Brian K. Snyder
Underwater diving, with or without the breathing of compressed gas, usually takes place without incident. However, injuries during diving can occur. These injuries are generally secondary to pressure changes (barotrauma) or the effect of gas bubbles in the vascular system and tissues (arterial gas embolism [AGE] and decompression sickness [DCS]). Other injuries associated with compressed air diving include gas toxicity and immersion pulmonary edema. Aviators and others exposed to hypobaric environments can be similarly injured, also as a result of atmospheric pressure changes.
Any discussion of diving injuries requires an understanding of gas physics (Table 362.1). In diving medicine, pressure is commonly referred to in units of atmospheres absolute (ATA) or feet of seawater (fsw) (Table 362.2). As the most basic concept, pressure and volume are inversely related (Boyle law). Changes of volume and pressure in gas-containing organs of the body during descent and ascent lead to barotrauma. According to Dalton law and Henry law, compressed gas breathing at depth will lead to an increase of partial pressures of gas within the lung, vascular system, and tissues of the diver. A subsequent decrease in ambient pressure allows the gas to expand in volume and this is what can lead to DCS.
TABLE 362.1
Gas Laws
TABLE 362.2
Pressure Units and Equivalents
Barotrauma occurs either during descent (more common) or ascent (more dangerous). Structures potentially injured during descent are the middle and inner ear and the sinuses. The lung is the structure most likely to be injured during ascent, but fortunately, this is uncommon.
DCS or “the bends” occurs during ascent and is the result of the occlusive and inflammatory effects of inert gas bubbles in the tissues and vascular system (1). At depth, inert gas will diffuse into and eventually saturate the tissues. During a controlled ascent, the gas leaches out of the tissue slowly in equilibrium with the saturation and does not form physical bubbles. If the ascent is too rapid, the ambient pressure decreases too quickly for the gas to stay dissolved and gas bubbles will form in the tissue and vascular system. The exact mechanism of bubble formation is unclear, although pre-existing micronuclei of gas may serve as the nidus for further bubble growth (1). In addition, inflammatory vascular microparticles resulting from decompression stress may be the mechanism of DCS (2). Given that bubbling often occurs without symptoms, the presence of bubbles are necessary but not sufficient to cause DCS, suggesting that there is a threshold beyond which symptoms occur.
Divers use decompression tables or special diving computers to determine safe dive exposures. Although unusual, DCS can occur even when dives conform to accepted decompression tables or computer algorithms. Factors that increase the risk of DCS include multiple dives, rapid ascent, and flying following a dive. Symptoms from DCS may improve during a subsequent dive (essentially recompression therapy) but can get worse on resurfacing (as the inert gas load increases). Because flying after diving further decreases pressure and may elicit or worsen DCS symptoms, divers are advised to refrain from flying for at least 12 to 24 hours after the last dive (3).
Bubbles may form in the circulation (usually the low-pressure venous system) or directly in tissues. Venous bubbles may cross right-to-left shunts in the heart (e.g., a patent foramen ovale) or the lungs and arterialize, leading to AGE. The pathophysiology of spinal cord DCS appears to be initial bubbling in the venous plexus system, causing first a decrease and then complete cessation of venous blood flow from the cord. Decreasing venous blood flow prevents dissolved nitrogen in spinal cord tissues from off-gassing, thereby forming in situ bubbles within the spinal cord (4).
Other mechanisms beside direct ischemic effects are prominent in DCS and AGE. The air–blood and air–endothelial interfaces are highly reactive, and initiate thrombotic and inflammatory processes. This causes leaky endothelium, leading to third spacing of fluids. Furthermore, adhesion and activation of neutrophils on the endothelium leads to the release of reactive oxygen species and other tissue-toxic neutrophil-derived moieties, causing a histopathology similar to an ischemia/reperfusion injury (5). Again, microparticles may be a mediator of this inflammation (2).
Inert gas, especially nitrogen, can cause narcosis at depth. Typically, symptoms start at depths of 100 ft or greater if breathing air. Further depth increases symptoms, including loss of fine motor skills and high-order mental processes and causes behavior similar to alcohol intoxication and may make activities at depth difficult or dangerous. Unconsciousness occurs below 300 ft. Symptoms improve on ascent. In addition, nitrogen narcosis may impair the diver’s memory of events during the dive (6).
Oxygen toxicity mainly affects the pulmonary system and the central nervous system (CNS). Pulmonary oxygen toxicity is unusual but can occur at partial pressures of oxygen at or below 1 ATA, as seen in patients requiring prolonged mechanical ventilation with high fractions of inspired oxygen. Symptoms include dyspnea, chest pain, cough, and decreased pulmonary function.
The CNS effects of oxygen usually begin to occur at depths when the partial pressure of oxygen in the breathing mixture is >1.6 ATA (220 fsw if breathing compressed air). Some divers may breathe oxygen-enriched air (“Nitrox”) with fractions of oxygen of 32% to 36%. Cerebral oxygen toxicity can occur at lesser depths and actually is the factor that limits diving depth with Nitrox. In addition, there are “oxygen rebreather” systems where the diver breathes in a continuous circuit of gas with more than 95% oxygen. With these systems, cerebral oxygen toxicity can occur at depths as little as 25 ft.
Clinical hyperbaric oxygen (HBO) treatments use oxygen partial pressures up to 3 ATA, although oxygen toxicity in hyperbaric chambers is unusual. Divers are more prone to cerebral oxygen toxicity as they are exerting themselves in a cold, wet environment. Cerebral oxygen toxicity is affected by cerebral blood flow and PaCO2. The mechanism is under investigation but may be caused by an increase in nitric oxide production (7).
CLINICAL PRESENTATION
The most common form of barotrauma seen in diving is a middle ear “squeeze.” During descent, air within the middle ear contracts as the pressure increases, causing inward movement of the tympanic membrane (TM). If the pressure in the middle ear is not equalized (by opening the eustachian tube with a Valsalva or other maneuver) the TM can be injured (8). Bleeding can occur within the TM or within the middle ear space, leading to a hemotympanum, or the TM may rupture. Similarly, a closed space in the external ear canal from occlusive material (e.g., wax or ear plugs) can bend the TM outward during descent and cause injury. The diver with otic barotrauma will present with a history of difficulty clearing the affected ear, pain, a conductive hearing loss, and sometimes vertigo.
Without adequate sinus ventilation during descent, pressure will increase in the sinuses, leading to pain and possibly a bloody nasal discharge as the mucosa is stripped from the periosteum. This may cause dramatic bleeding into the diver’s face mask.
The inner ear can also be injured secondary to pressure changes. During descent, a forceful Valsalva maneuver can damage the round or oval window of the cochlea, potentially forming a fistula. The diver with inner ear barotrauma will present with a history of difficulty clearing the ears, the use of a forceful Valsalva maneuver, and sudden onset of severe vertigo, tinnitus, and hearing loss. On examination, the patient will have severe vertigo, a sensorineural hearing loss, and possibly a positive “fistula test.” The fistula test involves insufflation of air onto the TM. The test is positive if eyes deviate to the contralateral side. The patient with inner ear barotrauma may also have signs of middle ear barotrauma (8).
During ascent, gas volumes increase as the pressure decreases. Generally, divers have no problems with their ears or sinuses during ascent (with some exceptions, see alternobaric vertigo below), because gas leaves the middle ear as the eustachian tube opens spontaneously or leaves the sinuses through the ostia. Barotrauma of ascent generally involves the lung. The most common scenario leading to pulmonary barotrauma is a panicked, rapid, or out-of-air ascent. With breath-holding during ascent, the glottis is closed, and the expanding gas cannot escape, causing rupture of alveoli. Congenital or acquired gas-trapping pulmonary processes (e.g., a cyst or bleb or asthma) may also result in lung barotrauma. Once the lung ruptures, gas can collect in the mediastinum (pneumomediastinum), interstitium of the lungs (pulmonary emphysema), in the pleural space (pneumothorax), or in the vascular system as an AGE. Divers with pneumomediastinum or pneumothorax will present with chest pain, dyspnea, and possibly subcutaneous emphysema. A chest radiograph will generally show the abnormal collection of gas but is not completely sensitive (4).
Although gas from an AGE will systemically embolize, the most prominent organ involved is the brain (cerebral arterial gas embolism or CAGE). A diver with CAGE will develop symptoms during ascent or immediately on surfacing. Symptoms include altered level of consciousness, hemiplegia or hemiparesis, seizure, or other cerebral dysfunction. Sudden death may occur. If the patient survives the initial event, he may spontaneously improve as gas is forced through the cerebral vascular system by a spike in blood pressure. Any neurologic symptoms in the setting of pulmonary barotrauma should be thought to be secondary to CAGE and appropriate therapy quickly initiated (4). CAGE can also be caused by the iatrogenic introduction of gas into the vascular system, such as the inadvertent injection of air, the insertion or removal of central vascular catheters, neurosurgical procedures or procedures requiring cardiopulmonary bypass, cesarean section, or peritoneal insufflation for laparoscopy. Symptoms and classification of DCS depend on the organs affected. Type I DCS (“pain only”) involves the joints, extremities, and skin. Lymphatic obstruction can cause lymphedema, which usually takes days to resolve despite recompression therapy. Type II DCS (or “serious” DCS) includes “neurologic DCS” involving the CNS (mainly the spinal cord in compressed-air sport divers), vestibular DCS (“staggers”), and cardiopulmonary DCS (“chokes”).
The symptoms of DCS usually occur minutes to several hours after surfacing, but cases of DCS symptoms occurring days after diving have been reported. The pain of type I DCS is typically described as deep and unrelieved, but not worsened, with movement. Since divers can injure themselves in other ways (strains, direct trauma), pain from DCS can be confused with or attributed to pain from these injuries. Distention from bubbles in ligaments, fascia, and long bones or the activation of stretch receptors caused by bubbles in tendons are thought to be the mechanism of pain. This mechanism is supported by the rapid improvement of type I DCS symptoms with recompression. The most common locations for type I DCS are knees and shoulders, and frequently only a single joint is involved. Diffuse and difficult to describe back pain may herald the more serious signs of spinal cord DCS.
The classic description of neurologic DCS (type II) begins with this sensation of truncal constriction or girdle-like pain. A “wooly feeling” may begin in the feet and develop into an ascending paralysis. This produces a presentation similar to a transverse myelitis. This form of neurologic DCS is usually rapid in onset and has a tendency to affect the lower cervical and thoracic regions.
In type II DCS, neurologic deficits do not necessarily follow distinct spinal cord syndromes seen with trauma or ischemia. Furthermore, because lesions are scattered throughout the spinal cord, a definitive “level” is frequently not found. Incontinence and sexual dysfunction from autonomic involvement is common.
Pulmonary DCS, or “the chokes,” is generally seen only after prolonged, deep diving. This syndrome is caused by large numbers of pulmonary artery bubbles and presents with cough, hemoptysis, dyspnea, substernal chest pain, or cardiovascular collapse. Vestibular DCS, or “the staggers,” also usually occurs after deep, long dives, although it is increasingly being reported in sport divers. It presents with vertigo, hearing loss, tinnitus, and disequilibrium. These symptoms are similar to inner ear barotrauma; however, they occur more gradually and after ascent whereas other historical clues are also helpful in distinguishing the two distinct processes (4).
Cerebral oxygen toxicity manifests itself with twitching, nausea, paresthesias, dizziness, and seizures. A seizure may be the initial manifestation of cerebral oxygen toxicity and may cause drowning when it occurs in the water. Immersion pulmonary edema can occur while diving and swimming. Typical symptoms include dyspnea, chest discomfort, and coughing of pink frothy secretions. The mechanism of this condition is unknown. It is not caused by decompression. Hydrostatic forces, thermal stress, and possibly increased capillary permeability may be involved (9,10).
DIFFERENTIAL DIAGNOSIS
The diver with vertigo may present a diagnostic challenge. Vertigo caused by transient unequal clearing of the ears is called alternobaric vertigo and can be confused with more dangerous processes such as inner ear barotrauma or vestibular DCS (Table 362.3). The diagnosis can be complicated by a combination of injuries: for example, a diver sustains inner ear barotrauma, causing panic, leading to a rapid ascent and CAGE. The major confusion in the diagnosis of vertigo is differentiating inner ear barotrauma from CAGE. Because HBO treatment for CAGE can worsen inner ear barotrauma, this distinction is important. However, if one cannot distinguish between the two conditions or both may have occurred, myringotomies to decompress the middle year can be performed before commencing HBO.
TABLE 362.3
Differential Diagnosis of Vertigo in the Diver
Another difficult distinction is between CAGE and DCS. In fact, the two conditions can occur concurrently (type III DCS) (4). Some authorities do not distinguish between the two entities and call all bubble-related diving injuries decompression illness (DCI). The argument for this approach is that sometimes DCS and AGE cannot be reliably distinguished and the primary treatment is the same. Some oppose the term DCI because although sometimes indistinguishable, the two processes can often be separated. In addition, although primary therapy may be the same, adjunctive therapies may be specific (e.g., lidocaine in CAGE), and research may be hindered by such a lack of distinction.
CAGE usually occurs immediately or soon on surfacing after a rapid or uncontrolled ascent with mainly cerebral symptoms, such as altered level of consciousness, seizure, or hemiplegia. On the other hand, symptoms of DCS begin minutes to hours after the dive and although cerebral symptoms can occur, neurologic symptoms and signs usually refer to the spinal cord. CNS trauma, near-drowning, and hypothermia should be considered in the differential diagnosis of these conditions.
ED EVALUATION
The history should include details regarding the dive profile, symptom latency, severity, progression, and pre-existing health. Vital signs should include measurement of oxygen saturation. The physical examination should focus on the cardiopulmonary and neurologic systems and the ears, nose, and throat. Patients with chest signs and symptoms or altered mental status should have an ECG and undergo continuous cardiac monitoring. Evaluation for cardiac ischemia or dysfunction should be considered in patients with an abnormal ECG, pulmonary edema, or unexplained chest complaints, particularly those with risk factors for cardiovascular disease. Although routine laboratory studies are not helpful in the diagnosis or treatment of diving injury, they may evaluate for other conditions, if clinically indicated.
KEY TESTING
A chest radiograph is likely the only “routine” test in evaluating injured divers with potential cardiopulmonary complaints, CAGE or DCS. CNS imaging should not delay definitive treatment (HBO).
ED MANAGEMENT
Patients with uncomplicated barotrauma to the middle ear or sinuses should be treated symptomatically with decongestants such as oxymetazoline (Afrin) or pseudoephedrine and analgesics. Antibiotics can be prescribed in the cases of a perforated TM or sinus barotrauma occurring in contaminated water.
Patients with inner ear barotrauma should constantly sit up and avoid maneuvers that increase intracranial pressure (nose blowing, etc.). Some otolaryngologists advocate conservative treatment with antivertigo and antiemetic drugs such as meclizine (Antivert), reserving surgical intervention to those who do not improve spontaneously, although others advocate for immediate surgical exploration (8).
Patients with pneumomediastinum but no sign of CAGE can be managed conservatively. Those with more than a very small pneumothorax should have it evacuated, and a chest tube must be inserted if HBO therapy is to be employed.
Patients with suspected DCS or CAGE should receive 100% oxygen by nonrebreather face mask or endotracheal tube if necessary to ensure an intact airway. Recompression with HBO should occur as soon as possible, with transfer to a recompression center if necessary. Outcomes seem to correspond to the timeliness of HBO therapy. Although there are several recompression treatment tables employed in the treatment of DCS or CAGE, the most common is the US Navy Treatment Table 6 (with a maximum treatment pressure of 60 ft or 2.8 ATA). Lower treatment pressures have also been used with good results (11). If symptoms do not fully resolve, some centers will continue HBO treatments daily or twice daily until symptoms plateau. Divers with DCS have responded to HBO days after injury, and therefore this should be instituted even if presentation is delayed.
There are several beneficial physiologic effects of HBO. Increased pressure reduces bubble size. Increased partial pressure of oxygen dissolved in serum creates a gradient, causing nitrogen to move from bubbles into serum, increasing off-gassing of inert gas. Oxygen, in turn, moves into bubbles, but because it is metabolically active, it subsequently moves into cells, leading to further dissolution of bubbles. HBO increases the oxygen dissolved in the plasma which increases oxygen delivery to ischemic tissues, as well as decreasing edema and intracranial pressure, and reducing the adherence and activation of leukocytes on vascular endothelium (12).
Divers with CAGE should be kept supine with the head in a neutral position. The Trendelenburg position should not be employed.
Nondextrose-containing isotonic intravenous (IV) fluids should be infused to preserve tissue perfusion in divers with DCS and CAGE. Various pharmaceutical adjuncts have been used in the treatment of DCS and CAGE, including aspirin, corticosteroids, and heparin but animal studies and human experience have generally shown no definite benefit (13). IV lidocaine in the treatment of CAGE has been shown to be effective in animal models and in a human study examining neuropsychiatric outcomes after cardiopulmonary bypass (where neuropsychiatric deficits are thought to be secondary to intravascular air) (14). Typical cardiac doses are generally used.
Oxygen and nitrogen toxicity and immersion pulmonary edema resolve spontaneously. Treatment is primarily supportive. If immersion pulmonary edema is severe or persistent, standard treatments for this condition can be administered (9).
Clinicians unfamiliar with the treatment of underwater diving injuries should consult a diving or hyperbaric medicine specialist or the Divers Alert Network (DAN; phone: 1-919-684-9111; website: http://www.diversalertnetwork.org). DAN has staff available 24 hours a day to provide assistance to divers and clinicians and can provide the location of the nearest hyperbaric facility.
CRITICAL INTERVENTIONS
• Obtain a chest radiograph on patients with cardiopulmonary complaints. If the chest radiograph is normal, consider evaluation for acute coronary syndrome or other cardiac or pulmonary process, especially if the dive profile and symptoms do not suggest a high probability of DCS or AGE
• Administer oxygen and IV fluids and arrange for HBO therapy for patients with DCS and CAGE.
• Remember that medical conditions not related to barotrauma or decompression can occur in or around the water and the physician must be careful to evaluate for such processes.
DISPOSITION
Patients with pulmonary barotrauma but without evidence of CAGE do not require recompression therapy. Those with suspected DCS or CAGE should be transferred to a facility capable of providing HBO therapy. A diver may require hospitalization or repetitive treatments after initial therapy.
Given that treatment of inner ear barotrauma is controversial, emergent otolaryngology consultation may be obtained for patients with this condition.
Patients with barotitis or sinus barotrauma should not return to diving until symptoms resolve. Those with a perforated TM must not dive until it heals. Otolaryngology referral in 4 to 6 weeks is warranted.
Ideally, divers with DCS or CAGE should be examined by a physician experienced or trained in diving medicine before returning to diving. Counseling of divers experiencing immersion pulmonary edema is difficult as it cannot be predicted who will experience another episode.
Common Pitfalls
• Failure to appreciate that significant barotrauma can occur at shallow depths.
• Failure to consider the possibility of DCS or CAGE in any patient with neurologic symptoms after underwater diving.
• Failure to consult a diving or hyperbaric medicine specialist or the Divers Alert Network for advice and to consider HBO even when the diagnosis is not clear.
• Failure to consider inner ear DCS or barotrauma in the vertiginous diver and failure to differentiate between the two processes.
• Failure to have divers’ follow-up with a physician experienced in diving medicine beforereturning to diving.
REFERENCES
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