A 22-year-old male recreational diver was performing an open-ocean dive using a closed-circuit rebreathing apparatus with a group of fellow recreational divers. When he surfaced, he was unconscious; observers do not recall if his mouthpiece was in place. He was immediately placed into a nearby dive boat.
On presentation, the patient states that he had difficulty maintaining a proper partial pressure of oxygen (PO2) throughout his dive. He believes that his PO2 was too low and that his vision was graying out as he ascended to the surface. According to the dive master, the group’s diving profile was consistent with a no-decompression dive, with a maximum depth of 75 feet of seawater. The divers are uncertain about how long the patient was unconscious, though they remember seeing him conscious at approximately 10 feet of seawater during the ascent. If correct, this would have meant that the patient was unconscious for about 20 seconds underwater at a standard ascent rate of 30 ft/min.
On physical examination, the patient’s face-mask reservoir contains approximately 20 mL of pink, frothy sputum. The patient is a healthy-appearing man in no acute distress, but his work of breathing is increased. He has a pulse of 80 bpm, a blood pressure of 104/89 mm Hg, and an oxygen saturation of 98% while breathing oxygen 10 L/min by face mask and 92% while breathing room air. The neurologic examination reveals no deficits. His speech is normal, and there is no fullness of the neck, jugular venous distention, or tracheal deviation. Auscultation of the left lower lung field reveals diminished breath sounds. The remainder of the physical examination yields no abnormalities.
A chest radiograph is unrevealing. A computed tomography (CT) scan of his chest is obtained (see Image 1).
What was the cause of the loss of consciousness on ascent?
HINT
The cause is similar to the cause of shallow-water blackout. By definition, the final diagnosis requires that the patient survive — at least temporarily — after the initial accident.
Author:
Bradley Hickey, MD,
Undersea and Diving Medical Officer,
United States Navy,
Naval Diving and Salvage Training Center,
Panama City, FL
eMedicine Editors:
Joe Alcock MD MS,
FAAEM, Assistant Professor,
Department of Emergency Medicine,
University of New Mexico,
Staff Physician,
Emergency Medicine Service,
Veterans Administration Medical Center,
Albuquerque, NM
Rick G. Kulkarni, MD,
Assistant Professor,,
Yale School of Medicine,
Section of Emergency Medicine,
Department of Surgery,
Attending Physician,
Medical Director,
Department of Emergency Services,
Yale-New Haven Hospital, CT
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ANSWER
A near-drowning is defined by Dorland’s as “survival for any length of time after submersion in water and temporary suffocation; it sometimes ends with secondary drowning”.3 The incident is further categorized as a wet near-drowning because the patient aspirated seawater. This is opposed to a dry process, in which laryngospasm prevents the aspiration of water.
The prognosis after near-drowning varies substantially. The 2 most influential factors are the time the patient was submerged and the temperature of the water (cold water decreases cellular metabolism). These factors are ultimately related to the pathophysiology progressing from initial asphyxia, to hypoxia with ischemia and reversible tissue injury, to irreversible tissue injury with potential death from secondary drowning. Near-drowning is typically the result of an underlying event or condition that contributes to unintentional immersion or immersion with incapacitation, such as trauma, intoxication, seizure, hypothermia, dysrhythmia, shallow-water blackout, and, for divers, a lost or improper breathing source.6
Auerbach emphasized the importance of determining if the near-drowning or drowning was wet (aspiration) or dry (no aspiration).1 Although the mechanism of injury remains unchanged, aspiration of water in a near-drowning can affect respiration by washing out surfactant or injuring the alveolar membrane. In addition, aspiration increases the risk of a secondary pneumonia, which can further diminish respiration. One theoretical effect of wet drowning, which has been demonstrated in animal models and has caused some controversy, is electrolyte disturbance; however, this has not been convincingly observed in humans.2
In this case, an improper breathing source resulted in hypoxia, which led to near-drowning. The diver was using a closed-circuit rebreathing apparatus, which adjusted the PO2 depending on his depth. PO2 is adjusted to avoid seizures caused by oxygen toxicity. The closed-circuit rebreathing system is essentially free of bubbles because the diver is inhaling and exhaling into a closed system. The closed system has a scrubber to remove carbon dioxide, an oxygen source, and a source of inert gas (eg, nitrogen). As a diver descends, increasing amounts of inert gas are introduced into the system, decreasing the amount of oxygen. This type of system is commonly used because it allows a diver to remain at depth for prolonged periods and because it reduces the amount of inert gas the tissues absorb. By comparison, the standard self-contained underwater breathing apparatus (SCUBA) used in most recreational dives is an open system, in which the exhaled breath is released into the water.
Although a closed-circuit rebreathing system can be advantageous, mechanical failure and operator error are inherent risks. The most common mechanical failures are scrubber failure and delivery of an improper PO2 mixture. With scrubber failure, a diver can be incapacitated by hypercapnia. With an improper PO2 mixture, a diver can be incapacitated from hypoxia or hyperoxia, resulting in oxygen toxicity.
Human error can occur when the PO2 is adjusted manually or when a diver is ascending or descending too quickly and does not let the apparatus adjust the pressures accurately. In the case of ascending too quickly, an event similar to shallow-water blackout occurs. In a shallow-water blackout, a person hyperventilates before breath-hold diving (diving without any external breathing apparatus) and metabolizes oxygen from the lungs while at depth. If the breath-hold diver metabolizes too much oxygen at depth, the PO2 is insufficient to sustain consciousness as he or she nears the surface, and blackout results. This event almost always ends in drowning, unless it is observed by others. The same mechanism can occur with a closed-circuit rebreathing apparatus if the PO2 is too low to sustain consciousness as the diver surfaces.
In this case, it was clinically impossible to determine if the cause of the diver’s hypoxia was mechanical failure or operator error. The diving apparatus must be thoroughly inspected to determine if a mechanical failure occurred. An arterial gas embolism (AGE) was clinically ruled out as the inciting event. The low PO2 during the ascent, the sensation of graying out, and the consistently normal neurologic findings after the incident were the key findings in this case. The patient’s labored breathing, pink sputum, and diminished breath sounds on the left side suggested pulmonary barotrauma—specifically, pneumothorax. Given the clinical picture, hyperbaric oxygen therapy was not indicated and was thought to be potentially harmful because of the possibility of pneumothorax.
The 2 most important principles of physics in regard to diving are the Boyle law and the Henry law. The Boyle law states that, at a constant temperature, the volume of a gas varies inversely with its pressure. The Henry law states that the amount of gas dissolved in liquid or in human tissues at a given temperature is a function of its partial pressure. The Boyle law and the Henry law are the underlying mechanisms responsible for the 2 major types of hyperbaric injury: pulmonary barotrauma and decompression sickness (DCS), respectively.
Also called pulmonary overinflation syndrome, pulmonary barotrauma occurs when gas expansion in the lungs ruptures the lung tissue. Typically, this is caused by breath-holding on ascent, by a rapid or unconscious ascent, or by air trapped in the lungs on ascent. Air trapping is most commonly caused by asthma, secretions, pneumonia, and blebs. AGE, pneumothorax, mediastinal emphysema, subcutaneous emphysema, and pneumopericardium can result. An AGE is the result of a lung rupture that also ruptures veins or capillaries, shunting gas to the left side of the heart and distributing it to end organs. The most common signs and symptoms are cranial nerve deficits, paralysis or weakness, sensory abnormalities, poor coordination, and unconsciousness. More than 98% of AGEs manifest within 10 minutes after the initial injury. Pneumothorax or tension pneumothorax can result if gas is released into the pleural space. Pneumopericardium, mediastinal emphysema, and subcutaneous emphysema occur when gas escapes through the connective tissues in the thorax.
DCS is also known as decompression illness, the bends, and Caisson disease. DCS is caused by the formation of microbubbles in the tissues as a result of decreasing ambient pressure. Its pathophysiology is based on the mechanical and nonmechanical effects of the bubbles. The mechanical effects are limited to hypoxic injury caused by blocked blood flow and compression of localized tissues and surrounding structures. The nonmechanical effects are diverse; however, those most widely studied and understood are an inflammatory response, an intravascular aggregation of platelets and leukocytes, and stimulation of the clotting cascade.
The mechanical and nonmechanical effects combine to create the clinical picture of DCS. Most cases become apparent within the first hour, and >98% manifest within 24 hours. DCS is clinically separated into 2 types: type I and type II. DCS type I causes musculoskeletal joint pain, skin itching and marbling, and lymphatic swelling or tender lymph nodes. DCS type II leads to pulmonary, vestibular, or neurologic signs and symptoms. Type I is by far more common than type II, and the prognosis is typically more favorable for type I than for type II. Treatment is the same for type I and type II. Hyperbaric oxygenation treats both the mechanical and nonmechanical effects, by crushing the bubbles in the blood or tissues and by increasing the oxygen levels in the injured tissue.
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