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1 1,2001 / VOLUME63,Nwww.aafp.org/afpAMI
1,2001 / VOLUME63,Nwww.aafp.org/afpAMILYHYSICIAN Dive-Related BarotraumaDuring descent and ascent in the water,thediver is constantly exposed to alterations of ecreational scuba diving,whichis defined as pleasure divingwithout mandatory decompres-sion to a maximum depth of130 ft,has become a popularactivity in the past 20 years.In the UnitedStates alone,there are almost 9 million certi-fied divers. Recreational scuba diving has become a popular sport in the United States, withalmost 9 million certified divers. When severe diving injury occurs, the nervoussystem is frequently involved. In dive-related barotrauma, compressed or expand-ing gas within the ears, sinuses and lungs causes various forms of neurologicinjury. Otic barotrauma often induces pain, vertigo and hearing loss. In pulmonarybarotrauma of ascent, lung damage can precipitate arterial gas embolism, causingblockage of cerebral blood vessels and alterations of consciousness, seizures andfocal neurologic deficits. In patients with decompression sickness, the vestibular Neurologic Complications ofScuba DivingHERBERT B.NEWTON,M.D.,Ohio State University Hospitals,Columbus,Ohio conductive hearing loss that lateralizes to theaffected side during the WeberÕs test.In severecases (usually during ascent),increased pres-sure in the middle ear can cause reversibleweakness ofthe facial nerve and BellÕs palsy(facial baroparesis).Vertigo can also be induced ifbarotraumadifferentially affects the two vestibular organs(alternobaric vertigo).The vertigo resolvesafter pressure equalization occurs.Treatmentofmiddle ear barotrauma involves deconges-tants (e.g.,intranasal oxymetazoline,oralpseudoephedrine),antihistamines,analgesicsand antibiotics (amoxicillin-clavulanate[Augmentin] in a dosage of500/125 mgthree times per day or clindamycin [Cleocin]in a dosage of300 mg three times per day for10 to 14 days) in patients with otorrhea andperforation.Inner ear barotrauma also can develop inpatients with middle ear barotrauma.pressure gradient between the perilymph oftheinner ear and the middle ear cavity can occur,causing rupture ofthe labyrinthine windows(round and oval) and leakage ofperilymphinto the middle ear (i.e.,fistula).Symptomsinclude the acute onset ofvertigo,sensori-neural hearing loss,tinnitus,nausea and eme-sis.The WeberÕs test will lateralize to the unaf-fected side in this group ofpatients.Reducingintracranial and perilymphatic pressuresthrough bed rest,head elevation and with stoolsofteners can help.Surgical exploration may benecessary for repair ofthe fistula ifconservat

2 ivetreatment is ineffective within five
ivetreatment is ineffective within five to 10 days(i.e.,the symptoms persist or worsen).PULMONARYBAROTRAUMAPulmonary barotrauma is the most severeform ofbarotrauma and occurs duringascent.In accordance with BoyleÕs law,asthe ambient pressure is reduced during ascent,gas inside the lungs will expand in volume.the expanding gas is not allowed to escape byexhalation,the alveoli and surrounding tissueswill tear.The most common cause ofpul-monary barotrauma among recreationaldivers is breath holding.Other causes arerelated to pulmonary obstructive diseases,such as asthma or bronchitis,which can leadto the trapping ofgas.Several forms ofpul-monary barotrauma can develop,includingmediastinal emphysema,subcutaneous em-physema,pneumothorax and arterial gasembolism.Arterial gas embolism is the mostdangerous form ofpulmonary barotraumaand accounts for nearly one fourth offatalitiesper year among recreational divers.In addi-tion,it is the only form in which neurologicsymptoms predominate over pulmonarysymptoms.Arterial gas embolism develops when freeair enters the pulmonary vasculature and iscarried to the heart and arterial circulation.A large proportion ofair bubbles can reachthe brain,occlude blood vessels and causestroke-like events.The most common signsand symptoms ofarterial gas embolism areneurologic (Table 1,although pul-monary symptoms may also be present.Inmore than 80 percent ofpatients,symptomsdevelop within five minutes ofreaching thesurface,but they also can occur during ascentor after a longer surface interval.AMILYHYSICIANwww.aafp.org/afpOLUME63,N11 / J1,2001 Pulmonary barotrauma is the most severe form of HERBERT B. NEWTON, M.D., is associate professor of neurology and director of thedivision of neuro-oncology at Ohio State University Medical Center and Arthur G.James Cancer Hospital and Solove Research Institute, Columbus, Ohio. He graduatedfrom the State University of New York at Buffalo School of Medicine and BiomedicalSciences, Buffalo. Dr. Newton received his neurology training at the University ofMichigan Medical School, Ann Arbor. He completed a fellowship in neuro-oncology atMemorial Sloan-Kettering Cancer Center, New York City. Dr. Newton is certified by theProfessional Association of Diving Instructors (PADI) as a DiveMaster and Instructor indive medicine (PADI 162347) and is a member of the DiverÕs Alert Network and theUndersea & Hyperbaric Medical Society. Address correspondence to Herbert B. Newton, M.D., Department of Neurology, OhioState University Medical Center, 465 Means Hall, 1654 Upham Dr., Columbu

3 s, OH43210 (e-mail: newton.12@osu.edu).
s, OH43210 (e-mail: newton.12@osu.edu). Reprints are available from the author. Almost two thirds ofpatients with arterialgas embolism have alterations ofconscious-ness (i.e.,coma or obtundation).Seizures,focal motor deficits,visual disturbances,ver-tigo and sensory changes are also common.Spinal cord lesions occur less frequently.Manypatients show initial improvement withinminutes to hours,secondary to partial clear-ance ofair emboli.Magnetic resonance imag-ing (MRI) may demonstrate focal lesions inthe brain after arterial gas embolism.Arter-ial gas embolism can mimic decompressionsickness,and the presentation ofthe two syn-dromes may be clinically indistinguishable(Table 2Arterial gas embolism anddecompression sickness can develop simulta-neously in some patients.In fact,the airemboli ofarterial gas embolism may act as anidus,or Òseed,Óto precipitate decompressionsickness.Therefore,the two syndromes areoften described and treated together using themore global term,decompression illness.Treatment ofarterial gas embolism con-sists ofbasic or advanced cardiac life sup-port,100 percent oxygen,rehydration andtransport to a recompression facility.Oxygen reduces ischemia in affected tissuesand accelerates the dissolution ofair emboli.Seizures,arrhythmias,shock,hyperglycemiaand pulmonary dysfunction should betreated,ifpresent.Recompression therapyshould be initiated immediately,using theUnited States Navy (USN) Table 6 algo-rithm.Recompression therapy reducesthe size ofair bubbles by increasing ambientpressure,expedites passage ofembolithrough the vasculature and re-establishesblood flow to ischemic tissues.Decompression SicknessDecompression sickness is caused by therelease ofinert gas bubbles (usually nitro-gen) into the bloodstream and tissues afterambient pressure is reduced.At depth,the partial pressures ofgasses in the breath-ing mixture increase in proportion to theambient pressure,according to DaltonÕs law.Although oxygen is actively metabolized,nitrogen is inert and becomes dissolved inbody tissues until saturation,proportional tothe ambient pressure as defined by HenryÕslaw.The propensity for the formation ofnitrogen bubbles depends on the depth ofthe dive,the length oftime at depth and therate ofascent.Ifambient pressure is releasedtoo quickly,the dissolved nitrogen gas thatcannot remain in solution will form air bub-bles within the blood,interstitial fluids and(Figure 1).Decompression sickness is traditionallyclassified into type I and type II.In type Idecompression sickness,symptoms are usu-ally mild and may manifest

4 as fatigue ormalaise (i.e.,constitutiona
as fatigue ormalaise (i.e.,constitutional decompressionsickness) or may be more specific,involvingthe muscles,joints and skin.Type II decom-1,2001 / VOLUME63,Nwww.aafp.org/afpAMILYHYSICIAN TABLE 1Presenting Signs and Symptoms in Patients with Arterial Gas Embolism Sign or symptomPercentageStupor or confusion24Coma without seizures22Coma with seizures18Unilateral motor deficits14Visual disturbances9Vertigo8Unilateral sensory deficits8Bilateral motor deficits8 Collapse4 Information from references 2,4,6 and 7. Treatment of arterial gas embolism consists of life support,pression facility. pression sickness is more severe and can affectthe lungs,vestibular apparatus and the ner-vous system.In inner ear and neurologic decompressionsickness,the formation ofbubbles affects thebrain,spinal cord,cranial and peripheralnerves,and the neural vasculature.Nitrogenbubbles can injure neural tissues by mechanicaldisruption,compression,vascular stenosis orobstruction,and activation ofinflammatoryAMILYHYSICIANwww.aafp.org/afpOLUME63,N11 / J1,2001 TABLE 2 Clinical Features, Dive Profile and Treatment of the Neurologic Complications of Scuba Diving DisorderClinical featuresDive profileTreatmentMiddle ear Acute pain, vertigo, hearing During descent usually, Improved equalization techniques, barotrauma loss, rupture or hemorrhage possible during ascentoral and nasal decongestants; of descentof tympanic membranewith otorrhea use antibioticsFacial baroparesisIpsilateral facial paralysis, During ascentNo treatmentresolves within hoursInner ear Acute vertigo, nausea, emesis, During descent usually, ENT evaluation, bed rest, head barotraumatinnitus, sensorineural hearing possible during ascentelevation, stool softeners; loss; often associated with consider surgical exploration middle ear barotraumaif symptoms persistArterial gasStupor, confusion, coma, Within five minutes of surfacing 100 percent oxygen, United embolismseizures, focal weakness, �( 80 percent) or during ascent; States Navy Table 6 algorithm visual losssignificant time-depth exposure recompression, supportive carenot requiredInner ear DCSAcute vertigo, nausea, emesis, Within 30 to 60 minutes of Same as abovenystagmus, tinnitus, �surfacing ( 50 percent), sensorineural hearing loss90 percent by six hours; significant time-depth exposure requiredCerebral DCSConfusion, focal weakness, Same as aboveSame as aboveabnormality, headacheSpinal cord DCSParesthesias/sensory loss in trunk Same as aboveSame as aboveand/or extremities, leg weakness, Headache (arterial Severe generali

5 zed headache Usually develops within min
zed headache Usually develops within minutes Same as above; analgesicsgas embolism associated with alteration of of ascent, may persist without or DCS)consciousness and other signsrecompression treatmentHeadache Pounding, throbbing pain; Usually precipitated during Avoid precipitating stimuli, (migraine)nausea, emesis, photophobiapre-dive activities or at depthdive conservatively, consider prophylactic therapyOxygen toxicityFocal seizures, visual constriction, Occurs at depthReduce depth and oxygen exposure, supportive care, seizure paresthesias, rare generalized management; see arterial gas seizuresembolism treatmentENT = ear, nose and throat; DCS = decompression sickness. Information from references 1 through 5 and 7 through 10. pathways (e.g.,cytokines,complement).Cerebral decompression sickness (30 to 40 per-cent ofcases) usually involves arterial circula-tion,while spinal cord decompression sickness(50 to 60 percent ofcases) involves obstructionofvenous drainage and the formation ofbub-bles within the cord parenchyma.The incidence ofdecompression sicknessamong recreational scuba divers is estimatedto be one case per 5,000 to 10,000 dives.Div-ing within the limits ofdive tables is no guar-antee against decompression sickness,becausemore than 50 percent ofcases ofdecompres-sion sickness occur after no-decompressiondives.In addition to the dive profile and rateofascent,other factors may influence the riskofdecompression sickness,including hypo-thermia,fatigue,increased age,dehydration,alcohol intake,female gender,obesity andpatent foramen ovale.In type II neurologic decompression sick-ness,more than 50 percent ofpatients developsymptoms within one hour ofascent;withinsix hours,90 percent ofdivers are sympto-Inner ear decompression sicknesspresents with acute vertigo,nausea,emesis,nystagmus and tinnitus.The pathophysiologyremains unclear;one mechanism is bubblerupture ofthe intraosseous membranes in thesemicircular canals.In many cases,inner eardecompression sickness is clinically indistin-guishable from otic barotrauma,although thedive profile and timing ofsymptoms may helpto clarify the diagnosis (Table 2).Neurologic decompression sickness canpresent with a wide spectrum ofsymptoms(Table 3).The most severe presentation is par-tial myelopathy referable to the thoracic spinalcord.Patients complain ofparesthesiasand sensory loss in the trunk and extremities,a tingling or constricting sensation around thethorax,ascending leg weakness ranging frommild to severe,pain in the lower back or pelvisand loss ofbowel and/or bladder c

6 ontrol.Theneurologic examination will of
ontrol.Theneurologic examination will often revealmonoparesis or paraparesis,a sensory level1,2001 / VOLUME63,Nwww.aafp.org/afpAMILYHYSICIAN with a recent history of diving and a consistent clinical TABLE 3Presenting Signs and Symptoms in Patients with Decompression Sickness Sign or symptomPercentageNumbness59Pain55Dizziness27Extreme fatigue25Headache24Weakness23Nausea14Gait abnormality12Hypoesthesia10Visual disturbance8 Itching5 Information from references 1,2,4,5 and 9. FIGURE 1. Experimental preparation of decom-pression illness (i.e., cerebral decompressionsickness and arterial gas embolism) demon-strating the presence of bubbles passing withinvasculature of the cortical subarachnoid space(arrow). Note the regions of surface hemor-rhage (upper right) on surrounding gyri. and sphincter disturbances.However,neuro-logic examination also may be normal.Pathologic features within the spinal cordinclude hemorrhagic infarctions,edema,bub-ble defects,axonal degeneration and demyeli-(Figure 2)Cerebral decompressionsickness can occur alone or in combinationwith spinal decompression sickness and mani-fests as an alteration ofmentation or confu-sion,weakness,headache,gait disturbance,fatigue,diplopia or visual loss.The neurologicexamination may show hemiparesis,dyspha-sia,gait ataxia,hemianopsia and other focalsigns.Behavioral and cognitive aspects ofcere-bral decompression sickness may be persistentor slow to improve.The pathologic featuresare similar to those ofspinal decompressionsickness,although not as pronounced.The diagnosis ofneurologic decompressionsickness is clinical and should be suspected inany patient with a recent history ofdivingwho has a consistent presentation.Neu-roimaging studies may further clarify thediagnosis but should not delay treatment.MRI demonstrates high-signal lesions ofthebrain and spinal cord in 30 to 55 percent of(Figure 3),which suggests ischemia,edema and swelling.The lesions do notenhance with contrast.However,images onMRI are often normal.The initial management ofneurologicdecompression sickness is similar to that ofarterial gas embolism and decompression ill-ness,and requires transport to a recompres-sion facility.Iftransport by helicopter isnecessary,the patient should be flown at analtitude ofless than 1,000 ft to minimize exac-erbation ofsymptoms.The definitive treat-ment is recompression therapy using the USNTable 6 algorithm.USN Table 6 consists ofinitial recompression to 60 ft ofsalt water with100 percent oxygen for 60 minutes.Thepatient is then decompressed to 30 ft ofsaltwater for t

7 wo additional periods each ofAMILYHYSICI
wo additional periods each ofAMILYHYSICIANwww.aafp.org/afpOLUME63,N1,2001 FIGURE 3. FIGURE 2. breathing pure oxygen and air.Recompressiontherapy reduces the size ofbubbles,allowingeasier reabsorption and dissipation,andincreases the nitrogen gradient to expediteoff-gassing.The majority ofrecreationaldivers with neurologic decompression sick-ness have an excellent recovery after promptrecompression therapy.The Divers Alert Network (DAN) at DukeUniversity Medical Center,Durham,N.C.,isavailable 24 hours a day to discuss arterial gasembolism or decompression sickness and pro-vide divers a referral to the nearest recompres-sion facility,ifnecessary.The emergency hotlinenumber is 919-684-8111.For nonemergencymedical questions,call DAN at 919-684-2948.Headache is a common symptom in divers.There are numerous benign causes,includingexacerbation oftension or migraine headaches,exposure to cold,mask or sinus barotrauma,sinusitis and a tight face mask.Migraines arenot often precipitated by diving,but can besevere when they occur.Ifa migraine develops,the dive should be terminated because ofthepotential for nausea,emesis and alteration ofconsciousness.Dangerous causes ofheadacheinclude cerebral decompression sickness,cont-amination ofthe breathing gas with carbonmonoxide,arterial gas embolism,severe otic orsinus barotrauma with rupture,and oxygentoxicity.Ifheadache occurs in a patientwith potential arterial gas embolism or decom-pression sickness,it should be considered anemergency,because it suggests the presence ofintracerebral bubbles.This type ofheadacheusually develops within minutes ofascent.Immediate use of100 percent oxygen and ofrecompression therapy is indicated.Oxygen ToxicityIn the recreational diver,the most likelycause ofoxygen toxicity is diving with oxygenenriched air (i.e.,Nitrox).Nitrox is a breathingmixture that contains more than 21 percentoxygen (usually 32 to 36 percent),and allowsextended bottom time.When diving withNitrox,the diver is at risk ofoxygen toxicity ifthe maximum oxygen depth limit and/or theoxygen time limit is exceeded.In general,thehigher the oxygen content in the Nitrox mix-ture,the shallower the dive to minimize thepotential for oxygen toxicity.Symptomsdevelop at depth without warning and consistoffocal seizures (e.g.,facial or lip twitchingoccurs in 50 to 60 percent ofpatients),vertigo,nausea and emesis,paresthesias,visual con-striction and respiratory changes.General-ized seizures or syncope can also occur in 5 to10 percent ofpatients.Although uncommon,generalized seizures at depth are often f

8 atal,because divers may drown or arteria
atal,because divers may drown or arterial gasembolism may be precipitated during rescueto the surface.The cause ofoxygen toxicity tothe nervous system mainly involves oxygen-free radical formation,as well as reduction ofthe inhibitory neurotransmitter,gamma-aminobutyric acid.Treatment consists ofreducing oxygen exposure and dive depthand,ifnecessary,managing seizures.tion. World Neurology 1998;13:6.Dr. Newton received support in part from a NationalThe author thanks Harrison Weed, M.D., for critical 1.Divers Alert Network. Report on decompression ill-ness and diving fatalities: DANÕs annual review ofrecreational scuba diving injuries and fatalities2.Melamed Y, Shupak A, Bitterman H. Medical prob-1,2001 / VOLUME63,Nwww.aafp.org/afpAMILYHYSICIAN Scuba Diving 3.Clenney TL, Lassen LF. Recreational scuba diving4.Moon RE. Treatment of diving emergencies. CritCare Clin 1999;15:429-56.5.Dick AP, Massey EW. Neurologic presentation ofdecompression sickness and air embolism in sportdivers. Neurology 1985;35:667-71.6.Brylske A. The gas laws. A guide for the mathe-matically challenged. Dive Training 1997;Septem-7.Farmer JC. Otological and paranasal sinus prob-8.Molvaer OI, Eidsvik S. Facial baroparesis: a review.9.Neuman TS. Pulmonary barotrauma. In: Bove AA,10.Greer HD, Massey EW. Neurologic injury fromundersea diving. Neurol Clin 1992;10:1031-45.11.U.S. Navy. Recompression treatments when cham-ber available. U.S. Navy Diving Manual Vol. 1 (AirDiving). Revision 1, ch. 8, rev. 15. February 1993;Naval Sea Systems Command Publication NAVSEA12.Francis TJ, Pezeshkpour GH, Dutka AJ, HallenbeckJM, Flynn ET. Is there a role for the autochthonousbubble in the pathogenesis of spinal cord decom-pression sickness? J Neuropathol Exp Neurol13.Knauth M, Ries S, Pohimann S, Kerby T, Forsting M,Daffertshofer M, et al. Cohort study of multiplebrain lesions in sport divers: role of a patent fora-14.Francis TJ, Pearson RR, Robertson AG, Hodgson M,Dutka AJ, Flynn ET. Central nervous system decom-pression sickness: latency of 1070 human cases.15.Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N,Melamed Y. Spinal cord decompression sickness insport diving. Arch Neurol 1993;50:753-6.16.Levin HS, Goldstein FC, Norcross K, Amparo EG,Guinto FC, Mader JT. Neurobehavioral and mag-netic resonance imaging findings in two cases ofdecompression sickness. Aviat Space Environ Med17.Palmer AC, Calder IM, Yates PO. Cerebral vascu-lopathy in divers. Neuropathol Appl Neurobiol18.Clark JM, Thom SR. Toxicity of oxygen, carbonAMILYHYSICIANwww.aafp.org/afpOLUME63,N11 / J1,200