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CHAPTER 21:  Hyperbaric Oxygen Ther apy      137 TABLE 20-7 Angiotensin II Pharmacokinetics Metabolism Excretion Half-Life Onset/Duration of Action Enzymes found in the plasma, red blood cells, kidney, liver, and lungs Not reported by manufacturer <1 min Onset 5 min with infusion (median); duration up to 3 h TABLE 20-8 Dobutamine Pharmacokinetics Metabolism Excretion Half-Life Onset of Action/ Peak Effect In tissues and hepatically to inactive metabolites Urine (as metabolites) 2 min Onset: 1–10 min Peak: 10–20 min TABLE 20-9 Milrinone Pharmacokinetics Metabolism Excretion Half-Life Onset of Action Hepatic (minor); majority is not metabolized Urine (83% as unchanged drug; 12% as metabolites) 2.3–2.4 h Onset: 5–15 min Indications Angiotension II is indicated for septic or other distributive shock when other drugs such as norepinephrine have failed to increase mean arterial pressure to target levels.4,20,21 Dosing and Administration See Table 20-1. Adverse Effects Adverse effects include thromboembolic events (12.9%), thrombocytopenia (9.8%), tachycardia (8.6%), fungal infection (6.1%), delirium (5.5%), and acidosis (5.5%). 21,22 INOTROPES  DOBUTAMINE Actions Dobutamine is a synthetic dopamine analogue with potent inotropic and mild vasodilatory and chronotropic effects. It competi tively binds and stimulates α- and β-receptors (β 1 > β 2 > α 1), resulting in increased contractility and heart rate with neutral effect or possible decrease in blood pressure. Pharmacokinetics See Table 20-8.4 Indications Dobutamine is indicated for the short-term management of patients with acute cardiac decompensation, particularly in patients presenting with cardiogenic shock. Dobutamine can also be used for patients with persistent hypoperfusion despite adequate fluid resuscita tion and the use of vasopressor agents. Dosing and Administration See Table 20-1. Adverse Effects Adverse effects include hypertension, tachyarrhyth mia, headache, angina, and hypokalemia.  MILRINONE Actions Milrinone is an inotrope with vasodilator properties (inodi lator) that selectively inhibits the phosphodiesterase type III enzyme, resulting in the inhibition of cyclic adenosine monophosphate break down in myocardial and vascular smooth muscle cells. Increased cyclic adenosine monophosphate levels result in increased cardiac contractil ity, peripheral arterial and venous vasodilation, increased cardiac out put, and reduced systemic vascular resistance. Pharmacokinetics See Table 20-9.4 Indications Milrinone is used for the short-term treatment of acute decompensated heart failure. It is typically encountered in the ED when used as a short-term bridge to heart transplant or left ventricular assist device placement or as a continuous pump infusion for patients at home. In the ED, it is most commonly ordered in conjunction with cardiology or the heart failure service. Dosing and Administration See Table 20-1. Adverse Effects Adverse effects include ventricular and supraven tricular arrhythmias, hypotension, angina, and headache. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Hyperbaric Oxygen Therapy Tracy Leigh LeGros Heather Murphy-Lavoie INTRODUCTION Hyperbaric oxygen (HBO) therapy is a medical intervention in which a patient breathes continuous or intermittent 100% oxygen while inside a hyperbaric chamber that is pressurized to an ambient pressure greater than sea level.

tinalliEM.com. Hyperbaric Oxygen Therapy Tracy Leigh LeGros Heather Murphy-Lavoie INTRODUCTION Hyperbaric oxygen (HBO) therapy is a medical intervention in which a patient breathes continuous or intermittent 100% oxygen while inside a hyperbaric chamber that is pressurized to an ambient pressure greater than sea level. 1 HBO therapy results in the systemic delivery of oxygen that produces supraphysiologic oxygen tension in perfused tissues. The effects of HBO therapy are due to the combined effects of both increased ambient pressure and increased oxygen tension. Monoplace chambers accommodate a single occupant. An attendant monitors the patient from the outside and communicates via intercom. Specially designed cardiopulmonary monitoring devices, IV infusion pumps, and ventilators enable critically ill patients to be treated in monoplace chambers. Multiplace chambers (Figure 21-1) can simultaneously treat multiple patients and will accommodate medical personnel inside the chamber to perform hands-on patient assessment and care. Monoplace chambers generally use 100% oxygen for pressurization, whereas multiplace units are pressurized with air and patients breathe oxygen using a tight-fitting facemask, a hood, or an endotracheal tube while inside. Ambient pressure is an important concept in HBO therapy. At sea level, the pressure exerted by the air column (the atmosphere) above is quantified as 1 atmosphere absolute of pressure (ATA), 760 mm Hg, 760 torr, or 101 kPa. Once a patient is placed inside a chamber, the ambient pressure is increased by the gradual inflow of compressed gas, either oxygen or air. Most HBO therapy uses pressures between 2.0 and 3.0 ATA (202 to 303 kPa). A typical HBO treatment lasts 90 to 120 minutes. HBO therapies are performed using preset protocols that define pres surization level, treatment duration, use of air breaks, and the number of HBO sessions in a course of therapy. The oxygen content of the blood is the sum of the oxygen carried by hemoglobin and oxygen dissolved in the plasma. Hemoglobin becomes fully saturated around a P o 2 of 100 mm Hg (13.3 kPa); fully saturated hemoglobin carries approximately 20 mL of oxygen per 100 mL of blood, which is expressed as 20 vol%. At 1 ATA breathing room air, dissolved oxygen in the plasma is typically only 0.3 vol%. At a pressure of 3 ATA inside an HBO chamber pressurized with 100% oxygen, the arterial oxygen tension (Pao 2) will approach 2200 mm Hg (293 kPa), which will bring the dissolved oxygen content up to about 5.4 vol%. 2 This amount of dissolved oxygen can sustain basal metabolic functions in the com plete absence of hemoglobin. PHYSIOLOGIC EFFECTS HBO therapy should be viewed as a drug and the hyperbaric chamber as a delivery device. HBO affects tissues in two ways: there are effects related to mechanical forces of increased pressure and effects due to CHAPTER Tintinalli_Sec03_p0053-0142.indd 137 8/2/19 2:57 PM

om plete absence of hemoglobin. PHYSIOLOGIC EFFECTS HBO therapy should be viewed as a drug and the hyperbaric chamber as a delivery device. HBO affects tissues in two ways: there are effects related to mechanical forces of increased pressure and effects due to CHAPTER Tintinalli_Sec03_p0053-0142.indd 137 8/2/19 2:57 PM 138 SECTION 3: Resuscitation FIGURE 21-1. The outer and inner configurations of a multiplace hyperbaric chamber at the University of Pennsylvania Department of Hyperbaric Medicine, Philadelphia, Pennsylvania. TABLE 21-1 Beneficial Effects of Hyperbaric Oxygen Therapy •   Provides hyperoxygenation: reverses tissue ischemia •   Limits toxin production: inhibits microbial endotoxin and exotoxin production •   Bacteriostatic and bactericidal: to obligate anaerobic microorganisms •   Reduces tissue edema: induces vasoconstriction-mediated reductions of inflow without reducing outflow in posttraumatic tissue beds •   Stimulates angiogenesis: promotes production of oxygen-dependent collagen matrix, increases wound growth factors synthesis, and mobilizes stem/progenitor cells from bone marrow •   Promotes osteogenesis: in hypoxic bone by providing osteoblast simulation and bone tissue regeneration •   Promotes wound healing:  by impairing B2 integrin function and the amplifying oxygen gradients surrounding ischemic wounds •   Diminishes inflammatory responses: by lowering monocyte chemokine synthesis and ischemic preconditioning changes in heme oxygenase-1, heat shock proteins, and hypoxia-inducible factor •   Augments fibroblast replication: increasing collagen formation •   Blunts ischemia-reperfusion injury: to endothelial tissue •   Increases red blood cell flexibility: facilitating increases in elastic deformation •   Enhances leukocyte bactericidal activity:  improves neutrophil oxygen-dependent peroxidase bactericidal activity •   Enhances antibiotic transport: increases antibiotic penetration into target bacteria •   Preserves intracellular adenosine triphosphate: supporting intracellular functions •   Terminates lipid peroxidation: obviating tissue destruction TABLE 21-2 Indications for Hyperbaric Oxygen Therapy Acute ischemic events Arterial gas embolism Decompression sickness Central retinal artery occlusion Sensorineural hearing loss Select problem wounds* Exceptional blood loss anemia Traumatic injuries Crush injury and compartment syndrome Other acute ischemias Acute thermal burns Compromised grafts and flaps* Gas toxicities Carbon monoxide poisoning Cyanide poisoning Infections Clostridial myonecrosis (gas gangrene) Necrotizing soft tissue infections Intracranial abscess* Refractory osteomyelitis* Radiation injuries* Osteoradionecrosis Soft tissue radionecrosis *These usual nonemergent indications for hyperbaric oxygen therapy are not discussed in detail. hyperoxygenation. Of the two, elevated tissue oxygen tension is thought to be the primary effect. Hyperoxygenation reverses tissue ischemia, but also induces the formation of reactive oxygen species, including superoxide, hydrogen peroxide, hypochlorous acid, hydroxyl, and reactive nitrogen species (primarily nitric oxide). This stimulates the body’s natural antioxidant defenses, strongly mobilizing the antioxidant enzyme system and thus improving defense from oxidative damage. 3 Highly elevated oxygen levels generated during HBO therapy have therapeutic beneficial effects seen after tissue oxygen levels return to normal ( Table 21-1). Reactive oxygen species are natural by-products of metabolism that can oxidize proteins and membrane lipids, damage DNA, and mediate tis sue and organ damage seen in oxygen toxicity.

n levels generated during HBO therapy have therapeutic beneficial effects seen after tissue oxygen levels return to normal ( Table 21-1). Reactive oxygen species are natural by-products of metabolism that can oxidize proteins and membrane lipids, damage DNA, and mediate tis sue and organ damage seen in oxygen toxicity. The body has scavenger antioxidant systems to reverse the oxidative damage caused by reactive oxygen species generated during HBO therapy (making oxygen toxicity rare) and that continue to protect the body against oxidative stress upon completion of HBO therapy. 4,5 INDICATIONS 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).  AIR OR GAS EMBOLISM Air or gas embolism can occur as a consequence of a deep-sea dive– related accident 6 or as the result of a medical procedure (Table 21-3),7-10 including emergent or urgent procedures performed within the ED. Diving accidents are discussed in Chapter 214, “Diving Disorders, ” and this chapter will focus primarily on iatrogenic embolism. Air or gas embolism can occur either on the venous or arterial side of the circula tory system. Venous gas embolism can occur after surgical procedures. 8,10 The amount of gas is typically small, and the air bubbles trapped in the pulmonary capillaries are resorbed without symptoms. Large quantities of gas in the pulmonary vasculature can stimulate cough, dyspnea, and pulmonary edema and, in severe cases, cause vapor lock. A paradoxical arterial gas embolism may develop when a venous gas embolism travels to the arterial system (right to left shunt) by way of an intrapulmonary shunt or through an atrial septal defect or a patent foramen ovale. The consequences of an arterial gas embolism depend on location and magnitude of arterial occlusion. Arterial gas embolism is a poten tially catastrophic event with a reported mortality rate of 20%.11 Skeletal muscle, connective tissue, and skin can often tolerate small emboli, but air entering the coronary, cerebral, or spinal circulation can precipitate Tintinalli_Sec03_p0053-0142.indd 138 8/2/19 2:57 PM

occlusion. Arterial gas embolism is a poten tially catastrophic event with a reported mortality rate of 20%.11 Skeletal muscle, connective tissue, and skin can often tolerate small emboli, but air entering the coronary, cerebral, or spinal circulation can precipitate Tintinalli_Sec03_p0053-0142.indd 138 8/2/19 2:57 PM CHAPTER 21:  Hyperbaric Oxygen Ther apy      139 acute coronary syndrome, stroke, or paralysis, respectively. The intro duction of intravascular sheaths, such as at the start of an interventional radiologic procedure, accounts for the greatest proportion of iatrogenic gas embolism. When suspected, administer supplemental oxygen to support arte rial 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 may be attempted in those rare instances when it is visualized and a preexisting catheter is in place; de novo placement of a vascular catheter to attempt air aspiration is controversial. HBO is definitive treatment for arterial gas embolism and is recom mended when there is neurologic or cardiovascular impairment. 10 Start treatment as soon as possible, but there is evidence of improved out comes out to 60 hours or longer.13-15 The most common protocol used is the U.S. Navy Treatment Table 6, which begins at 2.8 ATA, with a subsequent decompression to 1.8 ATA (total treatment time of 285 minutes). For patients whose symptoms are not improved or worsen, the U.S. Navy Treatment Table 6A (initial pressurization up to 6 ATA in a multiplace chamber) may be considered. For patients with residual symptoms after the initial HBO treatment, additional treatments are recommended until there is no further neurologic improvement.  DECOMPRESSION SICKNESS Decompression sickness is due to the formation of nitrogen bubbles in body tissue and circulation during decompression (see Chapter 214, “Diving Disorders”). These bubbles cause direct mechanical disruption of tissue, occlusion of blood flow, platelet deposition and activation of the coagulation cascade, endothelial dysfunction, capillary leakage, endothelial cell death, complement activation, and leukocyte-endothelial interaction. HBO treatment is the definitive treatment for decompression sickness and recommended in all cases of diving decompression sickness. If HBO therapy is not available, patients with mild symptoms who are stable for longer than 24 hours may be treated with supplemental oxygen alone. If a patient must be transported by air to a hyperbaric facility, use pres surized aircraft to maintain sea-level pressure or transport at the lowest possible altitude in a nonpressurized craft, such as a helicopter. A variety of HBO regimens are used to treat decompression sickness, but most centers use the U.S. Navy Treatment Table 6 and most patients with decompression sickness who receive rapid HBO therapy will respond to a single treatment. The U.S. Navy Treatment Table 9 may be used in patients with residual symptoms.  CENTRAL RETINAL ARTERY OCCLUSION Central retinal artery occlusion is rare, usually presenting as painless vision loss in one eye; without treatment, vision loss can be permanent. Poor outcomes occur because the occlusion is often the result of a cholesterol embolus that is not treatable with thrombolysis. HBO therapy produces a clinically significant visual improvement especially when instituted within 24 hours of onset.

s vision loss in one eye; without treatment, vision loss can be permanent. Poor outcomes occur because the occlusion is often the result of a cholesterol embolus that is not treatable with thrombolysis. HBO therapy produces a clinically significant visual improvement especially when instituted within 24 hours of onset. 18 There are no other central retinal artery occlusion therapies with similar outcomes.19,20 Adjunctive therapies (i.e., supplemental oxygen and lowering intra ocular pressure) are recommended until HBO can be initiated. The HBO central retinal artery occlusion protocol is 2.0 ATA for 30 minutes. If vision improves, the patient is treated for a total of 90 minutes. Treatments are done twice daily and continued until there is no visual improvement for 3 consecutive days. If vision does not improve at 2.0 ATA for 30 minutes, the pressure is raised to 2.4 to 2.8 ATA (titrating to effect with at-depth visual acuities) for a total of 90 minutes with air breaks. 20 If there is no improvement after eight treatments, visual recovery is unlikely.  SUDDEN SENSORINEURAL HEARING LOSS Sudden sensorineural hearing loss is hearing loss of at least 30 dB occurring over 3 days involving at least three contiguous auditory frequencies. 21 The usual presentation is of a patient awaking from sleep with a sudden unilateral hearing loss, aural fullness, and at times tinni tus and vertigo. The cause is unclear, and many mechanisms have been described, including ischemia, trauma, toxins, vascular occlusion, viral infections, immune-associated disease, abnormal tissue growth, and labyrinthine and/or cochlear membrane damage. HBO therapy is effective primarily by achieving extremely high arte rial perilymphatic oxygen concentrations. In combination with steroids, HBO therapy produces hearing gains over all frequencies. 22,23 HBO therapy is indicated for profound sudden sensorineural hear ing loss (>40 dB) within 14 days of symptom onset. 24 Patients with longer delays in presentation may benefit; the American Academy of Otolaryngology–Head and Neck Surgery advocates HBO therapy for up to 3 months after symptom onset. 25 It is essential that both corticosteroids (e.g., prednisone, 60 milligrams, orally, daily for 7 to 14 days and then tapered over 1 to 2 weeks) and HBO therapy (e.g., 100% oxygen at 2.0 to 2.5 ATA for 90 minutes daily for 10 to 20 sessions) be used together.  EXCEPTIONAL BLOOD LOSS ANEMIA In cases of acute severe anemia where transfusion cannot be used to improve oxygen content to sustainable levels (e.g., Jehovah’s Witness, Rh incompatibility/transfusion reactions, patient refusal), HBO aids in sustaining life. 26 The benefits of HBO include rectifying the oxygen debt, providing a bridge that corrects end-organ damage, and allowing time for the patient’s endogenous erythropoietin levels and baseline hemo globin to rise. The HBO treatment protocol is 100% oxygen at 2.5 to 3.0 ATA for 3 to 4 hours (with air breaks) up to four times daily to raise Pao 2 in plasma to meet metabolic needs until red blood cell concentra tion improves.27-30 Both animal studies and human clinical experience support the use of HBO for severe blood loss anemia. 31  CRUSH INJURIES Crush injuries damage multiple tissues, creating a cycle of edema and ischemia. Approximately half of patients with severe injuries develop complications such as osteomyelitis, fracture nonunions, amputations, and failed flaps despite optimal surgical and medical care. HBO treatment is effective in reducing complications and promoting healing in such patients. 32 The HBO protocol for crush injuries is 2.4 ATA for 100 minutes three times daily for 2 days, and then twice daily for 2 days, followed by once-daily sessions for 2 days.

ailed flaps despite optimal surgical and medical care. HBO treatment is effective in reducing complications and promoting healing in such patients. 32 The HBO protocol for crush injuries is 2.4 ATA for 100 minutes three times daily for 2 days, and then twice daily for 2 days, followed by once-daily sessions for 2 days.  COMPARTMENT SYNDROME Standard therapy for compartment syndrome is a fasciotomy to decompress the compartment and reverse ischemia of enclosed muscles and nerves. Fasciotomy itself has associated complications, and in the situation of impending compartment syndrome, HBO can improve oxygenation to hypoperfused tissues, promote arterial hyperoxia, decease vasoconstriction and edema, and prevent progression requiring TABLE 21-3 Iatrogenic Air or Gas Embolism Emergency Department Procedures Surgical Procedures Mechanical ventilation Chest tube placement Cardiopulmonary resuscitation Lumbar puncture Arterial or central line insertion/ removal Penetrating chest trauma Contrast mechanical injection Hemodialysis/dialysis catheter placement Cardiac surgery Bronchoscopy GI endoscopy Laparoscopy Hysteroscopy Cesarean section Prostatectomy Transurethral surgery Hip replacement Arthroscopy Spine surgery Neurosurgery in sitting position Endoscopic vein harvesting Vitrectomy Liver resection or transplantation Percutaneous organ puncture Tintinalli_Sec03_p0053-0142.indd 139 8/2/19 2:57 PM

y GI endoscopy Laparoscopy Hysteroscopy Cesarean section Prostatectomy Transurethral surgery Hip replacement Arthroscopy Spine surgery Neurosurgery in sitting position Endoscopic vein harvesting Vitrectomy Liver resection or transplantation Percutaneous organ puncture Tintinalli_Sec03_p0053-0142.indd 139 8/2/19 2:57 PM 140 SECTION 3: Resuscitation fasciotomy.34-36 After fasciotomy for established compartment syndrome, HBO can prevent wound healing complications and accelerate recovery. Approximately three to five HBO treatments are usually required.33  OTHER ACUTE TRAUMATIC ISCHEMIAS HBO therapy has been reported to be beneficial in other acute traumas that involve a self-perpetuating cycle of accelerating tissue damage from edema and ischemia, such as frostbite injuries 37,38; threatened grafts and flaps39; in-jeopardy digit amputations or replantations 33,40; ear amputations41-43; nose amputations44,45; penis injuries and amputations and postsurgical penile gangrene 46-49; snake envenomation 50; high-pressure water gun injection51; and electrical injury complications.52 HBO therapy is a noninvasive, economically advantageous, and clinically efficacious adjunc tive therapy to consider when complications or poor outcomes are likely despite appropriate surgical and medical care.  ACUTE THERMAL BURN INJURY Animal models have shown significant benefits of HBO for thermal burns, including reducing partial- and full-thickness skin loss, hastening epithelialization, and lowering mortality. 53 Although some uncontrolled series have reported mixed results,54-56 many clinical trials have reported significant improvement in healing, 57,58 decreased length of stay, 59-61 decreased mortality,58,59,62 reduced cost of care,59,60,62 improved morbidity,58,59 decreased fluid requirements (30% to 35%),58,62,63 and decreased surgical procedures.60,63,65 Overall, in clinical trials, HBO showed benefit in 20 or 22 studies. 66 The HBO protocol for the treatment of thermal burns is 2.4 ATA for 100 minutes with two air breaks. Treatments begin three times daily and then decrease to twice daily and then once daily as healing occurs.  CARBON MONOXIDE POISONING Carbon monoxide toxicity develops from impairment of hemoglobin function and direct carbon monoxide–mediated cellular damage that poisons the electron transport chain and inhibits adenosine triphos phate formation (see Chapter 222, “Carbon Monoxide”). After removal from continued carbon monoxide exposure, the carbon monoxide slowly dissociates from the hemoglobin and the electron transport chain and is metabolized or exhaled. Treatment with HBO enhances elimina tion of carbon monoxide from the body. Professional hyperbaric medicine organizations 66,67 recommend HBO treatment for appropriate carbon monoxide–poisoned patients. Two HBO protocols have been studied for carbon monoxide poisoning. The Salt Lake City protocol uses 3 ATA for 60 minutes, with two air breaks, followed by a reduction to 2 ATA for 65 minutes with one air break. Two additional treatments are given in 6- to 12-hour intervals. 68 The Philadelphia protocol uses a single treatment at 2.8 ATA for 30 minutes followed by 2.0 ATA for 90 minutes.  CYANIDE POISONING Concomitant cyanide and carbon monoxide poisoning may be seen in patients rescued from closed-space fires in which synthetic materials are burned. Experimental evidence suggests that cyanide and carbon monoxide can produce synergistic toxicity. 70-72 HBO may directly reduce cyanide toxicity73,74 and/or augment other antidote treatments. 75 However, clinical experience with HBO for pure cyanide toxicity is sparse, and there are no controlled trials.

ls are burned. Experimental evidence suggests that cyanide and carbon monoxide can produce synergistic toxicity. 70-72 HBO may directly reduce cyanide toxicity73,74 and/or augment other antidote treatments. 75 However, clinical experience with HBO for pure cyanide toxicity is sparse, and there are no controlled trials. 75-80 Cyanide is among the most lethal poisons, and toxicity is rapid, so standard antidotal therapy for isolated cyanide poisoning is of primary importance (see Chapter 204, “Indus trial Toxins”). HBO can be considered in case of dual carbon monoxide and cyanide poisoning and in cyanide poisoning when vital signs and mental status do not improve with antidote treatment.  NECROTIZING SOFT TISSUE INFECTIONS Necrotizing soft tissue infections, including necrotizing fasciitis and Fournier’s gangrene, are rapidly spreading, deep, typically mixed infections that result in profound morbidity and mortality (see Chapter 152, “Soft Tissue Infections”). Over the past 10 years, advances in surgical technique and antibiotic therapy and a higher index of suspicion regarding presentations and at-risk populations have improved survival. HBO is a valuable adjunct to surgical debridement and antibiotic therapy in necrotizing soft tissue infections, reducing mortality, improving recovery rates, and decreasing both amputation rates and the num ber of required surgical interventions. 81-90 HBO is beneficial due to its ability to suppress growth of anaerobic microorganisms, improve bactericidal action of leukocytes that function poorly in hypoxic conditions, and enhance antibiotic penetration into target bacteria. 91-94 The HBO protocol for necrotizing soft tissue infections is twice-daily treatments at 2.0 to 2.5 ATA for 90 minutes with two air breaks until the extension of the necrosis is halted, and then daily until the infection is well con trolled, for up to 30 sessions.  CLOSTRIDIAL MYONECROSIS (GAS GANGRENE) Gas gangrene is an acute, rapidly progressing clostridial infection of muscle tissue characterized by profound toxemia, edema, tissue death, and variable gas production. 95 The induction of gas gangrene requires only the presence of clostridial spores and a region of lowered oxidation reduction potential caused by local circulatory failure or extensive soft tissue damage and muscle necrosis. 96 Under the conditions of low oxy gen tension, the clostridial spores can develop into the vegetative form.96 The pathogenesis of gas gangrene involves the production of clos tridial exotoxins, of which more than 20 have been identified.97-99 Alpha toxin is the most prevalent exotoxin and causes platelet and leukocyte destruction, widespread capillary damage, hemolysis, tissue necrosis, and often death. 99 Alpha toxin can be detoxified within hours after its elaboration, with natural host defenses conferring active immunity with production of a specific antitoxin. 98,100 However, death often occurs because the infection is so rapidly progressive that the patient dies before immunity can develop. The primary benefit of HBO therapy for gas gangrene is that inducing an oxygen tension of 250 to 300 mm Hg (33.3 to 40 kPa), achieved at 3.0 ATA, 101-103 halts alpha-toxin production, inhibits clostridial growth, 104 and allows normal host factors to swiftly detoxify the patient so that a moribund patient can rapidly be made nontoxic. 97,104-110 The addition of HBO to standard treatment for gas gangrene shows consistently beneficial results, with survival rates between 72.9% and 81% 111-113 and limb salvage rates between 80% and 82% (compared to 40% to 50% with primary surgery). 111,114-117 Results decline progressively when HBO is delayed.

ontoxic. 97,104-110 The addition of HBO to standard treatment for gas gangrene shows consistently beneficial results, with survival rates between 72.9% and 81% 111-113 and limb salvage rates between 80% and 82% (compared to 40% to 50% with primary surgery). 111,114-117 Results decline progressively when HBO is delayed. Treatment begins with an index of suspicion and a positive gramstained smear of the wound fluid revealing gram-positive rods and a paucity of leukocytes. Although treatment with gas gangrene involves a three-pronged approach—antibiotics, surgery, and HBO—the initial surgery can be restricted to opening of the wound or an initial fasciotomy, followed by immediate HBO therapy. Lengthy and extensive procedures in gravely ill patients may be deferred, with necrotic tissue debridement performed between HBO sessions when a clear demarca tion between dead and viable tissues is appreciated. 96 The HBO protocol for treatment of gas gangrene is 3.0 ATA for 90 minutes three times a day in the first 24 hours and then twice daily for the next 2 to 5 days. In several series, no mortality has been shown after the third HBO session (end of day 1). 115,118 COMPLICATIONS OF HBO THERAPY  BAROTRAUMA Middle ear barotrauma is the most common adverse effect of HBO treatment. 119 As the ambient pressure within the hyperbaric chamber increases, a patient must be able to equalize the pressure within the middle ear by autoinsufflation or else ear pain, tympanic hemorrhage, serous effusion, or rupture will develop. Standard protocols include instruction on autoinsufflation techniques and medical therapy when needed. When these interventions fail, tympanostomy tubes must be placed in order for HBO therapy to continue. The reported overall Tintinalli_Sec03_p0053-0142.indd 140 8/2/19 2:57 PM

serous effusion, or rupture will develop. Standard protocols include instruction on autoinsufflation techniques and medical therapy when needed. When these interventions fail, tympanostomy tubes must be placed in order for HBO therapy to continue. The reported overall Tintinalli_Sec03_p0053-0142.indd 140 8/2/19 2:57 PM CHAPTER 21:  Hyperbaric Oxygen Ther apy      141 incidence of aural barotrauma is between 1.2% and 7% of patients who undergo HBO therapy.120,121 One series reported a 4% incidence of tym panostomy tube placement.122 Pulmonary barotrauma during HBO treatment is extremely rare but should be suspected when significant chest or hemodynamic symptoms occur during, or shortly after, decompression. If symptoms develop and the patient is in a multiplace chamber, stop decompression and evalu ate for pneumothorax. If the patient is in a monoplace chamber, slowly decompress and provide supplemental oxygen upon returning to ambient pressure.  OXYGEN TOXICITY Biochemical oxygen toxicity can injure the brain, lungs, and eyes. Acute oxygen toxicity manifests as a grand mal seizure, reported to occur approximately one to four times per 10,000 patient treatments. 120,123-125 The risk of seizure is higher in hypercapnic patients and possibly those who are acidotic or septic. Seizures are managed by reducing the inspired oxygen tension while leaving the patient at the same pressure (to avoid pulmonary overexpansion injury when a patient is in tonic convulsion phase). Chronic oxygen toxicity can impair lung mechanics (elasticity), vital capacity, and gas exchange. 126 These changes are typi cally observed only when treatment duration and pressures exceed typical HBO protocols. 127-129 Progressive myopia has been reported in patients who undergo prolonged daily therapy and typically reverses within 6 weeks after stopping HBO therapy. 130 There is a risk for nuclear cataract development, typically when treatments exceed a total of 150 to 200 hours, but they may arise with less provocative exposures. 131,132 Current evidence does not indicate that typical HBO protocols have detrimental effects on neonates or the unborn fetus.  MISCELLANEOUS COMPLICATIONS Confinement anxiety may occur and is typically managed with sedating agents. Any environment with an elevated concentration of oxygen presents a risk for fire. Scrupulous avoidance of an ignition source is standard in HBO therapy programs. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Tintinalli_Sec03_p0053-0142.indd 141 8/2/19 2:57 PM

with sedating agents. Any environment with an elevated concentration of oxygen presents a risk for fire. Scrupulous avoidance of an ignition source is standard in HBO therapy programs. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Tintinalli_Sec03_p0053-0142.indd 141 8/2/19 2:57 PM Tintinalli_Sec03_p0053-0142.indd 142 8/2/19 2:57 PM This page intentionally left blank