All" 0/018C: 197,






SUMMARY - Malignant external otitis is an infection which begins in the external auditory canal. It is uniformly caused by the Gram negative Pseudomonas aeruginosa organism and mainly affects elderly diabetics. It spreads to the soft tissues beneath the temporal bone and, if not properly treated leads to facial nerve palsy, mastoiditis, sepsis, osteomyelitis of the base of the skull, sigmoid sinus thrombosis, multiple cranial nerve palsies and death. Experience with 72 patients in varying stages of the disease is summarized. Stressed are the diagnostic criteria of nonresponsiveness to the usual methods of treatment, continued suppuration, and the continuing reformation of granulation tissue in the floor of the external auditory canal. Medical treatment is recommended with hospitalization and intravenous carbenicillin and gentamicin. Minor surgical debridement is helpful. All patients should be treated medically for as long as improvement continues, reserving surgical intervention only in the event a plateau is reached or symptoms and signs become worse under treatment. With or without a major surgical procedure, it is imperative to continue treatment for at least seven days after apparent cure in order to avoid recurrent disease possibly at a site distant from the canal.

A classic description of malignant external otitis and its pathogenesis was given in 1959 by Meltzer and Kelemen! in a report which escaped my attention prior to my own report in 1959.2 The disease should be suspected in any patient with an external otitis found to be unresponsive to the usual methods of treatment. 3 The diagnosis can not and should not be made on the basis of one examination only. AGE

Since first recogmzmg the disease in 1959, I have managed personally or been associated closely with the treatment of 72 patients. The average age of all of these patients was 72 with a median of 71 years. The youngest was a 35-year-old female in excellent health with the exception of insulin dependent diabetes since childhood. The oldest was 91 years of age. I have seen some children and babies with what appeared at first inspection to be infections in the external canal or at least which originated there. Subsequent examinations

and their clinical course demonstrated that they were in all instances really infections secondary to the Pseudomonas aeruginosa organism, but which originated in the middle ear rather than in the external auditory canal. However, a two-month-old infant has been reported to have developed an infection in the external auditory canal due to pseudomonas which progressed to necrosis of tissue and a permanent facial paralysis.' DIABETES

Diabetes mellitus is a chronic disorder of carbohydrate metabolism characterized by hyperglycemia and glycosuria. There are in the United States at this time some 3 million persons who are known diabetics and perhaps as many more with undiagnosed diabetes. Of these 3 million known diabetics, approximately 1 million are insulin dependent. According to a standard text there is "no evidence that a well-controlled diabetic is abnormal in his response to infection."5 This is stated in similar ways in other standard texts. Notwithstanding this, the general con-

From the Department of Otolaryngology, University of Miami, School of Medicine Miami Florida. ' , Presented at the meeting of the American Otological Society, Inc., Boston, Massachusetts, May 7-8,1977.


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Incidence Died Complete Recovery Partial Recovery Permanent Paralysis

._ __ ..






15/38 8/15 3/15 2/15 2/15

(39%) (53%) (20%) ( 13%) (13%)

cept of most physicians is that diabetic patients are indeed susceptible to more and more serious infections, presumably on the basis of increased blood sugar levels, decreased activity of formed blood elements such as white blood cells, etc" in response to antigen stimulation and lowered state of cellular nutrition. One of the primary pathologic changes of diabetes is its microangiopathy, a term which describes its effect on the small blood vessels. This takes the form of arteriosclerosis, which consists of a hyalin thickening of the capillary walls, primarily due to thickening of the basement membrane and intima. This process is a rather generalized one. The Pseudomonas aeruginosa is an ubiquitous opportunistic Gram negative organism not ordinarily found on normal skin or in the external auditory canal. However, with excessive moisture or minor trauma, such as scratching with foreign objects, the wearing of a hearing aid mold, etc., it colonizes in the external auditory canal and is responsible for most cases of acute external otitis." Ordinarily it does not gain access to tissues outside of the canal, but under certain conditions results in a cellulitis or furuncle.' As deeper structures become involved it has the capacity for "selective vasculitis" with invasion of arteriolar, capillary and venule walls with or without hemorrhage, accompanied by thrombosis with focal coagulation necrosis of surrounding tissues. The necrosis may lack the usual inflammatory cell response. 8 These characteristics of the organism in combination with the basic pathologic change of diabetes referred to above may account for the pathogenesis

8/34 4/8 2/8

(24%) (50%) (25%)



23/72 12/23 5/23 2/23 4/23

(32%) (52%) (22%) ( 9%)


and relentless course of what is usually a benign and self-limited disease in other individuals. In this series of 72 patients, there were only 4 who did not have diabetes on the basis of the usual laboratory tests, including a 5-hour glucose tolerance test. Of these four patients, two had chronic lymphatic leukemia. Another had granulocytopenia secondary to hypersplenism. The one other nondiabetic was an 80-year-old male who had been treated in another hosptial for two weeks on one occasion and again for three weeks with intravenous carbenicillin and gentamicin for malignant external otitis. Following his discharge from the hospital the second time, he had developed recurrent pain, primarily behind the ear over the mastoid process. Examination revealed that the skin of the external auditory canal was intact, but that there was redness, swelling and pain on palpation over the mastoid process. There was clinical evidence of an acute mastoiditis which was substantiated by x-ray studies. A complete mastoidectomy was performed at which time granulomatous disease was found only in the tip and perisinuous cells. The antrum and middle ear were normal. Pseudomonas aeruginosa was cultured from the tissue and he was treated accordingly for two weeks postoperatively with complete and permanent resolution of all symptoms. The patient had no history of diabetes and two 5-hour glucose tolerance tests were completely within normal limits. His general health was excellent. The reason for his failure to respond completely during the two previous periods of hospitalization and appropriate treatment and the subsequent development of a frank mastoiditis without re-

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TABLE 2. INFLUENCE OF SURGERY IN PATIENTS WITH FACIAL NERVE PARALYSIS Surgery Precarbenicillin (1959-1969 ) 10 Postcarbenicillin (1969-1977 ) 6

No Surgery





currence of the infection in the canal was and remains unexplained. Of the other 68 patients, 6 had chemical diabetes only, whereas 27 were insulin dependent. Other reports have suggested that the extent of the disease is related to the severity of the diabetes." I have been unable to confirm this in a thorough review of my own material. FACIAL P ARALYSIS

The incidence of facial paralysis in patients with malignant external otitis has decreased somewhat (Table 1). I think this can be attributed to a more general awareness of the nature of the disease, by its earlier identification and the availability of more effective' antibiotic agents. However, in those patients ~~o do develop a paralysis of the nerve, It IS a grave prognostic sign. Half died, and of those who survived, half had no return of facial function. Facial paralysis by itself is first due to a physiologic conduction block because of the infection about the nerve in the soft tissues just at its exit from the stylomastoid foramen." If this infection is not controlled, actual necrosis of the nerve follows. Return of facial function is not possible in such instances and should not be expected. The data is displayed in a somewhat different form in Table 2 which sum~arizes ~e in~uence of surgery in patients WIth facial nerve paralysis prior to . ~he development and general availability of carbenicillin in late 1969 and its use in patients treated since that time.

Nerve Recovery



( 10%)





2 4








In the first group all of the ten patients developing paralysis of the facial nerve were operated upon. The surgery comprised, in all instances, a radical mastoidectomy, usually of an extended type, with decompression of the facial nerve in its intratympanic and vertical segments. In three instances, the nerve could .not be found distal to the stylomas~Old foramen. There were only five survivors, and of these, only one patient recovered his facial function. One of the patients not operated upon developed hypotension and abrupt cardiopulmonary failure as preparations were being made to operate upon him. He was resuscitated but the contemplated procedure had to be abandoned and he subsequently expired of his disease. Another was treated medically and while it seemed that the infection in and about the external auditory canal.healed completely, he subsequently expired to what I now think, in retrospect, was sigmoid sinus thrombosis and septicemia. The one patient who was not operated upon and was treated medically without any recovery of facial nerve function was a 48-year-old Negro male, who had suffered a previous cerebrovascular accident. He was a very uncooperative veteran and had not reported for medical care until six weeks after the appearance of the facial paralysis. As soon as he started feeling better under therapy in the hospital, he signed out against medical advice after only 19 days of treatment. He returned five weeks later because of severe pain, and was rehospitalized for 29 days of intravenous carbenicillin and

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TABLE 3. INCIDENCE OF SIGMOID SINUS THRO~1BOSIS IN 72 PATIENTS Patients at risk Proven Suspected (in retrospect)

8 4

(I not at risk)


(2 not at risk)

gentamicin therapy. He left the hospital again against medical advice just as the external auditory canal completely healed. However, he has reported back to the Out-Patient Clinic at the Veterans Administration Hospital for checkup examinations since that time upon specific request, and to date, nine months later, he still has no evidence of facial function. Electromyographic studies show no evidence of reinnervation and a spinal accessory-facial nerve anastomosis has been recommended to him. Patients operated upon since carbenicillin has been available were obviously those with much more extensive disease, and in three instances, were those who had failed to demonstrate continued improvement with medical therapy alone. While neither surgery nor successful medical treatment can be expected to restore the integrity of a necrotic nerve, the superiority of the latter in regard to the return of facial nerve function is evident. SIGMOID SINUS THROMBOSIS

There were eight patients with paralysis of one or more nerves leaving the cranial cavity through the jugular foramen (Table 3). They could be considered to be at risk for a thrombosis of the dome of tbe jugular bulb and the sigmoid sinus. Three were found at surgery to have thrombosis of the sigmoid sinus and of the jugular bulb, and one proved to have a block in the sigmoid sinus and dome of the jugular bulb by arterio- and venographic studies. Another patient with no cranial nerve deficit at all was found at operation to have a sigmoid sinus thrombosis along with extensive osteomyelitis of the base of the skull. He succumbed to his disease in the precarbenicillin era.

There are three patients in this group of 72 patients who are considered, in retrospect, possibly to have had sigmoid sinus thrombosis. The second patient in this entire series of patients was seen in 1960. A paralysis of the X and XI cranial nerves appeared in the course of a steadily progressive illness which had begun with an external otitis. A radical mastoidectomy was performed, but perusal of the operative note and study of the hospital record reveal no definite statement regarding the sigmoid sinus or dome of the jugular bulb. He expired of a myocardial infarct in the postoperative period. An autopsy was performed but the report cannot be found. Is it possible that this patient had a thrombosis of his sigmoid sinus which was unsuspected and undetected at the time of his surgery? Another patient was a 54-year-old male who had a radical mastoidectomy during the course of his illness, and was discharged from the hospital in a greatly improved condition in the precarbenicillin era. No note at the time of surgery was made regarding the sigmoid sinus or the dome of the jugular bulb. His infection progressed, and he was readmitted to the hospital with persistent pain and after the appearance of a full blown jugular foramen syndrome. Work-up at that time revealed displacement of the internal carotid artery in a superior and medial direction just at its exit from the petrous apex. An abcess of Meckel's cave was diagnosed but he succumbed to an accompanying meningitis prior to any additional surgical procedure. An autopsy confirmed the preterminal diagnosis but there was no note regarding the sigmoid sinus. I suspect that he might very well have had a sigmoid sinus thrombosis in addition to the extensive extradural abcess, meningitis and osteomyelitis. The third patient was a 74-year-old Caucasian insulin dependent diabetic male with symptoms of two months duration and prior treatment, including two separate courses of treatment with carbenicillin and gentamicin in another hospital, along with several minor opera-

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tive procedures. Facial paralysis oc- slight clouding of the pneumatized curred just prior to his referral to this mastoid process, but nothing otherwise medical center where he became a pa- remarkable. His external auditory catient of one of my colleagues. He was nal and tympanic membrane remained felt to represent a typical case of malig- perfectly normal as did his facial nerve nant external otitis. He was hospitalized function. His hospital course was charand treated with 80 mg of gentamicin acterized by progressive deterioration. every eight hours and 1 gm of carbeni- He expired six weeks after admission cillin every hour (24 gm / da y ). There still receiving carbenicillin and gentawas prompt improvement with disap- micin, though in irregular amounts. He pearance of pain and gradual resolution never developed frank meningitis and of the facial paralysis. He was dis- several lumbar punctures and cerebrocharged at his own request 22 days spinal fluid examinations were unreafter admission, greatly improved, but markable. with a residual small nodule of granulaPermission for a full postmortem tion tissue still in the floor of his ca- examination was not granted. A limited nal. The pain returned in six days and autopsy was performed at which time the granulation tissue increased in size. the brain and floor of the cranial cavity He was readmitted and treated once ware reported as being normal. Through again for 29 days in identical fashion. a technical and administrative error the At the time of his discharge, again at sigmoid sinus and dome of the jugular his own insistence, he had no pain, but bulb were not examined, nor were the it was noted that the "ear canal ap- temporal bones removed for histologic peared to be healing." I suspect, in study. There was no evidence of basilar retrospect, that it was not completely meningitis nor any other abnormalities epithelialized. Within one week, recur- to account for his clinical course of rent headaches prompted hospitalization steady deterioration and death. I postufor nine days at another institution un- late that he had a smoldering low-grade der the care of a neurologist. No diag- osteomyelitis of the base of the skull. nosis was made. The pain continued The infection of bone and soft tissue and he began to have some difficulty about the jugular foramen resulted in in swallowing. Four weeks later he was an intense inflammatory reaction which readmitted here and then seen by me encased and compromised function of for the first time. I found him to have the involved cranial nerves. I suggest a completely normal canal and tvm- also that he had a septic thrombosis of panic membrane. There was no local the internal jugular vein, dome of the tenderness or pain. However, paralysis jugular bulb and the sigmoid sinus. I of the IX, X, XI and XII cranial nerves cannot imagine why we did not seek was clearly evident. I felt he had active to prove or disprove this diagnosis more osteomyelitis of the base of his skull diligently, but suppose it is because of but did not at that time suspect a sinus our own myopia at the time; or perhaps thrombosis. No material was available this theory is incorrect. for culture. It is not surprising that the gross and Intravenous carbenicillin and genta- microscopic examinations of his brain micin was begun once again with only and the inner aspect of the dural lining a transient response. His general condi- of the skull were normal, since the distion remained poor and he was febrile ease was at the base of the skull deep with temperatures up to 38.3 and 38.9 C to the meninges. It is most regrettable and on several occasions spikes as high that a full detailed autopsy could not as 39.4 C. Blood cultures were negative. be performed or that, at least, we did An arteriogram was reported as nega- not remove for detailed examination the tive, although there was no positive temporal bone on the affected side. statement regarding the venous phase One patient with no cranial nerve of the examination. A jugulogram was deficit proved at surgery to have signot done. Mastoid x-rays revealed a moid sinus thrombosis and extensive

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and carbenicillin. The minimum inhibitory concentration for gentamicin was 8 mcg/ ml and 62 meg/ ml of carbenicillin. He was treated for six weeks with the addition of probenecid, 0.5 gm Another was a 56-year-old congeni- twice daily for the last seven days. He tally deaf patient who was fond of wear- was completely asymptomatic with the ing a hearing aid in his left ear because canal again completely clean and healed of the vibratory and tactile sense it pro- for the three weeks prior to his disvided him and which assisted him in charge. Facial function was normal. communication. He was married to a One month later, he began to have similarly afflicted woman. He had developed an ear infection which had left-sided headaches again. He then bebeen previously treated for several gan to experience some difficulty in weeks without relief by several oto- swallowing. Paralysis of the IX, X, XI logists. He presented with the classical and XII cranial nerves was noted two picture of malignant external otitis and months after his previous discharge. His was scheduled for admission to the hos- ear remained well and there was nothing pital for treatment with intravenous to culture. Mastoid skull x-rays, CAT carbenicillin and gentamicin. Facial pa- brain scan and arteriograms were not ralysis appeared before he could be helpful. A thrombosed sigmoid sinus admitted three days later. The pain dis- was suspected and an extended radical appeared in three days and within three mastoidectomy and subtotal resection of weeks, the canal was completely epi- the temporal bone was accomplished. thelialized. He was treated for one more The sigmoid sinus and dome of the juguweek and discharged after 31 days of lar bulb were encased in a firm fibrinous treatment. Facial function had started coat of grey inflammatory tissue from to return. Ten days later, the pain re- 2-3 mm in thickness, most marked curred, followed closely by the appear- just at the base of the skull. The ance of a swelling in the external audi- thrombosed bulb was removed along tory canal. This ruptured spontaneously with all of the osteomyelitic bone to disclose a small abcess and a mound around it. Free bleeding was enof granulation tissue. Palpation elicited countered from the proximal transverse some tenderness over the mastoid pro- sinus and the inferior petrosal sinus. The cess and emissary vein. Repeat x-rays pseudomonas organism was recovered showed an increased clouding of the from the clot. He experienced immedipneumatized spaces of the mastoid pro- ate relief of pain following the surgery. cess. He was treated for four days with Antibiotic therapy was continued. For carbenicillin and gentamicin after which ten days he was given 10 gm of cara complete mastoidectomy and facial benicillin intravenously every four hours nerve decompression was performed. A for a total daily dose of 60 gm along granulomatous mastoiditis was en- with 80 mg of tobramycin intravenously countered. Antibiotic therapy was con- every eight hours. There was no evitinued for an additional 22 days in the dence of renal or CNS toxicity. Two hospital when he was discharged with weeks later, the internal jugular vein nearly normal facial nerve function, a was ligated in the neck and removed completely healed incision and an intact up to the previous operative site at the tympanic membrane with an air con- base of the skull. Antibiotic therapy in taining middle ear and a normal and the usual amounts was continued for completely healed external auditory six more weeks. During the last three canal. He was symptom free for one weeks of his hospitalization, he was week then began to have an aching pain cheerful and pleasant and appeared in his ear again. A small draining sinus perfectly well. In spite of his protracted in the canal appeared. Culture revealed illness and previous vicissitudes, it was the pseudomonas organism with an in- difficult to keep him in the hospital creased resistance to both gentamicin any longer.

osteomyelitis of much of the base of the skull. He died of multiple organ failure four weeks following an extended radical mastoidectomy.

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Following his discharge from the hospital, he was completely free of pain, but continued to experience marked difficulty in swallowing, coughing and with other symptoms of aspiration. He developed a febrile illness and was hospitalized elsewhere for eight days. He was discharged as improved, but readmitted here four days later with a massive pleural effusion. He died of pneumonia and respiratory failure ten weeks after his last surgical procedure. His anacusic wife was hysterical and remained adamant in refusing an autopsy. It seems clear that the antibiotic therapy finally and completely eradicated the soft tissue infection in the external auditory canal and soft tissue at the base of the skull and even in the mastoid process. However, at the same time that it cured the infection around the facial nerve, as evidenced by the complete return of facial nerve function, he developed a full-blown jugular foramen syndrome in association with thrombosis of the dome of the jugular bulb and the sigmoid sinus. This latter surely resulted from the osteomyelitis of the skull around the jugular foramen itself and was also responsible for the paralysis of the involved cranial nerves. Further studies had indicated that the responsible organism remained the Pseudomonas aeruginosa and that its original sensitivities (MIC for tobramycin, 0.9 mcg/ ml; 0.75 mcg/ ml for gentamicin and 31 mcg/ ml for carbenicillin) were such that complete cure with appropriate antimicrobial therapy might have been expected. He was treated with adequate amounts of antibiotics for what was considered an adequate amount of time, but yet the organism was not eliminated from the bone at the base of the skull. Final sensitivity studies of the isolate from the jugular bulb indicated that it remained sensitive to gentamicin at an MIC of 0.19 mcg/ml, but was relatively insensitive to carbenicillin at 250 mcg/ml. One final patient who was and remains an enigma was a 79-year-old Caucasian male with diabetes controlled with oral medications. He presented to one of my associates in this medical


center with a rather typical history and picture of malignant external otitis. He was hospitalized and treated with intravenous carbenicillin and gentamicin for two weeks and then discharged on oral carbenicillin (Geocillin®) for an additional ten days. Pain recurred in two weeks. I then saw him for the first time to find a relatively normal external auditory canal and tympanic membrane. There was little or no local tenderness, but he complained vociferously of headaches in the left temporal and parietal regions. I felt that he did have residual disease present which was not clinically apparent, and advised hospitalization for further study. He refused but returned in three weeks and was admitted at that time. No material was available for culture. Work-up in the hospital failed to disclose anything particularly significant. His pain disappeared promptly upon resumption of intravenous antibiotic therapy, and he was discharged at his own insistence two weeks later. Within three days, the pain had recurred, and he reported back for reexamination which was about the same as before. He was hospitalized for a complete work-up. The neurologic consultant could find no abnormality and suggested that his pain was psychogenic and that a trial of placebo therapy might be helpful. As before, there was no material available for culture. Because of his persistent pain which yielded only to Demerol® by injection, he was started once again on intravenous carbenicillin and gentamicin. It was continued in maximum therapeutic amounts for three weeks at which time he was again discharged at his insistence, one week before I felt it was desirable. However, his pain had disappeared three days after the institution of treatment, and never recurred thereafter. The exact etiology for his disabling headaches was never determined. I feel, in retrospect, that it was possibly due to a low-grade persistent smoldering osteomyelitis of the base of the skull perhaps with an unrecognized sigmoid sinus thrombosis. Could the last three

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week course of antimicrobial therapy have eliminated the infection? Any patient developing a paralysis of any of the cranial nerves IX-XII must be suspected as having a thrombosis of the sigmoid sinus and dome of the jugular bulb. This can be ascertained by either direct or indirect methods; the former, by injection of contrast media into the internal jugular vein, for a jugulogram demonstrates it most directly, although intrarterial injection can provide the same as well as additional information. At the time of this writing, I am not certain as to whether or not thrombosis of the sigmoid sinus in this disease is an indication for mandatory surgical intervention, but suspect that it may be. If so, the surgery should be no less than an extended radical mastoidectomy with removal of all of the mastoid air cells, mastoid tip, and exposure of the entire sigmoid sinus, dome of the jugular bulb and the internal jugular vein at its entrance into the skull. The clot and all inflammatory material about the vein and sinus, as well as their lateral walls should be removed. As much osteomyelitic bone around and adjacent to the foramen should be removed. Free bleeding must be obtained from the transverse, superior and inferior petrosal sinuses, and the internal jugular vein. If not, antimicrobial therapy should certainly be continued for no less than six weeks after the diagnosis is made during all of which time the temperature should be perfectly normal and there should be no signs of sepsis, pain, tenderness, or other evidence of active infection in the external auditory canal, the neck, or anywhere else. Can the intravascular thrombus (and osteomyelitic bone) be sterilized with antibiotics alone, if administered for a long enough period of time in sufficient doses? If sterilized, will the sigmoid sinus and jugular vein recanalize? There is no question as to the prognostic import upon the appearance of this syndrome. Seven of eight such patients died of their disease. Meyerhoff et al correctly identified the pathogenesis of multiple cranial nerve palsies and

emphasized its grave significance. Three of their four patients died." MASTOIDITIS

Although the infection usually extends through the floor of the canal into the soft tissues at the base of the skull, it may and frequently does extend posteriorly into the bony canal wall of the external auditory canal and into and through the mastoid cortex or its tip. In other words, necrosis and sequestration of bone permits the direct extension of the infection into the pneumatized air cells of the mastoid process. I think it can progress into a full blown mastoiditis with or without middle ear involvement." This has been seen in many patients in this series. Most of them have been operated upon, but some have been cured by medical therapy alone. The initial work-up of any patient hospitalized for treatment of malignant external otitis should include mastoid x-rays. These will disclose any unsuspected changes and provide a baseline record for possible progressive disease which would mandate surgical intervention. Even when there is no clinical evidence of middle ear effusion or mastoiditis, x-rays may reveal a slight clouding of what is usually a well-pneumatized mastoid process. I believe that this is secondary to venous and lymphatic engorgement and an inflammatory response without actual bacterial invasion. When the organism has gained access to the mucosal lining of the air cells, there is more clouding and in some instances evidence of bone destruction. Should a mastoidectomy be performed in these patients? I do not know, but it has been my policy in the past to operate upon most of them when evidence of frank mastoiditis is present. However, since carbenicillin became available in 1969, I have treated more and more of them with medical therapy alone. One of my most recent patients is an excellent example. He was a 77year-old Negro male with diabetes controlled with oral medications. He had severe pain and a purulent discharge for one month. The referring otologist felt that he had a carcinoma of the ear.

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Biopsy and microscopic examination procedures had failed to halt the prodisproved this possibility and the diag- gress of the disease. nosis of malignant external otitis was A 73-year-old insulin dependent male confirmed by culture and sensitivity diabetic continued to have pain and restudies. Pain rapidly disappeared under intravenous antimicrobial therapy at formation of granulation tissue after which time a more careful examination three weeks of specific treatment. A could be performed. X-rays demon- complete mastoidectomy revealed extenstrated definite and quite marked cloud- sive bone and mucosal disease. Coming of the mastoid process. A probe plete recovery ensued after three more could be passed directly through the weeks of therapy. granulation tissue into the mastoid air An 80-year-old nondiabetic male, discell system through the posterior canal cussed previously, was treated on two wall at its junction with the mastoid separate occasions elsewhere for maligcortex. I felt that a complete mastoidec- nant external otitis. Following his distomy would be necessary. However, his charge from the hospital for the second clinical course was characterized by time, pain recurred and was accomcontinuous and steady improvement un- panied by a swelling of the tissues betil his ear was completely normal in hind the ear. Examination revealed a one month. He was treated for an addi- frank mastoiditis, with the expected tional week and discharged as com- x-ray findings. A complete mastoidecpletely cured. tomy was performed two days after adTwo patients had been operated mission. It is my opinion now that this upon elsewhere and referred for con- patient would have recovered comsultation and treatment because of per- pletely on antimicrobial therapy alone. sistent pain and gross infection due to He was not given sufficient opportunity the pseudomonas organism. Both pa- to improve maximally, but at that time, tients responded with prompt disap- I was not yet convinced that carbenicilpearance of pain and gradual and lin could be relied upon to that degree. steady resolution of the infectious pro- At the surgical procedure, typical granucess with complete healing of the mas- lomatous mastoiditis with bone destructoid cavities. Contemplated additional tion was found only in the tip and surgery was never required. periantral cells. The antrum was only Perhaps the reader might ask what is slightly involved and the ossicles and lost by an operation? And whether or epitympanum were perfectly normal. not a good sound operative procedure A gO-year-old Caucasian male diamight not shorten the total duration of betic, controlled with oral medications, the illness? This is a valid question, but with persistent pain and reformation of it is my feeling that an operative pro- granulation tissue developed a facial cedure opens up new channels and palsy as he was being treated for three fascial spaces to the infectious process weeks. An extended radical mastoidecand that, in any event, the specific anti- tomy and facial nerve decompression microbial therapy should be continued were performed, at which time extenin the postoperative period until total sive bony and soft tissue disease was healing has occurred. This requires at found. He was treated for six weeks least three weeks after a complete mas- postoperatively with complete recovery toidectomy and up to 12 weeks follow- except for his facial nerve function. ing a radical mastoidectomy. An 83-year-old male diabetic conIn an attempt to answer this important question, I have reviewed critically trolled with oral medications had perthe eight patients operated upon here sistent pain and developed a weakness since carbenicillin cured the first pa- of his facial nerve under treatment in tient in whom it was used. Incidentally, the hospital. A radical mastoidectomy this was a patient with a vagal palsy and facial nerve decompression and conappearing after three major operative tinued therapy for six additional weeks

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resulted in complete cure and return of facial nerve function. A 91-year-old male with chemical diabetes was diagnosed only after hospitalization. His pain continued under treatment. He became severely dizzy and developed a facial nerve palsy after ten days of treatment. An extended radical mastoidectomy and facial nerve decompression was performed. He was treated for six weeks afterward and discharged as greatly improved. This is one of the few patients who was left with a moist mastoid cavity and pain. Some six months after surgery, he suesumbed to advanced cardiac disease in another institution. Three patients were found to have sigmoid sinus thrombosis at surgery; one has been discussed previously. The average age of these eight patients was 74 years and only four were insulin dependent diabetics. Perhaps in only one of these eight patients could recovery have been expected without surgical intervention. TREATMENT

Even an elderly diabetic with an external otitis should be given the benefit of the doubt, and treated as an outpatient with careful cleaning of the canal and the local use of various liquids and ointment medicaments. With severe pain, abcess formation and/or cellulitis, oral or systemic antibiotic therapy is usually indicated. Most instances of external otitis will clear promptly with or without such treatment. In those instances in which there appears a dehiscence in the canal accompanied by some granulation tissue, it can be removed gently, and local treatment and usual supportive measures continued. If the infection clears within several weeks of standard treatment, then it is certainly not the malignant variety of external otitis. On the other hand if it should prove unresponsive to such usual methods of treatment and the granulation tissue persists, recurs, or increases in size along with local pain and purulent discharge, then malignant external otitis must be considered as a possible diagnosis. Material should be taken

from the canal for culture and sensitivity studies. If there is no history of diabetes, a urinalysis and glucose tolerance test should be secured to document its presence or absence. In the presence of a positive culture for Pseudomonas aeruginosa and failure to respond after two weeks of intensive local therapy, then admission to the hospital for intensive intravenous antimicrobial therapy is indicated. Hospital work-up should include mastoid x-rays, routine urinalysis and blood counts, blood urea nitrogen (BUN), creatinine and blood sugar levels and an electrocardiogram. In the absence of any history suggestive of allergy to penicillin, treatment should be begun promptly with carbenicillin as an intravenous bolus of 5 gm every four hours. A continuous intravenous infusion of saline or dextrose in water is necessary to provide access for drug administration. One of the newer semisynthetic penicillin derivatives such as ticarcillin or pirbenicillin may be substituted. In addition to the carbenicillin an aminoglycocide antibiotic should b~ added. Gentamicin is the drug with which I have had the most experience. In the absence of renal disease and presence of normal blood creatinine levels, it should be given in the dosage of 80 mg every eight hours; it may be given intravenously as a bolus but should not be mixed with the carbenicillin. Tobramycin, which has a similar spectrum of antibacterial activity, and/ or amikacin or some other aminoglycocide derivative may be substituted." It is important to use such a drug together with the carbenicillin, as it may prevent the development of resistance of the organism to carbenicillin. In the event that the patient has a history of sensitivity to penicillin, treatment may be begun with intravenous gentamicin alone. The clinical course of the patient and further bacteriological and laboratory studies will determine whether or not this will be efficacious. In the event that it is not, or if the infection is in an advanced stage of the disease, perhaps with mastoiditis and/ or facial paralysis, then the

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patient should be desensitized to carbenicillin. The appearance of a skin eruption or reaction during therapy is usually due to the carbenicillin, but the drug should not be discontinued unless absolutely necessary. The administration of antihistamines and corticosteroids in therapeutic amounts is usually helpful in this regard. In addition, antipruritic medications can be used for local application.

very high level. However, the toxic dose is not known and probably little harm would come from continuing the drug in usual amounts. However, one must be extremely careful in such instances of urinary tract obstruction, preexisting renal disease or elevated BUN or creatinine levels from whatever cause. The amount of gentamicin given must be titrated carefully according to the creatinine clearance or serum creatinine levels. lf diuretics are necesI suggest that all patients be treated sary because of fluid retention, one medically for as long as improvement must avoid a rapid increase in serum continues and to consider surgical in- aminoglycocide levels. These can be tervention only in the event that a determined in the laboratory of most plateau is reached or symptoms and large hospitals. In the event that the signs become worse under treatment. infectious process seems not to be relf this policy is followed, most patients sponding as expected, then one must will get well and it is likely that many secure from the microbiology laboratory unnecessary and potentially harmful minimum inhibitory and minimum hacsurgical procedures can be avoided. tericidal concentration levels. A sensiMost of these patients are at an ad- tive pseudomonas organism responds to vanced age, and they are heir to all a concentration of gentamicin of less sorts of medical and other surgical prob- than 1 mcg/ml and to less than 32 lems developing while they are being mcg/ml of carbenicillin. In borderline treated for their ear infections. The instances, the sensitivity of the organism most recent death which occurred just should be studied more thoroughly by several months ago was in a 78-year-old tube dilution methods for determination male diabetic controlled with oral medi- of serum bactericidal levels and evalucations. By his own admission and by ated in light of the patient's clinical examination, his ear infection seemed course. to be improving steadily as he develAs all of these patients present a oped pulmonary edema, cardiac irreg- variety of medical problems which may ularities, urinary obstruction and reten- differ and vary in their severity and tion, renal failure, etc. He died of mul- significance, one requires the assistance tiple organ failure as his ear was of a good house staff and competent steadily improving. At least two others colleagues to carry them through what died of coronary infarcts, and three died may be an arduous program of treatof renal failure, related and aggravated ment. A serious problem is that of conin part by nephrotoxic aminoglycocide drugs. vincing the patient of the necessity for prolonged hospitalization and the anCarbenicillin is nontoxic to the kid- noying continuous intravenous infusion ney, although in renal failure patients, long after the pain in his ear has disapit can accumulate in the blood to a peared. REFERENCES 1. Meltzer P, Kelemen G: Pyocyaneous 4. Coser PL, DeCosta V: Otite externa osteomyelitis of the temporal bone, mandible, maligna em lactante apresentacao de urn caso. and zygoma. Laryngoscope 69:1300-1316, Rev Bras Oto-Rino-Laryngol 40:200-202, 1974 1959 5. Malins J: Clinical Diabetes Mellitus. 2. Chandler JR: Malignant external otitis. London, Eye and Spottiswoode, 1968 Laryngoscope 78: 1257-1294, 1968 6. Wright D, Alexander J: Effects of water 3. Chandler JR: Pathogenesis and treatment on bacterial flora of swimmer's ear. Arch Otoof facial paralysis due to malignant external laryngol 99:15-18, 1974 otitis. Ann Otol Rhinol Laryngol 81: 1-11, 1972 7. Chandler JR: Malignant external otitis

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and facial paralysis. Otolaryngol Clin North Am 7:375-383, 1974 8. Hubbard J, King H, Beamer P: The pathogenicity of pseudomonas aeruginosa (bacillus pyocyaneus) experimental studies and report of a case. Am J Clin Pathol 28:243-257,

1957 9. Meyerhoff WL, Gates GA, Montalbo PJ: Pseudomonas mastoiditis. Laryngoscope 87: 483-492, 1977 10. Neu H: Tobramycin: an overview. J Infect Dis 134:S3-S19, 1976

ACKNOWLEDGMENT - I gratefully acknowledge the unstinting support and assistance of a dedicated house staff in caring for this difficult group of patients. REPRIXTS - James R. Chandler, MD, P. O. Box 520875, Biscayne Annex, Miami, FL 33152.

GUIDELINES OF GRANTS TRUSTEES OF AMERICAN OTOLOGIC SOCIETY A matter of continual concern to the members of the Board of Trustees of the American Otological Society is the determination of guidelines for the funding of grants from its research fund. The following is our current formulation of policy. Our objective is clearly before us as the problem of otosclerosis: its diagnosis and management, the possible causes and underlying conditions (such as the hereditary background), and an understanding of the disorder that may lead eventually to its prevention and cure. Our present lack of understanding of the disorder and the absence, as far as known, of any similar condition in animals below man. makes research in this field particularly difficult. A direct attack on the disease is hardly feasible; therefore it seems to be sound strategy to try circuitous approaches, such as the investigation of bone development, growth, and repair under various conditions, and the study of other diseases that show suggestive correspondence. It is possible that directions of investigation that may seem initially somewhat remote from otosclerosis itself mav provide insights that will eventually lead to success in reaching our goal. The applicant should describe correlations between proposed research with the clinical pathological entity of otosclerosis. Therefore. our policv is to aid and encourage research in the immediate field of otosclerosis and also in adioining fields if in our considered opinion there is a substantial promise that the results ohtained will be of assistance in the ways just indicated, and may lead to the attainment of our objective. To stimulate the attainment of this obiective, the Board of Trustees wishes to remind the general otolaryngologic community that funds are still available for suitable grants. Application forms may be obtained from the office of the secretary, David A. Hilding, MD, 1855 West Taylor Street, Chicago, IL 60612. Grant requests should be submitted by January 31.

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Malignant external otitis: further considerations.

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