TUBERCULOMA a intresting case of tuberculoma

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1. An interesting case of head ache

2. data Name : Miss Nandhini Age:26 Gender : Female Address: CUDDALORE Chief complaints: Head ache since one week Fever since one week vomiting since 4 days Altered behaviour since 2 days

3. History of present illness patient developed headache which is band like, gradual onset, progressive type ,persistent through out the day associated with vomItings 4 to 5 episodes projectile not blood stained containing food particles ,associated blurring of vision fever, intermittent , of low grade, no diurnal variations, not associated with chills and rigors for 3 days Altered sensorium 3 days not obeying commands ,not able to identify relatives History of travel present to temple History of loss of weight History of loss of appetite

4. No history of yellowish discolouration of sclera skin No history of rash No history of cough with sputum expectoration No history of burning micturition no history of abdomen pain, loose stools No history of involuntary movements No history of photophobia No history of hydrophobia No history of animal bite

5. Past history no History of similar illness in the past Not known case of diabetes ,hypertension ,asthma ,tuberculosis Menstrual history Cycles are regular 5 days for 28 days moderate flow LMP 24/1/24 Obstetric history p1L1A0 Personal history Diet mixed

6. Bowel and bladder habits regular Family history not significant no history of contact of tb GENERAL PHYSICAL EXAMINATION Drowsy disoriented Dehydration present Moderately built, moderately nouRished No external markers of tuberculosis No pallor ,icterus clubbing cyanosis ,pedal edema ,lymphadenopathy Temp afebrile PR: 82bpm BP 120/90 mm hg RR 14cym

7. Systemic examination c vs S1 S2 present rs bilateral air entry present ,normal vesicular breath sounds , pA soft non tender, no organomegaly CNS Conscious, confused, agitated GCS E4 v4 M5 , left eye complete ptosis present Dilated pupil 6mm not reacting to light extra ocular movements couldn’t be elicited Right eye pupil size 4mm reacting to light NECK STIFFNESS PRESENT KERNINGS SIGN PRESENT .

8. Provisional diagnosis : Acute meningitis/encephalitis ? bacterial / ? viral ? tubercular

9. Forum open for discussion

10. Treament Iv antibiotics started inj ceftriaxone 2gm iv bd inj ampicillin 2 gm iv q6h inj acyclovir 5oomg iv tds inj vancomycin 500mg iv bd inj dexa 8mg iv bd Inj mannitol 100ml iv tds Inj phenytoin iv sos Neurologist opinion sorted sir asked to continue same treatment and review with mri report

11. ON OPTHALMOLOGICAL EXAMINATION THERE WAS NO EVIDENCE OF PAPPILEDEMA LP WAS PLANNED AFTER MRI contraindicated due to the location and size of the lesion

12. Blood investigations INVESTIGATION REPORT INVESTIGATION REPORT INVESTIGATION REPORT HB 12.3 SODIUM 135 HBSAg N-R PLATELET 1.25L POTASSIUM 3.7 ANTI-HCV N-R WBC 10350 CHLORIDE 99 VDRL N-R PMN 81% CALCIUM 9.5 LYMPHO 11% UREA 31 T BILI 0.9 CREATININE 0.6 D BILI 0.6 HBA1C 5.8% SGOT 19 ESR 30 SGPT 32 HIV N-R

13. Mantoux test

14. Mri t1

15. Mri report

16. MRS

17. FOLLOWED BY FOLLOWED BY MRI REPORT ATT WAS STARTED ON NEUROLOGIST SIR ADVICE RESPIRATORY MEDICINE SUGGESTED HRZE 3 FDC 3 TAB WITH INTENSIVE PHASE OF 2MONTHS

18. Ring enhancing lesions TubeRculoma Neurocysticercosis BRAIN ABSCESSES METASTASIS GLIOBLASTOMA SUBACUTE INFARCT/HEMORRHAGE /CONTUSION DEMYELINATION (INCOMPLETE RING) TUMEFACTIVE DEMYLINATING LESION RADIATION NECROSIS

19. ABSCESS Over 2 to 3 weeks Symptoms include :fever less than 50% Focal neurological deficit develops based on site Nuchal rigidity is present in 25% Pressure symptoms appear as size increases wall characteristics: thin and regular favors abscess intermediate to low T2 signal capsule favors abscess extensive edema relative to lesion size favors abscess central fluid content restricted diffusion favors abscess

20. Neurocysticercosis History of consumption of pork /uncooked meat size <20mm maigin Thin smooth wall edema Mild to moderate (t1 hypointense) t2 hyperintense Present at grey white matter junction fnd Usually none Mrs shows multiple amino acid peak Tuberculoma Subacute presentation 2 to 3 weeks Often >20mm Thick irregular wall edema Moderate to marked More common in posterior fossa Fnd Often present ,persistent Mrs shows lipid peak ,choline peak

21. Cns tb cns tb involves tb meningitis tuberculomas arachnoiditis

22. DIAGNOSIS 1Clinical assessment 2 CSF analysis : 3 Imaging : A. CNS imaging: i . NCCT/CECT head ii. MRI Brain + spine B. Imaging of other systems to evaluate for dissemination of disease

23. TBM diagnostic criteria A. Clinical Fever and headache lasting for more than 14 days (mandatory). Vomiting, alteration of sensorium or focal deficit (optional). B. Cerebrospinal fluid Pleocytosis with more than 20 cells, predominantly (greater than 60%) lymphocytes, protein greater than 100mg%, sugars less than 60% of corresponding blood sugars. Negative India ink studies and cytology for malignant cells (in relevant situations).

24. .c Radiological CT head showing 2 or more: 1. Exudates in basal cisterns or in Sylvian fissures 2. Hydrocephalus 3. Infarcts 4. Gyral enhancement D. Extra neural tuberculosis • Active TB of lungs, G.I.T, G.U.T, lymph nodes, skeletal system or skin - by radiological or microbiological tests or by presence of caseation necrosis on histopathological examination.

25. Based on presence of these features in combination of one or more, TBM can be clinically categorised as: 1 . Definite tuberculous meningitis ( i ) Clinical criteria (A) (ii) Bacterial isolation from CSF or diagnosis at autopsy 2. Highly probable tuberculous meningitis ( i ) Clinical criteria (A) (ii) All 3 of (B), (C) and (D) 3 . Probable tuberculous meningitis ( i ) Clinical criteria (A) (ii) Any 2 of (B), (C) and (D)

26. 4 . Possible tuberculous meningitis ( i ) Clinical criteria (A) (ii) Any one of (B), (C) and (D) Accuracy and positive predictive value were 91.7% 66.7% and 38.5% in the highly probable, probable and possible TBM groups respectively

27. British MRC Grading (Severity) • Grade 1 TBM: MILD - Glasgow coma score (GCS) of 15 with no focal neurological deficit; • Grade 2 TBM: MODERATE - GCS of 15 with a focal neurological deficit, or a GCS of 11–14; those with altered consciousness who are not comatose and those with moderate neurological signs, e.g. single cranial nerve palsies, paraparesis, and hemiparesis • Grade 3 TBM: SEVERE - GCS of ≤10; for comatose patients and those with multiple cranial nerve palsies, hemiplegia or paraplegia, or both. Severity assessment helps to stratify patients and is useful to predict prognosis

28. CSF analysis : A. Culture - LJ/MGIT: Using solid media (LJ) or liquid media (MGIT). The positivity of CSF culture varies from 25 - 70 % (LJ or MGIT).

29. csf Cob web coagulum in csf

30. sah

31. treatment ATT is the mainstay of medical therapy in any form of tuberculosis. The goal of therapy is CSF sterility with clinical and radiological improvement, the neurological deficit may persist. Intensive phase - 4 drugs HRZ + E/S x 2 months Continuation phase - 3 drugs HRE x at least 8-10 months Isoniazid 5-10mg/kg/day oral 90 – 95% Rifampicin 10-15g/kg/day oral 5 _ 25% Pyrazinamide 20-25mg/kg/day oral 95-100% Streptomycin 15-25mg/kg/day Injectable ( i.m ) 10 – 20%

32. Intensive phase duration based on index tb guide lines 2 months Continuation phase duration based on index tb 7months

33. RESPONSE therapeutic response - 6-8 weeks. Clinical response precedes radiological response. Follow Up : patients should be assessed for clinical improvement treatment compliance drug toxicities No need for repeat lp or mri . clinically indicated i.e worsening of symptoms

34. Role Of Steroids TBM is characterised by significant inflammation, in the form of meningeal reaction, basal exudates, vasculitis of intracranial vessels. According to a study by Prasad et al, the use of steroids was found to be associated with a reduced risk of death (32 v/s 41%) . • HIV negative patients – recommended for at least 4 weeks • HIV positive patients – may be used after ruling out opportunistic infections e.g., cryptococcal meningitis and cerebral toxoplasmosis – as these are associated with increased mortality with the use of steroids. Steroids are indicated in TBM at a dose of 0.4mg/Kg (dexamethasone), to be tapered over 6-8 weeks.

35. Following is the most accepted regimen – • IV dexamethasone – 0.4mg /Kg x 2 weekS …. 0.3mg/kg x 1 week followed by 0.2mg/Kg x 1 week followed by 4mg/day x 1 week followed by 3mg/day x 1 week followed by 2mg/day x 1 week followed by 1mg/day x 1 week and stoP

36. COMPLICATIONS AND MANAGEMENT Hydrocephalus: It is one of the commonest complications of TBM due to formation of basal exudates, which in turn impair CSF absorption. Medical - Anti-edema or osmotic agents-Mannitol, Acetazolamide, Frusemide, steroids . Surgical (CSF diversion ) – main modality of management. Ventriculoperitoneal shunt – best surgical approach

37. Raised Intracranial Pressure (ICP): Diffuse oedema , Infarcts, micro and macro, secondary to vasculitis • Space-occupying effect of associated tuberculomas This leads to decreased cerebral blood flow causing cerebral ischemia which is majorly responsible for poor outcomes. Osmotic agents (mannitol and hypertonic saline) and steroids are the mainstays of treatment

38. Hyponatremia (Sodium <135 mmol/L): 40 to 50% patients of TBM may develop hyponatremia. This may be secondary to SIADH or Cerebral salt wasting syndrome. Seizures : Benzodiazepines should be used as acute abortive treatment. Maintenance therapy with antiepileptic drugs may be required (levetiracetam is the most favourable drug) . Vasculitis/stroke

39. Experts recommend therapy for a duration of at least 12-18 months in case of tuberculomas or abscesses. the lesions may persist after therapy; therefore, extended therapy beyond 18 months may not be required in most of the cases If clinically no response within 6 - 8 weeks of effective therapy, further evaluation should be done to rule out the following: • Drug-resistant TB Other infectious causes • Neurocysticercosis, toxoplasmosis • Cryptococcomas • Malignancy – primary or metastatic • IRIS – usually within 3-6 months of therapY

40. TUBERCULOMA Tuberculomas And Abscess: • It is less common than TBM and has lower morbidity and mortality • It can arise anywhere in the brain or spinal cord • It may present as: • Mass lesion causing focal neurological deficits depending on anatomical location and/or seizure • It may be found in concurrence with TB

41. TUBERCULOMA Management of TB abscess or tuberculoma includes – Medical management - ATT with steroids is the mainstay • Surgery • Presence of associated obstructive hydrocephalus • Features of raised ICP • Large space-occupying tuberculomas with raised ICT

42. Case report Isolated cerebellar tuberculoma mimicking a malignant posterior cranial fossa tumor in a healthy child: A rare case report from Tanzania A 13-year-old female presented with headache, convulsions, blurry vision, and gait disturbance for six months.  Brain imaging  showed a left  cerebellar lesion  with  obstructive hydrocephalus . She underwent ventriculoperitoneal shunting on admission, then sub-occipital  craniotomy  with tumor resection one week later. Histology confirmed a diagnosis of tuberculoma. She was given anti-tuberculosis medications and she was discharged home healthy without any of the symptoms she had on admission.

43. CNS tuberculoma is a rare site for extrapulmonary tuberculosis and it can easily be misdiagnosed. The lesion can develop in any region of the brain as an isolated lesion even in unusual positions like cerebellum. They can also occur in immunocompetent patients with no history of systemic TB, leading to a wrong diagnosis. In high TB prevalent areas , physicians should keep a high degree of suspicion for CNS tuberculomas in patients presenting with features of intracranial space-occupying lesions regardless of the absence of risk factors.

44. Thank you

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