The Undersea and Hyperbaric Medical Society has defined clinical indications for HBO therapy, some of which are within the scope of emergency medicine practice (Table 21-2).3
TABLE 21-2Indications for Hyperbaric Oxygen Therapy ||Download (.pdf) TABLE 21-2 Indications for Hyperbaric Oxygen Therapy
Arterial gas embolism with neurologic symptoms*
Carbon monoxide poisoning*
Crush injury, compartment syndrome, and other acute traumatic ischemias*
Exceptional blood loss anemia*
Delayed radiation injury (osteoradionecrosis and soft tissue)
Compromised skin grafts and flaps
Acute thermal burns*
Arterial insufficiencies (enhancement of healing in selected problem wounds, central retinal artery occlusion)
Necrotizing soft tissue infections*
Clostridial myonecrosis (gas gangrene)*
Air or gas embolism can occur as a consequence of a deep sea dive–related accident4 or as the result of a medical procedure.5 Iatrogenic air or gas embolism has been reported in association with cardiovascular, obstetric/gynecologic, neurosurgical, and orthopedic procedures, generally associated with disruption of a vascular wall.6 Nonsurgical processes reported to cause air or gas embolism include overexpansion during mechanical ventilation, hemodialysis, and after accidental opening of central venous catheters. Air or gas embolism can occur either on the venous or arterial side of the circulatory system.
The consequences of an arterial gas embolism depend on location and magnitude of arterial occlusion. Often skeletal muscle, connective tissue, and skin can tolerate small emboli, but bubbles entering the coronary or cerebral arteries can precipitate acute coronary syndrome or stroke. Air entering the spinal cord circulation can produce weakness or paralysis. Any diver who surfaces with sudden onset of neurologic symptoms, such as confusion, speech difficulty, focal weakness, or paralysis, in less than 5 to 10 minutes should be assumed to have arterial gas embolism unless proven otherwise. Imaging with CT or MRI may help exclude an ischemic stroke or intracerebral hemorrhage. CT scan of the brain may show air in the cerebral vessels; however, this finding is variable and can be difficult to recognize (Figure 21-3).
Head CT demonstrating air in cerebral vessels before hyperbaric oxygen treatment (left) and eradication after treatment (right).
Venous gas embolism is common after compressed-gas diving and surgical procedures.6 The amount of gas is typically small, and the bubbles are trapped in the pulmonary capillaries and resorbed without symptoms. Large quantities of gas in the pulmonary vasculature can stimulate cough, dyspnea, and pulmonary edema. A paradoxical arterial gas embolism may develop when a venous gas embolism travels to the arterial system by way of an intrapulmonary shunt or through an atrial septal defect or patent foramen ovale.
Administer oxygen to support arterial oxygenation and hasten bubble resorption. Place the patient in the supine position; there is no proven benefit to a head-down position to lower the risk of additional cerebral air embolization or a left lateral decubitus position to trap gas within the apex of the right ventricle and minimize migration. Catheter aspiration of trapped air in the right ventricle may be attempted in those rare instances when it is visualized.
HBO is recommended for air or gas embolism with neurologic or cardiovascular impairment.3 The faster the patient receives HBO, the greater is the chance for complete neurologic recovery. Various protocols are used for air or gas embolism. A standard one is Treatment Table 6 from the U.S. Navy Diving Manual, which uses compression to 2.8 ATA for 75 minutes (with three air breaks), following by decompression to 1.8 ATA for 150 minutes (with two air breaks) for a total treatment time of 285 minutes. For patients whose symptoms are not improved or worsen, a protocol using pressurization up to 6 ATA (Treatment Table 6A) is recommended. For patients with residual symptoms after the initial HBO treatment, additional treatments are recommended until there is no further neurologic improvement, typically one to two additional treatments.
Decompression sickness is due to the formation of nitrogen bubbles in body tissue and circulation during decompression (see chapter 214, "Diving Disorders").7 During pressurization, inert gas (nitrogen if breathing air) is dissolved in body fluids. Upon reduction in ambient pressure, the dissolved gas comes out of solution and forms small bubbles in the tissue and circulation. HBO is an effective treatment because the increase in ambient pressure reduces gas bubble volume and the supplemental oxygen hastens inert gas diffusion out of the body.
Decompression sickness should be treated with HBO when such therapy is available and no contraindication exists. If HBO therapy is not available, patients with mild symptoms and neurologic stability for longer than 24 hours may be treated with supplemental oxygen therapy alone. If a patient must be transported by air to a hyperbaric facility, use pressurized aircraft to maintain sea-level pressure or transport at the lowest possible altitude in a nonpressurized craft, such a helicopter.
A variety of HBO regimens are used to treat decompression sickness,8 but most have in common pressurization to 2.8 ATA for 60 to 90 minutes, followed by stepwise decompression, similar to U.S. Navy Diving Manual Treatment Table 6. Most patients respond to a single treatment. Gas bubbles can persist for several days, and HBO may be beneficial even when begun after long delays.8
CARBON MONOXIDE POISONING
Carbon monoxide (CO) toxicity develops from impairment of hemoglobin function and direct CO-mediated cellular damage (see chapter 222, "Carbon Monoxide"). The affinity of CO for hemoglobin, forming carboxyhemoglobin, is more than 200-fold greater than that of oxygen. Carboxyhemoglobin cannot carry oxygen, so as the level rises, the oxygen-carrying capacity of blood decreases, inducing hypoxic stress initially on organs most dependent on oxidative metabolism—the brain and heart. After removal from continued CO exposure, the CO slowly dissociates from the hemoglobin and is metabolized or exhaled, and the carboxyhemoglobin levels fall. Treatment with HBO enhances the decline of carboxyhemoglobin levels, more rapidly restoring oxygen-carrying capacity of the blood. In animal models of CO poisoning, HBO treatment ameliorates pathophysiologic events associated with CNS injuries mediated by CO, such as improvement in mitochondrial oxidative processes,9 inhibition of lipid peroxidation,10 and impairment of leukocyte adhesion to injured microvasculature.11 Animals poisoned with CO and treated with HBO have more rapid improvement in cardiovascular status,12 lower mortality,13 and lower incidence of neurologic sequelae.14
Five prospective, randomized trials have assessed clinical efficacy of HBO for acute human CO poisoning.15,16,1718,19 Three did not find benefit,15,17,18 but have been criticized for methodologic weaknesses that may have affected results.20,21,22,23 The clinical trial from Salt Lake City found a significant reduction in neuropsychological sequelae at 6 weeks in HBO-treated patients.19 This study has been analyzed and debated by advocates and critics of HBO treatment.24 The results have been considered an outlier by meta-analysis that concluded there is no evidence that HBO reduces incidence of adverse CO-mediated neurologic outcomes.25,26 Despite the uncertainties, HBO treatment should at least be considered in cases of serious acute CO poisoning because 1) the neurologic sequelae can be severe, 2) retrospective analysis found that HBO was associated with diminished acute mortality,20 and the Salt Lake City trial found benefit.27
The Salt Lake City protocol for CO poisoning uses pressurization to 3 ATA for 60 minutes, with two air breaks, followed by a reduction in pressure to 2 ATA for 65 minutes with one air break.19 Two additional treatments are given in 6- to 12-hour intervals. An alternative protocol uses 2.8 ATA for 30 minutes followed by 2.0 ATA for 90 minutes.
Concomitant cyanide and CO poisoning may be seen in patients rescued from closed-space fires in which synthetic materials are burned. Experimental evidence suggests that cyanide and CO can produce synergistic toxicity.28,29,30 HBO may directly reduce cyanide toxicity31,32 or augment other antidote treatments.33 However, clinical experience with HBO for cyanide toxicity is sparse.34,35,36,37,38
Cyanide is among the most lethal poisons, and toxicity is rapid, so standard antidotal therapy for isolated cyanide poisoning is of primary importance. HBO can be considered in case of dual CO and cyanide poisoning and in cyanide poisoning when vital signs and mental status do not improve with antidote treatment.
EXCEPTIONAL BLOOD LOSS ANEMIA
In cases of severe anemia where transfusion cannot effectively improve oxygen content to sustainable levels (e.g., Jehovah's Witness, Rh incompatibility/transfusion reactions, patient refusal), HBO aids in sustaining life.39 Anecdotal reports describe using 100% oxygen at 2.5 to 3.0 ATA to raise PaO2 in plasma to meet metabolic needs.40,41,42,43 Treatments are administered for 3 to 4 hours, with air breaks, with sessions up to four times per day, and continued until red blood cell concentration improves.
ACUTE THERMAL BURN INJURY
Some burn centers use adjunctive HBO for severe burns. This is not a universal practice, and controversy persists.44 Animal models have documented benefits with HBO in reducing partial- to full-thickness skin loss, hastening epithelialization, and lowering mortality.2 Randomized clinical trials with small patient numbers have reported improved rates of healing with shorter hospitalization stays.45,46,47,48 Uncontrolled series have reported mixed results.49,50,51 A typical HBO protocol for thermal burns uses pressurization to 2.4 ATA for 100 minutes with two air breaks. Treatments are initiated at three sessions a day, then decreased to twice a day as healing occurs, and continued up to a total of 45 sessions.
NECROTIZING SOFT TISSUE INFECTIONS
Necrotizing soft tissue infections, such as necrotizing fasciitis and Fournier's gangrene, are typically mixed aerobic-anaerobic infections. HBO is potentially beneficial due to its ability to suppress growth of anaerobic microorganisms and improve bactericidal action of leukocytes that function poorly in hypoxic conditions.52,53,54,55
Variation in time of diagnosis and clinical status at time of admission make analysis of the six nonrandomized comparisons and four case series using HBO to treat necrotizing soft tissue infection too complex to yield a straightforward conclusion.56–65 Most studies have reported that when HBO is added to surgery and antibiotic therapy, mortality is reduced. Typical HBO therapy for necrotizing soft tissue infection uses pressurization to 2.4 ATA for 100 minutes with two air breaks, with treatments started at two sessions per day and then decreased to once a day for up to a total of 30 sessions.
CLOSTRIDIAL MYONECROSIS (GAS GANGRENE)
Gas gangrene is a serious infection with high morbidity and mortality. When tissue PO2 reaches about 250 mm Hg, α toxin production stops. Once production is halted, α toxin is rapidly cleared.66 In addition, HBO suppresses the growth of clostridial organisms.66 HBO therapy of gas gangrene has been the subject of five retrospective comparisons and 13 case series, along with separate analysis.2,67,68,69 Assessment of HBO therapy efficacy based on mortality or "tissue salvage" rates is difficult due to variation in patients and clinical practice. Most authors report clinical benefit from treatment, especially the often dramatic temporal improvement of vital signs. A typical HBO therapy protocol for gas gangrene follows the U.S. Navy Diving Manual Treatment Table 21-5: pressurization to 2.8 ATA for 45 minutes with one air break, followed by a slow reduction in pressure over 30 minutes to 1.8 ATA, maintaining pressure there for 30 minutes with two air breaks, followed by decompression, for a total treatment time of 135 minutes. Three treatments are done the first day, and two treatments are done each day for 4 to 5 days more.
CRUSH INJURY, COMPARTMENT SYNDROME, AND OTHER ACUTE TRAUMATIC ISCHEMIAS
The rationale for considering HBO therapy in crushed and ischemic tissues is to temporarily improve oxygenation to hypoperfused tissues and promote arterial hyperoxia, which will cause vasoconstriction and diminish edema formation.70 This latter mechanism has been convincingly demonstrated in experimental compartment syndrome.71 A single randomized controlled trial (involving 36 patients) with crushed limbs found that HBO therapy improved healing and reduced infection and wound dehiscence.72 In a case series of 23 patients, HBO resulted in limb preservation.73 Comparative evaluation of HBO treatment for complex extremity wounds sustained from bullets or explosions also showed considerable benefit.74 HBO therapy can be considered when complications or poor outcomes are thought to be likely despite appropriate surgical and medical care.
A typical HBO protocol for these injuries is pressurization to 2.4 ATA for 100 minutes, with two air breaks. Treatments are started at three sessions per day for 2 days, then decreased to twice a day for 2 days and then once a day for 2 days, for a total of 12 sessions.
CENTRAL RETINAL ARTERY OCCLUSION
Central retinal artery occlusion is rare yet devastating and can result in permanent vision loss. There is fair to good evidence based on retrospective case series that HBO therapy started with 24 hours after the onset of symptoms will improve outcome.3,75 Standard therapies, such as supplemental oxygen and lowering intraocular pressure, are recommended until HBO can be initiated.1,3
A typical HBO therapy protocol would be pressurization to 2.0 ATA; if vision improves with this pressure, the patient is treated for 90 minutes with two air breaks. Treatments are done twice a day and continued until there is no improvement in vision after 3 consecutive days. If pressurization to 2.0 ATA does not produce improvement, pressurization to 2.8 ATA is used.