Medical Science - Review Article

Intra cranial complications of tuberculous otitis media

M. Prakash, J. Carlton Johnny

Department of ENT, Sree ABSTRACT Balaji Medical College is one of the most common infections in the world. It is seen that tuberculous otitis media (TOM) and Hospital, Bharath University, Chromepet, is almost secondary to pulmonary tuberculosis. In this review we have tried to deal with all the aspects of the Chennai, Tamil Nadu, intra cranial complications of TOM such as tuberculoma, otitic hydrocephalus, brain abscess and tuberculous India meningitis. The aspects covered in this review are the pathology, clinical features, and investigations of the intra cranial manifestations. Address for correspondence: Dr. M. Prakash, E-mail: [email protected]

Received : 31-10-14 Review completed : 31-10-14 Accepted : 09-11-14 KEY WORDS: Intra cranial complications, tuberculosis, tuberculous otitis media

uberculosis is one the most common infections in the the growing resistance of the organisms to the antituberculosis T developing countries and its incidence are growing treatment (ATT). Early detection and prevention would be in developed countries due to the rise in HIV infection. the most appropriate step than dealing with the full blown Tuberculous otitis media (TOM) is one of the uncommon complication. complications of this systemic disease.[1-3] It is seen that TOM is always secondary to pulmonary tuberculosis.[4-6] Mode of Central Nervous System Infection WHO records an incidence of 8.6 million new cases in the world, but there is a global decline in the tuberculosis It is stated that most common mode of spread of tuberculosis incidence.[7] Recent studies show that the incidence has to the central nervous system is hematogenous. This focus declined by 2%.[8] Fall in incidence is attributed to increasing of infection may be either in the primary site of the lungs or in treatment for HIV infection. It usually manifests secondary infected middle ear (tuberculous otits media).[9] Other mode of to pulmonary infection and route of spread is mostly by blood- infection can also be due to direct spread from the middle ear borne metastasis.[9] The most common organism which is through the anatomical barriers through the tegmen tympani involved is mycobacterium tuberculosis and occasionally by where it may directly invade the dura mater and the middle Mycobacterium avium/Mycobacterium fortium. The intracranial cranial fossa. Another potential route of spread is through complications are very severe, life threatening and are unique the mastoid and then invading the sigmoid sinus. The close when compared with other complications of pyogenic otitis proximity of all these structures also aids in the rapid spread. media. The importance of knowing about the complications Another school of thought is that the tough meningeal layers are the difficulties in treatment of these complications and also prevent the extension of the infection into the cranial cavity. is mostly due to discharge of organisms form the tuberculous foci (rich focus), and the parenchymal lesion is mostly due to the hematogenous spread.[10] Access this article online Quick Response Code: Website: Intra Crainial Complications www.jpbsonline.org Classical tuberculoma DOI: 10.4103/0975-7406.155795 The incidence of tuberculoma has decreased in the past few years.[11] Figure 1 gives the CT image of a classical tuberculoma.[2]

How to cite this article: Prakash M, Johnny JC. Intra cranial complications of tuberculous otitis media. J Pharm Bioall Sci 2015;7:S51-4.

Journal of Pharmacy and Bioallied Sciences April 2015 Vol 7 Supplement 1 S51  Prakash and Johnny: Intra cranial complications of tuberculous otitis media

Since 1979,[12] tuberculomas are being diagnosed much earlier has many differential diagnoses so the definitive diagnosis must and in the majority of these, as there is no histopathological only be made by biopsy.[19] diagnosis, it is difficult to assess the true incidence. The response to ATT cannot also be taken as criteria because some of these Calcified tuberculoma disappear without any ATT drugs.[13] It may present as a calcified mass, and it must be noted that Pathology: It is usually 8-10 cm well circumscribed nodular, firm such lesions do not mean that it is not inactive or healed. A very to hard, Grey yellow vascular mass. It is surrounded by varying high incidence is seen in Eskimos and Canadian Indians.[20] degrees of edema and gliosis. There is no true fibrocollagenous capsule, but only the condensation of these materials resembles Tuberculous encephalopathy one. Histology reveals tuberculous granuloma, coagulative necrosis, epitheloid cells and Langerhans giant cells[14] [Figure 1].[2] It is usually an allergic reaction to the protein liberated by the lysed tuberculous bacilli. It is usually seen in children as diffuse Atypical tuberculoma/tuberculoma en plaque during surgery brain damage with minimal or no inflammation.[21,22] There mimics meningioma due to its adherence to the dura.[15] will be varying degrees of edema, perivascular myelin loss and hemorrhagic leucoenchepalopathy. Tuberculous abscess Investigations It is the most important differential for tuberculoma. A tuberculous brain abscess differs from tuberculoma by lacking ESR is often raised, may be normal. Mantoux is generally granulomatous changes and histologically resembles a chronic positive, if Mantoux is negative it does not rule out tuberculosis. pyogenic abscess, which is filled by acid-fast bacilli and pus.[16] Plain X-ray chest is mandatory. Computed tomography (CT) [23,24] This is mostly seen in immunocompromised individuals and scan findings depend on the morphology of the disease. AIDS patient.[9] The most common manifestations are small discs, rings <1 cm surrounded by edema. Centrally lucent, large ring lesions are [25,26] Cystic tuberculoma called target sign. There may be large nodular irregular masses. A magnetic resonance imaging (MRI) picture varies and it is mostly based on the degree of fibrosis, gliosis and lipid It was first reported in 1962 by Dastur et al.[17] in a 4-year-old content.[9] Magnetic resonance spectroscopy of hypo intense boy who presented with hemiparesis. The cyst contained clear lesions show characteristic lipid peak on stimulated echo yellow fluid, and the cyst wall had typical tuberculous pathology. [27-29] [18] acquisition mode and point resolved spectroscopy sequence. It may also mimic as cystic glioma. Stereotactic biopsy is essential for definitive diagnosis.[30]

Multiple grape like tuberculoma Tubercular meningitis

It is a very rare presentation, which is due to multiple immature The disease is usually caused by a cascade of proinflamatory [9] tuberculomas. It usually resembles a cluster of cysticercus cysts. cytokines like tumor necrosis factor-alpha, interferon, gamma cytokines due to cell-mediated response.[31] It is usually a Microtuberculoma meningio vasculo encephalitic than a pure meningitis. The plaque may stimulate a neoplasm as it becomes firm, adherent They are solitary small disc or rings of 5-7 mm in diameter. It to the brain, usually it stimulates a posterior fossa crainial tumor, foramen magnum lesion.[32] Figure 2 show the sequel of the associated meningitis.[1,3]

Clinical Features

Fever, meningismus, nausea, vomiting, focal neurological defect is manifested as cranial nerve involvement and motor paresis. Tubercular meningitis also mimics brain tumor, cerebral abscess or tuberculoma. There may be secondary rise in intracranial tuberculomas (ICT) usually by brain edema. There can be increased proteins in cerebrospinal fluid (CSF), with obstruction and poor absorption of the same.[9] Due to raised ICT impaired level of consciousness and de-cerebrate spasms can occur.[9]

Modified Ahuja criteria

The modified Ahuja criteria has been developed to diagnose Figure 1: Computed tomography scan of left temporal tuberculoma[2] tuberculous meningitis.[32,33]

 S52 Journal of Pharmacy and Bioallied Sciences April 2015 Vol 7 Supplement 1 Prakash and Johnny: Intra cranial complications of tuberculous otitis media

Figure 2: Contrast-enhanced fluid-attenuated inversion-recovery image shows hyperintensity along the/T1-weighted magnetic resonance imaging showing nodular meningitis meninges and within several sulci of the left parietal lobe

Clinical meningeal signs and focal signs can be elicited. In CT scan findings most specific for tuberculous meningitis is hyper intense in basal Fever for 2 weeks, loss of appetite, irritability, headache, cistern area to intravenous contrast medium administration and vomiting, meningeal signs, convulsions, and focal neurological the most sensitive feature is basal enhancements.[9] CT scan deficits. also helps us to identify presence or absence of infarcts. Single photon emission CT is also helpful. Cortical hypoperfusion with Cerebrospinal fluid analysis or without basal ganglia hypoperfusion is associated with frontal rhythmic intermittent delta activity and diffuse slowing on Pleocytosis >20 cells/mm, lymphocytes >60%, protein >100 mg% electroencephalogram, brainstem auditory evoked response and and sugar <60% of blood sugar. visual evoked potentials.[35,33] Magnetization transfer MRI is used to detect infectious diseases of different etiology.[36] Radiological Other rare complications Computed tomography scan findings include exudates in basal cistern, hydrocephalus, infarcts, gyral enhancements. Long term sequelae

Extra neural tuberculosis In usually seen in 78.5% of the patients with 55% having cognitive impairment, 40% having motor deficit, 37% optic Lungs, gastrointestinal tract, lymph nodes, skeletal system. atrophy and 23% having cranial nerve palsy.[36]

The scoring criteria have sensitivity of 83% and specificity of Syndrome of inappropriate antidiuretic hormone 63%. Syndrome of inappropriate antidiuretic hormone production, Investigations which is usually suspected if the polyuria, hyponatremia, volume depletion, and increased sodium excretion.[37-40] The first investigation to be done is CSF analysis and must be examined under Ahuja criteria. ELISA, polymerase chain Vision abnormalities reaction is also very useful. Other important investigations are microscopic observation drug susceptibility, IgG reactivity It is usually due to optic nerve ischemia process causing optic to lipoarabinomannon in CSF is used in early meningitis. atrophy, compression of the visual pathway by basal meningitis BACTEC 12B medium is used for quick growth of cultures.[9] or fibrosis of the optic cortex due to tuberculous sequelae. Other causes may also be optic chiasmal arachnoiditis and prolonged Hydro cephalus raised ICT.[9]

Secondary rise in ICT is usually by brain edema, increased Endocrine signs proteins in CSF, poor absorption and obstruction of CSF flow. Exudates get organized, and there is a fibrous obliteration of the Pituitary and hypothalamus involvement due to ischemia may subarachnoid space. Hydrocephalus is noncommunicating in lead to obesity, diabetes insipidus or hypo gonadism.[41-43] 58.5% and communicating in 41.5%.[34] Blockage of the arachnoid villi common site of obstruction is in the basal cisterns such as Conclusion cistern pontis, interpeduncularis and ambiens.[9] The presenting features are fever, altered senosorium, vomiting, and convulsions. The main aim of this review article that every physician in In later cases altered consciousness, de-cerebrate rigidity, tuberculosis endemic countries must come to know about these

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