Continuing Education Activity

Barotrauma is physical tissue damage caused by a pressure difference between an unvented space inside the body and surrounding gas or fluid. The damage is due to shear or overstretching of tissues. As a gas-filled space expands or contracts, it can cause damage to the local tissue. Occasionally, tears in tissue can allow gas to enter the body through the initial trauma site. This causes potential blockage of circulation at distant sites or interferes with normal organ function. Barotrauma can cause sinus injury, ear injury, facial injury, tooth injury, an acute abdomen, pneumothorax, pulmonary hemorrhage, and subcutaneous emphysema. This activity reviews the causes, presentation of barotrauma, and highlights the role of the interprofessional team in its management in order to improve outcomes.

Objectives:

• Identify the etiology of barotrauma.
• Outline the presentation of barotrauma.
• Review the treatment and management options available for barotrauma.
• Summarize interprofessional team strategies for improving care coordination and communication to advance the treatment of barotrauma and improve outcomes.

Introduction

Barotrauma is physical tissue damage caused by an unrelieved pressure differential between a surrounding gas or fluid and an unvented body cavity (e.g., sinuses, lungs), or across a tissue plane. The damage is due to compressive/ expansive forces and shear, leading to overstretching of tissues. Barotrauma most usually causes sinus injury or middle-ear injury, but may also cause facial injury, tooth injury, gastrointestinal (GI) rupture, pneumothorax, pulmonary hemorrhage, mediastinal and subcutaneous emphysema. Tears in pulmonary tissue can allow gas to enter the circulation. This causes embolic blockage of the circulation at distant sites or interferes with normal organ function.[1][2][3][4][5]

Etiology

According to Boyle’s Law of Gases, if the temperature of a gas is held constant, there is an inverse relationship between the volume of the gas and its pressure. A balloon that rises in the atmosphere will expand in volume as the ambient pressure decreases. Similarly, the compressed air held in a diver’s lung, if he holds his breath, will expand as the surrounding water pressure decreases on the ascent. Atmospheric pressure at mean sea level is 14.7 psi. This is also measured in millimeters of mercury as 760mmHg. Both of these measurements are equivalent to one atmosphere (1 Atm or 1 Barr). Due to the density of water, pressure during a dive increases one additional 1 Atm for every 33 feet of seawater depth. Barotrauma occurs most commonly while scuba diving, but also may occur during flying, mountain climbing, or skiing. During scuba diving, barotrauma may be caused by descending or ascending too rapidly. The ‘squeezes’ are caused by the inability to equalize pressure on the descent, classically across the face mask, sinuses, teeth, or ear. Mask squeeze can cause skin ecchymosis imprinting the mask pattern on the face, conjunctival hemorrhage, and rarely, orbital hemorrhage. Dental squeeze can cause an implosion of carious teeth. Ear squeeze can occur in the ear canal or middle ear. Sinus squeeze can be excruciating, usually in the setting of chronic sinusitis with occluded ostia. Barotrauma on ascent may similarly result in the ear, sinus, and dental trauma (tooth explosion). The most serious form of ascent barotrauma is pulmonary injury. Additionally, injury to the lung from positive airway ventilation is a special case of barotrauma. The most serious consequence of barotrauma is a pulmonary alveolar rupture with antecedent air gas embolism. Peripheral embolism of the gas bubbles occludes the circulation, with potential for cerebrovascular accident or cardiac ischemia. Risk factors for barotrauma include asthma, sinusitis, dental abscesses and caries, chronic obstructive pulmonary disease (COPD), seizures, ear problems, syncope, panic disorders, vertigo, poor training, inexperience, and Eustachian tube dysfunction. Any patient receiving mechanical ventilation is at risk for barotrauma, but it is most commonly seen in patients with acute respiratory distress syndrome (ARDS). 

Epidemiology

There are approximately five million certified SCUBA divers in the US. About 500 to 1000 nonfatal dive injuries in the United States and Canada each year. Many of these are related to barotrauma. Diving injuries tend to correlate with advancing age, alcohol usage, obesity, asthma and COPD, chronic sinusitis and otitis.

Pathophysiology

Barotrauma of descent is caused by a lack of pressure equalization in closed spaces in contact with the diver, typically the ear, teeth, sinuses, and face mask. The resulting pressure difference between the tissues and the gas space causes injury. The actual rupture of the tympanic membrane  (TM) is a consequence of ear ‘squeeze’ and usually occurs in divers with Eustachian tube dysfunction. On the descent, as pressure builds up between the ear canal, TM, and the nasopharynx, the Eustachian tube should function to equalize this. However, if the pressure gradient exceeds 30mm, pain will ensue. At 100mmHg gradient, the Eustachian tube cannot open, and TM hemorrhage and rupture may occur. Curiously this is heralded by a sudden decrease in pain. However, hearing loss, whirling vertigo, tinnitus, and bloody drainage may ensue. Occasionally the pressure gradients across the left and right TMs differ asymmetrically, usually due to eustachian tube mismatch. When this gradient differential exceeds 45mgHg, alternobaric vertigo may occur. This may present with disorientation, nausea, vomiting, vertigo, and tinnitus. Drownings have occurred due to disorientation or vomiting. Occasionally inner ear barotrauma may occur. This is usually in the setting of severe (locked) Eustachian tube, allowing a large pressure gradient. The round and oval windows of the inner ear may rupture, with a concomitant perilymphatic leak. Tinnitus, sensorineural hearing loss and vertigo are common. Dental pain is caused by similar pressure effects at the site of fillings, apical abscesses, or carious teeth. Root abscesses can expand, causing pain. Fillings may distort. And carious teeth may implode on the descent. Sinuses are truly closed spaces, except for the functioning of their ostia. Sinus squeeze usually occurs in divers with some degree of chronic sinusitis, allergies, URI, mucoperiosteal thickening, nasal polyps, and ostial occlusion. Pain may be severe. Bloody nasal discharge is seen.[6][7][8][9]Barotrauma of ascent is caused by the volume increase of gas containing spaces. Ear, sinus, and dental injury may occur on the ascent as well as descent. Pulmonary barotrauma on the ascent is the most serious and potentially life-threatening. Breathing gas at depth during SCUBA causes the in gas in the lungs to be at a higher pressure than the atmospheric pressure. A free diver (non-SCUBA) can dive to 33 feet or 10 meters and safely ascend without exhaling because the gas in the lungs had been inhaled at the surface at atmospheric pressure. However, a SCUBA diver who inhales compressed gas from his tank at 10 meters and ascends without exhaling (i.e., holding his breath) may rupture his lungs and have extensive pulmonary barotrauma (pulmonary overpressure syndrome -POPS). This may occur with an ascent from shallow depths.  This pulmonary barotrauma (PBT) of ascent is also known as a pulmonary over-inflation syndrome (POIS), lung over-pressure injury (LOP), and burst lung. Consequent injuries may include pneumothorax, mediastinal, interstitial, or subcutaneous emphysema, and possibly arterial gas embolism, not usually all at the same time. Alveolar rupture during ascent can lead to arterial gas embolism with air entering the pulmonary circulation, then entering the left heart, and therefor embolizing to the systemic circulation, and obstructing cerebral, coronary, or other essential beds.A rare form of barotrauma of ascent is ruptured abdominal viscus secondary to the rapid expansion of gas trapped in the GI system. These are surgical emergencies. The ingestion of carbonated drinks before dives is discouraged.

History and Physical

When taking the history, it is essential to note the events preceding the dive. What was the ambient temperature, the sea conditions, the depth and duration of the dive? When was the onset of symptoms with respect to the dive profile (on the descent, at the bottom, on ascent or after surfacing)? Was there chest pain, shortness of breath, hemoptysis, headache, epistaxis, tinnitus, vertigo, nausea, vomiting, or disorientation? Did the diver have trouble ‘clearing’ his ears? Was a Valsalva maneuver necessary? Does the diver remember holding his breath on ascent? Was there any precedent URI, sinus infection, nasal discharge, earache, allergy, asthma, or chest pain. Was there any prior history of nasal polyps, asthma, COPD, hearing loss. Was the diver on nasal or oral decongestants. Was the diver on bronchodilators or systemic steroids? On physical exam, check sinuses for percussion tenderness, nasal discharge, or epistaxis. Ears should be visually checked. Note any obstruction, swelling, or ecchymosis of the external canal. The TM must be examined for the presence of suffusion, hemorrhage, or rupture. An unruptured TM should undergo pneumatic tympanometry. Note the TEED scoring system below. Note any nystagmus. Perform vertigo analysis if indicated. Hearing deficits should be tested for conductive or sensorineural elements. Dental examination should specifically look for dental caries, abscesses, and carious teeth. Percussion of individual teeth may define injury. Signs and symptoms of the POP syndrome include shortness of breath, crackles, crepitance, subcutaneous emphysema, sore throat, dysphagia, change in voice, tachypnea, respiratory distress, substernal chest pain, pain radiating to back, shoulders, or neck and in the case of pneumothorax, diminished breath sounds. Patients with chest pain, diminished breath sounds, tracheal shift, and unstable vital signs must be immediately evaluated for tension pneumothorax. Similarly, any diver with signs of pneumopericardium with tamponade (soft heart sounds, Kussmaul sign, pulsus paradoxus, and reduced pulse pressure) must be stabilized immediately.A complete neurologic exam is indicated for anyone with pulmonary barotrauma to screen for signs of arterial gas embolism (AGE), which could include numbness, weakness, paralysis, visual deficits, ataxia, aphasia, sensory loss, nystagmus, and confusion. Any stroke-like presentation following a dive is POP with arterial gas embolism until proven otherwise. Funduscopic examination may reveal retinal artery bubbles. Additionally, cardiac insufficiency symptoms of chest pain, arrhythmia, or failure should suggest coronary artery gas embolism.

Evaluation

History and physical is the most important key to making this diagnosis. Laboratory studies are not as useful. Arterial blood gas may be of value to look for a-a gradient in those suspected of having an air embolism. Rising creatine phosphokinase (CPK) and troponin-I levels may signal worsening tissue damage due to gaseous microemboli in the coronary circulation.EKG may confirm myocardial ischemia, cardiac arrhythmia, or suggest pericardial effusion. Stat chest x-rays should be ordered for suspicion of pneumothorax, pneumomediastinum, or pneumopericardium. Bedside cardiac echo should be done with any suspicion of pneumopericardium or air in the heart. Head CTA or MRA should be ordered in any patient with stroke-like symptoms or frank coma. The TEED scale is used for the classification of ear barotrauma. Grade I is a slight injection of the TM, Grade II is a partial hemorrhage of the TM, Grade III is a total hemorrhage of the TM, Grade IV is a blue and bulging hemotympanum, Grade V is a perforated TM.

Treatment / Management

Treat supportively for mild injuries such as sinus squeeze, middle ear squeeze. Use NSAIDs, decongestants, or analgesics as needed. Mild middle ear disease may be treated with topical or systemic steroids and topical or systemic decongestants. For tympanic membrane (TM) rupture, prescribe oral amoxicillin/clavulanate and fluoroquinolone ear drops. Suppurative otorrhea should be treated with antibiotics. Otolaryngology referral is also warranted for TM ruptures. They may also be consulted to drain affected sinuses, to evaluate persistent tinnitus or vertigo, and to evaluate sensorineural hearing loss. Perilymph leaks in inner ear trauma may be surgically corrected by patching of the round or oval window. A delayed dental referral would be appropriate for specific dental injuries. Dental abscesses should be started on antibiotics. An acute gastrointestinal rupture would present as an acute abdomen, most likely in shock. Early sepsis must be treated immediately, and urgent surgical consultation obtained, with direction toward prompt exploration. Most pulmonary barotrauma can be treated conservatively with rest and oxygen as needed. High flow 100% oxygen hastens the absorption of subcutaneous, mediastinal, and pericardial nitrogen, thereby shrinking the emphysematous tissue. The exception is pneumothorax with often requires decompression (needle, pigtail, or chest tube). Tension pneumothorax must be decompressed promptly. Chest thoracostomy tube drainage should be employed for any patient with pneumothorax and arterial gas embolism. Recompression in a hyperbaric chamber (see below) would allow an otherwise (needle) reduced pneumothorax to expand. Any diver with arterial gas emboli should be expeditiously transferred to a center with a hyperbaric chamber. The transfer should be utilizing high flow oxygen. Recompression with high ambient pressure oxygen shrinks the size of gas bubble emboli, and also, by establishing a high nitrogen gradient between gas emboli and the blood, absorbs the emboli. A standard chamber protocol is rapid recompression to 6 Atm of air for thirty minutes and then continued recompression with 100% oxygen at 2.8 Atm for 30 minutes. Pulmonary barotrauma was the most common complication of mechanical ventilation, but modern strategies have mitigated the incidence of ventilator-associated ARDS by limiting tidal volume (6 to 8 mL/kg) and plateau pressure to less than 30 to 50 cm. As an indicator of trans alveolar pressure, which predicts alveolar distention, plateau pressure is the best predictor of risk, but there is no accepted safe pressure at which there is no risk.  Aspiration of stomach contents and pre-existing diseases such as pneumonia and chronic lung disease also increase risk.[10][11][12]

Differential Diagnosis

Differential diagnoses include acute coronary syndrome (ACS), substance abuse/intoxication, asthma exacerbation, myocardial infarction, stroke pulmonary embolism, head injury, hypothermia, shock, otitis media/externa, bacterial sinusitis, pneumothorax, pneumonia, acute abdomen, dental caries, dental infection, arterial gas embolism, and decompression sickness (DCS).

Prognosis

The prognosis for barotrauma is good, most of these conditions are self-limiting. Most TM and external canal injuries heal spontaneously. Inner ear trauma, especially with a perilymphatic leak or endolymph/ perilymph mixing, may lead to chronic hearing loss (cochlear), vertigo, and tinnitus. Acute arterial gas embolism may eventuate in completed stroke, myocardial infarction, and death. Acute gastrointestinal rupture may present in septic shock with peritonitis.

Pearls and Other Issues

• In diving, descending injuries include squeezes; ascending injuries include POPS or AGE.
• On resurfacing and immediate symptoms: AGE
• Delayed symptoms 1 to 6 hours: DCS
• Lower tidal volumes and plateau pressures can largely prevent pulmonary barotrauma during mechanical ventilation.
• Due to the major change in density between air and water, the largest increase (delta) in pressure occurs as the diver enters the water and begins descent. Most squeeze symptoms occur close to the surface on the descent.
• In diving, descending injuries include the squeezes whereas ascending injuries are more likely to include POPS which can lead to AGE.
• On resurfacing and immediate symptoms: AGE
• Delayed symptoms of 1 to 6 hours: Usually not barotrauma and more likely DCS
• Flying too soon after diving can precipitate DCS.
• Absolute contraindications to diving include spontaneous pneumothorax, acute asthma with abnormal PFTs, cystic or cavitary lung disease, obstructive or restrictive lung disease, seizures, atrial septal defect (ASD), symptomatic coronary artery disease (CAD), chronic perforated TM, inability to equalize sinus or middle ear pressure, or intraorbital gas.

Enhancing Healthcare Team Outcomes

Barotrauma can occur during diving, flying, skiing, patients undergoing hyperbaric chamber treatment, or in patients on a mechanical ventilator. Barotrauma is usually managed by an interprofessional team that includes a pulmonologist, emergency department physician, intensivist, ICU specialist, otolaryngologist, and a surgeon. Critical care, emergency department, and other specialty care nurses must be aware of the signs and symptoms of this condition to avoid catastrophic outcomes and report their concerns to the interprofessional team. Most mild cases in divers are treated supportively. NSAIDs, decongestants, or analgesics are used as needed. For tympanic membrane (TM) rupture, prescribe oral amoxicillin/clavulanate and fluoroquinolone ear drops. Otolaryngology referral is also warranted for TM ruptures. The pharmacist should assist with patient education regarding medications and compliance. They should also evaluate for potential drug-drug interactions and report to the interprofessional team their concerns. Most pulmonary barotrauma can be treated conservatively with rest and oxygen as needed. The exception is pneumothorax with often requires decompression (needle, pigtail, or chest tube). Also, in patients on a ventilator, barotrauma is always managed with a chest tube. Further, some specialists also insert a prophylactic chest tube on the contralateral side as the risk of pneumothorax in ventilated patients with high PEEP.[13] (Level V)