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Home , Alternobaric vertigo, Barotrauma, Breathing gas, Decompression (altitude), Decompression (diving), Decompression illness

Neurologic Complications of HERBERT B. NEWTON, M.D., Ohio State University , Columbus, Ohio

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers. When severe diving injury occurs, the nervous O A patient infor- system is frequently involved. In dive-related , compressed or expand- mation handout on complications of ing within the , sinuses and causes various forms of neurologic scuba diving, written injury. Otic barotrauma often induces pain, and hearing loss. In pulmonary by the author of this barotrauma of ascent, damage can precipitate arterial gas embolism, causing article, is provided on blockage of cerebral blood vessels and alterations of consciousness, and page 2225. focal neurologic deficits. In patients with sickness, the vestibular system, and are affected by the formation of bubbles. Common include vertigo, thoracic myelopathy with leg weak- ness, confusion, and hemiparesis. Other diving-related neurologic com- plications include headache and . (Am Fam 2001;63:2211- 8,2225-6.)

ecreational scuba diving, which is defined as pleasure diving Dive-Related Barotrauma without mandatory decompres- During descent and ascent in the , the sion to a maximum depth of diver is constantly exposed to alterations of 130 ft, has become a popular ambient . Barotrauma refers to Ractivity in the past 20 years. In the United damage that occurs when a gas-filled body States alone, there are almost 9 million certi- space (e.g., lungs, middle ) fails to equalize fied divers.1 Although divers are concentrated its internal pressure to accommodate changes along coastal regions, many others dive in in .2-4 The behavior of gasses inland lakes, streams, quarries and reservoirs, at depth is governed by Boyle’s law: the vol- or fly to distant dive sites. practic- ume of a gas varies inversely with pressure.6 ing almost anywhere in the United States may During descent, as ambient pressure increases, see a patient with a dive-related injury or the volume of gas-filled spaces decreases complaint. unless internal pressure is equalized. If the In general, severe injury and death are pressure is not equalized by a larger volume of uncommon in acci- gas, the space will be filled by tissue engorged dents.1-5 The Divers Alert Network1 reports with fluid and blood. This process underlies an average rate of 90 fatalities per year since the common “squeezes” of descent that affect 1980. Each year, between 900 and 1,000 the , external auditory canal, mask, divers are treated with recompression ther- sinuses and teeth. apy for severe dive-related complications. In many of these patients, one or more of the OTIC AND SINUS BAROTRAUMA major symptoms are neurologic in origin. Barotrauma to the middle or inner ear can The is frequently involved in occur during the descent or ascent phases of dive-related complications and fatalities.5 the dive and may cause vertigo and other neu- Physicians need to be aware of the broad rologic symptoms.2-5,7 Middle ear barotrauma spectrum of neurologic injuries that can of descent is the most common type of diving occur during dive accidents to ensure early injury and may involve hemorrhage and rup- recognition, accurate diagnosis and appro- ture of the tympanic membrane. Symptoms priate . include the acute onset of pain, vertigo and

JUNE 1, 2001 / VOLUME 63, NUMBER 11 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 2211 neural hearing loss, , and eme- Pulmonary barotrauma is the most severe form of sis. The Weber’s test will lateralize to the unaf- barotrauma and occurs during ascent. fected side in this group of patients. Reducing intracranial and perilymphatic through bed rest, head elevation and with stool softeners can help. Surgical exploration may be that lateralizes to the necessary for repair of the fistula if conservative affected side during the Weber’s test. In severe treatment is ineffective within five to 10 days cases (usually during ascent), increased pres- (i.e., the symptoms persist or worsen). sure in the middle ear can cause reversible weakness of the facial nerve and Bell’s palsy PULMONARY BAROTRAUMA (facial baroparesis).8 Pulmonary barotrauma is the most severe Vertigo can also be induced if barotrauma form of barotrauma and occurs during differentially affects the two vestibular organs ascent.2-4,9 In accordance with Boyle’s law, as (). The vertigo resolves the ambient pressure is reduced during ascent, after pressure equalization occurs. Treatment gas inside the lungs will expand in volume.6 If of middle ear barotrauma involves deconges- the expanding gas is not allowed to escape by tants (e.g., intranasal oxymetazoline, oral exhalation, the alveoli and surrounding tissues pseudoephedrine), antihistamines, will tear. The most common cause of pul- and antibiotics (amoxicillin-clavulanate monary barotrauma among recreational [Augmentin] in a dosage of 500/125 mg divers is breath holding. Other causes are three times per day or clindamycin [Cleocin] related to pulmonary obstructive diseases, in a dosage of 300 mg three times per day for such as or bronchitis, which can lead 10 to 14 days) in patients with otorrhea and to the trapping of gas. Several forms of pul- perforation.2,4,7 monary barotrauma can develop, including Inner ear barotrauma also can develop in mediastinal emphysema, subcutaneous em- patients with middle ear barotrauma.2-5,7 A physema, and arterial gas pressure gradient between the perilymph of the embolism. Arterial gas embolism is the most inner ear and the middle ear cavity can occur, dangerous form of pulmonary barotrauma causing rupture of the labyrinthine windows and accounts for nearly one fourth of fatalities (round and oval) and leakage of perilymph per year among recreational divers.3 In addi- into the middle ear (i.e., fistula). Symptoms tion, it is the only form in which neurologic include the acute onset of vertigo, sensori- symptoms predominate over pulmonary symptoms.9 Arterial gas embolism develops when free The Author air enters the pulmonary vasculature and is carried to the and arterial circulation.9,10 HERBERT B. NEWTON, M.D., is associate professor of and director of the division of neuro- at Ohio State University Medical Center and Arthur G. A large proportion of air bubbles can reach James Cancer and Solove Research Institute, Columbus, Ohio. He graduated the brain, occlude blood vessels and cause from the State University of New York at Buffalo School of and Biomedical -like events. The most common signs Sciences, Buffalo. Dr. Newton received his neurology training at the University of Michigan , Ann Arbor. He completed a fellowship in neuro-oncology at and symptoms of arterial gas embolism are Memorial Sloan-Kettering Cancer Center, New York City. Dr. Newton is certified by the neurologic (Table 12,4,6,7), although pul- Professional Association of Diving Instructors (PADI) as a and Instructor in monary symptoms may also be present. In dive medicine (PADI 162347) and is a member of ’s Alert Network and the Undersea & Hyperbaric Medical Society. more than 80 percent of patients, symptoms develop within five minutes of reaching the Address correspondence to Herbert B. Newton, M.D., Department of Neurology, Ohio State University Medical Center, 465 Means Hall, 1654 Upham Dr., Columbus, OH surface, but they also can occur during ascent 43210 (e-mail: [email protected]). Reprints are available from the author. or after a longer surface interval.

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Almost two thirds of patients with arterial gas embolism have alterations of conscious- Treatment of arterial gas embolism consists of life support, ness (i.e., coma or obtundation). Seizures, 100 percent oxygen, rehydration and transport to a recom- focal motor deficits, visual disturbances, ver- pression facility. tigo and sensory changes are also common. Spinal cord lesions occur less frequently. Many patients show initial improvement within minutes to hours, secondary to partial clear- Oxygen reduces ischemia in affected tissues ance of air emboli. Magnetic resonance imag- and accelerates the dissolution of air emboli. ing (MRI) may demonstrate focal lesions in Seizures, arrhythmias, shock, hyperglycemia the brain after arterial gas embolism.10 Arter- and pulmonary dysfunction should be ial gas embolism can mimic decompression treated, if present. Recompression therapy sickness, and the presentation of the two syn- should be initiated immediately, using the dromes may be clinically indistinguishable (USN) Table 6 algo- (Table 21-5,7-10).2,4,6 Arterial gas embolism and rithm.2-5,10,11 Recompression therapy reduces can develop simulta- the size of air bubbles by increasing ambient neously in some patients. In fact, the air pressure, expedites passage of emboli emboli of arterial gas embolism may act as a through the vasculature and re-establishes nidus, or “seed,” to precipitate decompression blood flow to ischemic tissues. sickness. Therefore, the two syndromes are often described and treated together using the Decompression Sickness more global term, .4 Decompression sickness is caused by the Treatment of arterial gas embolism con- release of bubbles (usually nitro- sists of basic or advanced cardiac life sup- gen) into the bloodstream and tissues after port, 100 percent oxygen, rehydration and ambient pressure is reduced.2-5,10 At depth, transport to a recompression facility.2,4,9,10 the partial pressures of gasses in the breath- ing mixture increase in proportion to the ambient pressure, according to Dalton’s law.6 TABLE 1 Although oxygen is actively metabolized, Presenting Signs and Symptoms nitrogen is inert and becomes dissolved in in Patients with Arterial Gas Embolism body tissues until saturation, proportional to the ambient pressure as defined by Henry’s 6 Sign or symptom Percentage law. The propensity for the formation of nitrogen bubbles depends on the depth of Stupor or confusion 24 the dive, the length of time at depth and the Coma without seizures 22 rate of ascent. If ambient pressure is released Coma with seizures 18 too quickly, the dissolved nitrogen gas that Unilateral motor deficits 14 cannot remain in will form air bub- Visual disturbances 9 bles within the blood, interstitial fluids and organs (Figure 1). Vertigo 8 Decompression sickness is traditionally Unilateral sensory deficits 8 classified into type I and type II. In type I Bilateral motor deficits 8 decompression sickness, symptoms are usu- Collapse 4 ally mild and may manifest as fatigue or malaise (i.e., constitutional decompression Information from references 2,4,6 and 7. sickness) or may be more specific, involving the muscles, joints and .10 Type II decom-

JUNE 1, 2001 / VOLUME 63, NUMBER 11 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 2213 pression sickness is more severe and can affect brain, spinal cord, cranial and peripheral the lungs, vestibular apparatus and the ner- nerves, and the neural vasculature. Nitrogen vous system. bubbles can injure neural tissues by mechanical In inner ear and neurologic decompression disruption, compression, vascular stenosis or sickness, the formation of bubbles affects the obstruction, and activation of inflammatory

TABLE 2 Clinical Features, and Treatment of the Neurologic Complications of Scuba Diving

Disorder Clinical features Dive profile Treatment

Middle ear Acute pain, vertigo, hearing During descent usually, Improved equalization techniques, barotrauma loss, rupture or hemorrhage possible during ascent oral and nasal ; of descent of tympanic membrane with otorrhea use antibiotics Facial baroparesis Ipsilateral facial , During ascent No treatment resolves within hours Inner ear Acute vertigo, nausea, emesis, During descent usually, ENT evaluation, bed rest, head barotrauma tinnitus, sensorineural hearing possible during ascent elevation, stool softeners; loss; often associated with consider surgical exploration middle ear barotrauma if symptoms persist Arterial gas Stupor, confusion, coma, Within five minutes of surfacing 100 percent oxygen, United embolism seizures, focal weakness, (> 80 percent) or during ascent; States Navy Table 6 algorithm visual loss significant time-depth exposure recompression, supportive care not required Inner ear DCS Acute vertigo, nausea, emesis, Within 30 to 60 minutes of Same as above nystagmus, tinnitus, surfacing (> 50 percent), sensorineural hearing loss 90 percent by six hours; significant time-depth exposure required Cerebral DCS Confusion, focal weakness, Same as above Same as above fatigue, visual loss, diplopia, speech dysfunction, gait abnormality, headache Spinal cord DCS /sensory loss in trunk Same as above Same as above and/or extremities, leg weakness, loss of bowel/bladder function Headache (arterial Severe generalized headache Usually develops within minutes Same as above; analgesics gas embolism associated with alteration of of ascent, may persist without or DCS) consciousness and other signs recompression treatment Headache Pounding, throbbing pain; Usually precipitated during Avoid precipitating stimuli, (migraine) nausea, emesis, photophobia pre-dive activities or at depth dive conservatively, consider prophylactic therapy Focal seizures, visual constriction, Occurs at depth Reduce depth and oxygen nausea, emesis, vertigo, exposure, supportive care, paresthesias, rare generalized management; see arterial gas seizures embolism treatment

ENT = ear, nose and throat; DCS = decompression sickness. Information from references 1 through 5 and 7 through 10.

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Decompression sickness should be suspected in any patient with a recent history of diving and a consistent clinical presentation.

semicircular canals. In many cases, inner ear decompression sickness is clinically indistin- guishable from otic barotrauma, although the dive profile and timing of symptoms may help FIGURE 1. Experimental preparation of decom- 2-5,7,10 pression illness (i.e., cerebral decompression to clarify the diagnosis (Table 2). sickness and arterial gas embolism) demon- Neurologic decompression sickness can strating the presence of bubbles passing within present with a wide spectrum of symptoms vasculature of the cortical subarachnoid space (Table 3). The most severe presentation is par- (arrow). Note the regions of surface hemor- tial myelopathy referable to the thoracic spinal rhage (upper right) on surrounding gyri. cord.10,15 Patients complain of paresthesias and sensory loss in the trunk and extremities, pathways (e.g., cytokines, complement).4,10 a tingling or constricting sensation around the Cerebral decompression sickness (30 to 40 per- , ascending leg weakness ranging from cent of cases) usually involves arterial circula- mild to severe, pain in the lower back or pelvis tion, while spinal cord decompression sickness and loss of bowel and/or bladder control. The (50 to 60 percent of cases) involves obstruction neurologic examination will often reveal of venous drainage and the formation of bub- monoparesis or paraparesis, a sensory level bles within the cord parenchyma.12 The incidence of decompression sickness among recreational scuba divers is estimated TABLE 3 to be one case per 5,000 to 10,000 dives.1 Div- Presenting Signs and Symptoms ing within the limits of dive tables is no guar- in Patients with Decompression Sickness antee against decompression sickness, because more than 50 percent of cases of decompres- Sign or symptom Percentage sion sickness occur after no-decompression Numbness 59 dives. In addition to the dive profile and rate Pain 55 of ascent, other factors may influence the risk of decompression sickness, including hypo- 27 thermia, fatigue, increased age, , Extreme fatigue 25 intake, female gender, obesity and Headache 24 patent foramen ovale.2-5,13 Weakness 23 In type II neurologic decompression sick- Nausea 14 ness, more than 50 percent of patients develop Gait abnormality 12 symptoms within one hour of ascent; within six hours, 90 percent of divers are sympto- 10 matic.1,4,14 Inner ear decompression sickness Visual disturbance 8 presents with acute vertigo, nausea, emesis, Itching 5 nystagmus and tinnitus. The pathophysiology remains unclear; one mechanism is Information from references 1,2,4,5 and 9. rupture of the intraosseous membranes in the

JUNE 1, 2001 / VOLUME 63, NUMBER 11 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 2215 FIGURE 2. FIGURE 3.

and sphincter disturbances. However, neuro- roimaging studies may further clarify the logic examination also may be normal. diagnosis but should not delay treatment. Pathologic features within the spinal cord MRI demonstrates high-signal lesions of the include hemorrhagic , , bub- brain and spinal cord in 30 to 55 percent of ble defects, axonal degeneration and demyeli- cases (Figure 3), which suggests ischemia, nation (Figure 2).12,15 Cerebral decompression edema and swelling. The lesions do not sickness can occur alone or in combination enhance with contrast. However, images on with spinal decompression sickness and mani- MRI are often normal.5,10,16 fests as an alteration of mentation or confu- The initial management of neurologic sion, weakness, headache, gait disturbance, decompression sickness is similar to that of fatigue, diplopia or visual loss. The neurologic arterial gas embolism and decompression ill- examination may show hemiparesis, dyspha- ness, and requires transport to a recompres- sia, gait ataxia, hemianopsia and other focal sion facility.2-5,10,16 If transport by helicopter is signs. Behavioral and cognitive aspects of cere- necessary, the patient should be flown at an bral decompression sickness may be persistent of less than 1,000 ft to minimize exac- or slow to improve.10,16 The pathologic features erbation of symptoms. The definitive treat- are similar to those of spinal decompression ment is recompression therapy using the USN sickness, although not as pronounced.10,17 Table 6 algorithm.11 USN Table 6 consists of The diagnosis of neurologic decompression initial recompression to 60 ft of salt water with sickness is clinical and should be suspected in 100 percent oxygen for 60 minutes. The any patient with a recent history of diving patient is then decompressed to 30 ft of salt who has a consistent presentation. Neu- water for two additional periods each of

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pure oxygen and air. Recompression extended bottom time. When diving with therapy reduces the size of bubbles, allowing , the diver is at risk of oxygen toxicity if easier reabsorption and dissipation, and the maximum oxygen depth limit and/or the increases the nitrogen gradient to expedite oxygen time limit is exceeded. In general, the off-gassing. The majority of recreational higher the oxygen content in the Nitrox mix- divers with neurologic decompression sick- ture, the shallower the dive to minimize the ness have an excellent recovery after prompt potential for oxygen toxicity. Symptoms recompression therapy. develop at depth without warning and consist The (DAN) at Duke of focal seizures (e.g., facial or lip twitching University Medical Center, Durham, N.C., is occurs in 50 to 60 percent of patients), vertigo, available 24 hours a day to discuss arterial gas nausea and emesis, paresthesias, visual con- embolism or decompression sickness and pro- striction and respiratory changes.18 General- vide divers a referral to the nearest recompres- ized seizures or syncope can also occur in 5 to sion facility, if necessary. The emergency hotline 10 percent of patients. Although uncommon, number is 919-684-8111. For nonemergency generalized seizures at depth are often fatal, medical questions, call DAN at 919-684-2948. because divers may drown or arterial gas embolism may be precipitated during rescue Headache to the surface.4 The cause of oxygen toxicity to Headache is a common symptom in divers. the nervous system mainly involves oxygen- There are numerous benign causes, including free radical formation, as well as reduction of exacerbation of tension or migraine , the inhibitory neurotransmitter, gamma- exposure to cold, mask or sinus barotrauma, aminobutyric acid. Treatment consists of sinusitis and a tight face mask. Migraines are reducing oxygen exposure and dive depth not often precipitated by diving, but can be and, if necessary, managing seizures. severe when they occur. If a migraine develops, the dive should be terminated because of the Figures 1 and 2 used with permission from James potential for nausea, emesis and alteration of PB. Bubbles, brain damage and hyperbaric oxygena- tion. World Neurology 1998;13:6. consciousness. Dangerous causes of headache include cerebral decompression sickness, cont- Figure 3 used with permission from Elliott DH, Moon amination of the with carbon RE. Manifestations of the decompression disorders. monoxide, arterial gas embolism, severe otic or In: Bennett PB, Elliott DH, eds. The and sinus barotrauma with rupture, and oxygen medicine of diving. 4th ed. London: Saunders, toxicity.2-5,10 If headache occurs in a patient 1993;17:481-505. with potential arterial gas embolism or decom- Dr. Newton received support in part from a National pression sickness, it should be considered an Cancer Institute grant, CA 16058. emergency, because it suggests the presence of intracerebral bubbles. This type of headache The author thanks Harrison Weed, M.D., for critical usually develops within minutes of ascent. review of the manuscript and David Carpenter for Immediate use of 100 percent oxygen and of his editorial expertise. recompression therapy is indicated. REFERENCES

Oxygen Toxicity 1. Divers Alert Network. Report on decompression ill- ness and diving fatalities: DAN’s annual review of In the recreational diver, the most likely recreational scuba diving injuries and fatalities cause of oxygen toxicity is diving with oxygen based on 1998 data. Durham, NC: Divers Alert enriched air (i.e., Nitrox). Nitrox is a breathing Network, 2000. 2. Melamed Y, Shupak A, Bitterman H. Medical prob- mixture that contains more than 21 percent lems associated with . N Engl J oxygen (usually 32 to 36 percent), and allows Med 1992;326:30-5.

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3. Clenney TL, Lassen LF. Recreational scuba diving JM, Flynn ET. Is there a role for the autochthonous injuries. Am Fam Physician 1996;53:1761-74. bubble in the pathogenesis of spinal cord decom- 4. Moon RE. Treatment of diving emergencies. Crit pression sickness? J Neuropathol Exp Neurol Care Clin 1999;15:429-56. 1988;47:475-87. 5. Dick AP, Massey EW. Neurologic presentation of 13. Knauth M, Ries S, Pohimann S, Kerby T, Forsting M, decompression sickness and in sport Daffertshofer M, et al. Cohort study of multiple divers. Neurology 1985;35:667-71. brain lesions in sport divers: role of a patent fora- 6. Brylske A. The . A guide for the mathe- men ovale. BMJ 1997;314:701-5. matically challenged. Dive Training 1997;Septem- 14. Francis TJ, Pearson RR, Robertson AG, Hodgson M, ber:26-34. Dutka AJ, Flynn ET. decom- 7. Farmer JC. Otological and paranasal sinus prob- pression sickness: latency of 1070 human cases. lems in diving. In: Bennett PB, Elliott DH, eds. The Undersea Biomed Res 1988;15:403-17. physiology and medicine of diving. 4th ed. London: 15. Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Saunders, 1993;11:267-300. Melamed Y. Spinal cord decompression sickness in 8. Molvaer OI, Eidsvik S. Facial baroparesis: a review. . Arch Neurol 1993;50:753-6. Undersea Biomed Res 1987;14:277-95. 16. Levin HS, Goldstein FC, Norcross K, Amparo EG, 9. Neuman TS. Pulmonary barotrauma. In: Bove AA, Guinto FC, Mader JT. Neurobehavioral and mag- ed. Bove and Davis’ . 3d ed. netic resonance imaging findings in two cases of Philadelphia: Saunders, 1997;13:176-83. decompression sickness. Aviat Space Environ Med 10. Greer HD, Massey EW. Neurologic injury from 1989;60:1204-10. undersea diving. Neurol Clin 1992;10:1031-45. 17. Palmer AC, Calder IM, Yates PO. Cerebral vascu- 11. U.S. Navy. Recompression treatments when cham- lopathy in divers. Neuropathol Appl Neurobiol ber available. U.S. Navy Diving Manual Vol. 1 (Air 1992;18:113-24. Diving). Revision 1, ch. 8, rev. 15. February 1993; 18. Clark JM, Thom SR. Toxicity of oxygen, carbon Naval Systems Command Publication NAVSEA dioxide, and . In: Bove AA, ed. 0994-LP-001-9110. Bove and Davis’ Diving medicine. 3d ed. Philadel- 12. Francis TJ, Pezeshkpour GH, Dutka AJ, Hallenbeck phia: Saunders, 1997;10:131-45.

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