Recreational scuba diving injuries - includes patient information sheet

Author: Timothy L. Clenney, Lorenz F. Lassen
Date: April, 1996

It is currently estimated that the United States has more than 2 million certified sport scuba divers.[1] As interest in recreational diving continues to grow, it is important for family physicians to develop a better understanding of common diving injuries.

Injured divers often seek medical attention hours after diving and are frequently seen by emergency department or ambulatory care physicians. Although these patients do not often require hyperbaric treatment, physicians in these settings must be able to recognize significant diving injuries if they are to provide appropriate initial treatment and timely referral.

Two gas laws form the physiologic basis for most diving injuries. The first is Boyle's law, which states that, at constant temperature, the volume of a gas varies inversely with pressure. This law underlies the mechanisms of arterial gas embolism and barotrauma.

The second, Henry's law, explains the mechanism for decompression sickness. This law states that the amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in contact with the liquid. For a diver to breathe at the elevated pressures encountered while diving, air must be delivered at increased pressure. In accordance with Henry's law, this increased pressure results in a greater amount of inert gas (nitrogen) being dissolved in body tissues.

The amount of nitrogen absorbed by the body while diving is a function of two major variables: the depth and duration of the dive. Dive tables incorporating these variables, which were developed by the U.S. Navy,[2] are used by virtually all divers. The tables set time limits at which a diver may stay at a given depth without accumulating excess tissue nitrogen. If these limits are exceeded, decompression stops are required during ascent to avoid bubble formation in body tissue. For obvious reasons, all scuba divers are trained to stay within these "no-decompression" limits.


Barotrauma is defined as tissue damage resulting from a pressure differential between the environment and a noncompressable gas-filled body cavity. During a dive, this pressure differential must be equalized or the resulting expansion or contraction of trapped gas will cause tissue injury. Table 1 lists some types of barotrauma.


Middle Ear Squeeze

Also referred to as barotitis media, middle ear squeeze is the most common diving injury. It occurs in 30 percent of divers undergoing their first dive and in 10 percent of experienced divers.[3] Typically, this disorder is caused by eustachian tube dysfunction resulting from an upper respiratory tract infection or allergies. The patient reports ear pain and, occasionally, hearing loss. Clinical findings range from mild congestion of the tympanic membrane to hemotympanum, with or without perforation. A complex system for grading middle ear barotrauma has been described,[4] although the popularity of this system has declined in favor of more simplified systems for grading the severity of a middle ear squeeze. Table 2 shows one such grading system.


Treatment options include the use of decongestants and analgesics. If the tympanic membrane has perforated, systemic antibiotics should also be considered.[1] Diving should be avoided for two to seven days. If the tympanic membrane has perforated, diving should be avoided until the perforation is completely healed. Follow-up is essential to verify resolution of otoscopic findings before the patient returns to diving.

Preventive measures include pretreatment with 60 mg of pseudoephedrine 30 minutes before a dive[3] and avoidance of diving with an upper respiratory tract infection or allergy symptoms.

When performing medical screening of a patient who is considering taking up scuba diving, the physician should ensure that middle ear inflation (clearing) can be easily achieved by the patient. Middle ear inflation is checked by observing the movement of the tympanic membrane while the patient performs a Valsalva maneuver or by interpreting the patient's report after the maneuver. Unfortunately, the ability to successfully autoinflate at surface pressure does not guarantee the ability to do so while diving.[5] This point should be emphasized to the patient.

Inner Ear Barotrauma

Inner ear barotrauma is the occasional result of unsuccessful attempts to equalize the middle ear space during a dive. If a diver descends without clearing, a pressure differential is created between the middle ear and the surrounding water pressure. If a difference in pressure of as little as 90 mm Hg is present, locking of the eustachian tube occurs, and venting of the tympanic cavity becomes impossible.[6] Forceful attempts to clear under these conditions raises intracranial pressure, which, if transmitted to the inner ear through the internal auditory canal, may result in a round-window fistula or inner ear membrane tear.[6]

If inner ear barotrauma has occurred, the patient will report the sudden onset of tinnitus, vertigo, sensorineural hearing loss and the sensation of fullness in the ear.[1] When this occurs, inner ear decompression sickness must also be ruled out. The physician should elicit a detailed history with attention to the dive profile, the time of onset of symptoms with respect to the dive, and the presence of associated symptoms of decompression sickness, such as joint pain. Generally, if inner ear symptoms develop after a dive that required decompression, inner ear decompression sickness is the likely diagnosis. Similar symptoms that arise immediately after a dive that did not require decompression are more suggestive of inner ear barotrauma.[7] If the physician is unable to differentiate between the two disorders, decompression sickness must be assumed and appropriate referral made, since a delay in treatment of inner ear decompression sickness may worsen the outcome.[8]

The treatment of inner ear barotrauma involves taking measures to avoid increased intracranial pressure, including strict bed rest with the head of the bed elevated and the use of stool softeners, for a maximum of five days.[7]

Although most patients recover spontaneously, otologic and audiometric evaluation are recommended, since worsening or persisting symptoms may signal the need for surgery to repair a perilymphatic fistula.[6]

Pulmonary Barotrauma

If a scuba diver fails to exhale while ascending from a dive, expanding air will eventually cause rupture of pulmonary alveoli. This may result in infiltration of air into the pleural space, causing a pneumothorax, or into the mediastinum, causing mediastinal or subcutaneous emphysema.[9] Presenting complaints include chest pain or tightness, which may be associated with swelling and crepitation in the neck. These conditions are rarely life-threatening and usually resolve with inhalation of 100 percent oxygen.

A pneumothorax may be treated with oxygen alone or with needle aspiration or tube thoracostomy, depending on the severity of the pneumothorax. If recompression is required for treatment of arterial gas embolism or decompression sickness with a coexisting pneumothorax, a chest tube should be placed to prevent the development of a tension pneumothorax.[10]

Decompression Sickness

As already mentioned, an excessively rapid ascent from a dive may result in the accumulation of excessive tissue nitrogen. If the return to surface ambient pressure is too rapid, tissue nitrogen tension may exceed local tissue pressure enough to form bubbles.[11] Decompression sickness results when bubbles obstruct arteries, veins or lymphatics, or cause mechanical distortion of tissues. Vascular obstruction may be further aggravated by activation of the clotting cascade, which is reported to occur at the interface of a bubble with blood.[1]

Although the risk for developing decompression sickness is markedly reduced if the diver stays within the no-decompression limits, many cases still occur. Contributing factors implicated in the development of decompression sickness include dehydration, alcohol consumption, fatigue, hypothermia and obesity, presumably as a result of the increased solubility of nitrogen in body fat.[11]

Decompression sickness has many manifestations (Table 3), ranging from mild pain to significant neurologic impairment. In about 80 percent of cases, symptoms develop within the first eight hours, although they may develop up to 24 hours after the dive.[2] Frequently, pain is the only symptom. The most common complaint is joint pain that involves the shoulder and elbow more often than the knee or hip.[10]


Cutaneous manifestations of decompression sickness include pruritus, skin rash and skin marbling (cutis marmorata). Pruritus and skin rash usually resolve without treatment; whether these are actually true forms of decompression sickness is a matter of debate. Some physicians advocate observation of the patient with pruritus for 12 to 24 hours to ensure that the symptom does not progress to skin marbling, which is a true form of decompression sickness. Skin marbling may be an indication of systemic involvement, and patients with this symptom should always be referred for treatment.

More serious presentations of decompression sickness may feature neurologic or pulmonary involvement. Neurologic symptoms are most often referable to the spinal cord and are correlated with pathologic findings of hemorrhagic infarcts, axonal degeneration and severe demyelination in affected areas.[12] Presenting complaints may include numbness, paresthesia, weakness and altered mentation. Bowel and bladder dysfunction have also been reported.[13]

Less common presentations of decompression sickness include pulmonary and inner ear disorders. Pulmonary decompression sickness, or "the chokes," usually develops within minutes of surfacing from the dive. It is characterized by substernal pain, coughing and dyspnea. Pathophysiologically, this disorder resembles adult respiratory distress syndrome (ARDS).[11] Emergency recompression is indicated for this potentially lethal condition.

Inner ear decompression sickness results when inert gas bubbles form in either the perilymph or endolymph spaces or in the internal auditory vascular system.[14] The affected diver presents with vertigo, sensorineural hearing loss and tinnitus. This disorder must be differentiated from inner ear barotrauma, as already noted.

The initial treatment of decompression sickness requires appropriate hydration and transport to a recompression facility on 100 percent oxygen. If transport by helicopter is necessary, it is advisable to fly below 1,000 feet, to prevent worsening of symptoms as a result of a reduction in air pressure. If spinal cord decompression sickness is suspected, the bladder should be catheterized and the urine output monitored. Recent data do not support the use of corticosteroids in patients with spinal cord decompression sickness.[15]

It should be emphasized that a patient with a history and presentation consistent with decompression sickness should be immediately referred for recompression. Seemingly minor symptoms may evolve into life-threatening problems in these patients.

Arterial Gas Embolism

Arterial gas embolism is a potentially life-threatening manifestation of pulmonary barotrauma that accounts for about 30 percent of recreational diving fatalities.[16] Rupture of pulmonary alveoli permits entry of air into the pulmonary capillary circulation. After passing through the heart, air bubbles may reach the cerebral circulation and cause an event similar to an acute stroke.[17] The presentation ranges from collapse and death immediately after the diver surfaces to focal neurologic deficits or mental status changes that develop hours after diving.[10]

Frequently, arterial gas embolism must be differentiated from decompression sickness. Arterial gas embolism usually manifests soon after surfacing, and the patient often has a history of an uncontrolled ascent during the dive. The diagnosis of decompression sickness is favored when symptoms evolve gradually and the dive required decompression.

The initial management of a diver with a suspected arterial gas embolism should include assessment of hemodynamic stability and initiation of advanced cardiac life support or basic life support, as indicated. Transportation to a recompression facility should be arranged as quickly as possible. Adjuncts to treatment include appropriate hydration and administration of oxygen.

Patients presenting with neurologic symptoms several days after diving and with a history consistent with arterial gas embolism should still be referred for recompression. The author has treated symptomatic persons as long as three to five days after diving, with full resolution of symptoms.

Referral for Recompression

The Divers Alert Network (DAN), at Duke University Medical Center, Durham, N.C., maintains a database of recompression facilities and provides referral to the nearest appropriate facility. In addition, the network can be contacted for consultation on suspected diving injuries on a 24-hour basis. Their telephone number is 919-684-8111.

Nonemergency consultation, such as questions regarding medical screening for diving, may also be obtained at this number, from 8:30 a.m. to 5:00 p.m., eastern standard time, Monday through Friday.


[1.] Jerrard DA. Diving medicine. Emerg Med Clin North Am 1992;10:329-38. [2.] U.S. Navy diving manual. Vol. 1. Washington D.C.: Department of the Navy, 1993. [3.] Brown M, Jones J, Krohmer J. Pseudoephedrine for the prevention of barotitis media: a controlled clinical trial in underwater divers. Ann Emerg Med 1992;21:849-52. [4.] Edmonds C, Freeman P, Thomas R, et al. Otological aspects of diving. Glebe, New South Wales: Australasian Medical Publishing, 1973. [5.] Shupak A, Sharoni Z, Ostfeld E, Doweck I. Pressure chamber tympanometry in diving candidates. Ann Otol Rhinol Laryngol 1991;100:658-60. [6.] Shupak A, Doweck I, Greenberg E, Gordon CR, Spitzer O, Melamed Y, et al. Diving-related inner ear injuries. Laryngoscope 1991;101:173-9. [7.] Pullen FW 2d. Perilymphatic fistula induced by barotrauma. Am J Otol 1992;13:270-2. [8.] Adkisson GH, Meredith AP. Inner ear decompression sickness combined with a fistula of the round window. Case report. Ann Otol Rhinol Laryngol 1990;99(9 Pt 1):733-7. [9.] Kol S, Weisz G, Melamed Y. Pulmonary barotrauma after a free dive - a possible mechanism. Aviat Space Environ Med 1993;64(3 Pt 1):236-7. [10.] Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992;326:30-5. [11.] Francis TJ, Dutka AJ, Hallenbeck JM. Pathophysiology of decompression sickness. In: Bove AA, Davis JC, eds. Diving medicine. 2d ed. Philadelphia: Saunders, 1990:170-83. [12.] Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Melamed Y. Spinal cord decompression sickness in sport diving. Arch Neurol 1993;50:753-6. [13.] Greer HD, Massey EW. Neurologic injury from undersea diving. Neurol Clin 1992;10(4):1031-45. [14.] Reissman P, Shupak A, Nachum Z, Melamed Y. Inner ear decompression sickness following a shallow scuba dive. Aviat Space Environ Med 1990; 61:563-6. [15.] Francis TJ, Dutka AJ. Methyl prednisolone in the treatment of acute spinal cord decompression sickness. Undersea Biomed Res 1989;16:165-74. [16.] Kizer KW. Dysbaric cerebral air embolism in Hawaii. Ann Emerg Med 1987;16:535-41. [17.] Kizer KW. Scuba diving and dysbarism. In: Auerbach PS, ed. Wilderness medicine: management of wilderness and environmental emergencies. 3d ed. St. Louis: Mosby, 1995:1176-205.

The Authors

TIMOTHY L. CLENNEY, LT, MC, USN is head of the Undersea Medicine Department at Naval School, Explosive Ordnance Disposal, Indian Head, Md. He graduated from the University of South Florida College of Medicine, Tampa, and the Naval Undersea Medical Institute, Groton, Conn.

LORENZ F. LASSEN, CDR, MC, USN is chairman of the Department of Otolaryngology at Naval Medical Center, Portsmouth, Va. He graduated from the Uniformed Services University of the Health Sciences, F. Edward Herbert School of Medicine, Bethesda, Md. He completed a residency in otolaryngology at Naval Hospital, San Diego, Calif., and a fellowship in neuro-otology at the University of Pittsburgh School of Medicine.

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