as determined by easy autoinflation)
2. McNicoll WD, Scanlon SG: The nose-ear syndrome. J R Nav Med Serv 161:27-29, 1975.
2. Normal-appearing EAC and TM (as determined by otoscopic examination)
3. Farmer JC lr: Ear problems in diving and their management. Read before the Annual Scientific Meeting of the Undersea Medical Society, Key Biscayne, Fla, May 30, 1979.
3. No stapes prosthesis (as determined by history) 4. Normal peripheral vestibular function (as determined by history, physical examination, and caloric testing, if indicated).
4. Lundgren CEG: Alternobaric vertigo-a diving hazard. Br Med J 2:511-513, 1965. 5. Ingelstedt S, Ivarsson A, Tjernstrom 0: Vertigo due to relative overpressure in the middle ear. Acta Otolaryngol 78:1-14, 1974. 6. Farmer [C jr: Diving injuries to the inner ear. Ann Otol 86(suppl 36);1-20, 1977. 7. Fagan P, McKenzie MB, Edmonds C: Sinus barotrauma in divers. Ann 010185:61-63, 1976.
REFERENCES 1. Edmonds C, Thomas RL: Medical aspects of diving. Med J AU5t 2:1300-1304, 1972.
8. Fascenelli FW: Maxillary sinus abnormalities. Radiographic evidence in an asymptomatic population. Arch Oto/aryngol 90:190193, 1969.
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
OTOLARYNGOLOGIC ASPECTS OF SCUBA DIVING GARY
D. BECKER, MD
LOS ANGELES, CALIFORNIA G. JOSEPH PARElL, MD PANAMA CITY, flORIDA
Among the most common injuries encountered by the 700,000 active sport scuba divers in the United States are sinus and otitic barotrauma. The management of these injuries and the identification of high-risk patients during their required pretraining physical examination are discussed.
INTRODUCTION OF the 2.5 million scuba divers in the United States, 700,000 are actively diving, and 200,000 more are trained and certified each year. The authors, both certified and experienced divers, have observed that the most common injuries to the diver are sinus and otitic barotrauma. Since the otolaryngologist is likely to be consulted regarding these injuries, he (she) should not only familiarize himself (herself) with their diagnosis and treatment, but also be able to identify those persons "at risk" for these injuries. The purpose of this paper is (1) to identify the high-risk divers during the required pretraining physical examination and (2) to briefly discuss the management of these injuries.
Submitted for publication Nov 27,1978. From the Section of Head and Neck Surgery, Veterans Administration, Wadsworth Hospital Center, Los Angeles, and the Department of Surgery, University of California, Los Angeles, School of Medicine. Presented as a Scientific Poster Presentation at the 1978 Annual Meeting of the American Academy of Otolaryngology, Las Vegas, Sept 10-13. Reprint requests to 6200 Wilshire Blvd, Suite 1710, los Angeles, CA 90048 (Dr Becker).
BAROTRAUMA (SQUEEZE) Barotrauma, commonly called "squeeze" by the diver, is an injury resulting from a pressure difference between the environment and an air-containing space within the body. While pressure changes encountered during the ascent in air are relatively minimal (18,000-ft elevation is one half atmosphere), pressure changes on descent in water are great (16.5-ft depth is one half atmosphere). Changes in volume of a gas vary inversely with pressure (Boyle's law). As the diver descends, the increased (water) pressure is transmitted throughout the body, and compressed air at ambient pressure is breathed from a pressure-sensitive regulator. As long as the diver is able to equalize the pressure of the various noncollapsible spaces within the body to ambient pressure, barotrauma does not occur.
EXTERNAL EAR SQUEEZE Occlusion of the external auditory canal (EAC) by cerumen, exostoses, or ear plugs prevents effective equalization during descent. This may cause vertigo, owing to unilateral caloric stimulation of the unaffected ear, or a squeeze, resulting in injection or hemorrhagic vesiculation of the EAC. No treatment of the injury is necessary. Insuring a patent EAC before diving will avoid this type of injury.
MIDDLE EAR SQUEEZE As the diver descends, increased water pressure results in an inward movement of the tympanic membrane (TM). Rupture of the normal TM occurs at a depth
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct> 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
570
BECKER AND PARELL
of between 4 and 17 ft unless there is equalization of pressure via the eustachian tube (ET). This is usually accomplished by the Valsalva maneuver, even though many divers have voluntary control over opening their ETs. While continuous equalization from the surface throughout the descent is ideal, equalization every 2 to 3 ft is usually sufficient to prevent a locked ET and possible TM rupture. Depending on the pressure difference between the water and the middle ear space owing to inability to equalize, varying degrees of injury (barotitis) take place. These may be graded from I through V according to Edmonds' classification.' Injection of the TM is the mildest injury (grade I), followed by contusion (grades II and 111), bleeding into the middle ear space (grade IV), and rupture of the TM (grade V). Management of all grades of barotitis is expectant. Ear drops, oral antibiotics, and nasal decongestants are not necessary unless subsequent infection occurs.' Depending on the severity of the injury, at least one month is necessary for satisfactory resolution before diving again. Divers at risk for barotitis include those with abnormal nasal (especially ET) physiology. All divers should be able to autoinflate their ears without difficulty before diving. Conditions such as allergic rhinitis, nasal polyposis, chronic sinusitis, or a deviated septum may need correction if autoinflation is not easily accomplished. Correction of a deviated nasal septum restores the ability to autoinflate the ears in most persons.! Patients with a perforated TM should not dive, since water in the middle ear space will cause vertigo and, probably, infection. Also, patients with a perforation healed by an atrophic membrane should not dive, because minimal pressure changes are likely to cause perforation.
INNER EAR SQUEEZE (WINDOW RUPTURE)
Perilymph fistula resulting from rupture of the oval or round window results in a variety of cochleovestibular symptoms, singly or in combination. Forceful autoinflation of the ears during descent is a common denominator of most fistulas. It is speculated that increased CSF pressure or violent movement of the stapes during a forceful Valsalva maneuver is causative. The result is an immediate but variable combination of hearing loss, tinnitus, and dizziness. Audiometry may reveal a sensorineural hearing loss, and electronystagmography (ENG), while often normal, may demonstrate a positional nystagmus or a hypoactive caloric response. Results of the fistula test are not specific. If other causes of vertigo are excluded, management should consist of bed rest with the head of the bed elevated and avoidance of increased CSF and middle ear pressure. If the cochleovestibular symptoms persist for several days, exploratory tympanotomy and repair of the fistula are indicated. Patients who are unable to easily autoinflate their ears are at risk for window ruptures. Although no documentation to this effect was found, patients with a stapes prosthesis should not dive for two reasons. First, many patients have a hypoactive caloric response after stapes surgery that may result in unequal caloric vestibular stimulation in the water, causing vertigo. Second, even if a predive caloric examination is normal, large movements of the TM owing to pressure changes in the water and autoinflation are likely to tear the oval window membrane (two patients with perilymph fistulas owing to scuba diving after stapes surgery were mentioned at a recent meeting).3 VERTIGO
Unequal caloric stimulation during diving may be the result of a preexisting
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
SCUBA DIVING peripheral vestibular deficit or of unequal douching of cold water in the EAC owing to a unilateral EAC obstruction, eg, cerumen, exostoses, ear plugs, or a tightfitting hood. This problem may be avoided by insuring that the diver has a patent EAC and a properly fitting hood, which may include cutting holes in the areas of the EAC. If the history or physical examination suggests the possibility of peripheral vestibular pathology, symmetric nystagmus responses to caloric testing should be demonstrated before diving is permitted. Alternobaric vertigo is a transient vestibular dysfunction occurring, by definition," on ascent, and is probably due to unequal equilibration of middle ear pressure.! Hearing loss and tinnitus are not components of this disorder, which has been noted to cause vertigo in 26% of sport divers.s Patients who cannot easily autoinflate their ears are at risk for alternobaric vertigo. Decompression sickness (bends) is the result of nitrogen coming out of solution in the blood and tissues in the form of bubbles after ascent to the surface. On descent, the increased (water) pressure causes a high partial pressure of gas (according to Dalton's law) that, depending on the time spent at depths greater than one atmosphere of gauge pressure (33 ft sea water), will come out of solution as bubbles on ascent. While the most common manifestation is pain (usually in the joints), otologic dysfunction as an isolated manifestation may occur. Any patient with cochleovestibular symptoms, isolated or not, occurring shortly after a dive in which the "no decompression limits" were exceeded and in which window rupture is unlikely, should be considered as having otologic decompression sickness and be recompressed in a hyperbaric chamber," Air embolism is the result of rapidly expanding air against a closed glottis
571
(during ascent) causing "alveolar rupture and escape of air into the intra-arterial system. This is usually a catastrophic event, and any otologic symptoms are overshadowed by life-threatening cardiac, pulmonary, and CNS disorders. Patients with roentgenographic evidence of pulmonary blebs or air trapping should not be allowed to dive, as these conditions may lead to overinflation and rupture on ascent. Breath holding on ascent must be avoided by any diver, as this may lead to pulmonary overinflation and possible air embolism. Treatment is immediate recompression in a hyperbaric chamber. Many authorities advocate transporting the patient in the head-down, left lateral position to prevent systemic embolism.
BAROSINUSITIS Injury to the mucoperiosteum of the sinuses may result from unequalization of the sinus air space to ambient water pressure. Pain is experienced on descent and disappears when the sinus fills with blood. Roentgenograms are nonspecific and reveal mucoperiosteal thickening, an air-fluid level, or an opaque sinus." The maxillary sinus is most frequently involved. Treatment is symptomatic. Prophylactic antibiotics and nasal decongestants are unnecessary, and sinus lavage may contaminate the contents of the sinus cavity. Any patient with abnormal nasal physiology is at risk for barosinusitis. Baseline roentgenograms of the sinus may be useful in detecting persons with abnormal roentgenograms as a normal varlant.s
SUMMARY The potential diver with a high risk of the described otolaryngologic injuries may be detected during the required physical examination if the following standards are observed:
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
BECKER AND PARELL
572
1. Normal nasal and ET function (as determined by easy autoinflation)
2. McNicoll WD, Scanlon SG: The nose-ear syndrome. J R Nav Med Serv 161:27-29, 1975.
2. Normal-appearing EAC and TM (as determined by otoscopic examination)
3. Farmer JC lr: Ear problems in diving and their management. Read before the Annual Scientific Meeting of the Undersea Medical Society, Key Biscayne, Fla, May 30, 1979.
3. No stapes prosthesis (as determined by history) 4. Normal peripheral vestibular function (as determined by history, physical examination, and caloric testing, if indicated).
4. Lundgren CEG: Alternobaric vertigo-a diving hazard. Br Med J 2:511-513, 1965. 5. Ingelstedt S, Ivarsson A, Tjernstrom 0: Vertigo due to relative overpressure in the middle ear. Acta Otolaryngol 78:1-14, 1974. 6. Farmer [C jr: Diving injuries to the inner ear. Ann Otol 86(suppl 36);1-20, 1977. 7. Fagan P, McKenzie MB, Edmonds C: Sinus barotrauma in divers. Ann 010185:61-63, 1976.
REFERENCES 1. Edmonds C, Thomas RL: Medical aspects of diving. Med J AU5t 2:1300-1304, 1972.
8. Fascenelli FW: Maxillary sinus abnormalities. Radiographic evidence in an asymptomatic population. Arch Oto/aryngol 90:190193, 1969.
Oto/aryngol Head Neck Surg 87:569-572 (Sept-Oct) 1979 Downloaded from oto.sagepub.com at University of Sussex Library on June 5, 2016
