Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 141. Dysbaric Injuries

Ira J. Blumen

Eric Beck


• An air embolism is the most serious dysbaric injury and requires aggressive care, which includes 100% oxygen, intravenous fluids, and hyperbaric treatment.

• Patients with suspected air embolism should be placed in the Trendelenburg or left lateral decubitus position to minimize the passage of air emboli to the brain.

• The treatment of choice for most air emboli and decompression illnesses is hyperbaric (recompression) therapy. This is initiated as soon as possible, ideally within 6 hours of the onset of symptoms.


Dysbaric injuries may be the result of several distinct events that expose an individual to a change in barometric pressure. The first possible etiology is an altitude-related event, which can be illustrated by the rapid ascent or descent during airplane transport or sudden cabin decompression at an altitude of 25,000 ft. The second type of dysbaric injury results from an underwater diving accident. A third dysbarism is caused by a blast injury that produces an overpressurization effect.

Scuba (self-contained underwater breathing apparatus) diving currently allows the recreational diver to descend to depths >100 ft. There are a number of recreational diving organizations that have minimum age requirements for certifications. In general, candidates must be 15 or 16 years old for full certification. Pool-based divers may be certified at the age of 8 years, and some organizations will certify 10-year olds for ocean diving to 40 ft (12 m). However, certification is not required to dive and it is the untrained or poorly trained individual who is at greater risk for injury.

Serious diving-related injuries and fatalities are rare and are often associated with human error, unsafe behaviors, or hazardous conditions. On the average, each year, the Divers Alert Network receives more than 2000 scuba-related emergency calls.1 From 1995 to 2006, there has been an average of 85 diving fatalities annually in the United States and Canada, but there was a noted increase in 2007 and 2008 to over 110 fatalities each year.2 The most common cause of death is from drowning. On average, there were 16 diving injuries requiring hyperbaric recompression therapy in scuba divers aged 19 years and younger in North America between 1988 and 2002.3 During this time period, the youngest diving fatality was 14 years old and the youngest injured diver was 11.3

Several terms are often used when discussing this topic. Dysbarism represents the general topic of pressure-related injuries. Barotrauma, the most common diving injury, refers to the injuries that are a direct result of the mechanical effects of a pressure differential. The complications related to the partial pressure of gases and dissolved gases are called decompression sickness.


Dysbarisms can best be explained by the physical gas laws and through an understanding of pressure equivalents that cause these injuries. The amount of pressure exerted by air at sea level and at different altitudes or depths can be described in several different ways, as shown in Table 141-1.

TABLE 141-1

Effect of Altitude or Depth on Air Pressure


Individuals and objects under water are exposed to progressively greater pressure due to the weight of the water. Small changes in underwater depth will result in large atmospheric pressure and volume changes. This is significantly different from the pressure and volume variation noted in air above sea level. Boyle’s law explains this relationship. Under water, the largest proportionate change in the volume of a gas is seen near the water surface. An air-filled cavity that is 33 ft below the water surface will double when it reaches the surface. In comparison, a volume of gas at sea level will need to rise to an altitude of 18,000 ft to double in volume.

Dalton’s law of partial pressure describes the pressure exerted by gases at various depths or altitudes. Each gas will exert a pressure equal to its proportion of the total gaseous mixture; Figure 141-1 depicts the gaseous composition of the atmosphere at sea level and the corresponding partial pressures.


FIGURE 141-1. Atmospheric composition at sea level.

Henry’s law states that the quantity of gas dissolved in a liquid is proportional to the partial pressure of the gas in contact with the liquid. The partial pressure of a gas and the solubility of the gas determine the amount of gas that will dissolve into a liquid. This law will help explain the increased absorption of nitrogen during descent.

The clinical findings of dysbaric injuries may be immediate or delayed in onset up to 36 hours or later. Most will occur during descent or in close proximity to ascent. A delayed presentation is possible, however, which may make diagnosis difficult.


Barotrauma is the direct result of a pressure difference between the body’s air-filled cavities, which are subject to the effects of Boyle’s law and the surrounding environment. While scuba diving, barotrauma can occur during ascent or descent, with most symptoms developing during a descent. On descent, a negative pressure develops within enclosed air spaces relative to the ambient surrounding pressure. If air is unable to enter these structures, equalization does not take place, and the air-filled cavities collapse. If the cavity is a rigid structure and unable to collapse, the negative pressure may result in fluid being displaced from the blood vessels of the surrounding mucosa into the intravascular space. The resulting injury pattern can include pain, hemorrhage, edema, vascular engorgement, and tissue damage.

If air is unable to escape on ascent, an expansion of gas within enclosed air spaces causes a positive pressure to develop. This may result in the rupture of such spaces or the compression of adjacent structures. Many of the symptoms of barotrauma in the human body result in a “squeeze” phenomenon. These trapped gas disorders are differentiated by the gas-filled part of the body that is affected.


Barometric pressure changes can result in disorders of the external, middle and inner ear. The tympanic membrane (TM) separates the middle ear from the outer ear. The eustachian tube functions as a valve allowing air pressure to equalize between the middle ear and ambient environment.

Barotitis media is the most common diving-related barotrauma and involves the middle ear. It is commonly referred to as middle ear squeeze or ear block. Equalization via the eustachian tube will occur when there is a pressure differential of approximately 15 to 20 mm Hg. The diver becomes symptomatic if equalization is unsuccessful and the pressure differential reaches or approaches 100 mm Hg.

Middle ear squeeze commonly develops on descent between 10 and 20 ft below the surface. The symptoms include a fullness in the ears, severe pain, tinnitus, vertigo, nausea, disorientation, and transient, conductive hearing loss. Up to 10% of divers may have no pain during descent but will become symptomatic after the dive. If the diver is unable to equalize the pressure and continues to descend, symptoms may be exacerbated and the TM may rupture and bleed. With perforation, the caloric stimulation of cold water entering the middle ear can cause vertigo, nausea, and disorientation. Physical examination may reveal erythema or retraction of the TM, blood behind the TM, a ruptured TM, or a bloody nasal discharge.

Treatment for middle ear squeeze should be directed toward its prevention before pain develops. Scuba divers should attempt to clear their ears every 2 to 3 ft during descent. Under normal situations, pressure in the middle ear is equalized without incidence by actively opening the eustachian tube, which opens and exposes the middle ear to ambient pressures. Divers must learn to open the eustachian tube through various maneuvers such as blowing the nose against pinched nostrils or repositioning the jaw (false yawning), while keeping a regulator in their mouth. Another suggested treatment for barotitis is the Frenzel maneuver. This is performed by pinching the nose closed, placing the tongue on the roof of the mouth, then moving the tongue backward and upward as when starting to swallow. This is repeated as many times as necessary until equalization occurs.

Equalization may be compromised if the eustachian tube is obstructed by swelling of the mucosa, the presence of polyps, previous trauma, allergies, upper respiratory infection, a sinus problem, or smoking. To decrease the incidence of ear discomfort and injury to the TM, a pre-dive treatment of a topical vasoconstrictor nasal spray (oxymetazoline hydrochloride, 0.05%) may be beneficial when used approximately 15 minutes before beginning a dive. The recommended pediatric dosage for ages ≥6 years is two to three sprays in each nostril. Oxymetazoline hydrochloride is not recommended for children younger than 6 years. Pseudoephedrine may also be considered as a pre-dive treatment. For ages 6 to 12, the recommended dose is 30 mg PO. For children older than 12 years, the adult dose of 60 mg PO may be used. If pain persists after the dive, analgesics may be used. If a pre-dive decongestant was not used, it may be considered at this time.

Any patient with barotitis media is to be instructed to refrain from diving until all signs and symptoms have resolved. Erythema generally resolves within 1 to 3 days, whereas it will take 2 to 4 weeks when there is blood behind the TM. A perforated TM must heal before any further diving is attempted. A 10-day course of oral antibiotics and otic suspension is indicated if there is a perforation of the TM. ENT follow-up is given upon discharge from the emergency department.

Barotrauma can occur during either descent or ascent. If air is unable to escape the middle ear through the eustachian tube during ascent, a diver may develop symptoms of reverse ear squeeze.

Alternobaric vertigo may develop during descent, but it is more common during ascent. A sudden change in middle ear pressure or asymmetrical middle ear pressure may result in decreased perfusion, affecting vestibular function. Symptoms include transient vertigo, tinnitus, nausea, vomiting, and fullness in the affected ear. Symptoms may last minutes to several hours after the completion of a dive. Decongestants, antiemetics, and medication for vertigo are recommended.

Barotitis externa occurs when the external auditory canal, which is normally a patent air-filled cavity that communicates with the surrounding environment, is occluded during descent. At the initiation of descent, the air would normally be replaced by water. If the external canal is obstructed, the enclosed air space will be subject to the increased ambient pressure, resulting in an external ear squeeze or barotitis externa. Obstruction can be caused by cerumen, ear plugs, or other foreign bodies. A diver may experience pain with or without bloody otorrhea.

Barotitis interna or inner ear squeeze is uncommon but may result in permanent injury to the structures of the inner ear. It often follows a vigorous Valsalva maneuver. In addition to sudden sensorineural hearing loss, symptoms include severe pain or pressure, vertigo, tinnitus, ataxia, nausea, vomiting, diaphoresis, and nystagmus. These patients must be seen emergently. The potential for recovery within a few months is very good in most patients treated conservatively. Others, however, may require surgical intervention.


Barotitis media is the most common barotrauma of air travel. During ascent to altitude, gas will normally escape through the eustachian tube every 500 to 1000 ft to equalize pressures. As altitude decreases, the gas within the middle ear will contract. As with diving, equalization may be accomplished by yawning, swallowing, or performing the Valsalva maneuver. Children who are asleep should be awakened 5 minutes before descent and instructed to swallow more frequently. For infants, a bottle should be given during takeoff and landing. Although this may reduce the likelihood of barotitis media, it may increase the incidence of gastrointestinal distress after takeoff from swallowed air.


Normally, air can pass in and out of the sinus cavities without difficulty. However, if a person has a cold or sinus infection, air may be trapped and will be subject to the barometric pressure changes. Barosinusitis is the second most common ailment among scuba divers. Failure of the air-filled frontal or maxillary sinuses to equilibrate results in headache, epistaxis and pain or pressure above, behind, or below the eyes, which is commonly referred to as sinus squeeze. Pain may persist for hours and may be accompanied by a bloody nasal discharge. The ethmoid and sphenoid sinuses rarely contribute to this type of barotrauma.

The treatment for barosinusitis is similar to the treatment of barotitis media. The most effective treatment involves the use of a vasoconstrictor nasal spray before initiating a dive or before starting a descent from altitude in an airplane. Antibiotics should be started and continued for 14 to 21 days.

Reverse sinus squeeze is felt during a diving ascent when an obstruction of the sinuses results in excessive pressure. A sharp pain will be felt in the affected sinus. Numbness may be felt along the infraorbital nerve if the maxillary sinus is affected. The diver should descend to a greater depth, relieving some of the discomfort, and then ascend at a slower rate.


Barodentalgia or tooth squeeze results from trapped air and is often associated with recent dental extraction, dental fillings, periodontal infection, periodontal abscess, or tooth decay. Although this is a rare problem, individuals with pre-existing dental or periodontal disease are more susceptible to this barotrauma. Treatment is directed toward preventative dental care and pain control. Following dental procedures, a minimum of 24 hours is advised before initiating a scuba dive.


During descent, the increased ambient pressure will tend to exert increasing pressure against the air-filled face mask of a scuba diver. The diver may develop facial or eye pain, subconjunctival hemorrhages, subconjunctival edema, epistaxis, and periorbital edema. Face mask squeeze is commonly prevented by using a low-volume face mask that minimizes the amount of air and allows for additional small amounts of air to be blown into the mask from the nose.


Under normal circumstances, the stomach and intestines contain approximately 1 quart of gas. Ingesting carbonated beverage, chewing gum (and swallowing air), eating large meals, and pre-existing gastrointestinal problems increase the amount of gas in the intestines. Gas expansion will cause discomfort, abdominal pain, belching, flatulence, nausea, vomiting, shortness of breath, or hyperventilation. Although aerogastralgia is rarely a serious problem, significant distention of the abdominal contents may result in venous pooling and syncope. In addition, tachycardia, hypotension, and syncope may result from a vasovagal response to severe pain. Gastric rupture has also been reported.

Symptoms are prevented or relieved by belching or passing flatus. Wearing clothes that are loose and nonrestrictive is also of benefit.


The second most common cause of death among scuba divers is pulmonary barotrauma. Air in the lungs can compress during descent. If the lung volume were to decrease below residual volume, hemoptysis, hemorrhage, and pulmonary edema could occur. However, breathing from a compressed air source, this loss of volume will be prevented. Pulmonary overpressurization syndrome (POPS) is an example of the positive-pressure barotrauma that can be seen during ascent. The alveoli become overinflated and can rupture, causing a pneumothorax in an estimated 10% of the pulmonary barotrauma victims. Ruptured pulmonary veins allow air emboli to enter the systemic circulation. These can occur if the scuba diver fails to exhale adequately on ascent or in the presence of predisposing lung disease. To reduce the risk of pulmonary barotrauma, divers are trained to not hold their breath. This is important not only during ascent, but also in the event a diver is not aware of an unintended decrease of depth. This holds true for novice divers who may not yet be skilled at managing depth regulation using a buoyancy device, or for children who may have smaller lungs and body mass making it more difficult to maintain a constant depth. Also at risk for pulmonary barotrauma are divers with obstructive airway diseases, including asthma and chronic obstructive pulmonary disease.


While it is rare to develop a pneumothorax during a dive, it represents a significant problem when it does. On ascent, air trapped in the pleural space will expand and a simple pneumothorax may progress to a tension pneumothorax, shock, and loss of consciousness. These complications may also occur during air transport in an unpressurized aircraft. At increased risk for a pneumothorax are patients with a past history of spontaneous pneumothorax, pulmonary bullae, or cystic lung disease.

Treatment of a scuba diving pneumothorax is no different than the treatment of other traumatic or nontraumatic pneumothoraxes. Hyperbaric (recompression) treatment is avoided since it can convert a simple pneumothorax to a tension pneumothorax. If hyperbaric treatment will be necessary, chest tubes must be placed before initiating recompression.


Pulmonary barotrauma can result in an air embolism, which is the most serious dysbaric injury. Specific signs and symptoms will be determined by the final destination of air emboli. Because of the buoyancy of air and the fact that scuba divers are usually upright during ascent, the brain is most commonly affected. The onset of symptoms can be immediately on ascent, or within 10 to 20 minutes of surfacing. Neurologic symptoms that develop later than this are more likely caused by decompression sickness. A rapid onset and severe symptoms are suggestive of a poorer prognosis with both air embolism and decompression sickness. These patients require aggressive care, which includes 100% oxygen, intravenous fluids, and hyperbaric treatment. They are placed in the Trendelenburg or left lateral decubitus position (Durant’s maneuver) to minimize the passage of air emboli to the brain. Air emboli affect the heart if they embolize to the coronary circulation, causing coronary artery occlusion, dysrhythmias, shock, and cardiac arrest. Although these complications are rare compared with other dysbaric injuries, they represent a significant risk to the victim.

Cerebral arterial gas embolism (CAGE) is air in the arterial system of the brain and is more common than air embolization to the heart or spinal cord. Neurologic symptoms are similar to those of a stroke and include numbness, dizziness, headaches, weakness, visual field deficits, confusion, behavioral changes, amnesia, paralysis, vertigo, blindness, aphasia, deafness, sensory deficit, seizures, focal deficits, and loss of consciousness. It should be noted that CAGE is not restricted to open water scuba diving. There have also been documented pediatric cases of CAGE in swimming pools,4,5 in water as shallow as 2 ft.


Gases coming out of solution result in decompression sickness. A diver breathing compressed air is exposed to nitrogen, oxygen, and carbon dioxide. Approximately four-fifth of the air is nitrogen. Oxygen is metabolized, and the carbon dioxide is expelled. Under normal circumstances, additional nitrogen gas will not be absorbed by the body during inhalation. However, when the body is exposed to a varying ambient pressure, uptake or removal of nitrogen gas from the blood occurs. As ambient pressure increases, the positive-pressure gradient between the alveoli and the blood will result in more nitrogen being dissolved. As the dive progresses, the gas in the blood will equilibrate quickly with the gas in the alveoli. Nitrogen gas, however, is almost five times more soluble in fat. It will take longer to saturate these tissues. Therefore, the body will absorb more nitrogen gas at a rate that is dependent on the depth and duration of the dive. The longer and deeper the dive, the more nitrogen gas will be accumulated within the body.

Since nitrogen is not metabolized, it remains dissolved until the nitrogen gas pressure in the lungs decreases, and the nitrogen can be removed. During a slow ascent, as the surrounding pressure decreases, the nitrogen that is absorbed into the tissues is released into the blood and the alveoli. If the ascent is too quick, nitrogen levels do not have the opportunity to equalize among the tissues, blood, and alveoli. The pressure outside the body will drop significantly below the sum of the partial pressures of the gases inside the body. This results in the gas coming out of solution and the formation of gas bubbles in the blood or tissue. Because of the increased dissolved nitrogen, it has a disproportionately higher partial pressure. Therefore, a significant difference in partial pressure occurs. It is the release of these nitrogen bubbles from solution that results in decompression sickness.

Diving tables are often used by scuba divers as a tool to minimize the risk of developing a decompression sickness. However, even if the dive tables are carefully followed, additional factors could precipitate a decompression sickness, such as increased physical activity during a dive, cold temperatures, obesity, alcohol ingestion, previous dives with inadequate surface time to equilibrate, and flying within 12 hours of a dive.

Decompression sickness can be classified as Type I or Type II. Type I is the milder complication and involves extravascular gas bubbles affecting the joints, skin, and lymphatics. Type II is the severe form of decompression sickness and involves the neurologic or pulmonary systems. These can lead to serious injury or death and are caused by intravascular nitrogen gas emboli. The presentation may be very similar to that of air emboli. Children are more prone to type II injuries.


The generic term “the bends” is often used to identify any form of decompression sickness. When used correctly, however, the term refers to the musculoskeletal syndrome involving the joints, which is a very common dysbarism. The bends occurs in up to 75% of all decompression injuries and is caused by the release of nitrogen gas bubbles from the blood into the tissues surrounding the joint.

Symptoms usually develop within 6 to 12 hours after the conclusion of a dive and may increase over the next 1 to 2 days. A sharp, throbbing, or dull achy pain is a common presentation. There may also be associated numbness or tingling (paresthesia). The pain commonly is diffused in its origin but will become more localized as the intensity increases. The joints that are most often affected are the elbows and shoulders, followed by the knees and hips. Symptomatic relief may be obtained by splinting the extremity or by applying pressure over the affected joint. Massaging or moving the affected extremity often exacerbates the pain associated with the bends. The physical examination is usually unremarkable. On occasion, crepitus, edema, or tenderness is noted.


The extravascular release of nitrogen gas bubbles from the blood into the skin usually results in benign dysbarisms. Rashes, with or without pruritus, can present with any of the following patterns: scarlatiniform, mottling (cutis marmorata), and erysipeloid. The release of nitrogen gas bubbles can cause subcutaneous emphysema, often involving the neck and other sites. When the neck is involved, the victim’s voice may be altered, and the individual may complain of difficulty breathing or swallowing. In such a case when there is subcutaneous emphysema above the collarbone, there is concern for ruptured alveoli, a sign of more serious pulmonary barotrauma. Treatment of individuals with subcutaneous emphysema begins with 100% oxygen. The patient is then carefully examined for more serious dysbarisms and admitted.


The decompression illness that affects the pulmonary system is referred to as the chokes. It is caused by arterial or venous nitrogen gas embolization that obstructs the pulmonary vasculature. The symptoms may begin immediately after a dive but often take up to 12 hours to develop. They last between 12 and 48 hours but can progress to a rapid deterioration. The classic triad of symptoms includes shortness of breath, cough, and substernal chest pain or chest tightness. The shortness of breath is described as a feeling of suffocation. The individual becomes tachycardic and tachypneic. There is a nonproductive, often uncontrollable paroxysmal cough, which is exacerbated by deep inspiration. The chest pain is most frequently appreciated with deep inspiration, increased activity, and smoking. There is no radiation of the pain to the neck, arms, or abdomen.


Nitrogen gas embolism is the most serious decompression sickness. Venous gas emboli can result in venous obstruction, and arterial gas emboli can cause ischemia as a result of arterial obstruction or induced vasospasm. As with air embolus, the brain is commonly affected. The onset of symptoms, however, will usually be delayed with symptoms developing within 1 to 6 hours after a dive is concluded. These victims require aggressive care that includes 100% oxygen, intravenous fluids, and hyperbaric treatment. They are placed in the Trendelenburg or left lateral decubitus position to minimize the embolization to the brain.

Cerebral decompression injuries are more common with altitude-related decompression than with diving injuries. The symptoms are also similar to those of the air embolus. Common symptoms are headaches, visual field deficits, scintillating scotoma, confusion, behavioral changes, restlessness, amnesia, paralysis, blindness, deafness, hallucinations, sensory deficit, and seizures. Children primarily present with abnormal behavior, disorientation, and memory loss. The headache that develops is often dull and pulsating in nature. It may be unilateral and is often on the opposite side of the visual field deficits or scotoma. The mild-to-moderate pain will usually last for several hours. Scotoma may be peripherally or centrally located but often appear to move peripherally. They are appreciated with the eyes opened or closed and are unilateral or bilateral, singular or multiple. They appear as visual distortions or as colored lines that are horizontal or V-shaped.

Spinal cord complications are seen more often than cerebral decompression injuries as a result of diving accidents. An air embolism affects the spinal cord by blocking the venous return in the epidural vertebral venous system. This results in back pain, numbness in the extremities, weakness, paralysis, and urinary retention.


Decompression shock may be secondary to hypovolemia or due to vasovagal responses. Hypovolemia is caused by fluid loss and third spacing. The patient may become agitated, restless, cool to the touch, tachycardic, tachypneic, and finally hypotensive. If vasovagal symptoms dominate initially, the victim may present with diaphoresis, nausea, vomiting, bradycardia, light-headedness, and hypotension. Aggressive and timely management with intravenous fluids, 100% oxygen and recompression therapy should be initiated as quickly as possible.


The morbidity and mortality for dysbaric injuries depend on the severity of the injury, rapid identification of the illness, and timely access to appropriate medical care. When the “system” works, the recovery rate is as high as 90%. Treatment begins with the administration of 100% oxygen, hydration, and rewarming.6 The patient should be positioned in the left lateral decubitus position with mild Trendelenburg. In addition, the treatment of choice for most air emboli and decompression illnesses is hyperbaric (recompression) oxygen therapy (HBO). This is initiated as soon as possible, ideally within 6 hours of the onset of symptoms. Treatment of cerebral air emboli is less successful if HBO is delayed over 4 to 5 hours.7 However, there is still benefit to providing delayed HBO treatment. In some cases of air emboli, hyperbaric therapy has been effective for patients who are not treated until 10 to 14 days after the onset of their symptoms.

The goal of recompression treatment is to reduce the size of the liberated gas bubbles (Boyle’s Law), facilitate the reabsorption of these air bubbles, prevent the formation of new bubbles, and improve oxygenation. The mechanism of HBO is complex, but by causing bubbles to decrease in size, hypoxia can be reduced downstream of blocked vessels. In addition, HBO removes the nidus for activation of the complement system.6 Giving 100% oxygen also helps to replace undissolved nitrogen with oxygen, which is easier for tissues to utilize and eliminate from the body. In addition, HBO is postulated to provide additional benefit through delivering oxygen to tissues damaged by ischemic-reperfusion injury.8

Before hyperbaric treatment is initiated, certain procedures should be followed. Endotracheal tube cuffs and Foley catheter balloons should be filled with saline rather than air. It is essential to identify any pneumothorax and insert a chest tube prior to recompression. Some physicians have found Auralgan® otic drops beneficial to anesthetize the TM of smaller children who may have difficulty equalizing middle ear pressure during hyperbaric treatment.

The initiation of hyperbaric treatment is similar for types I and II decompression injuries as referenced in the US Navy Diving Manual treatment tables.9 Victims are taken to a “depth” of 60 ft (FSW), which is equal to 2.8 atm. Supplemental oxygen at an FIO2 of 100% is provided at 20-minute intervals, alternating with room air. The hyperbaric pressure will be reduced at an ascent rate of 1 ft a minute to equal a depth of 30 ft for a period of time and then slowly brought back to “sea level.”

Victims of an arterial air embolus will commonly be brought to an initial hyperbaric depth of 165 ft (6 atm). After 30 minutes, the patient will be brought slowly “up” to a depth of 60 and then 30 ft before returning to the normal ambient pressure.

Adjunctive therapies to HBO such as NSAIDs, glucocorticoids, lidocaine, aspirin, and heparin have been tried, but there is currently insufficient data to support their use.

In addition to hyperbaric therapy, patients should be dried off immediately and kept warm to prevent hypothermia. A urine output should be maintained in the pediatric patient between 1 and 2 mL/kg/h. Intravenous fluids that are in plastic bags should be used instead of glass bottles. Some individuals may experience neurologic deterioration after cessation of recompression therapy, possibly caused by: slow reexpansion of residual gas bubbles; post-ischemic reperfusion; and reembolization from underlying pulmonary abnormality or injury.

Special precautions should also be taken for victims who must be transported by helicopter or airplane. In some cases, even the slightest elevation, which results in exposure to a decreased ambient pressure, may compromise the victim by causing further gas expansion. Helicopter transports should be done at as low an altitude as possible (less than 1000 ft), while ensuring the safety of the transport. Airplane transport should be conducted in aircraft that are capable of being pressurized to sea level.

Victims of type I decompression sickness are advised to abstain from any further scuba diving for at least 4 to 6 weeks and type II victims must wait at least 4 to 6 months. An air embolism or a second occurrence of any type II complications is serious enough to cease diving on a permanent basis.10,11


Scuba diving is made possible through the use of compressed air tanks. As a diver descends, ambient pressure will increase causing a proportionate increase in the partial pressure of the compressed gases (Dalton’s Law). As a result, the partial pressure of the inhaled gas will increase at greater depths. The increased partial pressure of nitrogen in nervous system tissue represents a significant danger to scuba divers. These symptoms are referred to as nitrogen narcosis.


The inhalation of nitrogen gas at elevated partial pressures may cause an interference with nerve conduction. As a result, nitrogen narcosis can produce a narcotic or intoxicating effect during a dive. Symptoms can include euphoria, uncontrollable laughter, impaired judgment, memory loss, light-headedness, hallucinations, loss of coordination, and impaired reflexes. The signs of nitrogen narcosis may become evident at depths beyond 80 ft. It is estimated that every 50 ft of depth during a dive can result in symptoms roughly equal to one martini on an empty stomach. The greatest risk of nitrogen narcosis is drowning. With any evidence or suspicion of confusion, disorientation, or altered mental status, the dive should be terminated. The affected diver should be escorted slowly to the surface by a second diver. No other treatment is required.


Practitioners of pediatric patients may be requested to screen a child for scuba diving. No concrete recommendations can be found in the medical literature for or against children participating in scuba diving.3Children with chronic sinusitis or otitis media should be adequately prophylaxed against congestion and potential difficulty with equalization. Lung conditions that might cause blebs, such as cystic fibrosis, α1-antitrypsin deficiency, or chronic obstructive pulmonary disease impart serious risk of pulmonary barotrauma. Children with active asthma exacerbations or cold- or exercise-induced asthma should be advised against diving. However, asthmatic children not currently experiencing an exacerbation are not at increased risk of pulmonary barotrauma. Any prior history of spontaneous pneumothorax or thoracic surgery is a contraindication; however, traumatic pneumothorax that is well healed may not preclude diving.12

Cardiac conditions, such as patent foramen ovale, or other situations creating a potential right-to-left shunt (e.g., ASD or VSD) cause increased risk of arterial embolism and decompression sickness. Furthermore, long QT syndrome may trigger fatal arrhythmias during swimming and diving.12 Other conditions including claustrophobia and unrepaired inguinal hernias are also considered contraindications. However, divers with sickle cell trait or Crohn’s disease appear to be unaffected. Insulin-dependent diabetes mellitus is often considered a contraindication, but the Divers Alert Network has presented guidelines for recreational diving with diabetes.13


Scuba diving can be one of the most enjoyable and memorable recreational activities for family outings and vacations. Ill-prepared, however, it can also be one of the most dangerous. This is especially true for children who may not have an understanding of the physics of scuba diving or an appreciation of the inherent risks.

When planning for a dive-related vacation or excursion, it is important to consider any recent changes in health, injuries, surgery, and medication. Special attention should be given to any of the medical conditions mentioned in this chapter that may predispose an adult or child to barotrauma or a decompression illness.

Proper training, education, vigilance, and situational awareness are necessary to remain safe while diving. This may prevent the most common events involved with decompression injuries and fatal accidents. These events include running out of gas, entrapment or entanglement, buoyancy control, equipment misuse, and emergency ascent.2 All scuba diving should be done with a companion and adults should carefully monitor children who are diving. Divers should be physically fit, well rested, well hydrated, and should dive within the limits of their training and comfort zone. Judicious attention should be given to decompression risk factors that include depth of a dive (especially if greater than 60 ft), length of a dive, rate of ascent, repetitive dives, and strenuous activity. With proper training, the recreational diver should also be able to recognize the signs of injury and know how to find qualified dive medicine assistance when needed.


There is an increased risk of developing decompression sickness when divers are exposed to increased altitude too soon after completing a dive. At a flight altitude of 35,000 to 40,000 ft, the cabin pressure of commercial aircraft may be the equivalent of 6000 to 8000 ft (1829–2438 m), which could cause subclinical gas bubbles to increase in size. To decrease the risk of a developing a decompression illness, divers should avoid flying or an altitude exposure higher than 2000 ft (610 m) for:

• 12 hours minimum after surfacing from a single no-decompression dive

• 18 hours minimum after multiple dives per day or multiple days of diving

• substantially >18 hours after dives where decompression stops were required14,15


1. Annual Divers Report 2008 Edition. Divers Alert Network. Accessed February 2013.

2. Vann RD, Lang MA, eds. Recreational Diving Fatalities. Proceedings of the Divers Alert Network 2010 April 8–10 Workshop. Durham, N.C.: Divers Alert Network, 2011. Accessed February 2013.

3. Tsung, JW, Chou KJ, Martinez CM, et al. Pediatr Emerg Care. 2005; 21(10):681–686.

4. Weiss LD, Van Meter KW. Cerebral air embolism in asthmatic scuba divers in a swimming pool. Chest. 1995;107:1653–1654.

5. Johnson V, Adkinson C, Bowen M, Ortega H. Should Children Be SCUBA Diving? Cerebral arterial gas embolism in a swimming pool. Pediatr Emer Care. 2012;28:361–362.

6. Tetzlaff K, Shank ES, Muth CM. Evaluation and management of decompression illness – an intensivist’s perspective. Intensive Care Med. 2003;29(12):2128–2136.

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