CASE STUDIES IN TOXICOLOGY ScubaSeries Editor: Diving Lewis S. Nelson, Safety: MD A Case Report of Diving Injury in the Red Sea Moses Washington, MD, and Michael Touger, MD Case severe joint pain but continued A 28-year-old, previously healthy to dive. She finally sought medi- woman presented to the ED of Ja- cal attention on day 10 of her trip. cobi Medical Center, New York After being informed that there City, with bilateral shoulder and were no emergency hyperbaric Moroz Shutterstock/Stas © knee pain and shortness of breath. facilities on the Egyptian-Israeli She had arrived at New York’s JFK border, and of an indefinite sus- International Airport from Mos- pension of flights between Egypt cow, Russia, 3 days before presen- and Israel, she flew to Moscow for tation. treatment. (The patient was un- A recreational scuba diver born FIGURE 1 The red Sea aware that, in fact, she could have in the Ukraine and currently resid- traveled by land to a nearby hy- ing in New York, she had been training in underwater perbaric facility in Eilat, Israel.) videography in the Red Sea off the coast of Egypt (Fig- Her symptoms became worse during the flight to ure 1). Her dive profile consisted of multiple daily dives Moscow; upon arrival, she learned that her health in- to 50 meters (approximately 150 feet), with computer- surance did not cover treatment abroad. She then con- calculated decompression times from her dive instructor. tacted the US-based Divers Alert Network (DAN) and On Day 5 of her trip, the patient descended to depth was referred to the Jacobi Hyperbaric Center in New with instruction that upon depletion of air, she would York. During the flight to New York City, joint pain per- ascend via buddy breathing with her instructor. Unfor- sisted, and she noted shortness of breath, confusion, and tunately, the instructor was not in proximity of patient an unsteady gait. when her air depleted, and she experienced a panicked, In the Jacobi ED, the patient was in no acute distress. uncontrolled ascent without any decompression stops. Vital signs were: temperature, 98.7 F; heart rate, 76 beats/ Within 12 hours of this event, patient noted persistent min; blood pressure, 123/74 mm Hg; respiratory rate, 14 Dr Washington is a resident in emergency medicine at Jacobi/Montefiore Emergency Medicine Residency Program in New York City. Dr Touger is an associate professor of clinical emergency medicine in the Department of Emergency Medicine at Albert Einstein College of Medicine, and medical director at the Jacobi Hyperbaric Chamber in New York City. www.emedmag.com april 2013 | EMErGENCY MEDiCiNE 9 Scuba Diving Safety breaths/min. Oxygen saturation was 99% on room air. Classically, DCS can be divided into three types. Physical examination was essentially normal except for a Type I, often referred to as “pain-only” bends, is the most marked left-leaning gait disturbance (patient could only common and least severe form of DCS. Patients typically walk by holding onto a wall). The rest of her neurologic, experience pain in the large joints and extremities that is cardiovascular, and musculoskeletal examinations were not affected by movement. Pain may be monoarticular normal. Although the patient’s sensorium appeared in- or polyarticular, and is believed to be the result of tissue tact, her speech subjectively seemed slow and hesitant to ischemia caused by the mechanical obstructive effects of both the patient and a friend. nitrogen bubbles on joint tissue. In addition to pain, skin changes such as mottling can also occur in type I and are What is the pathophysiology secondary to impaired lymphatic and venous drainage of decompression sickness? due to obstruction caused by nitrogen bubbles. As in this case of uncontrolled ascent, diving injuries result from rapid changes in environmental pressure. Decom- Type II DCS, or “serious” DCS, includes pulmonary, car- pression sickness (DCS) occurs when nitrogen bubbles diovascular, and neurologic effects. Pulmonary DCS, called form in body tissues and the vascular system, leading to “the chokes,” results from nitrogen bubbles in the pulmo- tissue hypoxia. A review of the gas laws of Boyle, Henry, nary vasculature, causing chest pain, dyspnea, cough, and and Dalton as they apply to scuba diving, helps explain even hemoptysis. Severe pulmonary DCS can lead to car- the pathophysiology of DCS (see the box below). diovascular collapse. Neurologic DCS includes sensory or The most important gases involved in DCS are nitro- motor deficits, or both, presenting in a patchy distribution, gen and, to a lesser degree, oxygen. In accordance with which reflects the effects of nitrogen-bubble obstruction on Henry and Dalton’s laws, when one breathes compressed peripheral nerves. Patients may also experience vestibular air in a pressurized environment, nitrogen gas dissolves DCS, which can result in vertigo, hearing loss, and gait dis- in tissues. During ascent from depth, gas bubble-size in- turbance. This form can be difficult to distinguish from in- creases as per Boyle’s law. These changes in pressure lead ner ear barotrauma because symptoms are similar in both; to obstruction of blood flow and a cascade of inflamma- treatment, however, is different for the latter. tory changes. To further illustrate the effects of increased pressure Acute gas embolism (sometimes referred to as type and depth, it also helps to understand the units and con- III DCS) is a combination of acute arterial gas embo- versions employed to describe pressure. With respect to lism (AGE) and DCS and is manifested by rapid onset pressure, 1 ATA (atmosphere absolute) equals 760 mm of stroke-like or other neurologic symptoms—usually Hg of ambient pressure at sea level, which equals 33 feet within 10 minutes after ascent. It typically results from a of seawater ambient pressure. Therefore, there is an in- pneumothorax caused by the rupture of pulmonary al- crease in pressure of 1 ATA for every 33 feet of depth.1 veoli in which intrathoracic nitrogen enters the vascular system either by crossing the pulmonary venous vessels to the arterial side or by passing through a patent fora- It's the Law: Gas and Pressure men ovale ([PFO]; a congenital condition that can permit Boyle’s law: Pressure and volume are right to left intracardiac shunting of gas bubbles, increas- inversely proportional to each other, given a ing the risk of DCS). If these nitrogen bubbles occlude constant temperature. spinal arteries or cerebral vessels, the patient may develop Dalton’s law: The total pressure of a mixture a stroke-like syndrome with motor paralysis or symp- of different gases is the sum of all partial toms of spinal cord dysfunction, including urinary or fe- pressures of each individual gas. cal incontinence or retention.2 If computed tomography Henry’s law: Gas in a solution of liquid is (CT) or magnetic resonance imaging of the brain is per- proportional to the partial pressure of that gas. formed early (usually within 4 hours after injury), mac- Continued on page 20 10 EMErGENCY MEDiCiNE | april 2013 www.emedmag.com Scuba Diving Safety Continued from page 10 Continued from page 10 a total treatment time of approximately 5 hours, begin- ning at 2.8 ATA with staged decompression (Figure 3).4 Is there any benefit to hyperbaric therapy for a patient with a delayed presentation of a diving injury? The more severe DCS symptoms are at the time of in- jury, the more likely they are to persist. Although mac- roscopic nitrogen bubbles reabsorb within 24 hours and hyperbaric oxygen treatment benefits are optimal with early initiation, clinical benefits may be seen in patients who seek care after considerable delay. For example, de- layed therapy may still resolve persistent ischemia as well as limit ongoing reperfusion injury. DAN recommends Courtesy of Jacobi Medical Center, Bronx, New York. New Bronx, Center, Medical Jacobi of Courtesy initiating emergent treatment to any diver presenting FIGURE 2 The Jacobi multiplace hyperbaric with signs and symptoms of DCS, regardless of delay, chamber employing the appropriate USN TT.3 This organization also recommends repetitive treatments until the patient’s roscopic air may be visualized; otherwise, imaging may symptoms resolve or show no further resolution. be nondiagnostic. The sensitivity of radiographic imag- ing for the detection of bubbles is poor, however, and What are the complications should not delay recompression therapy. of hyperbaric oxygen treatment? Hyperbaric oxygen therapy is generally safe. Common Case continued complications include claustrophobia and middle ear Based on the patient’s recent diving mishap, DCS was high barotrauma, which are usually not issues with scuba div- on the differential. Pulmonary embolism was thought to ers. Although rare, oxygen toxicity seizures can occur, be unlikely because symptom onset preceded air travel. as well as barotrauma of other anatomic structures, in- The patient was placed on a cardiac monitor and given cluding the sinuses, lungs, and gastrointestinal tract. The 100% oxygen. A chest radiograph ruled out pneumotho- only absolute contraindication to emergency hyperbaric rax and barotrauma, and brain CT, likewise, ruled out therapy is untreated pneumothorax. Relative contraindi- intracranial injury. Based on these findings, patient was cations include pregnancy, epilepsy, and prior inner ear immediately sent to the hyperbaric chamber for treat- and sinus pathology. ment of presumptive DCS (Figure 2). What precautions should scuba divers take What is the therapeutic benefit of hyperbaric to avoid injury? oxygen in decompression sickness"? Novice divers should seek formal training by the Profes- The definitive treatment of DCS and AGE is recompres- sional Association of Diving Instructors or the National sion therapy in a hyperbaric chamber. Hyperbaric ox- Association of Underwater Instructors. Recreational div- ygen decreases the size of nitrogen bubbles, allowing ers should always dive with experienced and competent oxygen to diffuse into tissues and displace nitrogen bub- supervising divers, and all recreational divers are strongly bles.