eMedicine Specialties > Emergency Medicine > Environmental

Barotrauma

Joseph Kaplan, MD, MS, FACEP, Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia
Marshall E Eidenberg, DO, Staff Emergency Physician, Via Christi Regional Medical Center

Updated: Sep 29, 2009

Introduction

Background

Diving as a profession can be traced back more than 5000 years, yet diving-related disease was not described until Paul Bert wrote about caisson disease in 1878. Symptoms of caisson disease were noted among bridge workers after finishing their shifts underwater and coming back to the surface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the joints or abdomen. The caisson workers often noted that they felt better while working. This was usually attributed to their being rested at the beginning of the shift as opposed to being tired when 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 a variety of manifestations, from ear or mouth pain and headaches 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 exposed to a significant change in barometric pressure. The 3 major manifestations of barotrauma include the following: (1) sinus or middle ear effects, (2) decompression sickness (DCS), and (3) arterial gas emboli.

Barotrauma has also reportedly been caused by an airbag rupturing during deployment, forcing high-pressure gas into a person's lungs. It has also reportedly been associated with rapid ascent in military aircraft and with pressure changes associated with space exploration.

The most current research in barotrauma has been dealing with ventilator-associated barotrauma and 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 subject and 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 vary inversely with the pressure," or P1 X V1 = P2 X V2. Pressure rises by 1 atmosphere for every 33 ft (10 m) of seawater depth. This means that a balloon (or lungs) containing a volume of 1 cubic foot of gas at 33 ft of seawater depth will have a volume of gas of 2 cubic feet at the surface. If this air is trapped, as occurs when a person holds his or her breath during rapid ascent, it expands with great force against the walls of that space (reverse squeeze). During rapid ascent, incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. Sinus squeeze occurs with eustachian tube dysfunction, which may result in inner ear hemorrhage, 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 pressure exerted 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's air tank dissolves in the diver's fatty tissues or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. This occurs slowly and gradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream to the lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidly and forms gas bubbles.

Once bubbles are formed, they can affect tissues in many ways. They can simply obstruct blood vessels 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 can travel to any part of the body, accounting for many disorders. A gas bubble forming in the back or 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 circulatory system 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 with subsequent 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 of DCS is joint pain, which begins mildly and worsens over time and with movement. DCS type II is serious and life threatening. Manifestations may include respiratory, circulatory, and, most commonly, peripheral nerve and/or CNS compromise.

Arterial gas embolism (AGE) is the most dangerous manifestation of DCS type II. AGE occurs after 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 from relatively 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.

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 is increased in divers with asthma or pulmonary blebs. Risk of DCS type II is increased 2.5 times in patients with a patent foramen ovale. Deaths due to DCS in military aircraft have been reported to occur at a rate of 0.024 per million hours of flight time. Rates of decompression incidents 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 Australian defense 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 with race.

Sex

Because of a generally greater percentage of body fat, females have a theoretically higher incidence 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 common group affected ranges between 21 and 40 years. However, direct correlation does exist between age and residual effects of barotrauma, which significantly rises after age 50 years.

Clinical

History

Patients with DCS present with a history of diving, generally within 24 hours of the onset of symptoms. Patients may also have a recent history of occupational pressurization or depressurization. For example, this occurs with aircraft mechanics who must test aircraft windows by working in pressurized aircraft. Air emboli have also occurred in mechanics who maintain training altitude chambers. Recently, military operations involving troops traveling from ground level to high-altitude environments in a relatively short time and operations involving soldiers doing strenuous activities at higher altitudes have resulted in many cases of DCS. Recent studies have indicated that aerobic exercise either prior to a dive or during decompression stops may decrease the post dive gas bubble formation.^1,2

• 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 descent or 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 ear infection.
• Decompression sickness type I
  • Patients often have a history of recent diving followed by a flight home. They may complain of slowly progressing pain or numbness in their limbs or back.
  • Patients present with joint, muscle, or back pain that worsens over time. The pain worsens with motion 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 day and 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 an increased 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 the medical 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, altered mental status, and shock. They also may complain of dizziness or weakness. Patients may rapidly deteriorate without emergent intervention.
  • Essential history to ascertain includes time since dive ended, the dive profile, when the symptoms began, and prior medical history. The dive profile consists of prior dives that day, depth of dive, bottom time, decompression stop depth, and length of stop.
  • 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 occurs within a few minutes of surfacing. Patients who experience AGE often die before reaching a medical facility. Air emboli have also recently been noted to occur iatrogenically in association with central venous monitoring during surgical procedures. Case reports have shown AGE occurring secondary to occupational rapid decompression in both aircraft maintenance and altitude-chamber maintenance personnel.³
  • Obtaining a history from these patients can be difficult because they often present with altered mental status or are in shock.
  • Witnesses often report that divers experience a sudden or immediate loss of consciousness or collapse, usually within minutes of surfacing.
  • Ask the patient or dive partner about a history of patent foramen ovale.
• Abdominal compartment syndrome:⁴ Divers can develop large amounts of intraperitoneal extraluminal gas, which can compress the intraperitoneal organs. This can lead to venous compression of these organs and secondary compartment 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
    • Teed 1 - Congestion around the umbo, occurs with a pressure differential of 2 pounds per square 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
• Decompression sickness type I
  • 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. The examination should include testing motor and sensory functions, cerebellar function, and mental status. The findings from this examination must be recorded and used as a baseline to determine improvement in postdive chamber treatment.
• Decompression sickness type II
  • 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 heart murmurs.
  • Evaluate neurologic status, including gross motor, sensory, and cerebellar examinations. Tandem walking (heel to toe, with eyes closed) is an excellent method of evaluation.
  • Document Glasgow Coma Scale and Mini Mental State Examination.
• Arterial gas embolism: 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 to diver error. Diver error includes the following practices:

• 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 altitude chamber mechanics who have depressurized too quickly while working on the altitude chambers have also been documented. Pilots and crewmembers performing high-altitude air drops on military missions and special-operations soldiers involved in such missions have also reported instances of DCS.

Differential Diagnoses

Other Problems to Be Considered

Surgical abdominal complaint
Sprain or contusion of any joint

Workup

Laboratory Studies

• Do not delay treatment while waiting for laboratory studies. Laboratory studies helpful in treating 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 sequelae 1 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: 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 potential candidate for these imaging studies.
  • Spiral CT is the most sensitive method to evaluate for pneumothorax. It should be performed in all patients suspected of having a barotrauma-related pneumothorax when chest radiograph findings are negative for pneumothorax.
• Echocardiography (ultrasonography) can be used to detect the number and size of gas bubbles in the 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 or shock.

Treatment

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 to maintain 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.⁵ Several in vitro studies have been promising, and there is hope 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 persistent hypoxia despite breathing 100% oxygen.
  • Perform tube thoracostomy to evacuate a pneumothorax or hemothorax.
  • Perform nasotracheal or orotracheal intubation when appropriate.
• 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 and hydration 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 void due to a neurogenic bladder.
• Continue intravenous hydration to maintain adequate blood pressure.
• 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 neurologic impairment.
• Sinus squeeze
  • Symptomatic therapy with decongestants, both oral and nasal, is indicated.
  • Pain control should be instituted with nonsteroidal anti-inflammatory drugs (NSAIDs) or narcotic 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. If TM has ruptured or water is contaminated, consider antibiotics that treat acute otitis media.
  • Severe (Teed 5): Treatment is same as above. Consider myringotomy if the above have failed. Control pain with Tylenol with codeine (acetaminophen 300 mg with codeine phosphate 30 mg) 1-2 tablets every 4-6 hours.
• Decompression sickness type I
  • 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 pain control.
  • 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 having DCS 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 atmospheric absolute [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 of altitude 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.
• Decompression sickness type II
  • 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.
• Arterial gas embolism
  • Patients with AGE can have mild symptoms from a small embolism that may improve with therapy for DCS type I, including intravenous hydration, high-flow oxygen, and aspirin.
  • Patients with severe AGE (ie, unstable blood pressure, respirations, neurologic status) require immediate recompression therapy in a hyperbaric chamber.

Consultations

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

• The recompression chamber specialist must be contacted prior to transfer to determine chamber 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

The primary medications in treatment of dysbaric injuries are oxygen, isotonic fluids, anti-inflammatory medications, decongestants, and analgesics.

Acetylsalicylic acid

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.

Dosing

Adult

325-650 mg/d PO

Pediatric

15 mg/kg/d PO

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, history of blood coagulation defects, or patients taking anticoagulants

Decongestants

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.

Dosing

Adult

2 sprays of 0.05% solution in each nostril bid

Pediatric

<6 years: 2-3 gtt of 0.025% solution in each nostril bid, am and hs
>6 years: Administer as in adults

Interactions

Hypotensive action of guanethidine may be reversed; concurrent administration with methyldopa may result in an increased vasopressor response; concurrent use of MAOIs and ephedrine may result in hypertensive crisis; pressor sensitivity to mixed-acting agents, such as ephedrine, may be increased; guanethidine potentiates effects of epinephrine and inhibits effects of ephedrine; phenothiazines may reverse action of nasal decongestants such as oxymetazoline; TCAs potentiate vasopressor response and may result in dysrhythmias

Contraindications

Documented hypersensitivity; MAOI therapy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, coronary artery disease, ischemic heart disease, diabetes mellitus, increased intraocular pressure, or prostatic hypertrophy; because of increase in vasoconstriction, patients with hypertension may experience change in blood pressure; do not use topical decongestants for longer than 3-5 d

Pseudoephedrine (Silfedrine, Sudafed)

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

Dosing

Adult

60-120 mg PO bid/qid

Pediatric

<6 years: Not established
6-12 years: 30 mg PO qid
>12 years: Administer as in adults

Interactions

Propranolol, MAOIs, and sympathomimetic agents may increase toxicity of pseudoephedrine; methyldopa and reserpine may reduce effects of pseudoephedrine

Contraindications

Documented hypersensitivity; severe anemia; postural hypertension and hypotension; closed-angle glaucoma; head trauma; cerebral hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, and increased intraocular pressure

Narcotic analgesics

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.

Dosing

Adult

1-2 tabs PO q4-6h prn

Pediatric

0.5-1 mg/kg/dose based on codeine PO q4-6h; 10-15 mg/kg/dose based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen

Interactions

Toxicity increases with CNS depressants or tricyclic antidepressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients dependent on opiates because this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction

Glucocorticoids

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 prostaglandin synthesis.

Dosing

Adult

30 mg/kg IV bolus initial, followed by 5.4 mg/kg/h IV

Pediatric

Administer as in adults

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Inert gas

Heliox may initially accelerate bubble shrinkage when administered on the surface. Heliox may be superior to 100% oxygen for treatment at sea level.

Inert Gas

Oxygen

First line of treatment in dysbaric injuries. Administer at high flow with a tight-fitting nonrebreather mask.

Dosing

Adult

15 L/min via a high-flow nonrebreather mask (In military operations, patient is administered oxygen via an aviator's mask labeled ground-level oxygen [GLO]; is standard treatment used in all cases of dysbarism involving military missions and patient descent)

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

None reported

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Inspired oxygen concentrations from 50-100% carry substantial risk of lung damage

Helium-oxygen (heliox)

Consists of 50% helium and 50% oxygen.

Dosing

Adult

Administer high flow via a tight-fitting nonrebreather mask

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

None reported

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Oxygen toxicity can be mistaken for pulmonary fibrosis

Follow-up

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 pressure recompressions 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 or diving 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.
  • Decongestants are used to reduce the pressure differential. Administer oxymetazoline (Afrin) 0.05%, 2 squirts each nostril bid. Performing the Valsalva maneuver immediately after 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 300 mg 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. The chamber 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 of the patient's condition to assist the pilot in keeping the aircraft fully pressurized before attaining altitude.

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 and should 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 eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education articles Barotrauma/Decompression Sickness; Ear Pain, Scuba Diving; and The Bends - Decompression Syndromes.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider the diagnosis of decompression sickness in a patient who has been diving or in a patient who has been found unresponsive in an environment that is frequented by divers
• Failure to consider this diagnosis in someone who has been performing training dives in a swimming pool (since most decompression injuries occur at relatively shallow depth)
• Failure to appropriately counsel a patient against flying after complaints and history suggestive of barotrauma
• Attributing extremity symptoms to hypothermic insult instead of DCS of the extremities or nerves
• Attributing musculoskeletal pain after a history of diving or being under compression to simple sprains or strains

Special Concerns

• Children younger than 12 years should not use self-contained underwater breathing apparatus (SCUBA) equipment. In this article, all patients are considered adults. Pulmonary barotrauma can occur even on the surface while training for other activities, so children are not exempt from these conditions.
• Newer dive computers that "promise" longer bottom times modify the US Navy dive tables, potentially causing an increased risk of DCS.
• Women are theoretically at a slightly higher risk for DCS as a result of the increased fat percentage in their bodies. More nitrogen gas can dissolve in the fat, which eventually must come out as the patient surfaces.
• Pregnant women should not dive due to the increased risk of birth defects and risk of fetal decompression disease. Therapeutic abortion is not recommended, and several normal uncomplicated pregnancies have been reported in women who continued to dive.
• During their training, divers are instructed not to fly for 24 hours after diving. This should be slightly modified to no flying for 24-48 hours after resolution of DCS type I injuries. The longer the interval between resolution of symptoms and flying, the greater the reduction of risk of DCS injuries in the air.

Multimedia

Media file 1: 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.

Media file 2: US Navy dive table for altitude diving used to compare the patient's dive profile with the standard dive profile at altitude. Reprinted with permission of the US Navy.

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Keywords

barotrauma, the bends, caisson disease, dive medicine, hyperbaric medicine, squeeze, sinus squeeze, decompression sickness, DCS, decompression sickness type I, decompression sickness type II, middle ear squeeze, arterial gas embolism, AGE, decompression chamber, recompression, diving-related disease, diving barotrauma

Contributor Information and Disclosures

Author

Joseph Kaplan, MD, MS, FACEP, Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning, Georgia
Joseph Kaplan, MD, MS, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Marshall E Eidenberg, DO, Staff Emergency Physician, Via Christi Regional Medical Center
Marshall E Eidenberg, DO is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Dana A Stearns, MD, Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital
Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David Eitel, MD, MBA, Associate Professor, Department of Emergency Medicine, York Hospital
David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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