Decompression Illness in Sports Divers: Part II, Chapter III
Abstract and Introduction
Decompression sickness (DCS) results from gas coming out of solution in the bodily fluids and tissues when a diver ascends too quickly. This occurs because decreasing pressure lowers the solubility of gas in liquid. Also, the expansion of gas in the lungs may lead to alveolar rupture, also known as “Pulmonary Overinflation Syndrome,” which may, in turn, result in arterial gas embolism (AGE). DCS, AGE, and all of their presentations are grouped together under the heading “decompression illness”. Joint pain is the most common complaint in DCS, especially in the elbow, shoulder, hip and knee. Blockage of vessels results in ischemia and infarction of tissues beyond the obstruction, and inflammatory changes can lead to extravasation into the tissues, resulting in edema and further compromising the circulation. Involved skin displays a mottled appearance known as “cutis marmorata.” In the lymphatic system, bubbles may result in regional lymphedema. More severe cases may involve the brain, the spinal cord, or the cardiopulmonary system. Neurologic manifestations may include sensory deficits, hemiplegia, paraplegia, paresthesias, and peripheral neuropathies. Possible cardiopulmonary effects include massive pulmonary gas emboli or myocardial infarction. Decompression sickness is treated with recompression in a chamber to 60 FSW or deeper, associated with hyperbaric oxygen breathing. In the US, this therapy is usually guided by a Navy Treatment Table. These tables are very effective, especially when recompression is begun promptly.
On the earth’s surface, the human body is exposed to an ambient pressure which is the result of the combined partial pressures of all the gases in the earth’s atmosphere. At sea level, the force of this pressure is described as 1 atmosphere absolute (ATA). As a diver descends, exposure to increasing pressure forces more gas to dissolve in the bodily fluids and tissues, as described by natural gas laws. Upon ascent through the water column, the solubility decreases again. Rapid ascent may lead to bubble formation and decompression sickness (DCS) or alveolar rupture (“Pulmonary Overinflation Syndrome” [POIS]), with resultant bubbles in the arterial circulation (arterial gas embolism [AGE]).DCS, AGE, and all of their presentations are grouped together under the heading “decompression illness” (DCI). Treatment consists of recompression in a chamber using air or a combination of helium-oxygen. Bubbles may form in blood vessels, where they may cause ischemia and infarct, and in tissues, where they may initiate an inflammatory response. Inflammatory changes can lead to extravasation into the tissues, further compromising the circulation and resulting in edema.
Hyperbaric exposures (situations where there are elevated pressures) can occur during construction and tunneling projects, in hyperbaric oxygen treatment facilities and in aviation. (The airman is subject to the same problem as divers, except that the situation is reversed–bubbles form on ascent, due to a decrease in pressure and supersaturation. Returning to the ground increases pressure and is analogous to recompression. However, DCS symptoms may occur after returning to the ground and sometimes require additional recompression.)
Recreational scuba diving is the most common type of hyperbaric exposure, especially since the explosive growth of sports scuba (self-contained underwater breathing apparatus) diving in the past decade. Hyperbaric oxygen (HBO) treatment is gaining popularity as the definitive therapy for a growing number of disorders, including decompression sickness, AGE, CO poisoning, clostridial infections, crush injuries, diabetic leg ulcers, skin graft failures, refractory osteomyelitis, thermal burns, necrotizing soft tissue infections, and osteoradionecrosis.
It is incumbent on physicians to be fully conversant with the diagnosis and treatment of decompression illness, especially because the hyperbaric chamber is now widely recognized as effective in reversing the sometimes-deadly changes that take place with DCI.
Medical Management of DCS and AGE
- Provide 100% oxygen through a tight-fitting mask. This helps to off-gas inert gases. Resuscitation equipment should be available on all dive boats and in all dive facilities. Divers should refuse to dive if this equipment is not readily available.
- Give copious fluids as needed to maintain good urinary output. Fluids should be administered at a rate greater than 0.5ml/kg/hr–usually 1 L qhr or 1 L q4hr, titrated against the hematocrit, which should be maintained at less than 50%. The hemoconcentration associated with decompression sickness is the result of increased vascular permeability mediated by endothelial damage and kinin release. The fluids can be given orally if the diver is conscious–if not, give fluids by intravenous, if available. Avoid using hypotonic fluids, such as D5W, using 0.9% saline instead. Insert a urinary catheter if there is spinal cord DCS.
- Give steroids if there is neurological DCS; dexamethasone 10 to 20 mg IV initially, followed by 4 mg every 6 hours; diazepam (5 to 10 mg) controls the dizziness, instability and visual disturbances associated with labyrinthine (vestibular) damage to the inner ear.
- Seizure activity is treated with a loading dose of Dilantin. Seizures result from damage incurred from cerebral bubbles formed from DCS or air embolism (resulting from pulmonary barotrauma); they can also result from oxygen toxicity associated with the treatment schedule. Dilantin (phenytoin) is given IV at 50 mg/min for 10 minutes for the first 500 mg and then 100 mg every 30 minutes thereafter. Blood levels of Dilantin should be monitored to maintain a therapeutic concentration of 10 to 20 mcg/mL. Levels over 25 mcg/mL are toxic.
Some people provide aspirin, 600 mg, for its anti-platelet effects; this modality is debatable because of the possibility of associated spinal cord hemorrhage. Lidocaine has been shown to be protective in animal models but has not been studied adequately in humans.
Attempting to treat the diver by returning him/her to the water, (known as in-water recompression), is hazardous not only to the diver, but to the caregivers who have to be re-subjected to pressure. This should not be attempted unless special arrangements have been made to do so. For example, in Australia, because of the great distances and time lags involved in reaching a recompression chamber, dive operators have a system of surplus air and oxygen tanks ready for in-water recompression.Transportation. Ascending to an altitude greater than 1000 feet should be avoided. Sea level aircraft that are acceptable for transportation include the military C9, the Cessna Citation and the Lear Jet. Commercial aircraft fly at 5000 to 8000 feet cabin pressure. The “ABCs” initiated at the dive site should be continued while in transport.
Treatment in the chamber. The treatment of choice for decompression illness, whether DCS or AGE, is recompression in a multiplace, hands-on chamber. It should have the capability of locking personnel and equipment in or out with trained attendants available for critical care monitoring.
Multiplace chambers. These units (Fig. 1) can accommodate between 2 to 18 patients, depending upon configuration and size. They incorporate a minimum pressure capability of 6 atmospheres absolute. Patients are accompanied by hyperbaric staff members, who may enter and exit the chamber during therapy via an adjacent access lock or compartment. The multiplace chamber is compressed on air and patients are provided with oxygen via an individualized internal delivery system. A dedicated compressor package and high volume receivers provide the chamber’s air supply.
Advantages include constant patient attendance and evaluation (particularly useful in treating evolving diseases such as decompression sickness), and multiple patients treated per session; disadvantages include high capitalization and staffing costs, large space requirements and risk of decompression sickness in the attending staff.
Figure 1. Multiplace chambers accommodate between 2-18 patients, depending upon configuration and size. They have a pressure capability of 6 atmospheres absolute. Reprinted from Hyperbaric Medicine, Brooks Airforce Base.
Monoplace chambers. These units (Fig. 2), first introduced in the 1960s are designed for single occupancy. They are constructed of acrylic, have a pressure capability of 3 atmospheres absolute and are compressed with 100% oxygen. Recent technical innovations have allowed critically-ill patients to undergo therapy in the monoplace chamber. The high flow oxygen requirement is supplied via the hospital’s existing liquid oxygen system.
Figure 2. Recent technical innovations have allowed critically-ill patients to undergo therapy in the monoplace chamber. Monoplace chambers are designed for single occupancy. They have a pressure capability of 3 atmospheres absolute and are compressed with 100% oxygen. Reprinted from Hyperbaric Chambers Systems & Management.
Outcome. The most recent DAN (Divers Alert Network) report (1994 data) suggests that complete resolution of symptoms occurred in only 56% of cases while 28% of divers had neurologic sequelae and 17% continued to experience pain. Travel after treatment of DCS should be delayed for at least 48 hours; 72 hours for arterial gas embolism. Recurrence of symptoms has occurred with flying more than one week after the initial event. Diving should not be resumed if there is any residual neurological damage.
Table I. US Navy Treatment Table 6: Oxygen treatment of Type II Decompression Sickness*¶
60† 20 O2§ 0:20‡ 60 5 Air 0:25 60 20 O2 0:45 60 5 Air 0:50 60 20 O2 1:10 60 5 Air 1:15 60 to 30 30 O2 1:45 30 15 Air 2:00 30 60 O2 3:00 30 15 Air 3:15 30 60 O2 4:15 30 to 0 30 O2 4:45
* Treatment of Type II or Type I decompression sickness when symptoms are not relieved within 10 minutes at 60 feet. † Descent rate–25 ft/min. Ascent rate–1 ft/min. Do not compensate for slower ascent rates. Compensate for faster rates by halting the ascent. ‡ Time at 60 feet begins on arrival at 60 feet. § If oxygen must be interrupted because of adverse reaction, allow 15 minutes after the reaction has entirely subsided and resume schedule at point of interruption. ¥ Caregiver breathes air throughout unless he has had a hyperbaric exposure within the past 12 hours, in which case he breathes oxygen at 30 feet. ¶ Extensions to Table 6: Table 6 can be lengthened up to 2 additional 25 minute oxygen breathing periods at 60 feet (20 minutes on oxygen and 5 minutes on air) or up to 2 additional 75 minute oxygen breathing periods at 30 feet (15 minutes on air and 60 minutes on oxygen) or both. If Table 6 is extended only once at either 60 or 30 feet, the tender breathes oxygen during the ascent from 30 feet to the surface. If more than one extension is done, the caregiver begins oxygen breathing for the last hour at 30 feet during ascent to the surface. Adapted from the US Navy Diving Manual.
- Polak B, Adams H: Traumatic air embolism in submarine escape training. U.S. Naval Med. Bull. 30: 165-177, 1932.
- Francis TJR, Smith D (eds): Describing Decompression Illness. Bethesda, Undersea and Hyperbaric Medical Society, 1987.
- Boussuges A: Hemoconcentration in neurological decompression illness. Int J Sports Med 17 (5): 351-55, 1996.
- Neurological Disorders (Section 11) and Seizure Disorders (Section 121) in Berkow R (ed): The Merck Manual of Diagnosis and Therapy, ed 16, Whitehouse Station, NJ, 1996-1997; http://www.merck.com/!!tMSNq2zF6tMSOn1CAu/pubs/mmanual/html/hjinkcff.htm.
- Gorman, D. The pathology and clinical features of decompression illness, DAN 21st Diving Accidents and Hyperbaric Medicine Course, Sharm-el-Sheik, Egypt, 1992.
- Berghage TE, Vorosmarti J JR, Barnard EEP: Background, in: Davis JC (ed): Treatment of Serious Decompression Sickness and Arterial Gas Embolism. Rep 34 WS (SDS). Bethesda, Undersea Medical Society, 1979, pp xi-xvii.
- Hart GB, Strauss MB, Lennon PA: The treatment of decompression sickness and air embolism in a monoplace chamber. J Hyperbar Med 1: 1-7, 1986.
- Kindwall EP, Goldman RW, Thombs PA: Use of the monoplace chamber in the treatment of diving diseases. J Hyperbar Med ; 3: 5-10, 1988.
- Zamboni WA: The microcirculation and ischemia-reperfusion: mechanisms of HBO, in: EP Kindwall (ed): Hyperbaric Medicine Practice, Flagstaff, AZ Best publishing, 1994, pp 551-564.
- Cianci, Paul: Pathophysiology of Decompression Sickness, Medical Seminars, Palua, May, 1996.
- Campbell ES: Danger! At Hotel Scuba. Scuba Times Online. http://www.scubatimes.com/medcntr/med_hotl.html. 1996.
Berghage TE, Durman D: US Navy Air Decompression Schedule Risk Analysis. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #80-1, 1980.
Boettger ML. Scuba diving emergencies: Pulmonary overpressure accidents and decompression sickness. Annals Emerg Med 12: 563-567, 1983.
Boussuges A, Thiriion P, Molenat F, et al: Neurologic decompression illness: A gravity score. Undersea and Hyperbaric Medicine 23:151-155, 1996.
Boycott AE, Damant GCC, Haldane JS: The prevention of compressed-air illness. J Hyg Camb 8: 342-443, 1908.
Bove AA, Moon RE, Neuman TS: Nomenclature of pressure disorders. Classification of the decompression disorders: time to accept reality. DCI/DCS: Does it matter whether the Emperor wears clothes? Undersea and Hyperbaric Medicine 24:1-4, 1996. Editorials.
Bove AA: The basis for drug therapy in decompression sickness. Undersea Biomed Res 9: 91-111, 1982.
Bracken MB, et al: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal injury. New Eng J Med 322: 1405-1412, 1990.
Catron PW, Flynn ET Jr: Adjuvant drug therapy for decompression sickness: A review. Undersea Biomed Res 9: 161-74, 1982.
Cross SJ, Thomson LF, Jennings KP, et al: Right-to-left shunt and neurological decompression sickness in divers.
Lancet ii 568, 1989. Letter.
Cross SJ, Lee HS, Thomson LFet al: Patent foramen ovale and subaqua diving . BMJ 304: 1312, 1992. Letter.
Davis JC, Kizer KW: Diving medicine, in: Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd edition. St. Louis, The C.V. Mosby Co., 1989.
Dewey AW, Jr: Decompression sickness, an emerging recreational hazard. N Engl J Med 267: 759-65; 812-20, 1962.
Dick APK, Massey EW: Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 35: 667-671. 1985
Edmonds C. Barotrauma, in Strauss R.(ed): Diving Medicine. New York, Grune & Stratton, 1976.
Gorman DF: Decompression sickness and arterial gas embolism in sports scuba divers. Sports Medicine 8: 32-42, 1989.
Green RD, Leitch DR: Twenty years of treating decompression sickness. Aviat Space Environ Med 58: 362-6, 1987.
Hall ED: Lazaroids: Mechanisms of action and implication for disorders of the CNS. Neuroscientist, 3:42-51, 1997.
Johnston RP, Broome JR, Hunt PD, et al: Patent foramen ovale and decompression illness in divers. The Lancet 348: 1515, 1996. Letter.
Kelleher PC, Pethybridge RJ, Francis TJR: Outcome of neurological decompression illness: development of a manifestation based model. Aviat, Space, and Environ Med 67: 654-658, 1996.
Kindwall EP: Diving emergencies, in Kravis TC (ed): Emergency Medicine Aspen Systems Corporation, Rockville, Maryland, 1983.
Kizer KW: Dysbaric cerebral air embolism in Hawaii. Ann Emerg Med 16: 535-41, 1987.
Knauth M, Ries S, Pohlmann S, et al: Cohort Study of multiple brain lesions in sport divers: Role of a patent foramen ovale. BMJ 314: 701-705, 1997.
Krzyzak J: A case of delayed-onset pulmonary barotrauma in a scuba diver. Undersea Biomed Res 14: 553-61, 1987.
Mebane GY, Dick AP: DAN Underwater Diving Accident Manual. Divers Alert Network, Duke University, 1985.
Mitchell SJ: The role of lignocaine in the treatment of decompression illness: A review of the literature. SPUMS Journal 25:182-194, 1995.
Moon RE, Sheffield PJ: Guidelines for Treatment of Decompression Illness. Aviat Space Environ Med 68:234-43, 1997.
Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and decompression sickness in divers. Lancet
1: 513-514, 1989.
Moon RE, Sheffield PJ, (eds.): Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996.
Neblett LM: Otolaryngology and sport scuba diving. Update and guidelines. Annals Otology, Rhin and Laryng. Supplement 115: 1-12, (a great article) 1985.
Rivera JC. Decompression sickness among divers: An analysis of 935 cases. Military Medicine, pp 314-334, April 1964.
Roydhouse N: 1001 disorders of the ear, nose and sinuses in scuba divers. Can J Appl Spt Sci 10: 99-103. 1985.
Schaefer KE, McNulty WP Jr., Carey C, Liebow AA. Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol 13: 15-29, 1958.
Strauss RH. Diving Medicine: State of the Art. Amer Rev Resp Dis 119: 1001-1023, 1979.
Thalmann ED in Moon RE, Sheffield PJ eds. Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996; pp 75-95.
Weeth JB. Management of underwater accidents. JAMA 192: 215-219, 1965.
Wilmshurst P, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers.
Lancet II: 1302-1306, 1989.
Weathersby PK, Homer LD, Flynn ET: On the likelihood of decompression sickness. J Appl Physiol 57: 815-25, 1984.
Weathersby PK, Survanshi SSM, Homer LD, Parker E, Thalmann ED: Predicting the time of occurrence of decompression sickness. J Appl Physiol 72:1541-1548, 1992.
Weathersby PK, Survanshi SS, Hays JR, et al: Statistically based decompression tables III. Comparative Risk Using US Navy, British, and Canadian Standard Air Schedules. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #86-50, 1986.
Wilmshurst: Patent foramen ovale and subaqua diving . BMJ 1312, 1992. Letter.
Wilmshurst P: Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. The Lancet 348: 752-753, 1996.
Wilmshurst P: Brain damage in divers (editorial). BMJ 314: 689-690, 1997.