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 various 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. Barotrauma has
also 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 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.

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 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.

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.[2, 3]

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 (see images below),
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.

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 standard
dive 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 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.[4]
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 [5]
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.

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
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.

Prehospital Care
Prehospital care should consist of assessing the ABCs and correcting any immediate lifethreatening 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.[6] 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
Needle decompression of the chest is indicated for suspected tension pneumothorax. A largebore 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.

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 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 30minute 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 Summary

Acetylsalicylic acid

Class Summary

Aspirin (Anacin, Ascriptin, Bayer aspirin)

Decongestants

Class Summary

Oxymetazoline (Afrin, Allerest)

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.

Narcotic analgesics

Class Summary

Acetaminophen with codeine (Tylenol #3)

Glucocorticoids

Class Summary

Methylprednisolone (Solu-Medrol, Depo-Medrol)

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

This agent is used to control pain and inflammation and to inhibit platelet aggregation.
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.

These agents are used to open blocked sinuses or eustachian tubes to allow for
equalization of pressure.

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.

These agents are used to treat severe pain resulting from dysbaric injuries.
Indicated for the treatment of mild to moderate pain.

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.

By reversing increased capillary permeability and suppressing PMN activity, may

decrease inflammation. May also prevent neuronal damage by inhibiting prostaglandin
synthesis.

Inert Gas

Class Summary

Oxygen

Helium-oxygen (heliox)

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

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

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 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 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 - Decompression
Syndromes.