Christian A. Tomaszewski
EPIDEMIOLOGY
Dysbarism is commonly encountered in scuba divers and refers to complications associated with changes in environmental ambient pressure while breathing compressed gases.
To understand diving injuries, one must be familiar with the three gas laws: Boyle’s, Dalton’s, and Henry’s.
Boyle’s law states that pressure and volume are inversely related. Therefore, if air-filled spaces that are fixed in size are not equilibrated during descent or ascent, barotrauma can ensue.
Dalton’s law states that the total pressure exerted by a mixture of gases is the sum of the partial pressures of each gas. This helps explains the uptake of inert gas into tissue with depth.
Henry’s law states that, at equilibrium, the quantity of gas in solution is proportional to the partial pressure ofthat gas. This, along with Dalton’s law, explains the release of inert gas, that is, nitrogen, from tissue with ascent.
Divers using compressed air, caisson (tunnel) workers, and high-altitude pilots can all present with decompression sickness (DCS). In divers, this usually results from exceeding the dive table limits for depth and time.
Sport divers are more prone to DCS of the spinal cord, while professional divers, caisson workers, and aviators tend more often to DCS of the joints.
DCS can occur within minutes to hours of surfacing, rarely days later. It may be precipitated by flying within 24 hours of diving.
PATHOPHYSIOLOGY
Barotrauma of descent includes squeezes of the ears, face, and teeth along with inner ear and sinus baro-traumas (Table 125-1).
Gas-filled areas are subjected to decreases in volume with descent. If such areas are not equilibrated, for example, by Valsalva maneuver for the middle ear, a “squeeze” can result with pain and injury to surrounding structures, that is, tympanic membrane.
Barotrauma during ascent is due to expansion of gas in body cavities.
Clinical conditions associated with ascent include alternobaric vertigo, pulmonary barotrauma, cerebral arterial gas embolism, and DCS (Table 125-1).
DCS is due to release of inert gas (nitrogen) within tissues or the circulation. This usually occurs from saturated tissue during or immediately after ascent. In extreme amounts, these bubbles can cause both acute occlusive and delayed inflammatory effects.
Spinal cord DCS, a form of type II DCS, occurs when autochthonous bubbles form in situ in various sites throughout the cord. Therefore, there may not be a distinct spinal cord syndrome and patients can present with ascending paralysis or spotty deficits with autonomic dysfunction, including incontinence or retention.
TABLE 125-1 Summary of Barotrauma of Descent and Ascent
CLINICAL FEATURES
BAROTRAUMA OF DESCENT (SEE TABLE 125-1)
The most common form of barotrauma occurs during descent and is middle ear squeeze, or barotitis media. It is caused by inability to equalize pressure causing tympanic membrane bleeding or rupture and may result in conductive hearing loss.
A forceful Valsalva during equalization can cause inner ear barotrauma with rupture of the round or oval window. Symptoms include tinnitus, sensorineural hearing loss, and vertigo.
If the sinus ostia are occluded on descent, an impending squeeze can cause bleeding from the maxillary or frontal sinuses, resulting in pain and epistaxis.
Other gas-filled areas can be subjected to squeeze with descent. Facial bruising and subconjunctival hemorrhages may result when air is not added to a face mask. A dry-suit squeeze can result when folds compress down on underlying skin producing painful red skin lines.
BAROTRAUMA OF ASCENT (SEE TABLE 125-1)
In the middle ear, the pressure differential from asymmetrical expansion can cause alternobaric vertigo. This is a temporary condition due to unequal pressure between both vestibular complexes.
Although rare, “reverse squeeze” may affect the ear or sinuses during ascent with rupture.
Pulmonary overinflation or burst lung can occur during rapid, panicked ascents if divers fail to exhale or if intrinsic pulmonary air trapping exists (eg, COPD). This may be manifested by pneumomediastinum, subcutaneous emphysema, or pneumothorax.
The most serious consequence of pulmonary over-inflation is cerebral arterial gas embolism (CAGE). Air transgresses into the pulmonary venous circulation, thereby embolizing to the brain. Any neurologic symptoms that occur on ascent or immediately upon surfacing should be considered secondary to CAGE. Such symptoms may include loss of consciousness, seizure, blindness, disorientation, hemiplegia, or other signs of stroke.
DECOMPRESSION SICKNESS (SEE TABLE 125-2)
DCS presents as one of two types. Type I is “pain only,” and type II is more “serious.”
Type I DCS includes mottled skin (“cutis marmorata”) or deep pain of the joints, usually the shoulder or knee, that is unaffected by movement.
Type II DCS is primarily associated with the central nervous system, typically the spine. Patients may initially complain of truncal constriction with ascending paralysis. Prolonged exposure at depth can also lead to cardiopulmonary “chokes” or vestibular “staggers.” In chokes, massive numbers of pulmonary artery bubbles can cause cough, hemoptysis, dyspnea, and substernal chest pain. Staggers, from vestibular DCS, is manifested by vertigo, hearing loss, tinnitus, and disequilibrium.
A third type of DCS has been described (Table 125-2). It occurs when arterial gas embolism promotes release of tissue gas and can have features of cerebral arterial gas embolism.
Because DCS and CAGE can be difficult to distinguish, or present simultaneously, the inclusive term “decompression illness (DCI)” is often typically used.
TABLE 125-2 Classification of Decompression Sickness
DIAGNOSIS AND DIFFERENTIAL
Dive profile (depth, duration, and repetitiveness) and time of symptom onset are the most useful historical factors in distinguishing dysbarism from other disorders.
During descent, the most common maladies are the squeezes. A fistula test, insufflation of the tympanic membrane on the affected side causing the eyes to deviate to the contralateral side, may help diagnose inner ear barotrauma.
During ascent, barotrauma or alternobaric vertigo is most likely to occur. A chest radiograph may reveal pneumomediastinum, pneumothorax, or subcutaneous air after pulmonary overinflation. If accompanied by early neurological symptoms, CAGE should be considered.
The differential diagnosis for DCS is broad. Musculoskeletal complaints could be joint strain or symptomatic herniated cervical disk. Chest pain may represent cardiac ischemia from overexertion. Immersion pulmonary edema from non-cardiogenic causes can occur during strenuous dives, particularly in cold water. Seizures at depth can result from breathing-enriched mixtures of oxygen exceeding 1.4 atmospheres absolute.
If DCS is suspected, a trial of pressure with hyper-baric oxygen usually results in some improvement.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Both middle ear and sinus barotrauma can be treated with decongestants and analgesics (Table 125-1). One can consider antibiotics. Advise patients against diving until healing is completed, especially for tympanic trauma. The patient should be able to equalize pressures within the ears effectively in order to return to diving.
Inner ear barotrauma requires bed rest with the head upright until otolaryngologic evaluation for possible surgical exploration.
Alternobaric vertigo requires no specific treatment because of its transient nature.
All cases of DCI, both DCS and CAGE, deserve immediate 100% oxygen and IV fluids.
If CAGE is suspected, place the patient in the supine position, not Trendelenburg. If vomiting occurs, readjust to the left lateral decubitus position to prevent aspiration.
In all cases of DCI, particularly if serious, rapidly arrange for recompression therapy (hyperbaric oxygen). Hyperbaric oxygen therapy can decrease bubble size, increase nitrogen washout, decrease tissue edema and ischemia, and prevent neutrophil adherence with inflammation. Divers Alert Network (1-919-684-8111) may help provide chamber locations.
Lidocaine 1 milligram/kg IV bolus followed by a continuous infusion at 1 milligram/min may provide neuroprotection, especially in cases of CAGE.
Pulmonary overinflation with ascent may require needle decompression or tube thoracostomy if a pneumothorax develops.
SPECIAL CONSIDERATIONS
Immersion pulmonary edema can occur during strenuous diving, particularly in cold water. Clinical features include dyspnea, chest pain, and frothy pink sputum, with pulmonary edema on radiography. Although a cardiac evaluation may be warranted, this condition is usually not associated with any abnormality and does not require treatment beyond symptomatic care.
Nitrogen narcosis occurs when breathing air at depths greater than 100 ft of seawater. High-order mental function and motor skills are temporarily disabled. This effect resolves with ascent or breathing of alternate gas mixtures.
Oxygen toxicity can affect the pulmonary and/or cerebral systems. Pulmonary oxygen toxicity is unusual in diving because prolonged exposures are required. But cerebral oxygen toxicity can occur with partial pressures of oxygen just exceeding 1.4 ATA. Manifestations of this include twitching, nausea, par-esthesias, dizziness, and even seizures. Although rare, cerebral oxygen toxicity can occur in divers breathing enhanced oxygen concentrations or patients during hyperbaric oxygen therapy sessions.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 208, “Dysbarism and Complications of Diving,” by Brain Snyder and Tom Neuman.