The pressure-related diving syndromes can be divided into problems caused by the mechanical effects of pressure (i.e., barotrauma) and problems caused by breathing gases at elevated partial pressures (i.e., gas toxicities and decompression sickness [DCS]).
Barotrauma is the most common affliction of divers. It is defined as tissue damage resulting from contraction or expansion of gas spaces that occurs when the gas pressure in the body, or its compartments, is not equal to ambient pressure. For purposes of discussion, barotrauma can be viewed according to whether it occurs during descent or ascent.
BAROTRAUMA OF DESCENT Barotrauma of descent, or "squeeze," as it is known in common diving parlance, results from the compression of gas in enclosed spaces as ambient pressure increases with underwater descent. Gas pressure in the various air-filled spaces of the body is normally in equilibrium with the environment; however, if something obstructs the portals of gas exchange, pressure equalization is precluded. If the air-filled space is not collapsible, the resulting pressure imbalance will cause tissue distortion, vascular engorgement and mucosal edema, hemorrhage, and other tissue damage. The ears and paranasal sinuses are most likely to be affected by such a process.
Aural barotrauma is the most common type of barotrauma and is a major cause of morbidity among divers, experienced by essentially all divers at one time or another. There are three main types of aural barotrauma, depending on which part of the ear is affected, and they may occur singly or in combination.
The first type involves the external auditory canal and is generally referred to as external ear squeeze, or barotitis externa. The external ear canal normally communicates with the environment and, consequently, the air in the canal is replaced by water when a diver is submerged. However, if the external ear canal is occluded (e.g., by cerumen, foreign bodies, exostoses, or earplugs), water entry is prevented, and compression of the enclosed air with descent will have to be compensated for by tissue collapse, outward bulging of the tympanic membrane, or hemorrhage. This is typically manifested by pain or bloody otorrhea. Physical examination may reveal petechiae or blood-filled cutaneous blebs along the canal, along with erythema or rupture of the tympanic membrane. Treatment involves keeping the canal dry, prohibiting swimming or diving until healed, and, in special cases, taking antibiotics and analgesics.
The next, and by far the most common, type of aural barotrauma is middle ear squeeze, or barotitis media. This results from a failure to equalize the middle ear and environmental pressures because of occlusion or dysfunction of the eustachian tube.
The eustachian tubes normally open and allow equalization of middle ear pressure when the pressure difference between the middle ear and pharynx reaches about 20 mmHg. This can be facilitated by yawning, swallowing, or using various autoinflation techniques (e.g., the Valsalva or Frenzel maneuvers). If middle ear pressure equalization is not achieved, the diver will notice discomfort or pain when the pressure differential reaches 100 to 150 mmHg or, roughly, when there has been a 20 percent reduction in middle ear gas volume. As the pressure differential is increased, mucosal engorgement and edema, hemorrhage, and inward bulging of the tympanic membrane develop. Eventually, these will be inadequate to compensate for the gas volume contraction, and the tympanic membrane ruptures. Fortunately, this is uncommon.
A number of factors may cause eustachian tube blockage or dysfunction—mucosal congestion secondary to upper respiratory infection, allergies, or smoking; mucosal polyps; excessively vigorous autoinflation maneuvers; and previous maxillofacial trauma. Persons with such conditions are at increased risk of middle ear barotrauma.
Divers having a middle ear squeeze usually complain of ear fullness or pain. As would be expected from the way that pressure changes with depth ( Table 19.2.-4), most problems occur near the surface. The pain is substantial and usually causes the diver to abort the dive. If not, it will continue to worsen until the eardrum ruptures, at which time the diver may feel air bubbles escaping from the ear and experience disorientation, nausea, and vertigo secondary to the caloric stimulation of cold water entering the middle ear. This sequence has been responsible for cases of panic and near drowning.
The otoscopic appearance of the tympanic membrane in cases of middle ear squeeze varies according to the severity of the injury and can be graded according to the amount of hemorrhage in the eardrum, with grades running from 0 (symptoms only) to 5 (gross hemorrhage and rupture). Physical examination may also disclose blood around the nose or mouth and a mild conductive hearing loss, which is usually only temporary.
Treatment of middle ear squeeze involves abstinence from diving until the condition has resolved and use of decongestants, which may be combined with antihistamines if there is an allergic component to the eustachian tube dysfunction. A combination of oral and long-acting spray decongestants is usually most efficacious. Antibiotics should be used when there is a tympanic membrane rupture or a preexisting infection. No diving should be done until a perforated eardrum has healed. Oral analgesics or topical aural anesthetics may be needed for a couple of days. In general, eardrops should not be used when there is a tympanic membrane perforation. Ideally, an audiogram should be obtained in anyone having more than a trivial middle ear squeeze, and serial audiograms should be obtained in patients having hearing loss. Most middle ear squeezes will resolve without complication in three to seven days. Prevention is preferable; a diver should refrain from diving when unable to easily equalize pressure in the ears and should always heed warning signs of ear pain.
Although less common, the third type of aural barotrauma, inner ear barotrauma, is much more serious than middle ear barotrauma because of possible permanently disabling injury to the cochleovestibular system. Inner ear barotrauma typically results from the sudden or rapid development of markedly different pressures between the middle and inner ear, such as may occur as a result of an overly forceful Valsalva maneuver intended to equalize the pressure in the middle ear or an exceptionally rapid descent during which the middle ear pressure is not equalized.
Patients with inner ear barotrauma typically are quite symptomatic, having a feeling of fullness or "blockage" of the affected ear, nausea, vomiting, nystagmus, diaphoresis, disorientation, or ataxia. The classic triad of symptoms indicating inner ear barotrauma is tinnitus, vertigo, and deafness. The onset of these symptoms may occur soon after the injury or may be delayed many hours, depending on the specific type of inner ear injury and the diver's activities during and after the dive. Findings on physical examination may be normal or may reveal signs of middle ear barotrauma or vestibular dysfunction, and audiometry may demonstrate a mild to severe sensorineural hearing loss. Any scuba diver with a hearing loss or vestibular symptoms following a nondecompression dive should be considered to have inner ear barotrauma until shown otherwise.
Clinically, there appear to be four categories or mechanisms for these injuries: hemorrhage within the inner ear (especially in the basal turn of the cochlea); rupture of Reissner's membrane, resulting in the mixing of endolymph and perilymph; fistulation of the round or oval window; and a mixed injury involving a combination of any or all of the other three. Injury to the membranous labyrinth may be either implosive or explosive.
Hemorrhage within the inner ear usually is associated with findings of middle ear barotrauma, no (or transient) vestibular symptoms, and a diffuse mild to severe sensorineural hearing loss (SNHL). Treatment of these patients should consist of bed rest with head elevated, avoidance of strain or strenuous activities, and symptomatic measures, as needed. The potential for full recovery is excellent, with the hearing loss usually completely resolved in three weeks to three months.
Manifestations of a tear in Reissner's membrane are similar to those of inner ear hemorrhage, although a persistent localized SNHL remains commensurate with the area of membrane tear. Treatment is similar to that of inner ear hemorrhage.
Inner ear fistulas typically present with a mild high-frequency SNHL or a marked cochleovestibular deficit and no or little evidence of middle ear barotrauma. Initially, these should be treated with bedrest, avoidance of strain, and other symptomatic measures, as needed. Worsening of hearing or vestibular symptoms or persistence of significant vestibular symptoms after a few days indicates the need for surgical exploration and repair. Some authorities, however, recommend immediate tympanotomy if severe symptoms are present initially. Importantly, recompression is contraindicated unless DCS or air embolism is also suspected to be present.
Any of the paranasal sinuses may fail to equalize pressure during descent. Manifestations of sinus squeeze include a sensation of fullness or pressure in the affected sinus, pain, or hemorrhage. Predisposing conditions for barosinusitis include upper respiratory infections, sinusitis, nasal polyps, or anything else that impairs the free flow of air from sinus cavity to nose. The maxillary and frontal sinuses are most often affected. Treatment for sinus squeeze is much the same as for middle ear squeeze, although antibiotics are usually indicated in cases involving the frontal sinuses.
Squeeze can also affect any other gas space that does not equilibrate with ambient pressure. For example, conjunctival, scleral, and periorbital hemorrhage may result if the diver fails to exhale into the mask during descent, resulting in telltale erythema, ecchymosis, and petechiae of the part of the face enclosed by the face mask—"face mask squeeze." If an area of skin is tightly enclosed by a dry diving suit a "suit squeeze" may occur. Although the appearance of these injuries may be spectacular, no special treatment is required, and they usually resolve in a few days.
Another special kind of squeeze may occur in divers who, while holding their breath, descend below the depth at which their total lung volume is reduced to less than residual volume. As occurs in other types of barotrauma of descent, the underventilated lung air spaces fill with tissue fluids and blood in an attempt to relieve the negative pressure. Clinical manifestations include chest pain, cough, hemoptysis, dyspnea, and pulmonary edema. Treatment includes administration of 100% oxygen, fluid replacement, and other supportive measures as clinically indicated. Because of the intrinsic lung injury and consequent potential for gas embolism, positive-pressure breathing (e.g., positive end-expiratory pressure or continuous positive airway pressure) should be avoided if possible. Very few divers attempt to free dive to depths likely to cause lung squeeze, and it is rare.
BAROTRAUMA OF ASCENT If there has been adequate equilibration of the pressure in the body's air-filled spaces during descent, the gas in those spaces will expand according to Boyle's law as ambient pressure decreases with ascent. The resulting excess gas is normally vented to the atmosphere. However, if this is prevented by obstruction of the air passages, the expanding gases will distend the tissues surrounding them; the resulting damage is known as barotrauma of ascent and is the reverse process of squeeze.
Although the ears and sinuses may be affected by barotrauma of ascent, this is unusual, because impediment of air egress is highly unlikely if pressure equalization is achieved with descent. However, middle ear and sinus barotrauma of ascent, or reverse squeeze, can occur, especially in divers having upper respiratory congestion treated with a short-acting nasal spray whose vasoconstrictive effect wears off while the diver is submerged. Similarly, alternobaric vertigo (ABV) resulting from unequal vestibular stimulation due to asymmetric middle ear pressure may occur during ascent. Although usually only transient, ABV may be severe enough to cause panic. Rarely, it may last for several hours, or even a day or two, after a dive.
Three other types of barotrauma of ascent should be discussed. The first may occur with either ascent or descent, although more commonly with ascent, and is known as barodontalgia, or, less accurately, "tooth squeeze." Several specific conditions are associated with this problem (e.g., pulp decay, peridontal infections, or recent extraction sockets or fillings), but it may be due to anything that causes a pressure disequilibrium in an air-filled space in or about a tooth. Although rare and usually self-limited, anyone presenting with a toothache after diving should be referred for dental evaluation after maxillary sinus squeeze has been excluded.
Another unusual type of barotrauma of ascent is gastrointestinal (GI) barotrauma, which is also known as aerogastralgia, or "gas in the gut." This occurs most commonly in novice scuba divers, who are more prone to aerophagia, and is caused by expansion of intraluminal bowel gas as ambient pressure is decreased during ascent. Other predisposing conditions include repeated performance of the Valsalva maneuver in the head-down position (which forces air into the stomach), drinking carbonated beverages or eating a heavy meal before diving (especially one containing legumes or other flatogenic substances), or chewing gum while diving. Symptoms of gastrointestinal barotrauma include abdominal fullness, colicky abdominal pain, belching, and flatulence. It is rarely severe because most divers will readily vent any excess bowel gas during ascent; however, it has been know to cause syncope and shocklike states. Actual gastric rupture from GI barotrauma has occurred, but this is exceedingly rare.
The last and most serious type of barotrauma of ascent is pulmonary barotrauma (PBT). Several different injuries can result from PBT of ascent, and these are collectively referred to as the pulmonary overpressurization syndrome (POPS) or "burst lung" ( Table 192-5).
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