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Journal of Symptoms and Signs 2012; Volume 1, Number 3

117

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Case Reports

Multifocal intracerebral mass lesions and diabetes insipidus: adiagnostic dilemma in absence of brain biopsy

Chaturaka Rodrigo MBBS1, Vijayabala Jeevagan MBBS

2, Prasad Katulanda MBBS, MD, DPhil

1

1Department of Clinical Medicine, Faculty of Medicine, University of Colombo, Sri Lanka,

2University Medical Unit, National Hospital of Sri

Lanka, Colombo, Sri Lanka.

Corresponding Author: Chaturaka Rodrigo, Lecturer in Medicine, Department of Clinical Medicine, Faculty of Medicine, University ofColombo, 25, Kynsey Road, Colombo 08, Sri Lanka. E-mail:[email protected].

AbstractIntroduction We report a patient with diabetes insipidus who had multiple mass lesions involving the corticaland suprasellar areas of the brain. In absence of consent for biopsy, we had to choose treatment judging the

pros and cons of treating the most likely diagnosis.

Case PresentationA sixty three year old male without any previously diagnosed comorbidities was admitted

in a state of disorientation plus cognitive impairment. He developed diabetes insipidus during the hospital stay.

Imaging of the brain showed mass lesions with minimum peri-lesional edema suggestive of a chronic granu-

lomatous infection in suprasellar and cortical areas. The pituitary dysfunction was limited to the hypothalamic

posterior pituitary axis. The epidemiological, historical evidence and biochemical analysis from cerebrospinal

fluid favored a diagnosis of tuberculosis. Still, it could not be confirmed. Anti-tuberculosis treatment was

started empirically and the patient made a dramatic improvement within 2 weeks. However, he suddenly de-

teriorated 6 weeks later and passed away.

Conclusions The dilemma in initiating anti-tuberculous treatment when a definite diagnosis cannot be estab-

lished is encountered by many neurologists. We narrate our experience and pitfalls in this regard as it would

be useful to clinicians who encounter similar situations.

Keywords:diabetes insipidus; tuberculosis; supracellar mass lesion.

Received:June 2, 2012; Accepted: July 9, 2012; Published:August 14, 2012

IntroductionWe report a case of a patient presenting with diabetes

insipidus who had multiple mass lesions involving the

suprasellar and cortical regions of the brain. The circum-

stantial evidence pointed to a diagnosis of tuberculosis

(TB). However, there was a diagnostic dilemma to dif-

ferentiate it from sarcoidosis.

Case PresentationA 63-year-old male without any previously diagnosed

comorbidities was admitted to his local hospital in a state

of disorientation plus cognitive impairment. Two months

prior to admission he had developed a chronic cough,

nocturnal fever and loss of appetite. He also com-

plained of an intermittent frontal headache. By the time

of admission to the hospital, he had severe headache, loss
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Multifocal intracerebral mass lesions and diabetes insipidus

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of memory (short and long term), polydipsia and polyuria.

On second day after admission, his disorientation got

worse and aggressive behavior with visual hallucinations

was noted. He became bed-bound, stopped taking oral

feeds and had urinary incontinence. He was transferred to

our unit at that time.

A detailed history did not reveal any significant clues

such as previously diagnosed comorbidities, surgical

procedures or drug sensitivities. However, he had a close

contact history for tuberculosis in the family. In addition,

he had been a heavy alcohol user and a smoker for more

than 20 years.

On admission to our unit, the patient was febrile and

drowsy with a Glasgow coma score of 10/15 (E-2, M-5,

V-3). However, he was hemodynamically stable with a

pulse rate of 96/min and a blood pressure of

120/90mmHg. The respiratory system was clinically

normal and a smooth non tender hepatomegaly (4 cm

from the costal margin) was noted on abdominal exami-

nation. The neurological examination did not reveal any

other abnormalities apart from disorientation, drowsiness

and cognitive impairment.

His hemoglobin level and platelets were within the

reference range since the start of illness but there was a

mild neutrophil leucocytosis throughout. His erythrocyte

sedimentation rate was 70 mm/h with a near normal C

reactive protein level 7 mg/L (< 6mg/L).

His serum sodium concentration was high at the time

of admission (152 meq/L; reference range: 135-148) and

it progressively rose during the course of illness. During

the second week of hospital admission, it increased up to

166 meq/L. The serum potassium was within reference

range (3.5-5.3 meq/L) though at times it dropped as low

as 3 meq/L. At the time of peak serum sodium concentra-

tion, he was having profuse polyuria sometimes exceed-

ing 5 liters per day. The urine specific gravity was 1.005

which was less than the normal value (1.010). He serum

osmolality was 320 mmol/kg (275-295) with a urine os-

molality of 122 mmol/kg (700-1500). The urinary sodi-

um concentration was also inappropriately low

(28 mmol/L; reference range: 80-200) establishing a di-

agnosis of diabetes insipidus. Given the clear constella-

tion of clinical features and biochemical indicators, a

water deprivation test was unnecessary to make the di-

agnosis. The anterior pituitary functions were not dis-

rupted. The serum cortisol, thyroid stimulating hormone,

free tri-iodothyronine (fT3) and free tetraiodothyronine

(fT4) levels were within normal ranges.

Figure 1.CT scan of the patient showing a hyperdense

mass in the suprasellar region.

Figure 2. MRI scan (sagittal section) showing the su-

prasellar mass and another mass in the anterior part of

corpus callosum.

CT scan of the brain showed a hyper-dense mass in

suprasellar region (Figure 1) plus multiple focal lesions

(contrast enhancing) in the left frontal, right fron-

to-parietal and right superior parietal region. The brain

stem and posterior fossa were spared. The magnetic res-

onance imaging (MRI) did not show a significant pe-

ri-lesional edema (Figures 2, 3). The biochemical analy-

sis of cerebrospinal fluid (CSF) showed a high protein

content of 185 mg/dl (10-40) with lymphocyte predomi-


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nance (15 cells/l). The glucose concentration was 40%

of the serum concentration. The direct smear was nega-

tive for organisms when stained with gram stain, Ziehl

-Neelsen stain (forMycobacteria) and Nigrosine stain for

Cryptococcus. Both the routine bacterial culture and tu-

berculosis cultures were negative on CSF. The polymer-

ase chain reaction (PCR) on CSF with appropriate pri-

mers failed to detect genomic material ofM. tuberculosis

as well as of common fungal pathogens. Cytological

analysis did not reveal any malignant cells as well.

Figure 3.MRI scan (coronal section) showing twoseparate mass lesions.

The chest roentgenogram was normal apart from a

small consolidation at the left lung base. There was no

hilar lymphadenopathy. These findings were confirmed

by a CT scan of the chest. The serum calcium and angio-

tensin converting enzyme inhibitor (ACEI) levels

(48 units/L) were within normal limits. Ultrasound scan

of the abdomen did not reveal any significant findings

apart from a cirrhotic liver which was attributed to his

long standing heavy alcohol use.The diabetes insipidus was managed with desmopres-

sin nasal puffs and anti-tuberculous therapy (ATT) was

started empirically since the most likely diagnosis was

tuberculosis. He was also started on intravenous (IV)

dexamethasone with ATT which was later converted to

oral therapy. The patient made a remarkable recovery

during the next two weeks and was discharged home.

However, 6 weeks later, he deteriorated suddenly and

passed away. His dexamethasone had been tailed off

about two weeks prior to his death.

DiscussionThere can be several differential diagnoses for the intrac-

erebral mass lesions in this patient. These include tuber-culosis, sarcoidosis, fungal infections (aspergillosis, coc-

cidiomycosis) and langerhan cell histiocytosis[1].

Several factors favored a diagnosis of central nervous

system tuberculosis including: contact history, chronic

constitutional symptoms, epidemiology and endemicity

of infection in the local population, biochemical and cy-

tological findings of CSF analysis and the initial response

to anti-TB therapy. Still, the direct smear of CSF for acid

fast bacilli, TB culture and TB-PCR on CSF were all

negative. The chest roentgenogram was also normal.

However, central nervous system tuberculosis may notalways coexist with pulmonary TB and the sensitivities

of diagnostic tests also vary. The diagnostic yield of CSF

culture forM. Tuberculosisvary between 25-70% in dif-

ferent studies[2]. Similarly, the diagnostic yield of

TB-PCR in CSF is shown to be low (sensitivity of 56%)

in a meta-analysis by Pai, et al[3].Some authors suggest

low bacterial load and presence of PCR inhibitors in CSF

plus difficulty in assessing low sample volumes as possi-

ble contributory factors to the low diagnostic yield of

TB-PCR on CSF [4].

However, similar CSF findings could have occurred insarcoidosis as well. There was no evidence of sarcoidosis

on the chest roentgenogram, chest CT and as per other

biochemical investigations such as serum calcium level

and ACEI level. Still, it doesnt exclude the possibility of

sarcoidosis. This diagnostic dilemma could have been

resolved if a biopsy from cerebral lesions was available.

Unfortunately, there was no consent for biopsy from

family.

Another theoretical way of differentiating the two con-

ditions would be a trial of steroids instead of anti-TB

drugs to assess the regression of lesions with treatment (if

the lesions were due to sarcoidosis). However, it would

have been definitely deleterious on part of the patient to

start on steroids alone, weighing on a less likely diagno-

sis of sarcoidosis against a more likely diagnosis of tu-

berculosis. Therefore, we took the safer option of treating

with anti-TB drug therapy combined with IV dexame-

thasone (steroids are indicated in the treatment of central

nervous system tuberculosis too). The initial improve-


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ment could have been due to anti-TB drugs and steroids

provided the diagnosis was tuberculosis or due to steroids

alone if the diagnosis was sarcoidosis.

One explanation for the sudden unexpected death of

the patient is the mass effect of the lesions. Previous ex-

perience with such multiple intra-cerebral lesions in tu-

berculosis as reported in literature show that a) anti TB

therapy is not always effective in securing a treatment

success [5] and b) deterioration can occur after starting

anti-TB therapy probably due to the reconstitution of the

cell mediated immunity and worsening cerebral edema[6].

This fact was anticipated and it was another reason to

maintain him on dexamethasone. His steroids were being

tailed off when he deteriorated.

Overall, we opted for a diagnosis of tuberculosis in

this patient. It is a rare cause of diabetes insipidus [7, 8].

Tuberculomas of pituitary sellar region often causes

hypofunction (or rarely hyperfunction) of the anterior

pituitary gland and instances of diabetes insipidus (poste-

rior pituitary involvement) are extremely rare[9]. Our

patient had isolated posterior pituitary/hypothalamic in-

volvement with sparing of the anterior pituitary func-

tions.In retrospect, judging by available evidence, we still

defend our decision to start anti-TB therapy but regret

that the dexamethasone was withdrawn too early.

Experience of previous authors show that sometimes

intravenous dexamethasone had to be continued for 2

months after starting anti-TB therapy for central nervous

system tuberculosis [10]. We also stress that whenever

possible, clinicians encountered with such diagnostic

uncertainty must push for a histological diagnosis with a

brain biopsy.

Disclosure

There are no conflicts of interest.

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mours: inflammatory and granulomatous expansive lesions of the

pituitary. Best Pract Res Clin Endocrinol Metab. 2009;23(5):639-650.

2. Garg RK. Tuberculosis of the central nervous system. PostgradMed J. 1999; 75:133-140.

3. Pai M, Flores LL, Pai N, Hubbard A, Riley LW, Colford JMJ.Diagnostic accuracy of nucleic acid amplification tests for tuber-

culous meningitis: a systematic review and meta-analysis. Lancet

Infect Dis. 2003; 3:633643.

4. Christie LJ, Loeffler AM, Honarmand S, Flood JM, Baxter R,Jacobson S, Alexander R, Glaser CA. Diagnostic challenges of

central nervous system tuberculosis. Emerg Infect Dis. 2008;

14:1473-1475.

5. Wang KC, Lin SM, Chen Y, Tseng SH. Multiple tuberculousbrain abscesses. Scand J Infect Dis. 2002; 34(12):931-934.

6. CNS Tuberculosis[http://www.springerimages.com/Images/RSS/2-PEDIA01-07-04

2]

7. Bajpai A, Kabra M, Menon PS. Central diabetes insipidus: clini-cal profile and factors indicating organic etiology in children. In-

dian Pediatr. 2008; 45(6):463-468.8. Dutta P, Bhansali A, Singh P, Bhat MH. Suprasellar tubercular

abscess presenting as panhypopituitarism: a common lesion in an

uncommon site with a brief review of literature. Pituitary. 2006;

9(1):73-77.9. Satyarthee GD, Mahapatra AK. Diabetes insipidus in sel-

lar-suprasellar tuberculoma. J Clin Neurosci. 2003;

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10. Hejazi N, Hassler W. Multiple intracranial tuberculomas withatypical response to tuberculostatic chemotherapy: literature re-view and a case report. Infection. 1997; 25:233-239.

Copyright:2012 Chaturaka Rodrigo, et al. This is an OpenAccess article distributed under the terms of the Creative Com-

mons Attribution License, which permits unrestricted use, dis-

tribution, and reproduction in any medium, provided the original

work is properly cited.

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