Scuba Diving and Dysbarism

Published on 20/05/2015 by admin

Filed under Emergency Medicine

Last modified 20/05/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 2.5 (2 votes)

This article have been viewed 5282 times

Chapter 143

Scuba Diving and Dysbarism

Perspective

Underwater free diving to salvage wrecks and to harvest seafood, sponges, coral, and mother-of-pearl has been practiced for more than 5000 years.1 Historically, divers also used breathing tubes, such as hollow reeds; however, it is nearly impossible to use these at depths of more than 3 feet because of the restriction of inspiration by underwater pressure. Subsequent inventions from the 16th to the 19th centuries, including diving dresses, allowed divers to remain underwater for prolonged periods at depths of up to 12 fathoms (72 feet).2 The first diving dress (1715) was a reinforced, leather-covered barrel with watertight armholes and a viewing porthole.2

With the advent of these technologies, the symptoms of diving-related illness began to be recognized. Colonel William Pasley, the officer in charge of a unit of the British Royal Engineers that salvaged the sunken warship HMS Royal George in 1840, observed symptoms in his divers.3 At approximately the same time, similar symptoms and even fatalities were observed among caisson workers.* The ailment became known as caisson disease, but the construction workers on the Brooklyn Bridge (built from 1870 to 1883) attached the name “the bends,” characterizing the symptoms that often caused the victim to bend forward in pain.3 The first clinical description of caisson disease was by Paul Bert in 1878.3 He correctly attributed the disease to nitrogen gas coming out of solution in the tissues during decompression. This led to the recommendation of slow ascents for pressurized workers and the development of the first recompression chambers.

The significant breakthrough allowing diving at depth was the invention of the aqua-lung by Jacques-Yves Cousteau and Emile Gagnan in 1943.2 The lighter and less expensive equipment, widely known by its acronym SCUBA (self-contained underwater breathing apparatus), does not require a surface supply of air or the support personnel that are necessary for helmet diving. This innovation allowed widespread deep-sea diving, and millions of divers have become certified to date.

Most amateur divers use compressed air, open-circuit scuba equipment at depths of less than 130 feet of seawater (fsw). Systems with artificial mixtures of various gases, however, are used to extend the depths to which divers can descend. Some of these are used in sport diving, but their use is uncommon and is primarily limited to commercial applications (Table 143-1).

Other variations of supplying air for divers are closed-circuit and semiclosed-circuit diving apparati (“rebreathers”) that use calcium hydroxide to absorb expired carbon dioxide. Oxygen is then added to the decarboxylated gas before rebreathing. The advantages of rebreathers over compressed air scuba are that they are more efficient (less gas is used for a given time), allow deeper dives and longer bottom times, and generate few if any bubbles.

The total number of diving-related injuries is unknown, but the absolute numbers of patients with decompression-related illnesses, one of the most serious dive-related injuries, continue to climb as the number of divers has increased despite the rate per 10,000 dives remaining relatively constant since 2001.4 This rate varies somewhat on the basis of the type of diver: 0.015% for scientific divers, 0.01 to 0.019% for recreational divers, 0.030% for U.S. Navy divers, and 0.095% for commercial divers.5 The rate of mortality in diving varies between 1.5 and 9 per 100,000 dives. With the popularity of diving and the relative ease of rapid travel from distant destinations, it behooves even the land-locked emergency physician to be aware of diving-related illnesses.

Principles of Disease

Scuba divers may encounter emergencies common to environmental exposures (e.g., hypothermia, sunburn, and physical trauma) or aquatic activities (e.g., submersion accidents, motion sickness, and marine envenomations), but they are also subject to the unique injuries related to dysbarisms and barotrauma. The pathophysiologic mechanism of these conditions primarily results from volume-pressure changes within the air-filled cavities of the body or from increased dissolution of gases, particularly nitrogen, in body tissues.

Atmospheric pressure varies with altitude and weather patterns, but 760 mm Hg (14.7 psi or 1 atm) is the standard used at sea level. Water is far denser than air. A mountain climber would need to ascend to 18,000 feet to reduce atmospheric pressure by 50% from sea level, but a diver needs to descend only 33 feet in seawater (34 feet in fresh water) to double the atmospheric pressure, an increase of 23 mm Hg per foot of depth.

To understand the pathophysiologic processes of dysbarisms and barotrauma, one should be familiar with several of the laws of physics that define the behavior of liquids and gases (Table 143-2; Figs. 143-1 to 143-5). The human body is composed mostly of water and behaves like a liquid subject to Pascal’s law, which states that a pressure applied to any part of a liquid is transmitted equally throughout. Pressure changes, however, do alter the volume within the air-filled spaces of the body, including the lungs, bowel, sinuses, and middle ear, according to Boyle’s law. This law states that at constant temperature, the absolute pressure and the volume of gas are inversely proportional (PV = k). In other words, as pressure increases (with descent), the gas volume is reduced; as the pressure is reduced (with ascent), the gas volume increases.

Table 143-2

Laws of Physics

GAS LAW FORMULA SIGNIFICANCE
Pascal’s law: A pressure applied to any part of a liquid is transmitted equally throughout. ΔP = ρg (Δh)
ΔP is the hydrostatic pressure.
ρ is the fluid density.
g is acceleration due to gravity.
Δh is the height of fluid.		 Pressure increases in a contained space are transmitted throughout; significant for inner ear barotrauma and middle ear barotrauma (see Fig. 143-1)
Boyle’s law: At a constant temperature, the absolute pressure and the volume of gas are inversely proportional. As pressure increases, the gas volume is reduced; as the pressure is reduced, the gas volume increases. P1 • V1 = P2 • V2 Relates to change in the volume of a gas caused by the change in pressure due to depth, which defines the relationship of pressure and volume in breathing gas supplies (see Fig. 143-2)
Charles’ law: At a constant pressure, the volume of a gas is directly proportional to the change in the absolute temperature. V1/T1 = V2/T2 Increasing pressure (filling a scuba tank) causes heat; cooling a tank decreases the pressure (see Fig. 143-3)
The general gas law combines these concepts to predict the behavior of a gas when the factors change. P1 • V1/T1 = P2 • V2/T2
P1 is the initial pressure.
V1 is the initial volume.
T1 is the initial temperature.
P2 is the final pressure.
V2 is the final volume.
T2 is the final temperature.		 A means of relating pressure, volume, and temperature together in one equation when variables are not constant
Dalton’s law: The total pressure exerted by a mixture of gases is equal to the sum of the pressures (partial pressures) of each of the different gases making up the mixture, with each gas acting as if it alone is present and occupies the total volume. PTotal 3 P1 + P2 + P3 + … + Pn Nitrogen under pressure acts as if other gases are not present (see Fig. 143-4)
Henry’s law: The amount of a gas that will dissolve in a liquid at a given temperature is directly proportional to the partial pressure of that gas. ep = ekc
e is approximately 2.7182818 (the base of the natural logarithm).
p is the partial pressure of the solute above the solution.
c is the concentration of the solute in the solution.
k is the Henry’s law constant.		 More nitrogen is taken into solution (e.g., serum) at high pressures than comes out of solution at lower pressures (see Fig. 143-5)

Temperature also affects the pressure and volume of a gas as described by Charles’ law. At a constant pressure, the volume of a gas is directly proportional to the change in the absolute temperature (V1/T1 = V2/T2). Thus with heat the volume increases, and with cold the volume decreases. The general gas law (P1 • V1/T1 = P2 • V2/T2) combines Boyle’s and Charles’ laws to predict the behavior of a given quantity of gas when any of these factors change.

Barotrauma results when a diver is unable to equalize the pressure within air-filled structures to the ambient pressure of the environment during ascent or descent. The fractional changes in volume are greater near the surface. Thus the greatest risk for barotrauma is in shallow water, where the proportional pressure changes are also the greatest.

Dalton’s law states that the total pressure exerted by a mixture of gases is equal to the sum of the pressures (partial pressures) of the individual gases making up the mixture, with each gas acting as if it alone is present and occupies the total volume (Ptotal = P1 + P2 + P3 + … + Pn). Henry’s law states that the amount of any gas that dissolves in a liquid at a given temperature is directly proportional to the partial pressure of that gas. At higher ambient pressures, the concentration of each component of air in solution with blood and tissues increases until a new steady-state concentration is achieved.

The gases in a diver’s breathing mixture are dissolved into the body in proportion to the partial pressure of each gas in the mixture. The length of time the diver is breathing the gas at the increased pressure and the inherent solubility of the gas also govern the quantity of a particular gas that dissolves. The dissolved gas remains in solution as long as the pressure is maintained. As the diver ascends, however, increasingly more of the dissolved gas comes out of solution. A rapid ascent may reduce the pressure at a rate higher than the body can accommodate, and the bubbles (particularly nitrogen) may accumulate and disrupt body tissues and systems, a phenomenon termed decompression sickness (DCS). This is similar to the way that rapid opening of a bottle of soda allows bubbles of carbon dioxide to come out of solution rapidly.

If the ascent rate is controlled (i.e., through the use of the safe decompression tables or submersible dive computers), the gas is carried to the lung vascular bed and is exhaled before it accumulates to form significantly large or numerous bubbles in the tissues, similar to how opening of a soda bottle slowly reduces the bubbling of the contained carbonated liquid.

Clinical Features

Disorders Related to Descent

Middle Ear Barotrauma

Middle ear barotrauma (MEBT), also known as barotitis or “ear squeeze,” is the most common complaint of scuba divers. It is experienced by 30% of novice scuba divers and 10% of experienced divers.6,7 The middle ear is an air-filled space with solid bone walls except for the tympanic membrane (Fig. 143-6). The eustachian tube is the only anatomic passage to the external environment.

As the diver descends, the water exerts increasing pressure against the intact tympanic membrane. Typically, the diver performs various maneuvers to force air into the middle ear through the eustachian tubes in an attempt to maintain equal pressure across the tympanic membrane. If the diver fails, the floppy medial third of the eustachian tube collapses shut, making any further attempts at equalization futile. This is typically painful and can be associated with tinnitus; some patients develop transient vertigo.

Further descent can cause the tympanic membrane to rupture. The pain may or may not resolve as the tympanic membrane ruptures. The ruptured tympanic membrane can cause caloric stimulation by exposure of the middle ear to cold water, inducing a transient nystagmus and vertigo. The pressure of the water in the middle ear may lead to a facial palsy in certain individuals where the seventh cranial nerve passes unexposed through this space. On occasion, this disorder can be life-threatening during a dive as the subject becomes disoriented and can drown.

Inner Ear Barotrauma

Inner ear barotrauma (IEBT) results in damage to the cochleovestibular apparatus. It is much less common than MEBT but is associated with greater morbidity. A large negative pressure gradient develops in the middle ear if the diver is unable to equalize pressure during descent, similar to MEBT. Inward deflection of the tympanic membrane is transmitted to the oval window of the cochlea through the ossicles. Movement of the oval window creates a pressure wave within the perilymph of the cochlea, which causes an outward distention of the round window into the middle ear. Sudden equilibration of pressure in the middle ear or a vigorous Valsalva maneuver may rupture the round window, lead to hemorrhage into the inner ear, or tear the labyrinthine (Reissner’s) membrane.9–11

Symptoms associated with IEBT include variable hearing loss, severe vertigo, nausea, tinnitus, and fullness in the affected ear. Signs include severe nystagmus, positional vertigo, ataxia, and vomiting. The degree of sensorineural hearing loss is variable. Distinguishing IEBT from inner ear DCS (a type of DCS II) can be challenging but should not delay recompression in a patient in whom the diagnosis is in doubt.

Barosinusitis

Obstruction of the sinus ostia by mucosal thickening, polyps, pus, or deviated septum predisposes to sinus barotrauma, the second most common complaint among divers.8,9 The air-filled maxillary, frontal, and ethmoidal sinuses are susceptible to volume-pressure changes on ascent or descent; the most commonly affected is the maxillary sinus, followed by the frontal.11 The most common symptom is facial pain; epistaxis is common.

Disorders Arising at Depth

Nitrogen Narcosis

Nitrogen narcosis, known as rapture of the deep, results from the intoxicating effects of increased tissue nitrogen concentration at depth. Symptoms include euphoria, false feeling of well-being, confusion, loss of judgment or skill, disorientation, inappropriate laughter, diminished motor control, and tingling and vague numbness of the lips, gums, and legs.3 With breathing of compressed air, symptoms typically begin to occur at approximately 100 feet and often become profound at depths of more than 150 feet.3 Because of these dangers, the use of compressed air is not recommended for sport diving to depths of more than 120 feet. Although the effects of nitrogen narcosis resolve with ascent to shallower depths and are variable between individuals, the diver may drown because of poor judgment or seriously impaired motor skills in the presence of a dive emergency.

Oxygen Toxicity

At elevated partial pressures for extended periods, oxygen can be toxic to the central nervous system (CNS) or lungs. Oxygen becomes toxic to the CNS when its partial pressure exceeds 1.6 ATA. Oxygen partial pressures below 1.4 ATA are unlikely to produce CNS toxicity. A diver breathing compressed air would attain a partial pressure of 1.6 ATA of oxygen at a depth of 218 fsw. This far exceeds the depth to which sport divers would go. Deep divers prevent oxygen toxicity by breathing mixed gases with decreased oxygen content (e.g., hypoxic trimix).

Pulmonary oxygen toxicity (low-pressure oxygen poisoning) can occur after 24 hours of exposure to partial pressures of oxygen in excess of 0.6 ATA. The symptoms of pulmonary oxygen toxicity include a burning sensation or pain on inspiration and coughing. Pulmonary function gradually becomes normal after the exposure is terminated, but pneumonitis and permanent fibrosis are possible. It is extremely unlikely that a sport diver would ever be exposed for the duration that is required to produce toxicity; however, long exposures to higher levels of oxygen, such as those administered for certain recompression protocols, may lead to pulmonary oxygen toxicity.

Contaminated Air

Rarely, other gases, such as carbon monoxide and carbon dioxide, can contaminate the air that is compressed into a tank. This can happen, for example, if the compressor intake is placed too close to the compressor’s engine exhaust. As in the case of oxygen and nitrogen, the partial pressure of these contaminants in the tissues increases dramatically with depth, potentiating their clinical effects. The symptoms of hypercarbia or carbon monoxide poisoning are more severe at elevated partial pressures. Hypercarbia increases a diver’s susceptibility to CNS oxygen toxicity.3

Rebreathers release microscopic calcium hydroxide or “soda lime” dust particles into the apparatus.12 These particles are small enough and have geometric characteristics that allow them to be deposited in the alveoli. When soda lime comes into contact with water, it forms a caustic liquid. In the event of a hose rupture allowing seawater contamination of the circuit, caustic burns to the mouth, throat, and airways may result. Chronic exposure to soda lime dust may contribute to long-term effects on respiratory function.

Disorders Arising on Ascent

Alternobaric Vertigo

Alternobaric vertigo (ABV) results from an inability to equalize pressure within the middle ear during ascent. Although equalization during descent requires active maneuvers to maintain eustachian tube patency, air normally exits the middle ear without difficulty during ascent because the pressure within the middle ear exceeds ambient pressure. In the setting of mucosal edema or thickening within the eustachian tube, however, the passage of air may be impeded. The problem is typically unilateral. When the pressure gradient within the middle ear reaches 60 cm H2O, increased labyrinthine discharge produces nystagmus. Clinically, the patient experiences a profound but transient sense of vertigo during ascent that may be associated with nausea and vomiting. Unlike those of IEBT, the symptoms are self-limited.

Gastrointestinal Barotrauma

Serious gastrointestinal barotrauma is a rare condition in scuba divers. It results from the expansion of bowel gas in the small intestine and colon on ascent after diving. Predisposing factors include consumption of carbonated beverages, large meals, or gas-producing foods before diving as well as performance of the Valsalva maneuver in the head-down position. Symptoms include eructation, flatulence, bloating, and crampy abdominal pain. In divers with inguinal or other hernias, the potential for expansion of trapped gas within the hernia exists, and expansion may result in incarceration or strangulation.13,14 Gastric rupture is a rare complication.14 Although gastrointestinal barotrauma is a rare entity, it should be suspected in the diver-patient with a provocative history and abdominal pain.

Pulmonary Barotrauma

Without continuously expiring on ascent, a scuba diver who takes a full breath at 33 fsw will have twice the lung volume at the surface (Boyle’s law). Because the volume expansion of the alveoli is limited, the increase in pressure either forces gas bubbles across the alveolar-capillary membrane or causes the wall of the alveoli to rupture. A differential pressure of only 80 mm Hg between the alveoli and chest wall, corresponding to a change in depth of 3 to 4 feet, is all that is required to force air bubbles across the alveolar-capillary membrane.

The greatest risk for pulmonary barotrauma occurs in less than 10 feet of water. It is therefore important for the clinician to evaluate patients with symptoms that are consistent with disease entities related to pulmonary barotrauma even after exposure to shallow depths. Pulmonary barotrauma can result in the following four conditions: pneumothorax, pneumomediastinum, subcutaneous emphysema, and alveolar hemorrhage. Risk factors elicited from the dive and medical history may suggest the diagnosis of pulmonary barotrauma. In most cases, fast ascent, panic, problems in regulating buoyancy, or running out of air is noted.

Asthmatics have a twofold increased risk for pulmonary barotrauma compared with the general diver population.15 There are six mechanisms that contribute to the increased risk in asthmatics:

1. Bronchospasm and mucus plugging predispose local regions of lung to injury.

2. When air is compressed, it becomes denser. This may contribute to greater turbulent flow through narrow airways.

3. During scuba diving, there is a reduction in breathing capacity related to the effects of immersion. At 33 feet underwater, the maximum breathing capacity of a normal scuba diver is only 70% of the surface value. At 100 feet underwater, the reduction is approximately 50%.

4. When compressed air (from the scuba tank) expands in the regulator before delivery to the lungs, it cools (Charles’ law). Breathing of chilled air may trigger bronchospasm in asthmatics who have a cold-induced component of their disease.

5. Scuba diving takes some effort; asthmatics who have an exercise-induced component of their disease may experience bronchospasm.

6. Compressed air may be contaminated by pollen and other allergens.

Buy Membership for Emergency Medicine Category to continue reading. Learn more here

Related posts:

Diarrhea Mechanical Ventilation and Noninvasive Ventilatory Support Monitoring the Emergency Patient Intimate Partner Violence Headache Seizure Disorders