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1368 SECTION 16: Environmental Injuries FIGURE 213-5. Box jellyfish sting. This 24-year-old woman was snorkeling off of Koh Tao, Thailand, when she was stung by a box jellyfish 15 minutes prior to this photograph being taken. She presented with severe extremity pain and chest tightness. [Photo contributed by Sittidet Toonpirom, MD, and Rittirak Othong, MD.] pain and erythema. Approximately 20 to 30 minutes later, severe gen eralized pain in the abdomen, back, chest, head, and limbs develops. The pain is usually associated with systemic signs of catecholamine excess, including tachycardia, hypertension, sweating, piloerection, and agitation. In severe cases, cardiogenic shock with pulmonary edema and serum troponin elevation occur. 40,44 Treatment consists of deactivation of attached nematocysts, tentacle removal, reversal of venom effects if possible, and symptomatic and pain relief. All victims with systemic signs or symptoms should be observed for ongoing envenomation or delayed reactions (Table 213-3). Irrigate with seawater or normal saline to remove and deactivate undischarged nematocysts. Remaining visible tentacles can then be removed. Do not irrigate with freshwater because the hypotonic solution is thought to stimulate nematocyst discharge. Best methods for removal are scraping the skin with a sharp object (e.g., razor or credit card) or application of adhesive tape. 38 If adhesive tape is used, the adherent nematocysts can later be identified. Treat with hot water immersion (111°F [43.3°C] to 114°F [45.6°C]) and apply topical lidocaine. Effective topical decontaminants appear to be species specific. 46,47 Because the species is often unknown, the geographic location of the envenomation guides decontamination. In Indo-Pacific waters, particularly those surrounding Australia, nematocyst deactivation therapy with 5% acetic acid (vinegar) is recommended, 43,48 and 5% acetic acid is the first-line management recommendation by the Australian Resuscitation Council.43,49,50 Treatment for severe Chironex envenomation consists of standard resuscitative measures and administration of sheep-derived antivenom specific for C. fleckeri (CSL Ltd., Melbourne, Australia). 39 Be prepared to treat anaphylaxis. Fatalities despite antivenom administration may be related to the rapidity of onset of cardiovascular collapse after Chironex envenomation. 27 Therefore, antivenom should be administered IV as early as possible. The initial dose may be repeated if there is no clinical response, and some clinicians recommend three or more doses in severe envenomations associated with cardiovascular collapse. 44 Magnesium improves outcome in animal studies and should be considered in refractory cases of severe Chironex envenomation with cardiac arrest.40,45 Severe generalized pain in Irukandji syndrome requires titrated IV opioid analgesia, often with large and repeat doses. Magnesium bolus and infusion have been used for treatment of the pain and hypertension associated with Irukandji syndrome. 45,51 However, adverse effects due to hypermagnesemia have been reported, and the treatment has not been as effective as originally suggested. 51,52 A recent systematic review of magnesium sulfate administration in the management of Irukandji syndrome found no clear evidence of benefit, and its use is not recommended. Obtain an ECG and troponin testing on admission; echocardiography is useful in patients with myocardial involvement.

e as originally suggested. 51,52 A recent systematic review of magnesium sulfate administration in the management of Irukandji syndrome found no clear evidence of benefit, and its use is not recommended. Obtain an ECG and troponin testing on admission; echocardiography is useful in patients with myocardial involvement. Manage pulmonary edema with oxygen supplementation, positive-pressure ventilation, and inotropes.  CONTROVERSIES IN JELLYFISH ENVENOMATION MANAGEMENT The application of topical commercial vinegar (4% to 5% acetic acid solution) in the treatment of jellyfish and stinging hydroid envenom ation is controversial. A 2012 systematic review and a 2013 Cochrane review both found no benefit from the intervention. 46,47 Further, an in vivo study observed increased jellyfish nematocyst discharge after application of vinegar, particularly from Physalis physalis tentacles. Similarly, in a randomized controlled trial of multiple topical treatments for Chrysaora chinesis stings in 96 human subjects, application of 5% acetic acid failed to improve pain as compared to placebo. 55 This appears to contradict field observations and recommendations by authorities in wilderness medicine. 56-58 It is possible that nematocysts from different jellyfish species respond differently to vinegar, and the intervention is a subject of ongoing scientific investigation. However, at this time, topical application of vinegar for jellyfish envenomation cannot be universally recommended as standard care. For jellyfish stings, “hot water and lidocaine appear more universally beneficial in improving pain symptoms and are preferentially recommended. ” 46 The venoms are heat labile, and heat reduces toxicity in most jellyfish envenomations. 36,41,47 Chironex stings are the exception. Recent evidence suggests hot water immersion is “no more effective than icepacks for reducing the acute pain of box jellyfish stings. ” 59 In waters surrounding the United States, application of 5% acetic acid solutions to tentacles from Chrysaora species appears to increase nematocyst discharge. 54,60 For Chrysaora (e.g., sea nettle) or Cyanea (e.g., lion’s mane) jellyfish, a slurry of baking soda (sodium bicarbonate) is thought to be effective. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Diving Disorders Charlotte A. Sadler Brian K. Snyder INTRODUCTION 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 rel evant 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: P 1V1 = P2V2. Pressure can be measured in a variety of units. The Interna tional 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): CHAPTER Tintinalli_Sec16_p1333-1418.indd 1368 8/2/19 8:23 PM

ssure can be measured in a variety of units. The Interna tional 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): CHAPTER Tintinalli_Sec16_p1333-1418.indd 1368 8/2/19 8:23 PM CHAPTER 214:  Diving Disorders      1369 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 that 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 circula tion 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 dissolved 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.  EVALUATION OF THE DIVER History There are several aspects of the history that are specific to the diver that need to be obtained. Ask the diver for their complete dive profile, including time, depth, number of dives done that day, and type of breathing gas used. Additionally, obtain history regarding the dive itself, including level of exertion, difficulty with equalization, any equipment difficulty, any history of rapid ascent, or if the dive buddy witnessed anything unusual. If there is a dive computer, it may be useful to see if there were any omitted decompression stops or evidence of rapid ascent. It is also very important to get an exact history regarding timing and onset of symptoms. For example, vertigo that occurs on descent with ear equalization is likely due to barotrauma and not inner ear decompres sion sickness.

y be useful to see if there were any omitted decompression stops or evidence of rapid ascent. It is also very important to get an exact history regarding timing and onset of symptoms. For example, vertigo that occurs on descent with ear equalization is likely due to barotrauma and not inner ear decompres sion sickness. Chest pain and shortness of breath that occur at depth are unlikely to be due to an arterial gas embolism and may be due to immersion pulmonary edema (see below) or other primary pulmonary or cardiac disease. Physical Exam All divers should undergo a thorough physical exami nation. Particular attention should be paid to the neurologic examina tion, including a full cerebellar and mental status exam. The patient may even be unaware of subtle cognitive abnormalities that may otherwise go undetected. 2 It is also important to note that neurologic signs may not present like other neurologic illnesses and may not localize to any one identifiable lesion or spinal cord level. Urinary retention may be an early sign of severe spinal cord decompression sickness, and ability to void should always be evaluated. BAROTRAUMA OF DESCENT The clinical conditions resulting from barotrauma of descent are baro titis (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 mem brane the tissue most commonly affected by this phenomenon, if active measures such as “clearing the ears” with a Valsalva or other maneu vers are not successful. 3 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 TABLE 214-1 Summary of Barotrauma of Descent and Ascent Barotrauma Clinical Features Treatment Barotrauma of descent Otic barotrauma (“ear squeeze”)

eeze. ”  BAROTITIS (EAR SQUEEZE) Barotitis can range from symptoms of pain or fullness without otoscopic changes, to hemorrhage within the tympanic membrane or hemorrhage TABLE 214-1 Summary of Barotrauma of Descent and Ascent Barotrauma Clinical Features Treatment Barotrauma of descent Otic barotrauma (“ear squeeze”) Sinus barotrauma (“sinus squeeze”) Inner ear barotrauma Pain, fullness, vertigo, conductive hearing loss from inability to equalize middle ear pressure Pain over affected sinus, possible bleeding from nares Sudden onset of sensorineural hearing loss, tinnitus, severe vertigo after forced Valsalva Decongestants, consider antibiotics Decongestants, consider antibiotics Head of bed up, no nose blowing, antivertigo medications, and urgent otolaryngology consultation as some surgeons advocate early exploration Barotrauma of ascent Pulmonary overinflation syndromes (pulmonary barotrauma) Arterial gas embolism Dyspnea, chest pain, subcutaneous air, extra-alveolar air on radiograph; usually occurring secondary to rapid or uncontrolled ascent Neurologic symptoms occurring immediately after uncontrolled or rapid ascent or neurologic symptoms in the setting of pulmonary barotrauma Pneumomediastinum requires only symptomatic care and does not require recompression Pneumothorax requires drainage and does not require recompression (if recompression is instituted for treatment of arterial gas embolism, then the pneumothorax must be drained before recompression) Airway, breathing, circulation, high-flow oxygen, IV hydration, immediate recompression (hyperbaric oxygen), consider adjunctive lidocaine Any neurologic symptom in the setting of documented pulmonary barotrauma must be treated as an arterial gas embolism Tintinalli_Sec16_p1333-1418.indd 1369 8/2/19 8:23 PM

ompression) Airway, breathing, circulation, high-flow oxygen, IV hydration, immediate recompression (hyperbaric oxygen), consider adjunctive lidocaine Any neurologic symptom in the setting of documented pulmonary barotrauma must be treated as an arterial gas embolism Tintinalli_Sec16_p1333-1418.indd 1369 8/2/19 8:23 PM 1370 SECTION 16: Environmental Injuries 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, trans mitted 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 combi nation 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 hear ing 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 and reproduction of the vertigo. 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.

auses 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 barotrau matic 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 re-create the same pressure differentials that caused the injury, potentially causing more perilymph leakage and, possibly, worsening the injury, as well as the symptoms.  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 under lying skin, producing local trauma manifested by painful red streaks. BAROTRAUMA OF ASCENT 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 pres sure 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 ves tibular impulses to the brain, resulting in vertigo (alternobaric vertigo). This is usually transient and generally requires no specific treatment. Symptoms should resolve shortly after surfacing. Prolonged symptoms of vertigo should prompt one to look for another cause of vertigo.  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. 4 Mediastinal air can track superiorly into the neck, resulting in subcutaneous air on physical examination or air on a cervical spine radiograph. Pulmonary overinflation injury can cause pneumothorax, requiring aspiration of air or tube thoracostomy.

res symptomatic treatment and may be subtle on the chest radiograph. 4 Mediastinal air can track superiorly into the neck, resulting in subcutaneous air on physical examination or air on a cervical spine radiograph. Pulmonary overinflation injury can cause pneumothorax, requiring aspiration of air or tube thoracostomy. If air enters the pulmonary venous circulation, embolization of the gas through the arterial system occurs. The most sensitive end-organ to such embolization is the brain, and cerebral arterial gas embolism is the term applied to this condition, although the air emboli distribute to other tissues and organs. 5 Any neurologic symptom or sign referable to the circulation to the CNS in the setting of barotrauma associated with ascent should be considered to be secondary to cerebral arterial gas embolism. The symptoms, signs, and treatment are discussed below in the section “ Arterial Gas Embolism. ” Isolated pneumomediastinum can be treated with surface oxygen, observation, and serial chest radiographs. Pulmonary barotrauma ( Figure 214-1) can occur without a rapid ascent or closed glottis in divers with congenital cysts, obstructive pul monary disease, or other processes that cause air trapping.  OTHER BAROTRAUMAS OF ASCENT An air pocket underneath a tooth may equilibrate with ambient pressure while diving, only to expand during ascent. This produces severe pain and may dislodge a filling or fracture a tooth. Swallowed air during diving may expand during ascent, rarely producing gastric distention and abdominal cramps. Tintinalli_Sec16_p1333-1418.indd 1370 8/2/19 8:23 PM

may equilibrate with ambient pressure while diving, only to expand during ascent. This produces severe pain and may dislodge a filling or fracture a tooth. Swallowed air during diving may expand during ascent, rarely producing gastric distention and abdominal cramps. Tintinalli_Sec16_p1333-1418.indd 1370 8/2/19 8:23 PM CHAPTER 214:  Diving Disorders      1371 DECOMPRESSION SICKNESS  PATHOPHYSIOLOGY The pathophysiology of decompression sickness is related to the obstructive and inflammatory effects of inert gas bubbles in tissues and the vascular system. 5 Decompression sickness may occur in div ers breathing compressed air, caisson workers, high-altitude pilots, or astronauts. Bubbles may form when a body with additional inert gas in solution experiences a decrease in ambient pressure that causes liberation of the gas. Uptake of inert gas occurs at different rates in different tissues. The U.S. Navy publishes dive tables to provide the limits to a dive (measured by bottom depth and time) that can be undertaken without a decompression stop (“no decompression” or “no stop” dives). Other Navy tables provide a variety of decompression schedules for longer dives. A multitude of dive computers, often using proprietary mathematical models, provide divers with relatively safe diving limits. Decompression sickness is less likely to occur if the limits of the dive tables or dive computer are followed, but compliance with dive table limits or a dive computer does not completely eliminate risk. Bubbles are necessary but not sufficient by themselves to cause decompression sickness; bubbling occurs after many dive profiles that do not lead to decompression sickness. Obviously, there must be a threshold at which the bubble load causes symptoms. The exact mechanism of bubble formation is not known, although preexisting gas micronuclei in the circulation likely form a nidus for gas accumulation. Bubbles may form directly in tissues or the circulation (usually the low-pressure venous circulation). Classically, it is thought that bubbles directly obstruct blood flow, leading to direct ischemia. Also, the air– blood and air–endothelial interfaces initiate a variety of inflammatory and thrombotic processes; activate the endothelium, leading to neutrophil adhesion and activation; and change the permeability of the endothelium, resulting in third spacing of fluid. In addition, decompression stress induces the production of microparticles, which are lipid bilayer– enclosed membranous vesicles extruded from vascular endothelial and other cells. Injection of these microparticles in animal models creates a clinical condition consistent with decompression sickness. 8 In humans, a positive relationship between microparticles and surface proteins associated with neutrophil activation and the occurrence of decompression sickness has been observed.  CLINICAL FEATURES OF DECOMPRESSION SICKNESS The most commonly used classification divides decompression sickness into two (or sometimes three) main groups ( Table 214-2). We focus on types I and II for clarity. Type I is also called “pain-only” decompression sickness and involves the joints, extremities, and skin (“cutis marmo rata”). Lymphatic obstruction can occur in type I, causing lymphedema, which usually takes days to resolve despite recompression therapy. Type II involves the CNS (mainly the spinal cord in compressed air divers and the brain in high-altitude decompressions), vestibular symptoms (“staggers”), and cardiopulmonary symptoms (“chokes”).

tic obstruction can occur in type I, causing lymphedema, which usually takes days to resolve despite recompression therapy. Type II involves the CNS (mainly the spinal cord in compressed air divers and the brain in high-altitude decompressions), vestibular symptoms (“staggers”), and cardiopulmonary symptoms (“chokes”). To further complicate the nomenclature and classification of decompression sick ness, it can also occur when an arterial gas embolism (see “ Artificial Gas Embolism”) causes inert gas to come out of solution after a dive profile that would otherwise not be expected to cause decompression sickness (called type III). 10 Some advocate the use of the alternate term FIGURE 214-1. Pulmonary barotrauma. Note the air in the mediastinum in this radiograph (arrow). There is also air in the soft tissues of the neck. TABLE 214-2 Classification of Decompression Sickness (DCS) Classification Clinical Features Comments Type I: “pain-only” DCS Deep pain in joints and extremities, unrelieved but not worsened with movement Skin changes—mottling, pruritus, and color changes Usually single joint, most commonly knees and shoulders Lymphatic obstruction can occur and takes days to resolve despite recompression therapy Type II: “serious” DCS Pulmonary (“chokes”)—cough, hemoptysis, dyspnea, and substernal chest pain Cardiovascular collapse can occur Neurologic—sensation of truncal constriction, ascending paralysis, usually rapid in onset Vestibular (“staggers”)—vertigo, hearing loss, tinnitus, and disequilibrium More commonly affects the lower cervical and thoracic regions; may see scattered lesions Autonomic dysfunction may be seen Usually occurs after deep, long dives Type III: combination of DCS and arterial gas embolism Symptoms of DCS II noted above plus a variety of stroke syndromes, symptoms, and signs Symptoms occur on ascent or immediately upon surfacing Symptoms of arterial gas embolism may spontaneously resolve Tintinalli_Sec16_p1333-1418.indd 1371 8/2/19 8:23 PM

long dives Type III: combination of DCS and arterial gas embolism Symptoms of DCS II noted above plus a variety of stroke syndromes, symptoms, and signs Symptoms occur on ascent or immediately upon surfacing Symptoms of arterial gas embolism may spontaneously resolve Tintinalli_Sec16_p1333-1418.indd 1371 8/2/19 8:23 PM 1372 SECTION 16: Environmental Injuries decompression illness, instead of differentiating between decompression sickness and cerebral arterial gas embolism, to encompass all pathologic syndromes following a reduction in ambient pressure.1 Generally, the symptoms of decompression sickness occur minutes to several hours after surfacing, but in rare cases, symptoms can occur days after diving. Symptoms occurring between dives may improve during a subsequent dive (as recompression has occurred), but get worse upon resurfacing (as the inert gas load has increased and ambient pressure has decreased). Flying with the resultant decrease in ambient pressure may precipitate or worsen symptoms. For this reason, divers are generally advised to refrain from flying for at least 12 to 24 hours after the last dive depending on the nature of the diving exposure. Pain Divers with type I decompression sickness typically describe a deep pain, unrelieved but not worsened with movement. This pain can be attributed to or confused with pain caused by injury, potentially making accurate diagnosis difficult. Pain is thought to be due to distention from bubbles in ligaments or fascia, intramedullary bubbles at the ends of long bones, or the activation of stretch receptors caused by bubbles in tendons. The mechanism of simple distention of tissues is supported by the rapid improvement of symptoms with recompression. Common pain locations are knees and shoulders, and most often, only a single joint is involved. Decompression sickness in commercial and military divers, caisson workers, and aviators tends to manifest most often as joint pain. Sport divers, who usually perform multiple dives often over a period of days, are more prone to spinal cord effects. Poorly localized and difficult-to-describe back or abdominal pain may herald the more serious signs of spinal cord involvement. Pulmonary Symptoms Pulmonary symptoms, generally seen usu ally only after more prolonged exposures, are caused by large numbers of pulmonary artery bubbles and include symptoms of cough, hemop tysis, dyspnea, and substernal chest pain. Cardiovascular collapse can occur. Neurologic Symptoms The classic description of divers with neu rologic decompression sickness (type II) can begin with a sensation of truncal constriction or girdle-like pain. Often a wooly feeling begins in the feet, developing into an ascending paralysis, producing symptoms of transverse myelitis. This form is usually rapid in onset and tends to affect the lower cervical and thoracic regions. However, in type II decompression sickness, neurologic deficits do not necessarily cause distinct spinal cord syndromes (i.e., an anterior or posterior spinal artery syndrome), nor will a definitive level necessarily be found, as lesions may be scattered throughout the spinal cord. 12 Autonomic involvement, with resulting incontinence and sexual dysfunction, is not uncommon. The pathophysiology of spinal cord decompression sickness seems to be initial bubbling in the low-pressure venous plexus system that first impedes and then obstructs venous outflow from the cord. Decreasing venous blood flow prevents dissolved nitrogen in spinal cord tissues from egressing, and in situ bubbles within the spinal cord develop (called autochthonous bubbles). Vestibular Symptoms Vestibular decompression sickness usually occurs after deep, long dives, although it has been reported in sport divers.

. Decreasing venous blood flow prevents dissolved nitrogen in spinal cord tissues from egressing, and in situ bubbles within the spinal cord develop (called autochthonous bubbles). Vestibular Symptoms Vestibular decompression sickness usually occurs after deep, long dives, although it has been reported in sport divers. Signs are vertigo, hearing loss, tinnitus, and disequilibrium. The vestibular syndrome can be differentiated from inner ear barotrauma mainly by the history, because patients with inner ear barotrauma develop symptoms in the water and, generally, immediately after a forced Valsalva maneuver to equalize the middle ear pressure. Other nonspecific symptoms such as headache, nausea, dizziness, or unusual fatigue are also reported. It may be difficult to differentiate fatigue from decompression sickness from the expected fatigue from the exertion of diving. Patent Foramen Ovale The association between decompression sickness and patent foramen ovale is unclear. There appears to be an increased prevalence in patients with inner ear and cutaneous decom pression sickness. It is reasonable to screen divers with recurrent, unexplained decompression sickness for a patent foramen ovale. Closure of a large defect will reduce arterialization of venous gas emboli, although it has yet to be shown if such closure will reduce the incidence of subsequent decompression sickness.  ARTERIAL GAS EMBOLISM Arterial gas embolism occurs when air enters the left side of the vascular system. In the setting of diving, this most often results from pulmonary barotrauma. Arterial gas embolism can also occur as a complication of certain medical procedures, such as central vascular catheterization and cardiac bypass. Air inadvertently introduced into the venous circulation can cross from the right side of the circulation from intracardiac or pulmonary arteriovenous shunts. Air bubbles may also arterialize through these same shunts, sometimes making the source of arterial bubbles difficult to determine. 15 Whatever the source, when air embolizes systemically, distribution depends mainly on blood flow and not gravity. Clinical Features of Arterial Gas Embolism The most dramatic effect of arterial gas embolism is on the brain, resulting in a variety of stroke syndromes, symptoms, and signs, depending on the part of the brain affected. Rarely, diving-related arterial gas embolism from pul monary barotrauma causes immediate apnea and cardiac arrest. The mechanism of cardiovascular collapse appears to be air in the entirety of the large arteries and veins of the central vascular bed. 16 The effects of arterial gas embolism secondary to pulmonary barotrauma usually occur on ascent or immediately upon surfacing. If the victim does not die immediately, the symptoms of cerebral arterial gas embolism often include loss of consciousness, seizure, blindness, disorientation, or hemiplegia. Symptoms may spontaneously improve as the gas enters the venous cerebral circulation after a spike in blood pressure. Sometimes, by the time the patient reaches the clinician, the only signs that remain are subtle defects. In particular, parietal lobe signs and symptoms are easily overlooked. A cascade of inflammatory processes also occurs in air embolism, just as in decompression sickness.  DIAGNOSIS OF DECOMPRESSION SICKNESS AND ARTERIAL GAS EMBOLISM Diagnosis is clinical, based on history and physical exam, with limited laboratory testing. There are no current definitive diagnostic criteria for decompression sickness. The San Diego Diving and Hyperbaric Organizations criteria uses a point system to identify dive injuries resulting in decompression sickness with a high degree of specificity (90%), 17 but a sensitivity of only 53%.

ited laboratory testing. There are no current definitive diagnostic criteria for decompression sickness. The San Diego Diving and Hyperbaric Organizations criteria uses a point system to identify dive injuries resulting in decompression sickness with a high degree of specificity (90%), 17 but a sensitivity of only 53%. This is helpful to create databases of divers with decompression sickness to study outcomes and allow study of adjunctive therapies. The San Diego Diving and Hyperbaric Organizations criteria for arterial gas embolism have been shown in a small study to be useful. Using a cut point of ≥2 points, the score has a 94.7% sensitivity (95% confidence interval, 71.9% to 99.7%) and 85.7% specificity (95% confidence interval, 42.0% to 99.2%) for the diagnosis of arterial gas embolism (Table 214-3). TABLE 214-3 San Diego Diving and Hyperbaric Organizations Criteria for Arterial Gas Embolism Time Criteria   Points* Any of the following signs or symptoms within 5 min of surfacing Disorientation Sudden loss of consciousness Aphasia Hemiplegia 3 points Any of the following signs or symptoms within 5 min of surfacing Hemiparesis or monoparesis Seizures (new onset) Cortical blindness 2 points With resurfacing or discovered during ED evaluation A rapid uncontrolled ascent, or any ascent with panic and the onset of symptoms Hemoptysis Presence of barotrauma on chest radiograph (pneumomediastinum, pneumopericardium, or pneumothorax) Creatine phosphokinase greater than 2 times normal in the absence of musculoskeletal trauma 1 point *Requires 2 or more points to suggest a diagnosis of arterial gas embolism. Tintinalli_Sec16_p1333-1418.indd 1372 8/2/19 8:23 PM

e of barotrauma on chest radiograph (pneumomediastinum, pneumopericardium, or pneumothorax) Creatine phosphokinase greater than 2 times normal in the absence of musculoskeletal trauma 1 point *Requires 2 or more points to suggest a diagnosis of arterial gas embolism. Tintinalli_Sec16_p1333-1418.indd 1372 8/2/19 8:23 PM CHAPTER 214:  Diving Disorders      1373 Using these criterial may be helpful to the clinician; however, until a larger study can validate this study, physician clinical judgment should supersede this scoring system. Laboratory Testing Laboratory testing is not always indicated in cases of very mild symptoms or presentations. If labs are obtained for evaluating either decompression sickness or arterial gas embolism, it is useful to obtain a CBC, creatine phosphokinase, liver enzymes, and possibly cardiac enzymes (if any chest pain or shortness of breath present). The hematocrit may increase due to hemoconcentration and third spacing of fluids. The creatine phosphokinase (and other enzymes such as lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase) will become elevated secondary to the systemic distribution of bubbles. The degree of elevation of creatine phosphokinase corresponds to the embolism severity. Cardiac troponins may also be elevated and most likely do not represent occlusive coronary artery disease. 5 However, arterial gas embolism and decompression sickness are clinical diagnoses and cannot be ruled in or out based on laboratory testing. Imaging Routine imaging is not indicated in all cases of decompres sion sickness or arterial gas embolism. If the patient is having any chest pain or shortness of breath, a chest radiograph is recommended to evaluate for possible pneumothorax, pneumomediastinum, or other possible causes of symptoms. An untreated pneumothorax is an abso lute contraindication to hyperbaric therapy. A head CT scan may be obtained in patients with neurologic symptoms, particularly if the cause of symptoms is unclear, to rule out other causes such as a hemorrhagic stroke or subarachnoid hemorrhage. Although there may be gas bubbles seen in cases of arterial gas embolism, a negative CT does not rule out the diagnosis. Findings from decompression sickness and arterial gas embolism may both be seen on MRI; however, there may be discrepancy between the timing of the appearance of the lesions on MRI and what is clinically observed—either worsening of lesions on MRI with clinical improvement or improvement on MRI with worsening symptoms. Obtaining an MRI should not delay hyperbaric oxygen therapy.  TREATMENT OF DECOMPRESSION SICKNESS AND ARTERIAL GAS EMBOLISM Treatment includes administering 100% oxygen, increasing tis sue perfusion with IV fluids, and rapid recompression. A supine position—not Trendelenburg position—is recommended for patients with arterial gas embolism. Patients may improve on surface oxygen and even have complete resolution of symptoms. However, it is imperative that these patients still be treated with hyperbaric oxygen due to risk of recurrence or relapse of symptoms. Recompression therapy with hyperbaric oxygen treats these conditions through several mechanisms. See Chapter 21, “Hyperbaric Oxygen Therapy, ” for detailed discussion. The administered pressure decreases the size of bubbles, and the high partial pressure of oxygen in solution increases inert gas washout from bubbles and tissue. Mass action dic tates a gas will travel down pressure gradients; therefore, nitrogen will move from bubbles with a high partial pressure of nitrogen into plasma, where it will travel to the lungs and be exhaled.

es, and the high partial pressure of oxygen in solution increases inert gas washout from bubbles and tissue. Mass action dic tates a gas will travel down pressure gradients; therefore, nitrogen will move from bubbles with a high partial pressure of nitrogen into plasma, where it will travel to the lungs and be exhaled. Conversely, oxygen from plasma with a high partial pressure of oxygen will enter bubbles, but ultimately will diffuse into cells and be metabolized, further reduc ing bubble size. Hyperbaric oxygen also decreases tissue edema and increases oxygen delivery to ischemic tissues. Additionally, it attenuates ischemia reperfusion injury by reducing neutrophil activation and adhesion to the endothelium. Recompression using U.S. Navy Treatment Table 6 is a commonly used method of management for decompression sickness, employing a maximal treatment pressure of 2.8 ATA (60 fsw). Table 6 is also used for air embolism, although some advocate an initial pressurization to 6 ATA (165 fsw) to maximize bubble compression, then continuation at 2.8 ATA (U.S. Navy Table 6A). Different treatment tables are used in other parts of the world, and there is some experience using lower treatment pressures for decompression sickness in monoplace chambers with reportedly comparable results. 21 Some patients may benefit from repeated treatments if symptoms do not fully resolve. Recompression should occur as soon as possible, and it should not be withheld in cases with delayed presentation. 5 Additionally, for divers who have missed needed decompression stops because of an emergency ascent or nonadherence to appropriate diving tables, it may be appropriate for them to undergo recompression therapy even if asymptomatic. U.S. Navy Table 5 recompression would usually be adequate in such a circumstance. The administration of IV lidocaine as a therapeutic adjunct for cere bral arterial gas embolism has been advocated because it appears to decrease neuropsychiatric deficits when given during anesthesia for cardiac procedures requiring bypass, 22-24 since bypass operations commonly cause the entry of air into the arterial system. Dosing of lidocaine in this setting is not standardized, although typical cardiac dosing is commonly used. 25 NSAIDs may also be helpful.22 The Divers Alert Network Emergency Hotline (telephone: 1-919- 684-9111; website: http://www.diversalertnetwork.org) has staff avail able 24 hours a day to provide assistance to divers and to help clinicians treat patients with decompression sickness or arterial gas embolism. The Divers Alert Network can provide information and the location of the nearest recompression facility around the world. SPECIAL CONSIDERATIONS  IMMERSION PULMONARY EDEMA Pulmonary edema can occur while diving or swimming. Because the first reported cases occurred in cold water, this condition was first described as “cold water” or “cold-induced” pulmonary edema. How ever, many cases have subsequently been reported in warm water, up to 27°C (80.6°F). 26 Typical symptoms of pulmonary edema (dyspnea, chest discomfort, coughing up pink frothy secretions) occur at depth and usually improve over time or with standard treatments for pulmonary edema. The cause is unknown despite human studies. 27 Initially, it was thought that there was no significant incidence of underlying cardiac disease, as many of these cases were initially reported in military trainees and triathletes who were significantly exerting themselves. However, as more cases are reported, it seems that there may be a relationship to underlying cardiac and pulmonary disease, particularly in middleaged and older divers without significant exertion. It is possible that the mechanism of disease may be different in these patients, though with a common final pathway of disease.

er, as more cases are reported, it seems that there may be a relationship to underlying cardiac and pulmonary disease, particularly in middleaged and older divers without significant exertion. It is possible that the mechanism of disease may be different in these patients, though with a common final pathway of disease. It may be prudent, particularly in older divers, to pursue a cardiac workup, including an ECG, cardiac markers, echocardiogram, and possible stress testing. 28-30 Interestingly, some divers will experience repeated episodes, whereas others may never experience another episode.  NITROGEN NARCOSIS Inert gas narcosis occurs when air is breathed at a depth of 100 fsw or greater. Symptoms include loss of fine motor skills and high-order mental processes and can cause divers to engage in dangerous or foolish activities during deep dives. At depths greater than 300 fsw, uncon sciousness may occur from the anesthetic effect of nitrogen.  OXYGEN TOXICITY Oxygen toxicity usually affects the lungs or brain, depending on the partial pressure of oxygen delivered and duration of exposure. Pulmonary oxygen toxicity generally occurs at lower partial pressures of oxygen but with longer exposures, whereas cerebral oxygen toxicity occurs at high partial pressures with generally short exposures. Pulmonary oxygen toxicity is unusual in diving due to the long exposure required to develop symptoms. Cerebral oxygen toxicity most often occurs with partial pressures of oxygen >1.4 ATA in the water. Some divers may breathe “nitrox” or oxygen-enriched air with fractions of oxygen of 32% to 36%. There fore, cerebral oxygen toxicity can occur at lesser depths and actually is the factor that limits diving depth with nitrox. Additionally, there are rebreather systems (closed-circuit systems), with the diver breathing within a continuous circuit of gas that has a very high fraction of oxygen (>95%), with carbon dioxide being scrubbed out. With these systems, cerebral oxygen toxicity can occur at depths as little as 25 ft. Signs and symptoms of cerebral oxygen toxicity include twitching, nausea, paresthesias, dizziness, and seizures. High partial pressures of Tintinalli_Sec16_p1333-1418.indd 1373 8/2/19 8:23 PM