Illness in Scuba Divers What You Need to Know

The initial compression and subsequent expansion of air during a dive can have serious adverse effects on a wide range of body systems. As the popularity of the sport has increased in recent times, so has the likelihood that an emergency will see novice divers with , arterial gas embolism, and even pulmonary . The authors explain how to be prepared.

By Mark Merlin, DO, EMT-P, FACEP, Amy Ondeyka, BA, EMT-B, and Andreia Marques-Baptista, MD

ecreational has become in- grown, so has the incidence of diving-related inju- creasingly popular since the 1980s, with ries—in particular, decompression sickness (DCS) more than 500,000 new certifications and arterial gas embolism (AGE), which are collec- awarded each year. As the sport has tively referred to as . R Decompression sickness results from gas bubbles Dr. Merlin is an assistant professor of emergency that form in the venous circulation and tissues as the and and of the New ambient decreases when a diver ascends to Jersey EMS/ Fellowship at University of Medicine and -Robert Wood Johnson Medical the surface. Arterial gas embolism occurs when gas School and EMS/critical care transport medical director bubbles causing circulatory and inflammatory de- at Robert Wood Johnson University in New rangements enter the arterial circulation, obstruct- Brunswick, New Jersey. He is also medical director of the New Jersey EMS Task and chair of the New Jersey ing blood flow to various organs. Emergency physi- MICU Advisory Board for the Department of Health cians need to be prepared to recognize and manage and Senior Services. Ms. Ondeyka, a medical student the effects that decompression illness can have on a at University of Medicine and Dentistry-Robert Wood Johnson , has been involved in emergency wide range of body systems. medical services for over five years, as both a paid and volunteer EMT in New Jersey and Pennsylvania, and is a OF CHANGING PRESSURE certified open diver. Dr. Marques-Baptista is the In recreational scuba diving, divers typically do not New Jersey EMS/Disaster Medicine Fellow at University of Medicine and Dentistry-Robert Wood Johnson Medical exceed a depth of 130 feet water (fsw). As div- School. ers descend, the exerted on them © 2009 Argosy

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increases. At a depth of only 33 fsw, the ambient pressure on a diver has TABLE 1. Symptoms of Decompression Sickness already doubled.1 As stated in Boyle’s Type 1 Type 2 law, when a gas is subject to increas- ing pressure, its volume will decrease. • rashes CNS Increased pressure is felt not only in • joint pain • the air-filled spaces of a diver’s body, • musculoskeletal pain • paraplegia mainly the middle ear and sinuses, but • ataxia also in the and intestines. Proper • unconsciousness equalization techniques are stressed in diver education to avoid pain and Pulmonary (chokes) damage to these spaces. • hemoptysis During ascent, the ambient pres- • cough sure decreases back toward that of • substernal chest pain the atmosphere and the volume of gas expands. If air becomes trapped • dyspnea in the lungs from disease or because a diver does not exhale during ascent, expanding air can cause the lungs to overinflate and safety stop should allow ample time for the excess burst, a condition called pulmonary barotrauma. to leave the tissues, enter the low-pres- Scuba divers usually breathe a mixture of sure venous circulation, move into the pulmonary and nitrogen, which becomes compressed due to capillary bed, and be exhaled and eliminated in the the increased pressure during descent. Compressed normal manner. air contains more molecules at depth, and thus a descending diver receives more air molecules with SEVERAL TYPES OF ILLNESS each breath. This causes larger amounts of gas to If divers ascend too rapidly, they may not allow become dissolved in the blood and tissues. Oxygen enough time for excess gas to leave the tissues and is continually used by the body and does not ac- blood. Rapid ascent can cause gas to come out of cumulate, but the excess nitrogen molecules are not and form bubbles, which remain in tis- readily used, and is left with greater residual sues or in the blood. With continued ascent, the amounts at increased depths. gas bubbles will expand as pressure decreases. The The Professional Association of Diving Instruc- expanded bubbles can obstruct blood flow directly tors, one of the largest organizations, or cause ischemia indirectly by activating recommends that scuba divers ascend slowly, no and the coagulation cascade. Gas bubbles faster than 60 fsw per minute.1 Recreational divers can also lead to vascular en- are encouraged to perform a safety stop for dives dothelial dysfunction with >>FAST TRACK<< deeper than 60 fsw. A safety stop is merely a recom- capillary leakage, resulting The central nervous mended precautionary stop performed during ascent in complement activation system is especially at a depth of 15 to 20 fsw for 3 to 5 minutes. This and pathogenic interaction susceptible to recommended stop is different from a required de- between leukocytes and decompression illness compression stop, which is necessary for divers who endothelial tissues. These because nitrogen descend to depths greater than 130 fsw or who ex- changes provoke swelling dissolves so readily in its ceed the maximum time limit at a given depth. These that leads to pain in mus- fatty tissues. divers, depending on how deep they go, may be re- cles, joints, and tendons.3 quired to make multiple decompression stops.2 DCS types 1 and 2. Two distinct forms of DCS The purpose of a safety stop is to compensate are recognized (Table 1). Type 1 DCS, also called for variation in ascent rate and individual differ- the bends, results from the rapid formation and ex- ences in nitrogen absorption and elimination. A pansion of gas bubbles in the musculoskeletal, cu- slow ascent time combined with a recommended taneous, and lymphatic systems. Possible symptoms www.emedmag.com JUNE 2009 | EMERGENCY MEDICINE 19 DECOMPRESSION ILLNESS

FIGURE. Pulmonary Barotrauma and Subsequent Complications

PULMONARY BAROTRAUMA

overinflation and rupture of alveoli

leakage of air bubbles

vessels surrounding tissue pleural cavity

arterial gas embolism

subcutaneous pneumomediastinum emphysema

altered mental status, pleuritic chest pain, coma, , chest pain, shortness of dyspnea, tachypnea, motor/sensory breath, hemoptysis deficits, visual decreased breath sounds disturbances, chest pain

include arthralgia, myalgia, and skin rash. Type 1 outflow from the cord. This prevents the dissolved DCS usually presents within hours of surfacing but nitrogen already in the cord from leaving, which can occur up to 48 hours later. can result in the formation of in-situ bubbles that Type 2 DCS is diagnosed when gas bubbles have cause severe damage to the . Type 2 DCS induced local ischemia in the central nervous, car- symptoms include severe headache, altered mental diovascular, pulmonary, and digestive systems.4 The status, paraplegia, motor weakness, ataxia, and loss central is especially susceptible to of consciousness.4 decompression illness because nitrogen dissolves Pulmonary DCS (the chokes) is caused by a large so readily in its fatty tissues. Spinal cord involve- number of gas bubbles entering the pulmonary . ment is usually the result of gas bubbles in the ve- Symptoms range from cough, hemoptysis, dyspnea, nous plexus system that eventually occlude venous and substernal chest pain to cardiovascular collapse.

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Pulmonary barotrauma. A very serious possible air , or cardiopulmonary or other consequence when a diver holds his or her breath symptoms of pulmonary barotrauma, including pneu- on ascent, causing air-trapping in the , is pulmo- mothorax and . In the case nary barotrauma. As pressure decreases, the trapped of suspected cerebral AGE, imaging can show air expands, which can lead to rupture of the alveolar intravascular cerebral air bubbles. Usually, however, lining, allowing air to leak into the interstitium of the imaging is normal even in the face of severe neurologic lungs. The intermediate consequence of this is pul- abnormalities. monary interstitial emphysema, usually asymptomatic unless further damage and air leakage occur. From WHAT TIPS THE SCALES? the interstitium, air can travel and cause three main Deep and repetitive dives, rapid ascent, cold water complications (Figure): mediastinal and subcutane- dives, and air travel after diving are all significant ous emphysema from accumulated air in the medias- risk factors for decompression illness. The deeper tinum, AGE from air bubbles in the arterial system, the dive, the more excess nitrogen is dissolved into and pneumothorax from accumulated air between the the body tissues and the greater the likelihood that lung and chest wall. Continuing, unrelieved accumu- bubbles will form. Repetitive dives (two or more lation of air may result in tension pneumothorax. 5 dives in one day) also result in excess nitrogen in Arterial gas embolism. In AGE secondary to the body, because residual nitrogen remains dis- DCS, the pulmonary capillary beds become over- solved in body tissues for at least 12 hours after whelmed with bubbles. If this occurs, some bubbles every dive. Air travel also heightens risk because may pass into the left side of the and subse- of the reduced ambient pressure inside the aircraft, quently into the arterial circulation. Gas bubbles can which increases the possibility of formation. also directly enter the left side of the heart if the It is recommended that divers wait a minimum of 12 patient has a septal defect or patent foramen ovale. hours after a single shallow dive or 24 hours after Bubble distribution in the arterial system mainly de- deep or repetitive dives before they fly. pends on blood flow but most commonly occludes Individual risk factors include , fa- the cerebral and coronary circulations.4,5 tigue, obesity, smoking, diabetes, patent foramen Cerebral AGE occurs when gas bubbles lodge in ovale, cardiovascular disease, and lung disease. Pa- the smaller cerebral . It can cause a variety tients with pulmonary diseases such as emphysema of neurologic and -like symptoms, including already have air-trapping in their lungs, which pres- altered mental status, loss of consciousness, hemi- ents a significantly high plegia, and seizures. Symptoms of cerebral AGE risk of pulmonary baro- secondary to pulmonary barotrauma usually present trauma and decompres- >>FAST TRACK<< during ascent or immediately upon surfacing.4 sion illness. Divers with a Deep and repetitive dives, Diagnosis of AGE is clinical and relies on the patent foramen ovale have rapid ascent, cold water diver’s history and symptoms. Three main criteria a much higher risk of de- dives, and air travel after are used to diagnose AGE: onset of symptoms less veloping decompression diving are all significant than 15 minutes after surfacing, presence of cerebral illness, especially type 2 risk factors. neurologic , and symptom dura- DCS, because the defect tion greater than 15 minutes. An absence of neuro- allows gas bubbles to be shunted directly from logic manifestations does not rule out AGE, how- the right side of the heart to the left, bypassing ever. The most common of these, a general stupor the lungs and entering the arterial circulation. or altered mental status, is observed in only 24% of These patients have a high risk of neurologic DCS patients with AGE, followed by coma without sei- and AGE. zures (22%), coma with seizures (18%), unilateral Smoking elevates plasma fibrinogen and factor motor deficits (14%), visual disturbances (9%), and XIII levels, which are associated with increased , unilateral sensory deficits, and bilateral mo- blood coagulation activity. This puts divers at risk tor deficits (all 8%).6 for decompression illness and has been a noted The diagnosis is strengthened when a diver’s his- risk factor for pulmonary embolism in the general tory includes a rapid ascent to the surface, out-of- population.4,5 www.emedmag.com JUNE 2009 | EMERGENCY MEDICINE 21 DECOMPRESSION ILLNESS

dient into tissues. Oxygen will also show * TABLE 2. US Navy Treatment Table enhanced movement into tissues, thus increasing . The reduction of Depth (feet) Time (min) Total time bubble size accelerates as the volume of media elapsed (hr:min) gas declines with increasing pressure in the chamber. 60a 20 O b 0:20c 2 The US Navy developed the most com- 60 5 Air 0:25 monly used treatment regimen for decom-

60 20 O2 0:45 pression illness, including initial treatment 60 5 Air 0:50 of AGE, (Table 2)10; it recommends recom- pression to 2.8 atmospheres absolute or 60 60 20 O 1:10 2 fsw while breathing 100% oxygen. The 60 5 Air 1:15 session lasts anywhere from 60 minutes to

60 to 30 30 O2 1:45 4 hours and 45 minutes, depending on the 30 15 Air 2:00 severity of illness. Additional recompres- 30 60 O 3:00 sion treatments are recommended until 2 there is no further improvement of symp- 30 15 Air 3:15 toms. The number of repeated treatments 30 60 O2 4:15 will be determined by the patient’s symp-

30 to 0 30 O2 4:45 toms, but most divers with mild to moder- ate decompression illness need two to three *Treatment of type II or type I decompression sickness when symptoms are repetitions.5,6 The ’s not relieved within 10 min at 60 ft. statistical analysis of 3000 decompression aDescent rate=25 ft/min. Ascent rate=1 ft/min. Do not compensate for slower ascent rates. Compensate for faster rates by halting the ascent. illness cases supports the effectiveness of bIf oxygen must be interrupted because of adverse reaction, allow 15 min no more than five to 10 repetitive treat- after the reaction has entirely subsided and resume schedule at point of 11 interruption. ments for most people. Transitioning to cTime at 60 ft begins on arrival. other US Navy treatment tables12,13 is an Adapted from US Department of the Navy Treatment Table 6.10 option, based on clinical response. Recompression should be initi- ated promptly upon clinical diagnosis of THE ROAD TO RECOVERY decompression illness. Long delays to treatment are Emergency management for a scuba diver experienc- associated with incomplete resolution of symptoms; ing signs and symptoms of decompression illness however, no cutoff point for therapeutic efficacy has includes intravenous fluids and administration of been established. 100% oxygen via a non- mask. The patient Certain adjunctive treatments have been suggested should be kept as motionless as possible in the supine in addition to the gold standard of hyperbaric re- position; the Trendelenburg position is no longer compression therapy.14 The addition of nonsteroi- recommended because it merely increases intracra- dal anti-inflammatory drugs (NSAIDs) to routine nial pressure and decreases cerebral perfusion.7-9 recompression therapy has not been shown to im- For any form of decompression illness or injury, prove the effectiveness of treatment15; however, it immediate transport to a hospital with a recom- did demonstrate a reduction in the number of re- pression chamber is recommended. Recompression peat recompressions needed. Likewise, a and therapy reduces the size of air bubbles, allowing oxygen mixture used in the recompression chamber, for easier reabsorption into tissues and subsequent instead of pure oxygen, also correlates with a re- dissipation. The patient is placed in an airtight hy- duction in the number of recompressions needed perbaric chamber and 100% oxygen is administered for symptom reduction.16,17 Neither the addition of while the pressure in the chamber is increased.7,8 NSAIDs nor the replacement of oxygen with the The increased pressure enhances the movement of helium-oxygen product appears to improve the pa- nitrogen out of bubbles and down its gra- tient’s odds of recovery. continued on page 48

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continued from page 22

Neurologic deficits, cardiovascular instability, or 8. Moon RE, Gorman DF. Treatment of the decompression dis- orders. In: Brubakk AO, Neuman TS, eds. The and both indicate treatment of AGE. If pulmonary baro- Medicine of Diving. New York, NY: W.B. Saunders; 2003:600-650. trauma is the suspected cause of AGE, a chest x-ray 9. Vann RD, Bute BO, Uguccioni DM, et al. Prognostic factors in decompression illness in recreational divers. In: Moon RE, Shef- should be obtained before hyperbaric recompres- field PJ, eds. Treatment of Decompression Illness. Kensington, sion to check for a pneumothorax. If one is found, MD: Undersea and Hyperbaric Medical Society; 1996:352-363. a chest tube should be placed to prevent the devel- 10. US Department of the Navy. US Navy Diving Manual. Rev 6 (Treatment Table 6). Washington, DC: Naval Sea Systems Com- opment of a tension pneumothorax during recom- mand; 2008. SS521-Ag-PRO-010; NAVSEA 0910-LP-106-0957. pression therapy. http://www.supsalv.org/pdf/DiveMan_rev6.pdf. Accessed June 1, 2009. If a patient with decompression illness develops se- 11. Divers Alert Network. Report on Decompression Illness. Div- vere hypoxemia and dyspnea, suspicion of pulmonary ing Fatalities and Project Dive Exploration. Durham, NC: Divers Alert Network; 2003. embolism should be aroused. Prompt treatment in a 12. US Department of the Navy. US Navy Diving Manual. Rev 6 hyperbaric chamber, anticoagulation, and, if indicated, (Treatment Table 5). Washington, DC: Naval Sea Systems Com- administration of fibrinolytics are necessary.18 Q mand; 2008. SS521-Ag-PRO-010; NAVSEA 0910-LP-106-0957. http://www.supsalv.org/pdf/DiveMan_rev6.pdf. Accessed June 1, 2009. REFERENCES 13. US Department of the Navy. US Navy Diving Manual. Rev 6 1. PADI Worldwide Entry-Level Certifications [Statistical Table]. (Treatment Table 9). Washington, DC: Naval Sea Systems Com- Professional Association of Diving Instructors Web site. http:// mand; 2008. SS521-Ag-PRO-010; NAVSEA 0910-LP-106-0957. www.padi.com/scuba/about-padi/PADI-statistics/default. http://www.supsalv.org/pdf/DiveMan_rev6.pdf. Accessed June aspx#Graph_3. Accessed May 29, 2009. 1, 2009. 2. Byrlske A, Richardson D, Shreeves JT, et al. Encyclopedia of Rec- 14. Catron PW, Flynn ET Jr. Adjuvant drug therapy for decom- reational Diving. Santa Ana, CA: International PADI, Inc.; 1989. pression sickness: a review. Undersea Biomed Res. 3. Tetzlaff K, Thorsen E. Breathing at depth: physiologic and clinical 1982;9(2):161-174. aspects of diving while breathing compressed gas. Clin Chest 15. Bennett M, Mitchell S, Dominguez A. Adjunctive treatment of Med. 2005;26(3):355-380. decompression illness with a non-steroidal anti-inflammatory 4. Strauss MB, Borer RC Jr. : contemporary topics drug (tenoxicam) reduces compression requirement. Undersea and their controversies. Am J Emerg Med. 2001;19(3):232-238. Hyperb Med. 2003;30(3):195-205. 5. Kindwall EP. Use of short versus long tables in the treatment of 16. Drewry A, Gorman DF. A preliminary report on a prospective decompression sickness and arterial gas embolism. In: Moon randomized, double-blind, controlled study of oxygen and oxy- RE, Sheffield PJ, eds. Treatment of Decompression Illness. gen-helium in the treatment of air-diving decompression illness. Kensington, MD: Undersea and Hyperbaric Medical Society; Diving Hyperb Med. 1992;22:139-43. 1996:122-126. 17. Drewry A, Gorman DF. A progress report on the prospective 6. Thalmann ED. Principles of US Navy recompression treatments randomized, double-blind, controlled study of oxygen and oxy- for decompression sickness. In: Moon RE, Sheffield PJ, eds. gen-helium in the treatment of air-diving decompression illness. Treatment of Decompression Illness. Kensington, MD: Undersea Undersea Hyperb Med. 1994;21(3):321-327. and Hyperbaric Medical Society; 1996:75-95. 18. Gaye U, Sevinc SU, Ozgur K, et al. Bilateral massive pulmonary 7. Moon RE, Sheffield PJ. Guidelines for treatment of decompres- embolism secondary to decompression sickness: a case report. sion illness. Aviat Space Environ Med. 1997;68(3):234-243. Heart Lung. 2007;36(6):450-453.

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