Allris' Nasl/s' Larynx (Tokyo) 18, 199-208 (1991)
TUBERCULOUS OTITIS MEDIA PRESENTING AS COMPLICATIONS: REPORT OF 18 CASES D. S. GREWAL, M.D., Brajendra BASER, M.D., R.N. SHAHANI, M.D., and S. KHANNA, M.D. Department of Otolaryngology, T. N. Medical College and B. Y. L. Nair Hospital, Bombay-B, India
Tuberculous otitis media is a rare but treatable disease; delay in its diagnosis usually leads to complications. In the last 15 years we have come across 18 cases of tuberculous otitis media, which presented various intraand extracranial complications. In the past, tuberculous otitis media had always been considered a discrete disease, but it is possible that tuberculosis may coexist or secondarily affect an already discharging ear. The following discussion illustrates the complications and clinical problems encountered in tuberculous otitis media. The incidence of tuberculosis of the middle ear and mastoid has faIlen sharply due to improvements in standards of living, the advent of more effective chemotherapy, and effective public health measures. Even in developing countries it is now uncommon to see cases of tuberculosis of the middle ear cleft. The diagnosis is usually made with the help of histopathological examination of granulation tissue removed during mastoidectomy or aural polypotomy. However, tuberculosis should be suspected after mastoid surgery whenever granulomata, slow and incomplete wound healing, persistent otorrhea, and formation of bony sequestra are encountered (HEBERT and RIORDOAN, 1964). PATIENTS AND FINDINGS
We reviewed the records of 18 patients who were admitted to our services between 1975 and 1989 with the diagnosis of chronic suppurative otitis media with complications and where diagnosis of tuberculosis was made only after histopathological examination of granulation tissue. Of these 18 patients, 12 were male and 6 female, age range was 8 years to 42 years, and the majority of the patients was below 30 years of age. Nine patients (50 %) were referred to us from the neurology and neurosurgical services where they were treated for brain abscess and/or meningitis. Details of the clinical Received for publication
October 22, 1990 199
200
D. S. GREWAL ef al. Table I . Clinical presentation. No. of cases 1. 2. 3. 4. 5. 6.
5
Meningitis Bezold's abscess Subperiosteal abscess Gradenigo's syndrome Facial palsy Citelli's abscess
4 3 3 2
18
Total Table 2.
Otogenic abscesses (intracranial and extracranial). No. of cases
1.
2. 3. 4.
(a) Cerebral (b) Cerebellar (c) Perisinus Bezold's abscess Subperiosteal abscess Citelli's abscess
Intracranial
Table 3.
2
3 8 4 3
Bone erosion . No. of cases
I. 2. 3. 4. 5. 6.
Lateral semicircular canal Lateral sinus plate Promontory Facial canal Petrous apex Tegmen tympani with dural herniation
13 8 6 2 2 2
presentation are listed in Tables 1 and 2. Only 50 % of the cases had active tuberculosis elsewhere in the body (lungs 4, tonsil 1, and cervical lymph nodes 4) . During surgery, bone erosion was seen in all cases (Table 3). ILLUSTRATIVE CASE REPORTS
Case I A 20-year-old male patient was referred to us from the affiliated hospital with the complaint of swelling of the right side of the neck with high fever for 8 days. There had been foul-smelling otorrhea with deafness in the right ear for 8 years. On examination, the patient was toxic and had a 40°C temperature. There was a huge subperiosteal abscess involving the entire scalp . Examination of the right ear showed a large polyp with cholesteatomatous flakes. Testing showed hemoglobin, 10%; WBC, 14,000/mm3 ; polymorphs, 50%; lymphocytes, 45 % ; eosinophils, 3 %; and monocytes, 2 %. Erythrocyte sedimen-
TUBERCULOUS OTITIS MEDIA
201
Fig. I. A huge subperiosteal abscess (Case I). CT scan showing huge sUbperiosteal abscess involving the right mastoid and the right temporoparietal region, going to the scalp and left parietotemporal region with marked hydrocephalus.
tation rate was 20 mm at the end of the first hour; urine and stool examination was normal; chest X-ray was normal. A CT scan showed a huge subperiosteal abscess in the right mastoid and right temporoparietal region going towards the left parietotemporal region with marked hydrocephalus (Fig. 1). The abscess was drained under general anaesthesia by giving multiple incisions on the both parietal regions and nearly 750 ml of pus was evacuated. Aural polypotomy was also done at the same time. Pus was sent for culture and antibiotic sensitivity. It showed Pseudomonas aeruginosa and Escherichia coli which were sensitive to Gentamycin® and Cloxacillin®. Mycobacterium tuberculosis was not seen. The patient was kept on regular dressings with suction clearance of the ear and injections of Gentamycin'Rl, Cloxacillin®, and Metronidazole®. After 2 weeks a tympanomastoidectomy was done. On exploration of the ear, the mastoid was seen to be full of granulations and cholesteatoma, with thrombosis of sigmoid sinus present along with perisinus abscess. Histopathology of granulation tissue from the mastoid showed features of tuberculosis. The patient was given a complete course of antitubercular therapy (Rifampicin'Rl, Ethambutol®, and isonicotinic acid hydrazide). After an interval of 2 weeks, the patient was referred to neurosurgical services for a shunt operation for hydrocephalus. The interesting point about this patient was the huge subperiosteal mastoid abscess of tuberculous origin with sigmoid sinus thrombosis and marked hydrocephalus. Case II An 8-year-old male patient came to us in acute respiratory distress along with stiffness of the neck, high fever, and dysphagia lasting for 2 days. On examination, the patient showed marked swelling of the floor of the mouth, tongue, and the right lateral pharyngeal wall, and torticollis. Emergency tracheostomy was done under local anaesthesia because passing
202
D. S. GREWAL el af.
Fig. 2. Citelli's abscess (Case II). (a) Eight-year-old boy 4 days after draining of the para pharyngeal abscess, with marked cellulitis of the neck. Note the gauze packed in the abscess cavity and profuse discharge coming out of the right ear. (b) X-ray of the neck and chest showing soft tissue shadow on right side of the neck with marked shift of trachea to the left. (c) Radical mastoidectomy cavity. Note the pick in the fistulous tract under the exposed digastric muscle which caused the parapharyngeal abscess. (d) Photograph showing the features of tuberculosis. Note the epitheloid giant cells. H&Ex450.
the endotracheal tube was not possible due to marked swelling of the tongue and cellulitis of the neck. General anaesthesia was then given and the abscess in the upper neck drained by an incision in its most prominent part. About 300 ml of foul-smelling pus was drained and sent for culture and antibiotic sensitivity, which showed mixed infection with E. coli and Pseudomonas pyocyaneus. Treatment was given by intravenous injections of Gentamycin®, Ampicillin®, and Metronidazole®, to which the organisms were sensitive. No M. tuberculosis was seen (Fig. 2, a and b). On subsequent E.N .T. examination, we detected a cholesteatoma in the right
TUBERCULOUS OTITIS MEDIA
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ear. Fifteen days later, a tympanomastoidectomy was done. There was a fistulous tract anterior to the sigmoid sinus near the mastoid tip through which infection had traveled beneath the posterior belly of the diastric muscle and then to the pterygomaxillary and parapharyngeal spaces (Fig. 2c). The histopathology of granulations from the mastoid showed features of tuberculosis (Fig. 2d), and the patient was given complete courses of antituberculous drugs. The interesting point about this patient was that the mastoid tip was eroded by the tuberculous granulation tissue from where the pus extended to involve the parapharyngeal space leading to the parapharyngeal abscess. This lead to compression of the airway for which the emergency tracheostomy was required. Case III A 25-year-old male patient had complained of left earache and otorrhea for twenty years. Examination revealed a polyp in the left ear with foul-smelling discharge and left mastoid tenderness, which were suggestive of acute mastoiditis. Central nervous system examination showed that the patient was drowsy with neck stiffness, astereognosis, and positive Kernig's sign. Mastoid X-rays showed an area of rarefaction in the attic, antral, and periantral regions on the left side. CSF examination was suggestive of pyogenic meningitis (clear fluid with 16 mg% protein, markedly reduced sugar, 260 mm 3 cells (polymorphs), and no organisms). Patient was treated conservatively with antibiotics for 7 days, after which the ear was explored under general anaesthesia. A huge cholesteatoma that was eroding the sigmoid sinus and dural plates, with prolapse of the dura into the mastoid cavity, was seen. A modified radical mastoidectomy was done. The dural defect was closed with a mastoid cortical bone graft removed from the mastoid tip (Fig. 3, a and b). The postoperative recovery was smooth.
Fig. 3. Dural herniation (Case III). (a) Radical mastoid cavity with dural herniation and granulations. This was obscuring the view of the mastoid antrum and attic. This patient had a history of 5 attacks of meningitis. (b) Dural herniation reduced and bony defect closed with mastoid cortical bone removed from the tip of the mastoid. Attic and antrum are now visible.
204
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On the 18th postoperative day, the patient suddenly became drowsy. A carotid angiography was done, which was suggestive of left temporal lobe abscess. A CT scan was not done as this facility was not available at that time. A temporal burr hole was done and 50 ml of pus aspirated, which showed the presence of tuberculous bacilli. After improvement of the general condition of the patient, a craniotomy was done, and the temporal lobe abscess was excised. Histopathological examination of tissues from the mastoid cavity and wall of the temporal lobe abscess showed features of tuberculosis. A complete course of antituberculous therapy was given. In this case, there was no tuberculosis of lungs, lymph node, or bones, and thus we presume it to be primary tuberculosis of the middle ear. The patient had suffered since childhood from chronic suppurative otitis media with cholesteatoma, which later on might have secondarily become infected with tuberculous bacilli. COMMENT
Tuberculous bacilli find their way to the middle ear and mastoid through the Eustachian tube, the blood stream, and, rarely, through the external auditory meatus. Though tuberculous otitis media is usually secondary to tuberculous infection elsewhere in body, one occasionally encounters cases where no other tuberculous lesion in the body can be demonstrated. It is possible that tuberculosis may secondarily invade an already discharging ear, and in countries where the incidence of both tuberculosis and discharging ears is relatively high, at times it becomes difficult to say which of the infections was primary. Tuberculous otitis media, whether primary or secondary, is more prone to develop intra- and extracranial complications. In developing countries, discharging ears are frequently neglected by the patient but surprisingly the ratio of discharging ears to complications rate is quite low. Perhaps the more frequent use of antibiotics has changed the clinical picture of yesteryear, because although antibiotics alone are insufficient to cure most cases of discharging ears they are to some extent able to reduce the incidence of intracranial complications. This is in contrast to tuberculous otitis media, which is now uncommon even in developing countries. These days, clinical diagnosis of tuberculous otitis media is rarely made in the outpatient department. Histopathology of granulation tissue from patients who presented complications showed that about 12 % of all these cases were due to tuberculosis. This suggests that perhaps the clinical picture is changing: the more frequent use of Neomycin® and Gentamycin® ear drops might be responsible for masking the initial clinical picture as they are weakly antituberculosis. A low rate of positive staining or culture of aural discharge and delay in diagnosis may also be due to use of those eardrops (OLUJIMI, 1988). In our opinion, the delay in diagnosis is due to changes in the histopathological
TUBERCULOUS OTITIS MEDIA
205
picture due to use of the ear drops. In tuberculous otitis media the tympanic membrane is initially dull and lusterless; later it shows yellowish spots which are tuberculous deposits undergoing disintegration. After a few weeks multiple perforations through which a thin, scant, and odorless discharge of pale granulation tissue may be seen emerging. Later, mastoid air cells are replaced by tuberculous granulation tissue which may perforate the mastoid cortex, leading to a postaural abscess and subsequent fistula, which are often mUltiple (Fig. 4). Complications are common due to tuberculous granulation tissue and sequestration of bone (Fig. 5). Tubercular otitis media may give rise to facial paralysis, labyrinthitis, petrositis, lateral sinus thrombophlebitis, and thrombosis, meningitis, brain abscess (cerebral or cerebellar), and tuberculoma of the brain. There is no fixed route for the spread of the disease to these structures. Facial paralysis is much more common in children than in adults and appears to be due to pressure from granulation tissue (Fig. 5) and sequestration of bone around the facial c'lnal (ORMEROD, 1931). The disease involves the labyrinth, either by eroding the semicircular canals promontory or through the round window membrane. The labyrinthine involvement ranges from superficial erosion of semicircular canals to softening and sequestration of the entire labyrinth (Figs. 6 and 7). Because of the gradual spread of the disease to the labyrinth, tinnitus of varying degrees is most common, whereas vertigo, nystagmus, and ataxia are rare. At times, because
Fig. 4. A non-healing sinus. Sevenyear-old child showing non-healing sinus following incision and drainage of Bezold's abscess. Radical mastoidectomy with fascia grafting was done. Note the haemostat in the sinus.
Fig. 5. Radical mastoid cavity with exposed facial nerve which is surrounded by granulations. Note that the facial nerve is dividing into two branches in the mastoid. This patient had a history of facial nerve palsy since 8 months and ear discharge since 10 years.
206
D. S. GREWAL el af.
there is a gradual involvement of the labyrinth and because of adaptation, none of the above symptoms may be present and the labyrinth m':ly be dead.
Fig. 6. Radical mlstoid cavity showing erosion of all three semicircular canals.
Fig. 7. Radical mlstoid cavity with promontory erosion (2 x 1 mm). Note that the basal turn of the cochlea is exposed (marked t).
Fig. 8. Gradenigo's syndrome. (a) Note the left lateral rectus palsy. (b) CT scan showing small abscess at left petrous apex (marked t). (c) Radical mastoidectomy showing Frankner's approach to the petrous apex.
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Fig. 9. Radical mlstoid cavity showing posterior fossa dural defect (marked
n.
The petrous apex may get infected by direct extension of disease from the mastoid or by way of the bloodstream from the focus of tuberculosis elsewhere (Fig. 8, a-c). Miliary tuberculosis of the petro us apex without involvement of middle ear can occur, leading to Gradenigo's syndrome (MYERSON, 1944). The involvement of meninges is usually due to direct extension of the disease process (Fig. 9), while the brain is involved via communicating veins or perivascular spread along the Virchow Robin space. We conclude that suspicion of tuberculosis of the middle ear cleft should arise when, during mastoid surgery, the mastoid cavity formed is very large or much larger than expected. This is due to the following reasons: 1. In the presence of a normal middle ear with a well-pneumatized mastoid, the middle-ear cleft can get infected via the hematogenous or eustachian tube routes. In such a case the mastoid cavity formed is very large. 2. In the presence of a pre-existing chronic suppurative otitis media with acellular mastoid, a superimposed tuberculous infection can occur via the hematogenous, eustachian tube, or a perforation of the tympanic membrane, which gives rise to a larger mastoid cavity than expected. There are two ml in concepts in mastoid surgery, one the conventional outside-in and the other more fashionable but older inside-out. In our opinion, mastoid surgery is three dimensional, involving both depth and area. We normally do a mastoidectomy from lateral to medial and at the same time keep lowering the ridge. Ideally, at the end of surgery, the shape to the outlet of the mastoid cavity is round to oval. When the facial ridge is taken into consideration it is bean shaped . The aim of this canal-wall down technique is to divide the middle ear cleft into two parts at the level of the additus by fascia grafting, the middle ear communicating with the eustachian tube and the mastoid cavity with the external auditory canal. By this technique we simplify the complex middle ear cleft, thereby considerably increasing the cure rate. At the end of surgery we place a slightly thicker graft over the middle ear as this prevents formation of retraction
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packets. In combined approach tympanoplasty technique the middle ear cleft is made more complex hence it does not have good cure rates. The classical signs described for tuberculous otitis media, such as multiple perforations of the tympanic membrane or pale granulation tissue, are not seen these days because such cases are diagnosed and treated late, and by the time they are diagnosed and treated they already have complications. Hence we feel that the most common presenting feature of tuberculous otitis media is complications. The two important characteristic features of tuberculosis are abscess formation and bone erosion, which lead to complications. REFERENCES HEBERT, F., and RIORDOAN, D.: Tuberculosis of the middle ear. Laryngoscope 74: 198-204, 1964. MYERSON, M. c.: Tuberculosis of the middle ear and mastoid. III Tuberculosis of the Ear, Nose and Throat, 1st ed. (Myerson, M.C., ed.), Charles C. Thomas, Springfield, Ill., pp. 155-178, 1944. OLUJIMI, 0.: Early diagnosis of tuberculous otitis media. J. Laryngol. 0(01. 102: 133-135, 1988. ORMEROD, F. C.: Tuberculous disease of the middle ear. J. Laryngol. 0(01. 46: 449-459, 1931.
Request reprints to:
Dr. D. S. Grewal, 1/5 Doctor's Quarters, Government Colony Near Mahalaxmi Race Course, Haji Ali, Bombay 400 034, India
TUBERCULOUS OTITIS MEDIA PRESENTING AS COMPLICATIONS: REPORT OF 18 CASES D. S. GREWAL, M.D., Brajendra BASER, M.D., R.N. SHAHANI, M.D., and S. KHANNA, M.D. Department of Otolaryngology, T. N. Medical College and B. Y. L. Nair Hospital, Bombay-B, India
Tuberculous otitis media is a rare but treatable disease; delay in its diagnosis usually leads to complications. In the last 15 years we have come across 18 cases of tuberculous otitis media, which presented various intraand extracranial complications. In the past, tuberculous otitis media had always been considered a discrete disease, but it is possible that tuberculosis may coexist or secondarily affect an already discharging ear. The following discussion illustrates the complications and clinical problems encountered in tuberculous otitis media. The incidence of tuberculosis of the middle ear and mastoid has faIlen sharply due to improvements in standards of living, the advent of more effective chemotherapy, and effective public health measures. Even in developing countries it is now uncommon to see cases of tuberculosis of the middle ear cleft. The diagnosis is usually made with the help of histopathological examination of granulation tissue removed during mastoidectomy or aural polypotomy. However, tuberculosis should be suspected after mastoid surgery whenever granulomata, slow and incomplete wound healing, persistent otorrhea, and formation of bony sequestra are encountered (HEBERT and RIORDOAN, 1964). PATIENTS AND FINDINGS
We reviewed the records of 18 patients who were admitted to our services between 1975 and 1989 with the diagnosis of chronic suppurative otitis media with complications and where diagnosis of tuberculosis was made only after histopathological examination of granulation tissue. Of these 18 patients, 12 were male and 6 female, age range was 8 years to 42 years, and the majority of the patients was below 30 years of age. Nine patients (50 %) were referred to us from the neurology and neurosurgical services where they were treated for brain abscess and/or meningitis. Details of the clinical Received for publication
October 22, 1990 199
200
D. S. GREWAL ef al. Table I . Clinical presentation. No. of cases 1. 2. 3. 4. 5. 6.
5
Meningitis Bezold's abscess Subperiosteal abscess Gradenigo's syndrome Facial palsy Citelli's abscess
4 3 3 2
18
Total Table 2.
Otogenic abscesses (intracranial and extracranial). No. of cases
1.
2. 3. 4.
(a) Cerebral (b) Cerebellar (c) Perisinus Bezold's abscess Subperiosteal abscess Citelli's abscess
Intracranial
Table 3.
2
3 8 4 3
Bone erosion . No. of cases
I. 2. 3. 4. 5. 6.
Lateral semicircular canal Lateral sinus plate Promontory Facial canal Petrous apex Tegmen tympani with dural herniation
13 8 6 2 2 2
presentation are listed in Tables 1 and 2. Only 50 % of the cases had active tuberculosis elsewhere in the body (lungs 4, tonsil 1, and cervical lymph nodes 4) . During surgery, bone erosion was seen in all cases (Table 3). ILLUSTRATIVE CASE REPORTS
Case I A 20-year-old male patient was referred to us from the affiliated hospital with the complaint of swelling of the right side of the neck with high fever for 8 days. There had been foul-smelling otorrhea with deafness in the right ear for 8 years. On examination, the patient was toxic and had a 40°C temperature. There was a huge subperiosteal abscess involving the entire scalp . Examination of the right ear showed a large polyp with cholesteatomatous flakes. Testing showed hemoglobin, 10%; WBC, 14,000/mm3 ; polymorphs, 50%; lymphocytes, 45 % ; eosinophils, 3 %; and monocytes, 2 %. Erythrocyte sedimen-
TUBERCULOUS OTITIS MEDIA
201
Fig. I. A huge subperiosteal abscess (Case I). CT scan showing huge sUbperiosteal abscess involving the right mastoid and the right temporoparietal region, going to the scalp and left parietotemporal region with marked hydrocephalus.
tation rate was 20 mm at the end of the first hour; urine and stool examination was normal; chest X-ray was normal. A CT scan showed a huge subperiosteal abscess in the right mastoid and right temporoparietal region going towards the left parietotemporal region with marked hydrocephalus (Fig. 1). The abscess was drained under general anaesthesia by giving multiple incisions on the both parietal regions and nearly 750 ml of pus was evacuated. Aural polypotomy was also done at the same time. Pus was sent for culture and antibiotic sensitivity. It showed Pseudomonas aeruginosa and Escherichia coli which were sensitive to Gentamycin® and Cloxacillin®. Mycobacterium tuberculosis was not seen. The patient was kept on regular dressings with suction clearance of the ear and injections of Gentamycin'Rl, Cloxacillin®, and Metronidazole®. After 2 weeks a tympanomastoidectomy was done. On exploration of the ear, the mastoid was seen to be full of granulations and cholesteatoma, with thrombosis of sigmoid sinus present along with perisinus abscess. Histopathology of granulation tissue from the mastoid showed features of tuberculosis. The patient was given a complete course of antitubercular therapy (Rifampicin'Rl, Ethambutol®, and isonicotinic acid hydrazide). After an interval of 2 weeks, the patient was referred to neurosurgical services for a shunt operation for hydrocephalus. The interesting point about this patient was the huge subperiosteal mastoid abscess of tuberculous origin with sigmoid sinus thrombosis and marked hydrocephalus. Case II An 8-year-old male patient came to us in acute respiratory distress along with stiffness of the neck, high fever, and dysphagia lasting for 2 days. On examination, the patient showed marked swelling of the floor of the mouth, tongue, and the right lateral pharyngeal wall, and torticollis. Emergency tracheostomy was done under local anaesthesia because passing
202
D. S. GREWAL el af.
Fig. 2. Citelli's abscess (Case II). (a) Eight-year-old boy 4 days after draining of the para pharyngeal abscess, with marked cellulitis of the neck. Note the gauze packed in the abscess cavity and profuse discharge coming out of the right ear. (b) X-ray of the neck and chest showing soft tissue shadow on right side of the neck with marked shift of trachea to the left. (c) Radical mastoidectomy cavity. Note the pick in the fistulous tract under the exposed digastric muscle which caused the parapharyngeal abscess. (d) Photograph showing the features of tuberculosis. Note the epitheloid giant cells. H&Ex450.
the endotracheal tube was not possible due to marked swelling of the tongue and cellulitis of the neck. General anaesthesia was then given and the abscess in the upper neck drained by an incision in its most prominent part. About 300 ml of foul-smelling pus was drained and sent for culture and antibiotic sensitivity, which showed mixed infection with E. coli and Pseudomonas pyocyaneus. Treatment was given by intravenous injections of Gentamycin®, Ampicillin®, and Metronidazole®, to which the organisms were sensitive. No M. tuberculosis was seen (Fig. 2, a and b). On subsequent E.N .T. examination, we detected a cholesteatoma in the right
TUBERCULOUS OTITIS MEDIA
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ear. Fifteen days later, a tympanomastoidectomy was done. There was a fistulous tract anterior to the sigmoid sinus near the mastoid tip through which infection had traveled beneath the posterior belly of the diastric muscle and then to the pterygomaxillary and parapharyngeal spaces (Fig. 2c). The histopathology of granulations from the mastoid showed features of tuberculosis (Fig. 2d), and the patient was given complete courses of antituberculous drugs. The interesting point about this patient was that the mastoid tip was eroded by the tuberculous granulation tissue from where the pus extended to involve the parapharyngeal space leading to the parapharyngeal abscess. This lead to compression of the airway for which the emergency tracheostomy was required. Case III A 25-year-old male patient had complained of left earache and otorrhea for twenty years. Examination revealed a polyp in the left ear with foul-smelling discharge and left mastoid tenderness, which were suggestive of acute mastoiditis. Central nervous system examination showed that the patient was drowsy with neck stiffness, astereognosis, and positive Kernig's sign. Mastoid X-rays showed an area of rarefaction in the attic, antral, and periantral regions on the left side. CSF examination was suggestive of pyogenic meningitis (clear fluid with 16 mg% protein, markedly reduced sugar, 260 mm 3 cells (polymorphs), and no organisms). Patient was treated conservatively with antibiotics for 7 days, after which the ear was explored under general anaesthesia. A huge cholesteatoma that was eroding the sigmoid sinus and dural plates, with prolapse of the dura into the mastoid cavity, was seen. A modified radical mastoidectomy was done. The dural defect was closed with a mastoid cortical bone graft removed from the mastoid tip (Fig. 3, a and b). The postoperative recovery was smooth.
Fig. 3. Dural herniation (Case III). (a) Radical mastoid cavity with dural herniation and granulations. This was obscuring the view of the mastoid antrum and attic. This patient had a history of 5 attacks of meningitis. (b) Dural herniation reduced and bony defect closed with mastoid cortical bone removed from the tip of the mastoid. Attic and antrum are now visible.
204
D. S. GREWAL et al.
On the 18th postoperative day, the patient suddenly became drowsy. A carotid angiography was done, which was suggestive of left temporal lobe abscess. A CT scan was not done as this facility was not available at that time. A temporal burr hole was done and 50 ml of pus aspirated, which showed the presence of tuberculous bacilli. After improvement of the general condition of the patient, a craniotomy was done, and the temporal lobe abscess was excised. Histopathological examination of tissues from the mastoid cavity and wall of the temporal lobe abscess showed features of tuberculosis. A complete course of antituberculous therapy was given. In this case, there was no tuberculosis of lungs, lymph node, or bones, and thus we presume it to be primary tuberculosis of the middle ear. The patient had suffered since childhood from chronic suppurative otitis media with cholesteatoma, which later on might have secondarily become infected with tuberculous bacilli. COMMENT
Tuberculous bacilli find their way to the middle ear and mastoid through the Eustachian tube, the blood stream, and, rarely, through the external auditory meatus. Though tuberculous otitis media is usually secondary to tuberculous infection elsewhere in body, one occasionally encounters cases where no other tuberculous lesion in the body can be demonstrated. It is possible that tuberculosis may secondarily invade an already discharging ear, and in countries where the incidence of both tuberculosis and discharging ears is relatively high, at times it becomes difficult to say which of the infections was primary. Tuberculous otitis media, whether primary or secondary, is more prone to develop intra- and extracranial complications. In developing countries, discharging ears are frequently neglected by the patient but surprisingly the ratio of discharging ears to complications rate is quite low. Perhaps the more frequent use of antibiotics has changed the clinical picture of yesteryear, because although antibiotics alone are insufficient to cure most cases of discharging ears they are to some extent able to reduce the incidence of intracranial complications. This is in contrast to tuberculous otitis media, which is now uncommon even in developing countries. These days, clinical diagnosis of tuberculous otitis media is rarely made in the outpatient department. Histopathology of granulation tissue from patients who presented complications showed that about 12 % of all these cases were due to tuberculosis. This suggests that perhaps the clinical picture is changing: the more frequent use of Neomycin® and Gentamycin® ear drops might be responsible for masking the initial clinical picture as they are weakly antituberculosis. A low rate of positive staining or culture of aural discharge and delay in diagnosis may also be due to use of those eardrops (OLUJIMI, 1988). In our opinion, the delay in diagnosis is due to changes in the histopathological
TUBERCULOUS OTITIS MEDIA
205
picture due to use of the ear drops. In tuberculous otitis media the tympanic membrane is initially dull and lusterless; later it shows yellowish spots which are tuberculous deposits undergoing disintegration. After a few weeks multiple perforations through which a thin, scant, and odorless discharge of pale granulation tissue may be seen emerging. Later, mastoid air cells are replaced by tuberculous granulation tissue which may perforate the mastoid cortex, leading to a postaural abscess and subsequent fistula, which are often mUltiple (Fig. 4). Complications are common due to tuberculous granulation tissue and sequestration of bone (Fig. 5). Tubercular otitis media may give rise to facial paralysis, labyrinthitis, petrositis, lateral sinus thrombophlebitis, and thrombosis, meningitis, brain abscess (cerebral or cerebellar), and tuberculoma of the brain. There is no fixed route for the spread of the disease to these structures. Facial paralysis is much more common in children than in adults and appears to be due to pressure from granulation tissue (Fig. 5) and sequestration of bone around the facial c'lnal (ORMEROD, 1931). The disease involves the labyrinth, either by eroding the semicircular canals promontory or through the round window membrane. The labyrinthine involvement ranges from superficial erosion of semicircular canals to softening and sequestration of the entire labyrinth (Figs. 6 and 7). Because of the gradual spread of the disease to the labyrinth, tinnitus of varying degrees is most common, whereas vertigo, nystagmus, and ataxia are rare. At times, because
Fig. 4. A non-healing sinus. Sevenyear-old child showing non-healing sinus following incision and drainage of Bezold's abscess. Radical mastoidectomy with fascia grafting was done. Note the haemostat in the sinus.
Fig. 5. Radical mastoid cavity with exposed facial nerve which is surrounded by granulations. Note that the facial nerve is dividing into two branches in the mastoid. This patient had a history of facial nerve palsy since 8 months and ear discharge since 10 years.
206
D. S. GREWAL el af.
there is a gradual involvement of the labyrinth and because of adaptation, none of the above symptoms may be present and the labyrinth m':ly be dead.
Fig. 6. Radical mlstoid cavity showing erosion of all three semicircular canals.
Fig. 7. Radical mlstoid cavity with promontory erosion (2 x 1 mm). Note that the basal turn of the cochlea is exposed (marked t).
Fig. 8. Gradenigo's syndrome. (a) Note the left lateral rectus palsy. (b) CT scan showing small abscess at left petrous apex (marked t). (c) Radical mastoidectomy showing Frankner's approach to the petrous apex.
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Fig. 9. Radical mlstoid cavity showing posterior fossa dural defect (marked
n.
The petrous apex may get infected by direct extension of disease from the mastoid or by way of the bloodstream from the focus of tuberculosis elsewhere (Fig. 8, a-c). Miliary tuberculosis of the petro us apex without involvement of middle ear can occur, leading to Gradenigo's syndrome (MYERSON, 1944). The involvement of meninges is usually due to direct extension of the disease process (Fig. 9), while the brain is involved via communicating veins or perivascular spread along the Virchow Robin space. We conclude that suspicion of tuberculosis of the middle ear cleft should arise when, during mastoid surgery, the mastoid cavity formed is very large or much larger than expected. This is due to the following reasons: 1. In the presence of a normal middle ear with a well-pneumatized mastoid, the middle-ear cleft can get infected via the hematogenous or eustachian tube routes. In such a case the mastoid cavity formed is very large. 2. In the presence of a pre-existing chronic suppurative otitis media with acellular mastoid, a superimposed tuberculous infection can occur via the hematogenous, eustachian tube, or a perforation of the tympanic membrane, which gives rise to a larger mastoid cavity than expected. There are two ml in concepts in mastoid surgery, one the conventional outside-in and the other more fashionable but older inside-out. In our opinion, mastoid surgery is three dimensional, involving both depth and area. We normally do a mastoidectomy from lateral to medial and at the same time keep lowering the ridge. Ideally, at the end of surgery, the shape to the outlet of the mastoid cavity is round to oval. When the facial ridge is taken into consideration it is bean shaped . The aim of this canal-wall down technique is to divide the middle ear cleft into two parts at the level of the additus by fascia grafting, the middle ear communicating with the eustachian tube and the mastoid cavity with the external auditory canal. By this technique we simplify the complex middle ear cleft, thereby considerably increasing the cure rate. At the end of surgery we place a slightly thicker graft over the middle ear as this prevents formation of retraction
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packets. In combined approach tympanoplasty technique the middle ear cleft is made more complex hence it does not have good cure rates. The classical signs described for tuberculous otitis media, such as multiple perforations of the tympanic membrane or pale granulation tissue, are not seen these days because such cases are diagnosed and treated late, and by the time they are diagnosed and treated they already have complications. Hence we feel that the most common presenting feature of tuberculous otitis media is complications. The two important characteristic features of tuberculosis are abscess formation and bone erosion, which lead to complications. REFERENCES HEBERT, F., and RIORDOAN, D.: Tuberculosis of the middle ear. Laryngoscope 74: 198-204, 1964. MYERSON, M. c.: Tuberculosis of the middle ear and mastoid. III Tuberculosis of the Ear, Nose and Throat, 1st ed. (Myerson, M.C., ed.), Charles C. Thomas, Springfield, Ill., pp. 155-178, 1944. OLUJIMI, 0.: Early diagnosis of tuberculous otitis media. J. Laryngol. 0(01. 102: 133-135, 1988. ORMEROD, F. C.: Tuberculous disease of the middle ear. J. Laryngol. 0(01. 46: 449-459, 1931.
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