Intra cranial complications of tuberculous otitis media

Abstract

Tuberculosis is one of the most common infections in the world. It is seen that tuberculous otitis media (TOM) is almost secondary to pulmonary tuberculosis. In this review we have tried to deal with all the aspects of the intra cranial complications of TOM such as tuberculoma, otitic hydrocephalus, brain abscess and tuberculous meningitis. The aspects covered in this review are the pathology, clinical features, and investigations of the intra cranial manifestations.

Tuberculosis is one the most common infections in the developing countries and its incidence are growing in developed countries due to the rise in HIV infection. Tuberculous otitis media (TOM) is one of the uncommon complications of this systemic disease.[1,2,3] It is seen that TOM is always secondary to pulmonary tuberculosis.[4,5,6] WHO records an incidence of 8.6 million new cases in the world, but there is a global decline in the tuberculosis incidence.[7] Recent studies show that the incidence has declined by 2%.[8] Fall in incidence is attributed to increasing in treatment for HIV infection. It usually manifests secondary to pulmonary infection and route of spread is mostly by blood-borne metastasis.[9] The most common organism which is involved is mycobacterium tuberculosis and occasionally by Mycobacterium avium/Mycobacterium fortium. The intracranial complications are very severe, life threatening and are unique when compared with other complications of pyogenic otitis media. The importance of knowing about the complications are the difficulties in treatment of these complications and also the growing resistance of the organisms to the antituberculosis treatment (ATT). Early detection and prevention would be the most appropriate step than dealing with the full blown complication.

Mode of Central Nervous System Infection

It is stated that most common mode of spread of tuberculosis to the central nervous system is hematogenous. This focus of infection may be either in the primary site of the lungs or infected middle ear (tuberculous otits media).[9] Other mode of infection can also be due to direct spread from the middle ear through the anatomical barriers through the tegmen tympani where it may directly invade the dura mater and the middle cranial fossa. Another potential route of spread is through the mastoid and then invading the sigmoid sinus. The close proximity of all these structures also aids in the rapid spread. Another school of thought is that the tough meningeal layers prevent the extension of the infection into the cranial cavity. Tuberculous meningitis 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]

Intra Crainial Complications

Classical tuberculoma

The incidence of tuberculoma has decreased in the past few years.[11] Figure 1 gives the CT image of a classical tuberculoma.[2] Since 1979,[12] tuberculomas are being diagnosed much earlier and in the majority of these, as there is no histopathological diagnosis, it is difficult to assess the true incidence. The response to ATT cannot also be taken as criteria because some of these disappear without any ATT drugs.[13]

Figure 1.

Computed tomography scan of left temporal tuberculoma[2]

Pathology: It is usually 8-10 cm well circumscribed nodular, firm to hard, Grey yellow vascular mass. It is surrounded by varying degrees of edema and gliosis. There is no true fibrocollagenous capsule, but only the condensation of these materials resembles one. Histology reveals tuberculous granuloma, coagulative necrosis, epitheloid cells and Langerhans giant cells[14] [Figure 1].[2]

Atypical tuberculoma/tuberculoma en plaque during surgery mimics meningioma due to its adherence to the dura.[15]

Tuberculous abscess

It is the most important differential for tuberculoma. A tuberculous brain abscess differs from tuberculoma by lacking granulomatous changes and histologically resembles a chronic pyogenic abscess, which is filled by acid-fast bacilli and pus.[16] This is mostly seen in immunocompromised individuals and AIDS patient.[9]

Cystic tuberculoma

It was first reported in 1962 by Dastur et al.[17] in a 4-year-old boy who presented with hemiparesis. The cyst contained clear yellow fluid, and the cyst wall had typical tuberculous pathology. It may also mimic as cystic glioma.[18]

Multiple grape like tuberculoma

It is a very rare presentation, which is due to multiple immature tuberculomas. It usually resembles a cluster of cysticercus cysts.[9]

Microtuberculoma

They are solitary small disc or rings of 5-7 mm in diameter. It has many differential diagnoses so the definitive diagnosis must only be made by biopsy.[19]

Calcified tuberculoma

It may present as a calcified mass, and it must be noted that such lesions do not mean that it is not inactive or healed. A very high incidence is seen in Eskimos and Canadian Indians.[20]

Tuberculous encephalopathy

It is usually an allergic reaction to the protein liberated by the lysed tuberculous bacilli. It is usually seen in children as diffuse brain damage with minimal or no inflammation.[21,22] There will be varying degrees of edema, perivascular myelin loss and hemorrhagic leucoenchepalopathy.

Investigations

ESR is often raised, may be normal. Mantoux is generally positive, if Mantoux is negative it does not rule out tuberculosis. Plain X-ray chest is mandatory. Computed tomography (CT) scan findings[23,24] depend on the morphology of the disease. The most common manifestations are small discs, rings <1 cm surrounded by edema. Centrally lucent, large ring lesions are called target sign.[25,26] 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 content.[9] Magnetic resonance spectroscopy of hypo intense lesions show characteristic lipid peak on stimulated echo acquisition mode and point resolved spectroscopy sequence.[27,28,29] Stereotactic biopsy is essential for definitive diagnosis.[30]

Tubercular meningitis

The disease is usually caused by a cascade of proinflamatory cytokines like tumor necrosis factor-alpha, interferon, gamma cytokines due to cell-mediated response.[31] It is usually a meningio vasculo encephalitic than a pure meningitis. The plaque may stimulate a neoplasm as it becomes firm, adherent 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]

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 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 tuberculous meningitis.[32,33]

Clinical

Fever for 2 weeks, loss of appetite, irritability, headache, vomiting, meningeal signs, convulsions, and focal neurological deficits.

Cerebrospinal fluid analysis

Pleocytosis >20 cells/mm, lymphocytes >60%, protein >100 mg% and sugar <60% of blood sugar.

Radiological

Computed tomography scan findings include exudates in basal cistern, hydrocephalus, infarcts, gyral enhancements.

Extra neural tuberculosis

Lungs, gastrointestinal tract, lymph nodes, skeletal system.

The scoring criteria have sensitivity of 83% and specificity of 63%.

Investigations

The first investigation to be done is CSF analysis and must be examined under Ahuja criteria. ELISA, polymerase chain reaction is also very useful. Other important investigations are microscopic observation drug susceptibility, IgG reactivity to lipoarabinomannon in CSF is used in early meningitis. BACTEC 12B medium is used for quick growth of cultures.[9]

Hydro cephalus

Secondary rise in ICT is usually by brain edema, increased proteins in CSF, poor absorption and obstruction of CSF flow. Exudates get organized, and there is a fibrous obliteration of the subarachnoid space. Hydrocephalus is noncommunicating in 58.5% and communicating in 41.5%.[34] Blockage of the arachnoid villi common site of obstruction is in the basal cisterns such as cistern pontis, interpeduncularis and ambiens.[9] The presenting features are fever, altered senosorium, vomiting, and convulsions. In later cases altered consciousness, de-cerebrate rigidity, meningeal signs and focal signs can be elicited. In CT scan findings most specific for tuberculous meningitis is hyper intense in basal cistern area to intravenous contrast medium administration and the most sensitive feature is basal enhancements.[9] CT scan also helps us to identify presence or absence of infarcts. Single photon emission CT is also helpful. Cortical hypoperfusion with or without basal ganglia hypoperfusion is associated with frontal rhythmic intermittent delta activity and diffuse slowing on electroencephalogram, brainstem auditory evoked response and visual evoked potentials.[35,33] Magnetization transfer MRI is used to detect infectious diseases of different etiology.[36]

Other rare complications

Long term sequelae

In usually seen in 78.5% of the patients with 55% having cognitive impairment, 40% having motor deficit, 37% optic atrophy and 23% having cranial nerve palsy.[36]

Syndrome of inappropriate antidiuretic hormone

Syndrome of inappropriate antidiuretic hormone production, which is usually suspected if the polyuria, hyponatremia, volume depletion, and increased sodium excretion.[37,38,39,40]

Vision abnormalities

It is usually due to optic nerve ischemia process causing optic atrophy, compression of the visual pathway by basal meningitis or fibrosis of the optic cortex due to tuberculous sequelae. Other causes may also be optic chiasmal arachnoiditis and prolonged raised ICT.[9]

Endocrine signs

Pituitary and hypothalamus involvement due to ischemia may lead to obesity, diabetes insipidus or hypo gonadism.[41,42,43]

Conclusion

The main aim of this review article that every physician in tuberculosis endemic countries must come to know about these unique disease manifestations which are uncommon with other known diseases. The review about the treatment is beyond the scope of this article as there are many extensive methods for treatment, and they grossly vary from country to country. Thus, we have reviewed the outline of the intracranial complications of tuberculous otitis media. It may not be common way of spread of infection, but in endemic countries even a small population, which are affected adds up to be a large number, especially in India.