Hyperbaric Indications and Patient Selection Criteria Part 4 of 4

Hyperbaric indications and patient selection criteria part 4 of 4

Patient selection criteria for HBO2 treatment of specific indications: Part 4 of 4

Currently 14 indications for HBO2 are recognized by the UHMS, with recommendations for treatment. What follows is an abbreviated description of each.

NOTE: While these are effectively ‘snapshots’ of each indication we strongly recommend a thorough reading of each chapter in the UHMS Indications book to appreciate the full view for HBO2 treatment of these conditions.


Approximately 88% of sudden sensorineural hearing loss (SSNHL) has no identifiable etiology: Termed idiopathic sudden sensorineural hearing loss, ISSHL is the abrupt onset of hearing loss, usually unilaterally and upon wakening, that involves a hearing loss of at least 30 decibels (dB) occurring within three days over at least three contiguous frequencies. The historical incidence of ISSHL ranges from five to 20 cases/100,000 population, with approximately 4,000 new cases each year in the United States. The mean age of ISSHL presentation to be ages 46-49 with an equal gender distribution. It does not appear to have seasonal variations, uneven distributions of presentation throughout the year, or an association with upper respiratory infections, either prior to or following symptom onset. Spontaneous recovery is currently thought to be 30-60%.

Interestingly, a recurrence of ISSHL has been observed in those with comorbid conditions, principally diabetes), hypertension and dyslipidemia. ISSHL has been shown to be an early marker for an increased risk of stroke.

In the realm of otolaryngology, few topics are more controversial than the treatment of ISSHL. Treatment is often regionally specific and may be treated in the outpatient setting or upon hospital admission. More than 60 protocols have been proposed for the treatment of ISSHL. Of these, the greatest efficacy is in the combination of corticosteroids and HBO2. Corticosteroids have a primary role in protecting the cochlea from inflammatory mediators, increase cochlear blood flow and ameliorate cochlear ischemia, favorably altering the inner ear milieu.

Although there is a paucity of literature regarding the use of HBO2 as a primary treatment for ISSHL, it is usually an adjunctive treatment with medical therapies or as salvage therapy following failure of medical treatment. The Undersea and Hyperbaric Medical Society Committee Report advocates that for patients with moderate to profound ISSHL hearing loss (>40 dB) who present within 14 days of symptoms onset, treatment with HBO2 should be considered. However, the literature shows that patients presenting later than 14 days may show improvement with HBO2, and the American Academy of Otolaryngology Head and Neck Foundation advocates for the consideration of HBO2 therapy for up to three months following symptom onset – important, as the National Guideline Clearinghouse Clinical Practice Guidelines for Sudden Hearing Loss lists this reference as the entirety of their guidelines (guidelines.gov). However, the majority of the medical literature supports the notion that early intervention is associated with improved outcomes.

Continued consultation and follow-up with an otolaryngologist are recommended for the ISSHL patient. Additional testing and therapy may be recommended by the otolaryngologist, and the patient should be followed by the otolaryngology specialist during and following HBO2 therapy.


The term “intracranial abscess,” or ICA, includes cerebral abscess, subdural empyema, and epidural empyema, which share many diagnostic and therapeutic similarities and, frequently, similar etiologies. Infection may occur and spread from a contiguous infection such as sinusitis, otitis, mastoiditis, or dental infection; hematogenous seeding; or cranial trauma. Brain abscess usually results from predisposing factors such as HIV infection, systemic infection, immunosuppressive drug treatment, surgery, or contiguous infection as noted above. Approximately 50% of infections are caused by contiguous spread of local infections. Hematogenous spread is responsible in around a third of cases, with the mechanism for the remainder not identifiable.

In the United States the incidence of brain abscess is estimated to be 0.4-0.9 cases per 100,000 people per year. The mortality of intracranial abscess remains substantial but appears to have decreased from 40% in 1960 to 15% in recent years. Factors responsible for this decrease might include earlier and more accurate diagnosis through better imaging techniques; advances in minimally invasive surgery (e.g., stereotactic fine-needle aspiration); and improved understanding of the bacteriology of ICA, leading to more appropriate antibiotic therapy.

Following the diagnosis of ICA, adjunctive HBO2 should be considered under the following conditions: multiple abscesses; abscesses in a deep or dominant location; compromised hosts, particularly with fungal abscesses; in situations where surgery is contraindicated or where the patient is a poor surgical risk; no response or further deterioration in spite of standard surgical (e.g. one to two needle aspirates); and antibiotic treatment.

Because of improving mortality, there is a general trend toward a more conservative therapeutic approach in the management of ICA patients. Specimen from surgical tissue or needle aspirate should be sent for histopathology and microbiological cultures. Prior to identification of the offending organism, empiric antibiotic therapy is warranted, and targeted antimicrobial therapy will be dictated by microbial culture result. Early in the diagnosis, it is prudent to involve a multidisciplinary team to direct management including neurosurgery, neurology and infectious disease.

Under these circumstances, adjunctive HBO2 may confer additional therapeutic benefit for these reasons:

  • High partial pressures of oxygen can inhibit the growth of anaerobic organisms which are often present in intracranial abscesses.
  • HBO2 can cause a reduction in perifocal brain swelling without steroid use which might adversely impact anti-infective penetration of the blood-brain barrier.
  • HBO2 enhances neutrophil-mediated phagocytosis of infecting organisms.
  • HBO2 can improve the metabolic environment of acidosis and low oxidation-reduction potential due to angioinvasive fungi, promoting the activity of antifungal therapy.

In addition HBO2 augments the oxygen-dependent active transport of certain antibiotics such as cephalosporins and aminoglycosides across the bacterial cell wall. Finally, HBO2 has been reported to be of benefit in cases of concomitant skull osteomyelitis.


Necrotizing soft tissue infections (NSTIs) remain among the highest sources of morbidity and mortality. NSTIs include necrotizing fasciitis, necrotizing myositis, Fournier’s gangrene, necrotizing infection of the head and neck, non-clostridial myonecrosis, crepitant anaerobic cellulitis, progressive bacterial gangrene, and zygomycotic gangrenous cellulitis.

Confirmed cases within the United States approximate the overall mortality rate at 20%. NSTIs are often considered one of the most difficult diseases facing treating physicians and surgeons. Their ability to produce considerable tissue damage in a rapidly progressive manner underscores the importance of timely recognition and initiation of aggressive therapeutic interventions.

A number of clinical scenarios, specific lesions and syndromes have been described, based on the affected tissues and location of infection, the etiologic organism or combination of organisms involved in the infection, and particular host immunologic and vascular risk factors. In all of these clinical situations, the common denominator is the development of hypoxia resulting in tissue necrosis, with purulent discharge and gas production.

From a physiological viewpoint, all necrotizing soft tissue infections should benefit from HBO2 treatments, considering all the physiologic steps that enhance host response to infection. Hyperbaric oxygen is a recognized accepted adjunct to early judicious surgical debridement(s), appropriate broad-spectrum parenteral antibiotic therapy and a multidisciplinary approach to the management of NSTIs. HBO2 can reduce the amount of hypoxic leukocyte dysfunction occurring within an area of hypoxia and infection, and provide oxygenation to otherwise ischemic areas, thus limiting the spread and progression of infection. The diffusion of oxygen dissolved in plasma in the circulation, where it is initially carried in large vessels, proceeds to areas of poorly perfused tissue, from regions of very high O2 saturation down a gradient to lower oxygen levels in tissue. Integrin inhibition decreases leukocyte adherence, reducing systemic toxicity. HBO2 can act to enhance antibiotic penetration into target bacteria. Enhancement of the post-antibiotic effect by hyperbaric oxygen has been demonstrated for aminoglycosides and Pseudomonas. Amputation rates of 26% up to 50% are reported in cases of necrotizing fasciitis of the extremities, without hyperbaric therapy.

Twice-a-day hyperbaric oxygen treatments during the acute phase of necrotizing soft tissue infections are advised until extension of necrosis has been halted. This is often seen within seven to 10 treatments. Due to the natural history of often relentless progression and undetected foci of necrosis, these treatments would then be followed by once-daily treatments over an extended period until the infection is well controlled, which may take up to 30 treatments. Utilization review should be requested after 30 treatments.

Refractory Osteomyelitis

Refractory osteomyelitis is a chronic osteomyelitis that persists or recurs after appropriate interventions or where acute osteomyelitis has not responded to accepted management. The disease has several presentations, including mandibular osteomyelitis, spinal osteomyelitis, cranial osteomyelitis, malignant external otitis, and osteomyelitis as a consequence of diabetic foot ulcers.

As a result, osteomyelitis can be considered either a primarily medical or surgical disease depending upon the timing of presentation, source of infection, identified organism, degree of bony involvement, and overall status of the host. Initial management typically centers on starting culture-directed antimicrobial therapy. Where present, infected sinus tracts, sclerotic bone, and sequestra should be debrided.

Overall, resolution rates for primary osteomyelitis treated with surgery and antibiotics range between 35-100%. Despite the wide range of reported results, it can be estimated that a 70-80% cure rate can be achieved using routine surgical and antibiotic management techniques. This finding is in agreement with corresponding estimates for long-term osteomyelitis recurrence, which range between 20-30%. It is when appropriate surgical and antibiotic interventions fail and osteomyelitis progresses, recurs, or presents a high probability for morbidity or mortality that HBO2 therapy should be considered for inclusion in the patient’s treatment regimen.

The total number of required treatments varies with the severity and location of the patient’s infection, the presence or absence of coexisting diseases and the patient’s individual responsiveness to treatment. In the studies available for review, treatments ranged from 14 to more than 100 total sessions, with the majority of studies reporting between 20 and 50 total sessions. As would be expected, variability in clinical presentations and concurrent management strategies render specific treatment number recommendations impractical. Instead, it is recommended that clinicians carefully consider each patient’s disease severity, clinical responsiveness, and risk for osteomyelitis recurrence in guiding such determinations.


Patients who have marked loss of red blood cell mass due to hemorrhage, hemolysis or aplasia run the risk of lacking adequate oxygen-carrying capacity by blood. Clinical research has demonstrated that patients who within the first four hours of hemorrhage have sustained a severe hemorrhage have no chance of survival if the accumulative oxygen debt exceeds 33 L/m2. In patients of similar circumstance multiorgan failure occurs if the accumulative oxygen debt exceeds 22 L/m2, and most all patients who have an accumulative oxygen debt of 9 L/m2 survive without residual disability.

HBO2 should be considered in severe anemia when patients cannot receive blood products for medical, religious, or strong personal preferential reasons or situational blood inavailability. Its use should be guided by the patient’s calculated accumulating oxygen debt rather than by waiting for signs or symptoms of systemic or individual end-organ failure. HBO2 should be considered as a bridge therapy until stabilization of severe life-threatening acute anemia can be resolved. HBO2 has repeatedly allowed survival in what would have otherwise clearly been unsurvivable clinical circumstances without blood transfusion, providing a way to successfully correct accumulating oxygen debt in untransfusible patients or in patients for whom blood products are not immediately available.

Hyperbaric oxygen can be administered rapidly at pressures up to 200-300 kPa for periods of three or four hours three times a day to four times a day if intra-treatment air breaks are used. Hematinics should be co-administered along with nutritional support to correct protein energy malnutrition. HBO2 should be continued with taper of both individual treatment to the time and frequency of treatment tables until red blood cells have been replaced adequately by patient regeneration or patient acceptance of transfusion if possible.


The burn wound is a complex and dynamic injury. A significant and consistently positive body of evidence from animal and human studies of thermal injury supports the use of hyperbaric oxygen as an adjuvant treatment. HBO2 is a means of promoting healing. The majority of clinical reports have shown reduction in mortality, length of hospital stay, number of surgeries and cost of care. It has been demonstrated to be safe in the hands of those thoroughly trained in rendering this therapy in the critical care setting and with appropriate monitoring precautions. Careful patient selection is mandatory.

The National Burn Repository reviewed the combined data of acute burn admissions for the time period between 2006 through 2015. Patients age 60 or older represented 14% of burn cases. More than 75% of reported total burn cases involved less than 10% total body surface area and resulted in a mortality of 0.6%. Mortality rates were 3.3% for all cases and 5.8% for fire/flame injuries.

Infection remains the leading overall cause of death from burns. Susceptibility to infection is greatly increased due to the loss of the integumentary barrier to bacterial invasion, the ideal substrate present in the burn wound, and the compromised or obstructed microvasculature, which prevents humoral and cellular elements from reaching the injured tissue. Deaths increased with advancing age and burn size as well as presence of inhalation injury. A 20-39% burn in patients younger than 60 confers a mortality rate of 2.5%; the mortality rate increases to 14% with inhalation injury. The same injury in a 60-year-old shows a mortality of 32%, which increases to 55.8% in the presence of inhalation injury.

Pneumonia was the most frequent, clinically related complication, occurring in 5.4% of fire/flame- or flame-injured patients. The frequency of pneumonia and respiratory failure was greater in patients with four days or greater of mechanical ventilation, and the rate of complications increased with age.

Ongoing tissue damage is a major factor in thermal injury. It is due to multiple factors, including the failure of surrounding tissue to supply borderline cells with oxygen and nutrients necessary to sustain viability. Complete capillary occlusion may progress by a factor of 10 during the first 48 hours after injury. Local microcirculation is compromised to the greatest extent during the 12 to 24 hours post-burn. Burns are in this dynamic state of flux for up to 72 hours after injury. Ischemic necrosis quickly follows.

Hyperbaric oxygen treatment

after burns has shown reversal of the zone of stasis, reduction of ischemia and ischemic necrosis, prevention of progression of partial- to full-thickness injury, moderation of inflammation, lessening of capillary leak, preservation of dermal elements, a reduced need for grafting, shortened hospital stay, and a reduction in cost of care. HBO2 is recommended to treat serious burns – i.e., greater than 20% total body surface area and/or with involvement of the hands, face, feet or perineum – that are deep partial- or full-thickness injury. Patients with superficial burns or those not expected to survive are not accepted for therapy. Transfer of patients for HBO2 treatment should be considered carefully and should be sent only to a facility that has both a hyperbaric chamber and a burn unit. Utilization review is recommended after 30 hyperbaric oxygen sessions.

Given our current understanding of the uniquely beneficial effects of hyperbaric oxygenation on the cellular and molecular mechanisms of wound healing, it is suggested that the formal integration of HBO2 in early burn wound management be considered, as well as further investigated in well-designed multicenter studies that provide data for burn wound healing and burn patient outcomes.

Taken from Moon RE, ed. Hyperbaric Oxygen Therapy Indications, 14 ed. North Palm Beach: Best Publishing, 2019: 1-13.

Adapted by Renée Duncan, Communications, UHMS


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