With the advent of “extreme sports” that involve water contact, sport diving, and the increasing number of people engaging in breath-hold diving, a sharp increase in diving injuries has been seen in EDs (Box 133.2). Deaths from breath-hold diving alone have almost doubled in the last 5 years, thus illustrating the potential for injury associated with this form of diving.¹ With acute DCI, rapid assessment and treatment are the foundation of management. Three keys to successful ED treatment are having a high index of suspicion (DCI may have nonspecific findings), performing a thorough neurologic examination, and obtaining hyperbaric medicine consultation when DCI is suspected.

Box 133.2

Fatality Statistics for Diving

Deaths: 120 diving fatalities in the United States and Canada (2007)

Death analyses: men (85%); median age 50 years (men) and 43 years (women)

Obesity: 76% of deaths involved overweight or obese divers

Causes of death: drowning (86%); acute heart condition (9%); arterial gas embolism (3%); decompression sickness (1%)

Activities: 66% of deaths during pleasure of sight-seeing diving

Data from Divers Alert Network. DAN report on decompression illness, diving fatalities and project dive exploration, 2008. Available at www.diversalertnetwork.org/.

Pathophysiology

Dysbarism refers to the effects of variations in ambient (surrounding) pressure on the body. Hypobaric (low-pressure) exposure, such as that experienced by climbers, pilots, and astronauts, can result in symptoms and injuries similar to those found in divers with DCI who are exposed to high pressure while at depth. Decompression injuries during high-pressure (hyperbaric) exposure are far more common.

Diving Physiology

Evaluation of a diver with a water-associated injury requires a basic understanding of diving physiology and the physics of pressure and gases. Different gases have different properties at different depths, which allows gases to be used alone or in combination for different types of diving. The gases of most interest are air, oxygen, nitrogen, helium, and occasionally argon. Deep diving (past 180 feet of sea water [fsw]) often requires helium-oxygen combinations (heliox) to mitigate the effects of nitrogen narcosis (discussed later). Moreover, enriched nitrogen-oxygen combinations (nitrox) may be used to reduce obligations for decompression stops, which is the time spent at more shallow depths to help divers offload the nitrogen built up in the body before exiting a dive.

In general, most recreational divers breathe compressed air and use a self-contained underwater breathing apparatus (SCUBA) when diving to depths of less than 135 fsw. Nitrogen represents about 78% of the gas inhaled with compressed air diving. During diving, hydrostatic pressure “pushes” nitrogen into tissues; nitrogen (an inert gas) then becomes dissolved in plasma and permeates tissues. While at depth, gases remain in solution, and most divers experience minimal difficulty. The deeper that divers travel and the longer that they remain at depth, the more saturated the blood and tissues become with nitrogen (or other inspired inert gases). One of the tenets of diving is to ascend slowly when resurfacing. Doing so allows the dissolved (inert) gases to escape the tissues slowly and be cleared via normal respiration. If a person ascends to the surface too quickly, the dissolved gases come out of solution and form bubbles in tissues or within the vasculature. When these bubbles are not cleared by the lungs (“blown off”) they can embolize and cause downstream injury or they can cause local damage at the site of formation (autochthonous bubbles). When bubbles cause symptoms, the disorder is called DCI. Depending on the size, number, and location of the bubbles, DCI has a wide range of manifestations, from pain (most common symptom), numbness, and fatigue to severe neurologic symptoms such as seizure, paralysis, and loss of consciousness (LOC).

Bubble Physiology

Knowledge of bubble mechanics and the effects of bubbles in various tissues is critical to understanding the pathophysiology and treatment of DCI. Venous bubbles are not usually problematic because the lungs can filter large gas loads. Bubbles have damaging effects when they remain within tissues or embolize. Bubbles can pass from the venous circulation to the arterial circulation via a right-to-left shunt (patent foramen ovale or arteriovenous malformation). Bubbles can grow from “nucleation sites” within body tissues, such as the joint spaces, tendon sheaths, periarticular sheaths, and peripheral nerves.² Once inside these areas, bubbles can act as emboli and block perfusion of distal tissues or act as foreign bodies with resultant vascular damage through activation of the inflammatory and clotting cascades. Interestingly, scientists are now evaluating a possible biologic marker of DCI. As gas emboli within the circulation induce decompression stress, endothelial cells release microparticles in response to cellular activation or cell death. These microparticles may, in the future, reflect a biologic marker of decompression stress that can be used to gauge the extent of disease, efficacy of treatment, or prophylaxis.³

Principles of Gas Laws and Dysbarism

An understanding of the pertinent diving gas laws, units of measurement, abbreviations, and mathematic conversions helps facilitate the treatment and disposition of dive-injured patients. At sea level, the pressure of the atmosphere on the body (ambient pressure) is 760 mm Hg, which equals 1 atm. The term for the absolute pressure on a diver at sea level is called atmospheres absolute (ATA), and it represents the total sum of the pressure on a diver. Therefore, at sea level, a dive computer gauge reads zero, but sea level also represents one surrounding atmosphere of pressure (1 ATA). This knowledge helps the physician better comprehend the circumstances surrounding a dive injury. Although there are a large number of gas laws, the two that are the most important in diving medicine are Boyle’s law and Dalton’s law.

Boyle’s Law

Boyle’s law aids in understanding why a diver needs to exhale while ascending from depth. According to Boyle’s law, the volume of a quantity of gas (V) varies inversely with the pressure on that gas (P) if it is kept at a constant temperature. It is often represented by the following formula:

where the subscripts 1 and 2 indicate two different combinations of pressure and volume; in other words, the product of pressure and volume will always remain a constant.

Usually, as a diver descends deeper, the surrounding pressure increases in linear fashion. Water pressure at the surface is referenced as 1 ATA. In general, for every 33 fsw that the diver descends, there is an increase in pressure of 1 ATA. Therefore, a descent to 33 fsw would equal 2 ATA, a descent to 66 fsw would equal 3 ATA, and so on. Furthermore, for the first 33 fsw descended, the volume of gas present is reduced by half the original amount of gas at the surface. At 66 fsw, the volume is one third the original volume. The greatest changes in volume occur closest to the water surface and represent a significant vulnerability to injury (Fig. 133.1).

Fig. 133.1 Boyle’s law.

ATA, Atmospheres absolute.

Dalton’s Law

Dalton’s law of partial pressures is critical to understanding the mechanisms for DCS, nitrogen narcosis, and oxygen toxicity. It is represented by the formula

where P_total is the total pressure of the gases that a diver breathes and the subscripts 1, 2, and 3 indicate the partial pressure of each individual gas. This law explains why the effects of the individual gases increase as a diver travels deeper during a dive. Put simply, as a diver descends, the amount of each gas inhaled increases proportionally with increasing depth. When diving with air tanks, divers are exposed to higher partial pressures of both oxygen and nitrogen the farther down that they travel. Importantly, nitrogen at high concentrations has a narcotic effect (nitrogen narcosis), and oxygen at high concentrations can be toxic (oxygen toxicity). Both problems are described in further detail later in the chapter.

Presenting Signs and Symptoms

Barotrauma

Barotrauma is sustained from failure to equalize the pressure of an air-containing space with that of the surrounding environment. The most common examples of barotrauma occur during air travel and scuba diving.^1,⁴ Barotrauma occurs only in gas-containing (compressible) body spaces. More than 95% of the body is composed of water (incompressible). Typical gas-filled spaces include the sinuses, middle and inner ears, air-filled areas within carious or filled teeth, and hollow viscous organs such as the intestines and lungs. Barotrauma incurred during descent is called a “squeeze.” Barotrauma incurred during ascent is called a “reverse squeeze,” “reverse block,” or expansion injury.

Differential Diagnosis and Medical Decision Making

Table 133.1 lists the differential diagnosis for dive injuries based on the time of onset of symptoms.

Table 133.1 Differential Diagnosis of Dive Injuries Based on the Onset of Symptoms

SYMPTOM ONSET	INJURIES TO CONSIDER
Descent	Ear or sinus barotrauma Inner ear barotrauma
Bottom	Nitrogen narcosis Oxygen toxicity Trauma
Ascent	Arterial gas embolism Pneumothorax Pneumomediastinum Subcutaneous emphysema Severe decompression sickness Ear or sinus barotrauma Barodontalgia Gastrointestinal barotrauma Trauma Alternobaric vertigo Alternobaric facial palsy
15 min after resurfacing	Arterial gas embolism
15 min to 24 hr after resurfacing	Decompression sickness

Ear Barotrauma

With an intact tympanic membrane (TM), the only communication for equilibration of pressure between the middle ear and the ambient atmosphere is through the eustachian tube (ET).⁵ Divers typically perform Valsalva maneuvers during decent to equalize pressure in the middle ear. Failure to equalize leads to pain and damage from injury to the middle or inner ear and results in TM edema, rupture, or hemorrhage, as well as rupture of the oval or round window (may lead to a perilymphatic fistula).⁵ Table 133.2 summarizes the types of ear barotrauma.

Table 133.2 Barotrauma of the Ear