decompression syndrome

8/10/2019 Decompression Syndrome

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Background

Diving as a profession can be traced back more than 5000 years, yet diving-related disease wasnot described until Paul Bert wrote about caisson disease in 1878. Symptoms of caisson diseasewere noted among bridge workers after finishing their shifts underwater and coming back to thesurface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the jointsor abdomen. The caisson workers often noted that they felt better while working. This wasusually attributed to their being rested at the beginning of the shift as opposed to being tiredwhen the workday was through. The workers would often have severe back pain that left them

bent over, which is how caisson disease earned the nickname "the bends."

Diving barotrauma can present with various manifestations, from ear or mouth pain andheadaches to major joint pain, paralysis, coma, and death. As a result of the wide variety of

presentations, these disorders must be considered in any patient who has recently been exposedto a significant change in barometric pressure. The 3 major manifestations of barotrauma includethe following: (1) sinus or middle ear effects, (2) decompression sickness (DCS), and (3) arterialgas emboli.

Barotrauma has also reportedly been caused by an airbag rupturing during deployment, forcinghigh-pressure gas into a person's lungs. It has also reportedly been associated with rapid ascent inmilitary aircraft and with pressure changes associated with space exploration. Barotrauma hasalso been reported with both tracheal intubation and fiberoptic endotracheal intubation.Fiberoptic endotracheal intubation requires insufflated oxygen, which increases airway pressure.This leads to alveolar rupture with pneumothorax and subcutaneous emphysema .[1]

The most current research in barotrauma has been dealing with ventilator-associated barotraumaand barotrauma prevention.

Recently, there has been a significant rise in articles dealing with combat-associated barotrauma.These articles deal mainly with blast injury patterns and ballistics. This is an extensive subjectand is not covered in this article.

Pathophysiology

Injuries caused by pressure changes are generally governed by the Boyle and Henry laws of physics.

The Boyle law states, "For any gas at a constant temperature, the volume of the gas will varyinversely with the pressure," or P1 X V1 = P2 X V2. Pressure rises by 1 atmosphere for every 33ft (10 m) of seawater depth. This means that a balloon (or lungs) containing a volume of 1 cubicfoot of gas at 33 ft of seawater depth will have a volume of gas of 2 cubic feet at the surface. Ifthis air is trapped, as occurs when a person holds his or her breath during rapid ascent, it expandswith great force against the walls of that space (reverse squeeze). During rapid ascent, incidentsof pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can
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occur. Sinus squeeze occurs with eustachian tube dysfunction, which may result in inner earhemorrhage, tearing of the labyrinthine membrane, or perilymphatic fistula.

The Henry law states that the solubility of a gas in a liquid is directly proportional to the pressureexerted upon the gas and liquid. Thus, when the cap is removed from a bottle of soda pop, the

soda begins to bubble as gas is released from the liquid. In addition, when nitrogen in a diver'sair tank dissolves in the diver's fatty tissues or synovial fluids at depth, nitrogen will be releasedfrom those tissues as the diver ascends to a lower pressure environment. This occurs slowly andgradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream tothe lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidlyand forms gas bubbles.

Once bubbles are formed, they can affect tissues in many ways. They can simply obstruct bloodvessels leading to ischemic injury. This can be devastating when occurring in critical areas in the

brain. The bubbles can also form a surface to which proteins in the bloodstream can cling,unravel, and begin a clotting/inflammatory cascade. This cascade can lead to endothelial

breakdown and permanent tissue damage.

Decompression sickness

Decompression sickness (DCS) usually results from the formation of gas bubbles, which cantravel to any part of the body, accounting for many disorders. A gas bubble forming in the backor joints can cause localized pain (the bends). In the spinal cord or peripheral nerve tissues, a

bubble may cause paresthesias, neurapraxia, or paralysis. A bubble forming in the circulatorysystem can lead to pulmonary or cerebral gas emboli.

Some gases are more soluble in fats. Nitrogen, for example, is 5 times more soluble in fat than in

water. Approximately 40-50% of serious DCS injuries involve the central nervous system(CNS). Women may be at an increased risk of DCS because they have more fat in their bodies.DCS also may occur at high altitudes. Those who dive in mountain lakes or combine diving withsubsequent flying are at increased risk as well.

DCS is classified into 2 types. Type I is milder, is not life threatening, and is characterized by pain in the joints and muscles and swelling in the lymph nodes. The most common symptom ofDCS is joint pain, which begins mildly and worsens over time and with movement. DCS type IIis serious and life threatening. Manifestations may include respiratory, circulatory, and, mostcommonly, peripheral nerve and/or CNS compromise.

Arterial gas embolism (AGE) is the most dangerous manifestation of DCS type II. AGE occursafter a rapid ascent, when a gas bubble forms in the arterial blood supply and travels to the brain,heart, or lungs. This is immediately life threatening and can occur even after ascent fromrelatively shallow depths. However, AGE can also occur from iatrogenic causes.

Patients with a patent foramen ovale (up to 30% of the population) are at higher risk of gas passing from a right-to-left shunt and causing CNS injuries.


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Epidemiology

Frequency

United States

The average risk of severe (type II) DCS is 2.28 cases per 10,000 dives. The number of minor(type I) injures is not known because many divers do not seek treatment. Risk of DCS isincreased in divers with asthma or pulmonary blebs. Risk of DCS type II is increased 2.5 timesin patients with a patent foramen ovale. Deaths due to DCS in military aircraft have beenreported to occur at a rate of 0.024 per million hours of flight time. Rates of decompressionincidents for civilian aviation average about 35 per year, and less than half are significant.

International

No information is available on the incidence of diving barotrauma worldwide. The Australiandefense force has averaged 82 incidents per million hours of flying time.

Race

No significant differences in the incidence of dive-related injuries have been associated withrace.

Sex

Because of a generally greater percentage of body fat, females have a theoretically higherincidence of barotrauma injuries than males. However, no data support this hypothesis.

Age

Although no direct correlation exists with age and frequency of barotrauma, the most commongroup affected ranges between 21 and 40 years. However, direct correlation does exist betweenage and residual effects of barotrauma, which significantly rises after age 50 years.

History

Patients with DCS present with a history of diving, generally within 24 hours of the onset ofsymptoms. Patients may also have a recent history of occupational pressurization ordepressurization. For example, this occurs with aircraft mechanics who must test aircraftwindows by working in pressurized aircraft. Air emboli have also occurred in mechanics whomaintain training altitude chambers. Recently, military operations involving troops travelingfrom ground level to high-altitude environments in a relatively short time and operationsinvolving soldiers doing strenuous activities at higher altitudes have resulted in many cases ofDCS. Recent studies have indicated that aerobic exercise either prior to a dive or duringdecompression stops may decrease the post dive gas bubble formation .[2, 3]


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Sinus squeeze

Patients usually present with complaints of facial or oral pain, nausea, vertigo, or headache.

Other important information to gather includes any history of recent upper respiratory infections,

allergic rhinitis, sinus polyps, and sinus surgeries and whether the pain worsened during descentor ascent.

Middle ear squeeze

Patients often have a history of sudden vertigo, nausea, tinnitus, ear pain, deafness, or headache.

They may have a history of previous diving ear injury or a history of previous or current earinfection.

Decompression sickness type I

Patients often have a history of recent diving followed by a flight home. They may complain ofslowly progressing pain or numbness in their limbs or back.

Patients present with joint, muscle, or back pain that worsens over time. The pain worsens withmotion but is always present. The pain may range from mild (tickles) to severe (the bends).

Patients may have a history of previous decompression illness and multiple dives in the same dayand frequently have not followed the dive tables closely. New dive computers that offer more"bottom time" do so by modifying the US Navy dive tables and possibly place divers at anincreased risk for DCS injuries. Divers should be questioned as to the method of computing

bottom and ascent times with safety stops. This information should be recorded as part of themedical record.

Decompression sickness type II

DCS type II usually presents sooner than DCS type I.

Patients may present with shortness of breath (the chokes), chest pain, severe headache, alteredmental status, and shock. They also may complain of dizziness or weakness. Patients mayrapidly deteriorate without emergent intervention.

Essential history to ascertain includes time since dive ended, the dive profile (see images below),when the symptoms began, and prior medical history. The dive profile consists of prior dives thatday, depth of dive, bottom time, decompression stop depth, and length of stop.


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Basic US Navy dive table used to compare the patient's dive profile to

the standard dive profile. Reprinted with permission of the US Navy. US Navy dive table for altitude diving used to compare the patient's dive profile with the standarddive profile at altitude. Reprinted with permission of the US Navy.

Diver should be asked about his or her prior dive category.

Inquiry should be made specifically about previous decompression injuries, pulmonary blebs,Marfan syndrome, asthma, congenital pulmonary illnesses, HIV status, chronic obstructive pulmonary disease (COPD), lung tumors, histiocytosis X, cystic fibrosis, pregnancy, and any prior pulmonary injuries or surgeries.

Arterial gas embolism

AGE usually occurs shortly after ascending very rapidly, often from fairly shallow depths.People may be described to scream suddenly and lose consciousness. Onset of AGE often occurswithin a few minutes of surfacing. Patients who experience AGE often die before reaching amedical facility. Air emboli have also recently been noted to occur iatrogenically in association

with central venous monitoring during surgical procedures. Case reports have shown AGEoccurring secondary to occupational rapid decompression in both aircraft maintenance andaltitude-chamber maintenance personnel .[4]

Obtaining a history from these patients can be difficult because they often present with alteredmental status or are in shock.
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Witnesses often report that divers experience a sudden or immediate loss of consciousness orcollapse, usually within minutes of surfacing.

Ask the patient or dive partner about a history of patent foramen ovale.

Abdominal compartment syndrome [5]

Divers can develop large amounts of intraperitoneal extraluminal gas, which can compress theintraperitoneal organs. This can lead to venous compression of these organs and secondarycompartment syndrome.

Physical

The physical examination should be tailored to the patient's history.

Perform a general physical examination on all patients, with initial emphasis on ears, sinuses,and neck as well as on the pulmonary, cardiovascular, and neurologic systems. AGE often

presents with signs and symptoms of acute stroke.

Inspect and palpate the extremities, and test range of motion in all joints.

Sinus squeeze

Inspect nasal mucosa for polyps, hemorrhage, or lesions.

Palpate and transilluminate sinuses to inspect for hemorrhage.

Percuss upper teeth with a tongue blade to inspect for severe sinus tenderness.

Ear squeeze

Carefully inspect the tympanic membrane (TM), looking in particular for the following signs:

Amount of congestion around the umbo Percent of TM involvement Amount of hemorrhage noted behind eardrum Evidence of TM rupture

Palpate the eustachian tube for tenderness.

Test the patient's balance and hearing.

Evaluate the TM on the Teed scale:

Teed 0 - No visible damage, normal ear


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Teed 1 - Congestion around the umbo, occurs with a pressure differential of 2 pounds persquare inch (PSI)

Teed 2 - Congestion of entire TM, occurs with a pressure differential of 2-3 PSI Teed 3 - Hemorrhage into the middle ear Teed 4 - Extensive middle ear hemorrhage with blood bubbles visible behind TM; TM

may rupture Teed 5 - Entire middle ear filled with dark (deoxygenated) blood


Inspect for swelling or effusion in the affected joint.

Test for range of motion both actively and passively.

Palpate the affected area for crepitus and compartment tightness.

Evaluate neurovascular status by performing a complete neurologic examination. Theexamination should include testing motor and sensory functions, cerebellar function, and mentalstatus. The findings from this examination must be recorded and used as a baseline to determineimprovement in postdive chamber treatment.


Evaluate cardiovascular and pulmonary systems.

Note neck vein distention or petechiae on the head or neck.

Palpate the skin for crepitus.

Auscultate the lungs and heart for decreased breath sounds, muffled heart tones, or heartmurmurs.

Evaluate neurologic status, including gross motor, sensory, and cerebellar examinations. Tandemwalking (heel to toe, with eyes closed) is an excellent method of evaluation.

Document Glasgow Coma Scale and Mini Mental State Examination.


Use the same examination used for decompression sickness type II.

Causes

The causes of DCS are related to predisposing medical or genetic factors, as listed above, and todiver error. Diver error includes the following practices:


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Multiple daily dives Poor adherence to the dive tables Breath holding (most common scenario for pulmonary barotrauma) Rapid ascent - This can occur from relatively shallow depths. For example, pilots

undergoing rapid ascent while performing underwater escape training after flight may

experience DCS. Flying or traveling to high altitudes within 24 hours after diving Occupational causes - These causes include rapid depressurization by maintenance

workers and mechanics after working in pressurized aircraft cabins. Reports of altitudechamber mechanics who have depressurized too quickly while working on the altitudechambers have also been documented. Pilots and crewmembers performing high-altitudeair drops on military missions and special-operations soldiers involved in such missionshave also reported instances of DCS.

Laboratory Studies

Do not delay treatment while waiting for laboratory studies. Laboratory studies helpful intreating patients with DCS include a complete blood count (CBC) and arterial blood gas (ABG) determination.

Complete blood count

In one study, patients who had a hematocrit of 48% or higher had persistent neurologic sequelae1 month after the injury.

White blood cell (WBC) count with differential may help to determine infectious causes.

ABG determination

Determine the alveolar-arterial gradient in patients suspected of having an embolism.

Serum creatine phosphokinase level

Increases in creatine phosphokinase (CPK) levels indicate tissue damage associated with DCS.Rising CPK levels indicate increasing tissue damage due to microemboli.

Imaging Studies

Chest radiography

Obtain a chest radiograph if the patient complains of chest discomfort or difficulty breathing.

Obtain inspiratory and expiratory views if a pneumothorax is suspected clinically.

Radiographs of joints or extremities
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When indicated clinically, obtain these to evaluate for the presence of a fracture or dislocation.

Computed tomography (CT) scans and magnetic resonance imaging (MRI)

Patients who may benefit the most from these diagnostic modalities are often the most unstable,

making their transport to the radiology suite potentially dangerous.

Any patient who presents with a severe headache or severe back pain after a dive is a potentialcandidate for these imaging studies.

Spiral CT is the most sensitive method to evaluate for pneumothorax. It should be performed inall patients suspected of having a barotrauma-related pneumothorax when chest radiographfindings are negative for pneumothorax.

Echocardiography

Echocardiography (ultrasonography) can be used to detect the number and size of gas bubbles inthe right side of the heart. This can be used both for diagnosis and prognosis.

Other Tests

ECG is useful for determining potential cardiac causes of the altered mental status orshock.

Prehospital Care

Prehospital care should consist of assessing the ABCs and correcting any immediate life-threatening conditions while maintaining adequate oxygenation and perfusion. Patients should be

placed on high-flow oxygen and have large-bore venous access with isotonic fluid infusion tomaintain blood pressure and pulse. Although research is being done on the use of surfactants

being given prior to high-risk activities such as deep dives or space missions, it is still in the bench research stage of development .[6] Several in vitro studies have been promising, and there ishope that surfactant use will someday greatly decrease the frequency of barotrauma.

Emergency Department Care

Stabilize the airway, breathing, and circulation.

Intubation

Perform endotracheal intubation on a patient who has an unstable airway or has persistenthypoxia despite breathing 100% oxygen.

Perform tube thoracostomy to evacuate a pneumothorax or hemothorax.


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Perform nasotracheal or orotracheal intubation when appropriate.

Needle decompression

Needle decompression of the chest is indicated for suspected tension pneumothorax. A large-

bore needle is inserted over the rib in the second intercostal space, midclavicular line.

Foley catheterization

Place a Foley catheter in patients who present with shock to assist in assessing volume andhydration status. Normal urine output is 1 mL/kg of body weight per hour.

Place a Foley catheter in patients with spinal cord manifestations of DCS who are unable to voiddue to a neurogenic bladder.

Hydration

Continue intravenous hydration to maintain adequate blood pressure.

Recompression therapy

Recompression therapy should be performed at a dive chamber by a dive medical officer or personnel certified in hyperbaric medicine. Indications include spinal cord injury and neurologicimpairment.

Sinus squeeze

Symptomatic therapy with decongestants, both oral and nasal, is indicated.

Pain control should be instituted with nonsteroidal anti-inflammatory drugs (NSAIDs) ornarcotic analgesic medications.

Middle ear squeeze

Severity and treatment are based on the Teed scale.

Mild (Teed 0-2): Decongestants, both nasal (0.05% oxymetazoline hydrochloride spray bid for 3 d) and oral (pseudoephedrine 60-120 mg bid/qid) are administered.

Moderate (Teed 3-4): Treatment is same as above, but a short course of oral steroids,such as prednisone 60 mg/d for 6 days then tapering over 7-10 days, may be needed. IfTM has ruptured or water is contaminated, consider antibiotics that treat acute otitismedia.

Severe (Teed 5): Treatment is same as above. Consider myringotomy if the above havefailed. Control pain with Tylenol with codeine (acetaminophen 300 mg with codeine

phosphate 30 mg) 1-2 tablets every 4-6 hours.


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These patients should receive high-flow oxygen via a nonrebreather mask.

After establishing intravenous access, administer isotonic fluids (isotonic sodium chloride

solution or lactated Ringer solution) to maintain urine output at 1-2 mL/kg/h.

These patients should also receive aspirin 325-650 mg for antiplatelet effects as well as paincontrol.

Obtain appropriate radiographs to evaluate for fractures or dislocations.

If a patient's medical condition continues to deteriorate, he or she is then classified as havingDCS type II.

Currently, the United States Air Force is developing a new, shorter Treatment Table 8 (TT8) that

allows for dives of shorter duration (lasting 30 min with air breaks between each 2 atmosphericabsolute [ATA] dive). This is done with 4 dives each for 30 minutes with 10-minute air breaks.The TT8 should only be used to treat DCS type I when symptoms occur within 2 hours ofaltitude chamber or flight and when partial response on oxygen after 10 minutes has occurred.Treatment Table 6 (TT6) should be used immediately if symptoms persist after the first 30-minute interval or recur within 24 hours.


All of the interventions for DCS type I are appropriate for DCS type II.

These patients need recompression therapy to resolve their symptoms.

The most appropriate management is to transfer the patient to the nearest hyperbaric chamber.


Patients with AGE can have mild symptoms from a small embolism that may improve withtherapy for DCS type I, including intravenous hydration, high-flow oxygen, and aspirin.

Patients with severe AGE (ie, unstable blood pressure, respirations, neurologic status) requireimmediate recompression therapy in a hyperbaric chamber.

Consultations

Consult a specialist at a recompression chamber for any patient with DCS type II or an unstableAGE.


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The recompression chamber specialist must be contacted prior to transfer to determinechamber availability.

A complete list of recompression chambers is available from the Divers' Alert Network and is only provided by calling (919) 684-8111 or (919) 684-4326.

Medication Summary The primary medications in treatment of dysbaric injuries are oxygen, isotonic fluids,

anti-inflammatory medications, decongestants, and analgesics. Acetylsalicylic acid Class Summary This agent is used to control pain and inflammation and to inhibit platelet aggregation. Aspirin (Anacin, Ascriptin, Bayer aspirin) Blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis

and prevents formation of platelet-aggregating thromboxane A2. By inhibiting prostaglandin synthesis, aspirin may also inhibit key steps in the inflammation process.

Decongestants Class Summary These agents are used to open blocked sinuses or eustachian tubes to allow for

equalization of pressure. Oxymetazoline (Afrin, Allerest) Stimulates alpha-adrenergic receptors and causes vasoconstriction when applied directly

to mucous membranes. Decongestion occurs without drastic changes in blood pressure,vascular redistribution, or cardiac stimulation.

Pseudoephedrine (Silfedrine, Sudafed)

Stimulates vasoconstriction by directly activating alpha-adrenergic receptors of therespiratory mucosa. Induces bronchial relaxation and increases heart rate and contractility

by stimulating beta-adrenergic receptors. Narcotic analgesics Class Summary These agents are used to treat severe pain resulting from dysbaric injuries. Acetaminophen with codeine (Tylenol #3) Indicated for the treatment of mild to moderate pain. Glucocorticoids Class Summary In studies of patients with spinal cord trauma, methylprednisolone has been shown to

improve long-term neurologic outcome. It has not yet been approved for DCS but should be considered a treatment option.

Methylprednisolone (Solu-Medrol, Depo-Medrol) By reversing increased capillary permeability and suppressing PMN activity, may

decrease inflammation. May also prevent neuronal damage by inhibiting prostaglandinsynthesis.
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Inert Gas Class Summary Heliox may initially accelerate bubble shrinkage when administered on the surface.

Heliox may be superior to 100% oxygen for treatment at sea level. Oxygen First line of treatment in dysbaric injuries. Administer at high flow with a tight-fitting

nonrebreather mask. Helium-oxygen (heliox) Consists of 50% helium and 50% oxygen.

Further Inpatient Care

Patients may require multiple recompression "dives" in a hyperbaric oxygen chamber to reverse

neurologic impairment or to treat air emboli.

Patients with continued pain despite appropriate treatment at sea level require recompression.

Patients who are seriously ill or do not respond to initial treatment may require higher pressurerecompressions at 4-5 atm of absolute pressure and may need breathing gas of 50% helium/50%oxygen mixture (heliox).

No definitive studies have proven that other modalities provide increased long-term benefit.

Further Outpatient Care

Outpatient care is based on the type of dysbaric injury.

Adequate hydration and pain control are the hallmarks of outpatient care.

Of key importance, the patient must be warned against either traveling to significant altitudes ordiving again too soon after barotrauma.

Recommendations for recovery time vary depending on the individual and amount of barotrauma.

Consult a dive medical officer (hyperbaric specialist) prior to giving recommendations to patients.

Inpatient & Outpatient Medications

Sinus and middle ear squeeze are treated identically.


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Decongestants are used to reduce the pressure differential. Administer oxymetazoline(Afrin) 0.05%, 2 squirts each nostril bid. Performing the Valsalva maneuver immediatelyafter spray forces the medication into the osteo and helps to open them quickly.

Administer pseudoephedrine (Sudafed) 60-120 mg PO bid/qid. Anti-inflammatory medications treat the pain. Administer aspirin 325-650 mg PO q4-6h.

NSAIDs also may be used in standard dosages. Narcotic analgesics may be appropriate to treat more severe pain, eg, acetaminophen 300mg with codeine 30 mg (Tylenol #3) 1-2 tablets PO q4-6h.

Transfer

Patients with DCS type II or severe AGE should be transferred to a recompression chamber. Thechamber specialist must be contacted prior to any transfer to determine availability. When

presenting the case, the dive medical officer needs to know the following signs and symptoms:

Vital signs Pertinent medical symptoms (especially neurologic) Time last dive finished Onset of symptoms Length of dive Depth of dive Decompression stops (length of time and depth) Any flight or change in altitude after dive

If the patient is to be transferred by air, the aircraft must stay below 1000 ft if possible,depending on the terrain, or be transported in a pressurized aircraft. Flight crew must be aware ofthe patient's condition to assist the pilot in keeping the aircraft fully pressurized before attainingaltitude.

Deterrence/Prevention

Any patient who sustains pulmonary barotrauma should not dive again.

Patients with asthma, Marfan syndrome, or COPD are at very high risk of pneumothorax andshould be warned against diving.

Avid divers should be warned against multiple daily dives, diving and flying on the same day,

and trying to "shave" their dive profile.

Patient Education

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center . Also, see eMedicineHealth's patient education articles Scuba Diving:Barotrauma/Decompression Sickness , Scuba Diving: Ear Pain , and The Bends - DecompressionSyndromes .
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