A Case of TB meningitis with Pituitary TBPresentation Transcript
An interesting case of Tuberculosis DevendraPatil Dr. Prof. Magheshkumar Unit M1 unit
We sincerely thank Dr. Chenthil ( IMCU chief ) Dr. Gowrishankar and M3 team Dept of Neuro-Surgery Department of chest medicine Endocrinology dept, SMF Apollo Hospital Labs
Case history A 21 year old unmarried girl came to GSH with chief complains of Fever ( low grade, evening rise)…………..10 days Altered behavior………..4 days Increased drowsiness…….3 days
No h/o convulsions Neck pains , headache , vomiting Fall/trauma to head Weakness in any on the limbs , diplopia Cough with expectoration Abdominal pains Join pains / swelling Body rash Swellings in neck , axilla , groin Jaundice in past TB in past / family
o/e She is drowsy , responding to painful stimuli , GCS – 10/15 Temp 100 F P- 94 /min regular RR – 16 / min regular BP – 130/80 mm Hg No pallor / ict / cyn /club / LN / pedal oedema Neck veins – normal Skin -normal No external markers of TB CVS : NAD RS : NAD PA : NAD
CNS Higher mental function Drowsy Disoriented Responding to painful stimuli Cranial : Pupils – B/L equal reacting to light Fundus : b/l normal, no e/o papillodema no other cranial nerve involvement Spinomotor: tone is normal in all 4 limbs power is 3+/5 in all limbs all DTR are present and normal B/L plantar - flexor Sensory : response to pain present, Cerebellar : no signs present Meningeal : neck rigidity +nt Kernigs –ve , Brudzinki –ve Skull and spine - normal
Investigation Hb – 9.8 gm% TC – 5600/cc DC – P56,L32 ESR – 22mm/hr Platelet – 2.3 lac RBS – 84 mg% Urea – 21 mg% Cr – 0.7 mg% Na – 139 meq/L K – 3.7 meq/L CSF analysis : Physical : clear Pressure : high ( not measured ) Protein : 140 mg% Sugar - 34 mg % Cells - 8-10 lymphocytes seen ADA - 7 IU/L Cytology – lymphocytes seen Grams Stain - negative AFB stain – negative PCR ( MTB )– not sent IMPRESSION : Suggetsive of TB meningitis
NEUROIMAGING What to expect in a case of TB meningitis ? Infarcts ( due to vascuitis ) Granuloma Arachnoiditis Subpial / subependymal foci of TB Ependimitis Leptomenigealenchancement Exudation Choriodplexitis Hydrocephaleus
Neuro imaging CT Brain : Normal study MRI BRAIN : Right thalamus infarct Pontine , occipital , parietal SOL Ring enhancement present Lepto-meningeal enhancement Occiptal exudates f/s/o--- CNS tuberculosis
ATT registration and commencment Antibiotic policy changed Steroids continued Patient general condition improved Shifted to ward and accordingly discharged She was asked to continue ATT at nearby DOTS centre
5 months later…………. She came with chief complains of Secondary Amenorrhea …….. 5 months Excessive Weight gain ……….. 5 months Altered behaivour …………..2 weeks Drowsiness , Headache , Vomiting …………… Excessive sleepiness…………………. 2 weeks
O/e She is drowsy , responding to oral stimuli , T- afebrile P – 86 /min RR- 14 / min BP – 100/70 mm Hg No pallor / icterus / cyn /club /nodes Facial puffiness seen Decreased frequency of urination No pedal edema CVS - NAD RS - NAD PA - NAD
CNS : Higher mental function: Drowsy Not oriented Responding to painful stimuli CRANIAL NERVES: Pupils – B/L equal reacting to light. no ophtalmoplegia no papillodema No other cranial nerve involvement SPINOMOTOR : tone and reflexes were normal SENSORY : pain sensation preserved Meningeal : neck stiffness present Kernig sign - absent Cerebellar : couldn’t be assessed Spine , Skull - normal
Problems c/o TB meningitis on ATT since 5 months Non – compliance Incomplete steroid treatment Meningeal signs Secondary Amenorrhea Altered behaivour Weight gain with reduced urine frequency
Possibility TB relapse TB Hydrocephalus Hyponatremia Chronic meningitis of different etiology
Investigation Hb – 10 gm % TC – 6500 /cc DC – P60,L35 ESR – 25 mm/hr Platelet – 1.2 lac RBS - 90 mg% Urea – 27 mg% Cr- 0.6 mg% Na - 124 meq/L K – 3.6 meq/L CSF analysis : Physical - clear Pressure – high ( not measured ) Protein - 120 mg % Sugar - 29 mg% Cells - few lymphocytes ADA – not sent Cytology - acellular Grams Stain - negative AFB stain – negative Impression : Suggestive of TB meningitis Or incompletely treated pyogenic meningitis
On the 3rd day of re-admission patient developed precipitous neurological detoriation and complained on binocular diplopia Causes: Cerebral edema Hyponatremia Raised ICT hydrocephalus She was given iv. mannitol and iv. steroids An emergency CT brain was requested and promptly done.
An emergency call - over to neuro surgery dept was given and they took over the patient for an immediate ventricular decompression surgery. Post surgery patient recovered Became more responsive and there was a dramatic reduction in the facial and pedal odema. Patient was shifted back to medicine wards 10 days later.
Siadh There is a strong suspicion that part of the delirium in our patient could be due to SIADH secondary to CNS tuberculosis and the ensuing communicating hydrocephalus The points that are in favour are Hypo-osmolarHyponatremia Reduced urinary frequency Urine 24 hr Na+ levels 916 meq/L Altered behaivour Clear-cut etiology brisk diuresis following relief of hydrocephalus pt lost weight and became as she was about 5 months back However the points not in favour are : Presence of f/s/o overhydrated state Urine osmolality studies not done
Problems that were still persisting Patient still drowsy Prefered to sleep most of the day Reduced appetite Secondary Amenorrhea Lower range of BP Generalised apathy to surroundings
Possibilites: TB of the pituitary gland TB exudation causing Hypothal pituitary axis supression ( stalk – section effect ) Further plan: MRI imaging of the pituitary gland
Treatment given: ATT under cat 1 to be continued Repeated counselling regarding the compliance T. Eltroxin 50 ug/day T. Hydrocort 20mg/8am and 10 mg/8pm T. Estrogen T. Progesterone Her condition improved to an extent that she was able to do her work independently.
Final Diagnosis TB chronic meningitis Sequaelae Communicating hydrocephaleus VP shunt in situ and functioning anterior - Hypopitutarism Pituitary tuberculosis On hormone replacement therapy
What is so different in this case The propensity of TB to affect the pituitary is rare.
What is so different in this case The lesion is primarily in the pitiutary or the hypothalamus is quite uncertain.
Why a ACTH stimulation and GHRH stimulation test not done
Why was a PCR not done
Most of the case reports have a histopathological diagnosis. Hence a trans spenoidoidal biopsy should be done as an ultimate proof of the pathology
What is so different in this case The development of clinically apparent TB hypopituitarism when the patient is already on ATT is puzzling.
KEY MESSAGE…. TB pituitary is rare but known entity Recent onset of altered behaivour , apathy , secondary amenorrhea especially in endemic regions should suggest possibility of tuberculous involvement of hypophysiscerebri. It is important for us to keep a high index of suspicion in managing cases of CNS tuberculosis to pick up its complications very early in the course
Thank you References : Harrison’s 16/e Sharma – tuberculosis K Sunil, et.al.,Pituitary Tuberculosis. JAPI 2007.