Adjuvant Hyperbaric Oxygen


Malignant External Otitis

Jefferson C. Davis, MD; George A. Gates, MD; Charles Lerner, MD; Merrit G. Davis, Jr, DO; Jon T. Mader, MD; Alan Dinesman, MD

Necrotizing invasive pseudomonal infection of the exauditory canal (malignant external otitis) is an uncommon but important disorder in the elderly. The high morbidity, and even mortality, of this disorder has been reduced by the early and intensive use of combination antipseudomonal antibiotics. However, in severely immunocompromised patients or in infection involving the base of the skull, multiple cranial nerves, or the meninges, conventional therapy has been prolonged, intensive, and relatively ineffective. We treated 16 patients with malignant external otitis with adjuvant hyperbaric oxygen therapy. In six patients, infection was in advanced stages, infections were recurrences after previous treatment, and repeated treatment with antipseudomonal antibiotics had failed. All 16 cases responded promptly when a 30-day course of hyperbaric oxygen was added to the antibiotic regimen, and all patients remained free of infection or neurologic deficit during 1 to 4 years of follow-up. No complications of this treatment modality were noted. Hyperbaric oxygen therapy reverses tissue hypoxia, which enhances phagocytic killing of aerobic microorganisms, and stimulates neomicroangiogenesis. In addition, hyperbaric oxygen augments the action of aminoglycoside antibiotics. Adjuvant hyperbaric oxygen therapy should be considered in advanced or recurrent cases of malignant external otitis. (Arch Otolaryngol Head Neck Surg. 1992;118:89-93) \s=b\


pseudomonal infections of the tempo¬ ral bone Invasive highly morbid, progressive, that ear




occur primarily in elderly life-threatening processes diabetic patients.1 The process may be primary or sec¬ ondary. Primary infection most often begins in the exter¬ nal auditory canal and rarely in the middle ear.2 Second¬ ary infections are generally complications of chronic suppurative otitis media in susceptible patients. Regard-


for publication May 9, 1991. From the Departments of Hyperbaric Medicine (Drs J.C. Davis and M.G. Davis) and Medicine (Dr Lerner), Southwest Texas Meth-

Hospital, the Department of Otolaryngology, Washington University School of Medicine, St Louis, Mo (Dr Gates), the Department of Medicine, University of Texas Medical Branch at Galveston (Dr Mader), and the Department of Otolaryngology, odist

Northside Presbyterian Deceased.

Hospital, Albuquerque, NM (Dr Dinesman).

Reprint requests to the Department of Otolaryngology, Washington University School of Medicine, 517 S Euclid, Box 8115, St Louis, MO 63110 (Dr Gates).

less of the initiating event, the infectious process resists conventional treatment for external otitis and may result in osteitis of the skull base, multiple cranial neuropathy, and intracranial infection. Death may occur due to inani¬

pulmonary aspiration secondary to vagai neuropa¬ thy, meningitis, cerebritis, or vascular rupture or throm¬ tion,

bosis. Before the advent of combination antimicrobial therapy with an aminoglycoside agent plus an antipseudomonal penicillin drug, this process was associated with a poor outcome. Even with optimal antimicrobial therapy, the mortality rate remains high in patients with multiple cranial neuropathy,3 and recovery is rare when extension into the meninges occurs.4 The most common form of invasive pseudomonal infection of the ear and temporal bone, called malignant external otitis (MEO) by Chandler, ' begins as an insidious polymicrobial inflammation of the external auditory ca¬ nal. The cardinal clinical feature is deep-seated, intense, and unrelenting pain that persists despite adequate local therapy. Purulent discharge and infected granulation tis¬ sue in the floor of the external auditory canal are typical early physical findings. These may persist for weeks to months before facial paralysis, the most common cranial neuropathy, occurs. The air spaces of the middle ear and mastoid generally remain clear. We define this clinical picture (with or without facial paralysis) as stage I MEO. In stage II MEO, the process extends into the soft tis¬ sues under the base of the skull and involves the poste¬ rior cranial nerves (cranial nerves IX through XII) as they exit their respective foramina. Pseudomonal osteitis of the skull base usually coexists with and often precedes the neuropathy. Radionuclide bone scans are usually diag¬ nostic. Spread to the opposite side occurs occasionally, usually through the soft tissues of the skull base or nasopharynx. If untreated or if unresponsive to treat¬ ment, intracranial extension may occur, which is defined as stage III MEO. Table 1 describes the staging of malignant external otitis. Cultures of the infected tissue invariably reveal Pseudomonas aeruginosa, the archetypal bacterial opportunist. Its pathogenesis is enhanced by a polysaccharide (slime) coat¬ ing and the elaboration of exotoxins and enzymes. Exotoxin is believed to be responsible for the reversible neurotoxicity of this disorder. A variety of enzymes promote spread by enzymatic destruction of tissue. The immune status of the host is an important cofactor. Ninety percent of the patients are diabetic, and the

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majority are aged 60 years or older; 10% have undergone chemotherapy for malignant disease. Concurrent vascu¬

In vivo studies have demonstrated low oxygen tension in infected and hypoperfused bone and soft tissue, and impaired phagocytic killing of aeruginosa in hypoxic environments.1219 Because wound Po2 is substantially in¬ creased when oxygen is breathed at hyperbaric pressures, we have employed daily, 2-hour oxygen

lar disease is common. Known immune defects in the di¬ abetic patient that may predispose these patients to MEO include altered macrophage chemotaxis and leukocyte phagocytosis. Outcome appears to be related to the severity of the underlying disorder and to the promptness and intensity of parenteral antibiotic treatment. In cases limited to the external auditory canal, with or without in¬ volvement of cranial nerve VII, prolonged antipseudomonal therapy is generally successful.511 How¬ ever, recurrence within 3 to 6 months, which may indicate inadequate therapy, is not uncommon. Table

1.—Staging of Malignant


Herein, cases


Infection of


External Otitis






Type, 172°



of this


PATIENTS AND METHODS treated for 4 to 6 weeks with parenteral antipseudomonal antibiotics and daily HBO treatments adminis¬ tered in a chamber in which the entire patient can be exposed to pressures greater than those at sea level. The patients breathed 100% oxygen from a head tent at 2.4 atm absolute (20.1 psi greater than sea level pressure) for 90 minutes once or twice daily, on a schedule that provided three 30-minute periods of oxygen breathing interrupted by 10 minutes of breathing room air. Arterial P02 under these conditions averages 1300 mm Hg, and transcutaneous oxygen measurements confirm skin Po2 levels of 1100 to 1300 mm Hg.20

Table 2. —Pretreatment Case NoV Age, y


of MEO treated in two centers with



deep pain



adjunct to antibiotic therapy. experience with 16 consecutive

as an


canal and contiguous soft tissue or without facial paralysis II: Extension of the above infection to include osteitis Stage of the skull base or multiple cranial neuropathy Stage III: Further extension intracranially: meningitis, epidural empyema, subdural empyema, or brain abcess





Osteitis Gallium 67/ Technetium Tc 99m/ Indium 111 CT Scan

Neural Pathology Cranial Nerves Affected



VII, IX-XII 1/59


GaTc + CT +

VII, Vili, Xl-Xll


Cisternogram +



CT + No bone




Epidural abscess pleocytosis

Ca + CT +











Ga+ CT +


CT +



GaCT +




GaCT +




Tc + Ga not done CT +



No bone CT +













1 3 R 1 L






Temporal CT +

11/72 12/67

Tc + ,

13+/54 14/68




CT- Tc not done









0 0 CT-, Tc not done 1 CT+, Tc+, lnd + VII, XII 17/71 VII 1 CT+, Tc+, lnd + *DM indicates diabetes mellitus; MEO, malignant external otitis; Ga, gallium; CT, computed tomographic; Tc, technetium; CSF, brospinal fluid; and CSOM, chronic suppurative otitis media; plus sign, positive; and minus sign, negative.

15/80 16/70

tPreviously reported


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Fig 1. —Case 7. Left, Pretreatment gallium 67 citrate scan showing marked uptake in the temporal bone area. Right, A second scan obtained 3 weeks later, after 7 week of hy¬ perbaric oxygen therapy, shows improvement.

Fig 2. —Case

7. Gallium 67 citrate scan ob¬ tained 4 months after treatment shows no uptake in the left temporal bone area.


REPORT OF CASES Two cases are presented to highlight the treatment details. See Table 2 for additional information concerning these and other cases.

CASE 1.—A 59-year-old woman had a 22-year history of type I diabetes mellitus with angiopathy manifested by retinopathy and peripheral vascular disease, which necessitated a left-sided below-knee amputation. She also had chronic otitis media with purulent otorrhea and developed pain and facial paralysis in October 1982. Pseudomonas aeruginosa was cultured from the ex¬ ternal ear canal. She was treated for 4 weeks with parenteral tobramycin sulfate and piperacillin sodium, with the use of serum concentrations to ensure therapeutic doses. During this period, she underwent extensive débridement of the ear canal, includ¬ ing the mastoid cortex. Her condition improved, and facial function returned. Three weeks later, she underwent an elective radical mastoidectomy to control her primary middle-ear dis¬ ease, and piperacillin therapy was administered for 10 days


The patient did well for 3 months and then developed fever, nuchal rigidity, and paralysis of the 7th, 9th, 11th, and 12th cra¬ nial nerves. Computed tomography of the temporal bone revealed an active, ongoing petrous osteomyelitis and epidural abscess. The cerebrospinal fluid was cloudy and had a white blood cell count of 1.7 x 109/L, of which 75% were polymorphonuclear neutrophils. A gallium scan showed increased uptake in the left temporal bone (Fig 1). The clinical diagnosis was stage III MEO, and the prognosis was guarded. A third course of antimicrobial therapy was begun, consisting of parenteral tobramycin (60 to 110 mg every 8 hours) and piper¬ acillin (3 g every 4 hours). There was little change in her clinical course. After 14 days of persistent dizziness, recurrent nausea and vomiting, and no improvement in her cranial nerve palsies, daily HBO treatment was begun. Antibiotic therapy continued unchanged. After 4 days of HBO therapy, dizziness and nausea and vomiting ceased. After 15 days of HBO therapy, function returned in all involved cranial nerves. After 30 HBO treatments, she was completely free of any manifestations of MEO, except for mild weakness of her face. A gallium scan 4 months later showed full resolution (Fig 2). She remained free of disease throughout 4 years of follow-up and had normal cranial nerve function until her sudden death due to an acute myocardial in¬ farction at age 64 years. Case 4.—A 74-year-old man with type I diabetes mellitus be¬ gan to experience ear pain and drainage in June 1984. There was no response to oral and topical antibiotic therapy and cleaning of the external ear canal. A modified radical tympanomastoidectomy was performed at another institution in July 1984, followed by débridement of the temporal bone and a 4-week course of parenteral tobramycin sulfate and ticarcillin disodium therapy.

Facial paresis persisted, and he developed progressive dyspha¬ and hoarseness. Examination showed left-sided arytenoid fullness and left-sided cranial nerve VII, IX, and XII deficits. By October 1984, he had developed diplopia and a left-sided exter¬ nal rectus paresis. A computed tomographic scan showed destruction of the left petrous ridge with involvement of the left jugular foramen and extension into the nasopharynx. A gallium scan showed involvement of the left pterygoid plates, left mas¬ toid, and parapharyngeal region. Cultures yielded aeruginosa, and he was again treated with parenteral tobramycin and ticarcillin. Hyperbaric oxygen treatment was begun, and during the course of 30 such treatments his symptoms and all cranial nerve palsies resolved. He has been free of infection during a follow-up period of 5 years.


RESULTS Table 2 summarizes the patients' history, disease stage, and clinical course. patients had recurrences after one to three previous treatment trials without HBO therapy. Nine patients had stage I disease and had no prior treatment. Fourteen patients had osteomyelitis of the skull base, demonstrated by technetium Tc 99m, gal¬ lium 67, indium 111, or computed tomographic scans. In all patients, cultures yielded aeruginosa, and all patients were diabetic. One patient (patient 13) has been described



Four patients débridement as

(patients 4, 12, 16,


17) underwent

and two and with mastoid disease 1 7) primary patients (patients underwent a radical mastoidectomy and postoperative HBO therapy. Seven of the patients with stage II or stage III disease underwent prior surgical excision of infected tissue in an attempt to control the pseudomonal infection or underwent primary mastoid surgery as the event lead¬ ing to invasive pseudomonal infection. All patients recovered as defined by 90% or greater re¬ turn of cranial nerve function and freedom from symp¬ toms and signs of infection for at least 1 year. One patient (patient 5), a brittle diabetic, developed contralateral MEO and required a second course of HBO therapy; he is free of disease 6 years later but has residual facial weakness as a result of prior mastoid surgery and severe hearing loss secondary to prolonged treatment with gentamicin sul¬ fate. There were no harmful side effects from the 620 HBO treatments given to these patients. Four patients required

part of




placement of tympanostomy tubes to allow middle-ear pressure equilibration during chamber compression.

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COMMENT familiar disorder to the infectious MEO a is Although disease specialist and to the otolaryngologist, it is unfa¬ miliar to most primary care physicians. However, because the prevalence of MEO appears to be increasing, proba¬ bly due to the aging of the diabetic population4 and because early treatment can prevent substantial morbid¬ ity in diabetic patients, a heightened awareness of this problem is warranted. In patients with stage I disease, early aggressive combination antipseudomonal antibiotic treatment for 6 weeks coupled with limited débridement is successful in the vast majority of cases. The indolent nature of the initial physical findings may lead to an er¬ roneous diagnosis and delay in therapy. Similarly, the pain response to treatment may lead to a shortened treat¬ ment duration. In these circumstances, the infectious process may recur in a minority of cases. Thus, strict ad¬ herence to the full course of treatment is recommended. With modern antipseudomonal drugs, facial paralysis does not worsen the prognosis. Therefore, we classify these patients as having stage I MEO, unlike Corey et al,3 who categorized them as having higher-stage disease. Multiple cranial neuropathy, which has a 28% mortality rate,4 does affect outcome substantially. Because nearly all patients with multiple cranial neuropathy in our series had radionuclide scan evidence of skull base osteitis, we group these two clinical findings into stage II disease. Treatment should be extended beyond the standard reg¬ imen if pain persists, if the wound cultures remain pos¬ itive for Pseudomonas, or if the gallium scan has not returned to normal by the end of the 6 weeks of treatment. Intensive therapy is warranted in stage II disease to avoid intracranial extension (stage III disease), in which there has been a 100% mortality rate.4 In the series reported herein, three patients with stage III disease had a downhill clinical course that was reversed promptly when HBO therapy was added to the standard treatment regimen. They remained free of disease after a follow-up period of 3 to 4 years. These three patients with stage III disease and four of the six patients with stage II disease had recurrences after previous treatment. Local débridement of necrotic tissue and drainage of abscesses are integral parts of the standard treatment, but extensive surgical resection should be considered only as a last resort if at all.22 Advanced disease indicates poor host resistance, and resection of infected tissue may break down tissue barriers and expose new areas. Although ex¬ tensive resection has been reported,23 we have not found it to be necessary since we began using adjuvant HBO


The reason that diabetic patients are prone to develop invasive pseudomonal infection of the ear and temporal bone is unknown. Local tissue hypoperfusion and hypoxia secondary to diabetic microangiopathy is a possible

explanation. Doroghazi et al11 demonstrated substantial thickening of the subendothelial basement membrane of cutaneous capillaries in biopsy specimens of the skin from the contralateral ear of a diabetic patient with MEO, which not evident in nondiabetic controls of the same age. In addition, infection is also known to cause wound hypoxia: Niinikoski et al24 noted a decrease in wound fluid oxygen to unmeasurable levels in rats injected with Pro¬ teus mirabilus, presumably due to (1) bacterial oxygen up¬ take, (2) high oxygen consumption of the inflammatory process,25 and (3) reduced local circulation.


Hypoxia impairs the oxygen-dependent bacterial kill¬ ing by phagocytes.12"17 Oxidative killing of aerobic bacte¬ ria by phagocytes depends on the availability of molecu¬ lar oxygen to form free radicals (Superoxides, hydroxyls, peroxides, aldehydes, hypochlorites, and hypoiodites), which are toxic to bacteria. The rate of production of these toxic radicals and therefore the adequacy of oxidative bacterial killing is directly proportional to the local tissue oxygen tension.18 Inspiring hyperoxic gas mixtures in¬ creases wound Po2 levels and the killing of aerobic bacte¬ ria by phagocytes.14"16 Hypoperfused tissue (ie, secondary to microangiopathy) is highly susceptible to infection, which further de¬

oxygen levels and, in turn, lowers the bacterial killing by leukocytes. Once infection is established, a vi¬ cious cycle is completed: swelling, decreased perfusion, increased oxygen consumption, tissue hypoxia, and lack of oxygen needed by leukocytes to form free radicals re¬ sult in impaired killing of aeruginosa. In early-stage dis¬ ease, before infection becomes too extensive and before vascular damage becomes too severe, aggressive parent¬ eral antibiotic treatment will adequately penetrate and sterilize infected tissue. However, in extensive disease, additional treatment is needed, and hyperoxygenation appears to be a logical adjunct. In hypoxic and hypoperfused human tissue with a proliferative endarteritis induced by prior radiation ther¬ apy, Marx and Johnson26 demonstrated capillary angiogenesis following hyperbaric oxygénation. A similar phe¬ nomenon in patients with MEO may, in part, explain their rapid healing and prolonged freedom from recurrence af¬ ter HBO therapy. Aminoglycoside antibiotics lose antibacterial activity as oxygen tension decreases.27 Under various levels of oxy¬ gen tension in an in vitro rabbit model of osteomyelitis, Mader et al28 demonstrated that HBO therapy enhanced the activity of tobramycin in the eradication of aeruginosa from infected bone. We have used historical controls to demonstrate the value of HBO therapy. Although stronger evidence of ef¬ ficacy might result from a randomized clinical trial, factors such as the effectiveness of the current treatment proto¬ col, the lower costs and increasing availability of home intravenous therapy, and the development of newer an¬ tipseudomonal agents8 make such a study possibly pre¬ creases





investigational setting,


would be difficult to justify withholding HBO therapy from control patients with stage III disease given the poor prognosis with conventional therapy and the good results reported herein. Our experience suggests that adjuvant HBO therapy should be considered in patients with MEO in advanced stages (stages II and III), in recurrent cases, and when the process becomes refractory to appropriate antibiotic treat¬ ment. Shupak et al29 have suggested the routine use of HBO therapy in patients with MEO. Although we stress its value in patients with advanced disease, with newer oral agents now available,9 we would withhold HBO therapy in most patients with stage I MEO. The fluorinated quinolones, which were not available when our patients were treated, appear to offer efficacy, ease of ad¬ ministration, and greater safety than the intravenous agents used in our patients.30"32 The early use of these agents should minimize the incidence of cases of latestage disease. The use of mono therapy vs poly therapy33

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monotherapy to use34-35 remain as unsettled issues. We propose that staging based on prognosis, such as presented herein, be used as a basis for the selection of therapy. The intensity and duration of treatment should reflect the a priori prognosis as well as the response to and which


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Adjuvant hyperbaric oxygen in malignant external otitis.

Necrotizing invasive pseudomonal infection of the external auditory canal (malignant external otitis) is an uncommon but important disorder in the eld...
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