Millions of recreational, commercial, and scientific dives are logged annually, and the vast majority of dives are completed without incident. However, there are physiologic effects and injuries relatively unique to the underwater environment. Generally, these effects and injuries are secondary to pressure changes on the submerged human body and the breathing of compressed gas.¹ This chapter outlines the most common diving injuries: barotrauma of descent (otic, sinus, and pulmonary), barotrauma of ascent (pulmonary overinflation syndromes and arterial gas embolism), decompression sickness, immersion pulmonary edema, oxygen toxicity, and nitrogen narcosis.

THE GAS LAWS

Understanding diving injuries requires familiarity with the three relevant gas laws most pertinent to diving: Boyle’s law, Dalton’s law, and Henry’s law.

Boyle’s law states that given a constant temperature, the pressure and volume of an ideal gas are inversely related. That is, if pressure is doubled, the volume of gas is halved. This law is stated as: P₁V₁ = P₂V₂.

Pressure can be measured in a variety of units. The International System of Units defines pressure using the pascal (Pa). Other commonly used units of pressure include millimeters of mercury (mm Hg), torr, pounds per square inch (psi), bar, or atmosphere (atm): 1 atm = 760 mm Hg = 760 torr = 14.7 psi = 1.013 bar = 101,325 Pa = 101.325 kPa. Additionally, pressure in diving settings is often described using feet of seawater (fsw) or meters of seawater (see below). In this chapter, we use atm, mm Hg, and fsw for pressure units.

Because of the high density of water, a relatively small change in depth causes a great change in pressure. The weight of seawater produces a change of 1 atm for each 33 ft of depth. For freshwater, pressure increases 1 atm for each 34 ft of depth. Therefore, the pressure exerted on a diver at a depth of 33 ft in seawater = 1 atm for the seawater + 1 atm for the atmosphere above the water = 2 atmospheres absolute (ATA). A diver at 165 ft of seawater would experience 6 ATA of pressure (1 atm for each 33 ft of seawater = 5 atm + 1 atm for atmospheric pressure at sea level).

Thus, Boyle’s law dictates as a diver descends in the water column, the volume of air-containing structures will decrease. For example, if the lungs contain volume V at the surface, a diver who descends to 33 ft of seawater holding his or her breath would have a lung volume of ¹/₂V. If the diver then breathes compressed air at this depth (from scuba equipment or from a surface-supplied source of gas), lung volume would return to V. If the diver then ascends to the surface without exhaling, lung volume would be 2V at the surface. This pressure–volume relationship governed by Boyle’s law is important in the etiology of injuries due to barotrauma and produces the volume changes of bubbles in the tissues and circulation that are associated with recompression (hyperbaric) therapy.

Dalton’s law states that the total pressure exerted by a mixture of gases is the sum of the partial pressures of each gas. Therefore, the partial pressure of a given component of a gas mixture will increase as the ambient pressure increases, although the proportion of gas in the mixture remains constant. The partial pressure of nitrogen in air at sea level is approximately 600 mm Hg or 0.79 ATA (the fraction of nitrogen in air, 0.79 × 760 mm Hg or 1 ATA). At a depth of 99 fsw, the partial pressure of nitrogen in air would be 4 × 600 = 2400 mm Hg (or 3.16 ATA).

Henry’s law, which states that at equilibrium the quantity of a gas in solution in a liquid is proportional to the partial pressure of the gas, along with Dalton’s law, explains the uptake of inert gas into tissues when breathing compressed air at depth. It is the uptake of inert gas that is intrinsic to the development of decompression sickness.

The clinical conditions resulting from barotrauma of descent are barotitis (ear squeeze), external ear squeeze, sinus barotrauma, inner ear barotrauma, and face, tooth, or dry-suit squeeze (Table 214-1).

PATHOPHYSIOLOGY

During descent, the volume of gas in all air-containing body cavities decreases. The air space in the middle ear makes the tympanic membrane the tissue most commonly affected by this phenomenon, if active measures such as “clearing the ears” with a Valsalva or other maneuvers are not successful.² As the volume of gas decreases, the tympanic membrane is bent inward, causing a feeling of fullness or pain in the ear. Forcing air through the Eustachian tube with a Valsalva maneuver will equalize the pressure between the middle ear and external ear canal by filling the middle ear with additional gas. Generally, divers who experience pain in an ear during descent will attempt to clear the ear and, if unsuccessful, will ascend to decrease the pressure differential and attempt equalizing again. If the diver is unsuccessful in equalizing and continues the descent, prolonged pain and injury to the tympanic membrane may result, known as barotitis or “ear squeeze.”

BAROTITIS (EAR SQUEEZE)

Barotitis can range from symptoms of pain or fullness without otoscopic changes, to hemorrhage within the tympanic membrane or hemorrhage into the middle ear with hemotympanum. Ultimately, the tympanic membrane may rupture, resulting in relief of the pain but also possibly causing an influx of water into the middle ear. This, in turn, might cause calorically induced vertigo and potential panic, drowning, or other injury.

Barotitis is treated conservatively with analgesics and decongestants. If tympanic membrane rupture occurs, antibiotics can be prescribed, especially if the diving occurred in contaminated water. Divers with perforated tympanic membranes should refrain from diving until the perforation heals. Most such perforations heal without difficulty, but referral to an otolaryngologist is appropriate for individuals with larger perforations or when healing does not occur. Divers with barotitis without perforation should refrain from diving until the diver is again able to equalize the pressure in the affected middle ear.

EXTERNAL EAR SQUEEZE

If the external canal is occluded by cerumen or an ear plug, the inability to equalize pressure between the external canal and the tympanic membrane causes the bending of the tympanic membrane outward, producing an injury called “external ear squeeze” that produces pain and tympanic membrane hemorrhage.

SINUS BAROTRAUMA

If the ostia to the sinuses are occluded, air cannot enter the sinuses during descent to equalize the increasing pressure. This causes pain and mucosal edema and can lead to submucosal hemorrhage and stripping of the sinus mucosa from bone, hemorrhage (often causing bleeding from the nose into the mask), and, rarely, paresthesias in the infraorbital nerve distribution. A similar traumatic neuropathy can occur to the facial nerve with middle ear barotrauma. Sinus barotrauma is treated with conservative measures, including decongestants and, possibly, antibiotics.

INNER EAR BAROTRAUMA

The inner ear is also susceptible to barotrauma, occasionally causing significant, long-term damage. If a diver attempts a forceful Valsalva maneuver to equalize the middle ear against an occluded Eustachian tube, the pressure differential between the cerebrospinal fluid, transmitted through the vestibular and cochlear structures and the middle ear air space, can cause rupture of the oval or round window, fistulization of the window, tearing of the vestibular membrane, or a combination of such injuries. Additionally, if the diver is able to open the Eustachian tube in this situation, a rapid increase in middle ear pressure may occur. This pressure wave is transmitted to the inner ear and can also cause a similar injury. Divers with inner ear barotrauma will generally present with unilateral roaring tinnitus, sensorineural hearing loss, and profound vertigo. A “fistula test” may be positive—that is, insufflation of the tympanic membrane on the affected side causes the eyes to deviate to the contralateral side. Because this injury usually occurs on descent and divers will provide a history of difficulty clearing the ears, this condition can usually be easily differentiated from other causes of vertigo, such as inner ear decompression sickness, cerebral arterial gas embolism, or alternobaric vertigo (discussed below).

Immediate complications of inner ear barotrauma are potential panic or disorientation, leading to possible drowning or a rapid ascent that predisposes the diver to pulmonary barotrauma. Divers with barotraumatic injuries to the inner ear require urgent otolaryngologic evaluation. Treatment is controversial, with some authors advocating immediate exploration and others suggesting a trial of bed rest (head upright), medications to control vertigo, and mechanical measures to reduce cerebrospinal fluid pressure spikes (e.g., stool softeners, no nose blowing). These authors reserve exploration for patients whose symptoms do not respond to conservative therapy or patients with severe hearing defects or significant abnormalities on an oculo-nystagmogram. Divers with potential inner ear barotrauma who will be treated with hyperbaric oxygen for decompression sickness or cerebral arterial gas embolism require emergent tympanostomy, because hyperbaric treatment will recreate the same pressure differentials that caused the injury, potentially causing more perilymph leakage and, possibly, worsening the injury.²

FACE SQUEEZE, TOOTH SQUEEZE, AND DRY-SUIT SQUEEZE

Other air-containing structures can be compressed during descent, producing “squeeze” symptoms. A face squeeze occurs when air is not added to the facemask during descent, causing the face and eyes to be forced into the collapsing mask. This can produce facial bruising, conjunctival injection or hemorrhage, changes in vision, and, rarely, retrobulbar hemorrhage. The latter could be a true ophthalmologic emergency. A tooth squeeze occurs when air spaces inside a tooth—due to decay, a filling, or an abscess—become compressed during descent. A dry-suit squeeze occurs when suit folds are compressed into the underlying skin, producing local trauma manifested by painful red streaks.

The clinical conditions of barotrauma of ascent are alternobaric vertigo, pulmonary barotrauma, arterial gas embolism, and decompression sickness (Table 214-1).

ALTERNOBARIC VERTIGO

During ascent, the physics of gas in air-containing organs is, of course, opposite that of descent—that is, air will expand as the pressure decreases. Air will flow through the ostia of the sinuses, and the expanding air in the middle ear will open the Eustachian tube (much like during takeoff in an airplane). Should air be trapped temporarily in one middle ear cavity, the pressure differential may cause unequal vestibular impulses to the brain, resulting in vertigo (alternobaric vertigo). This is usually transient and generally requires no specific treatment.

PULMONARY BAROTRAUMA

Air also expands within the lungs with ascent. If a diver breathing compressed air ascends with a closed glottis (holds breath, coughs, vomits), most frequently seen in a rapid, panicked, out-of-air ascent, the expanding air may cause parenchymal lung injury. This can occur even in shallow water (e.g., a swimming pool). Pulmonary barotrauma, also called pulmonary overinflation or burst lung syndrome, can lead to pneumomediastinum. This generally only requires symptomatic treatment and may be subtle on the chest radiograph.³

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