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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 7  |  Issue : 6  |  Page : 331-335

Disseminated tuberculosis presenting as hypovolemic shock, hypernatremia with central diabetes insipidus


1 Department of Pediatrics, Aditya Birla Memorial Hospital, Pune, Maharashtra, India
2 Department of Pediatrics, Dr. Bidari's Ashwini Hospital and Postgraduate Center, Vijayapura, Karnataka, India

Date of Submission18-Apr-2020
Date of Decision23-May-2020
Date of Acceptance01-Jun-2020
Date of Web Publication11-Nov-2020

Correspondence Address:
Dr. Ramaning Loni
Aditya Birla Memorial Hospital, Pune - 411 033, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPCC.JPCC_62_20

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  Abstract 


Disseminated tuberculosis (TB) not uncommon in children in developing countries like India, and the spectrum of the disease varies in the different age groups. Tubercular meningitis can present as central diabetes insipidus, which is rare in children characterized by polydipsia and polyuria, because of the inability to concentrate urine secondary to defective synthesis of antidiuretic hormone. Here, we present 7-year-old girl child who was admitted with polyuria, polydipsia for the last 2–3 months with respiratory problems for 2–3 weeks with a family history of active pulmonary TB in a completely unimmunized child. She had disseminated TB involving the respiratory system and central nervous system, So, presented with hypovolemic shock with severe hypernatremia with dilute urine with encephalopathy. She was resuscitated and managed for a hypovolemic shock with metabolic derangement such as hypernatremia, requiring deficit fluid correction, vasopressin therapy, and antitubercular therapy to respond clinically. The child recovered completely without a neurological deficit.

Keywords: Central diabetes insipidus, polyuria, tubercular meningitis


How to cite this article:
Loni R, Anitha B, Tapal S, Kamale M, Bidari LH. Disseminated tuberculosis presenting as hypovolemic shock, hypernatremia with central diabetes insipidus. J Pediatr Crit Care 2020;7:331-5

How to cite this URL:
Loni R, Anitha B, Tapal S, Kamale M, Bidari LH. Disseminated tuberculosis presenting as hypovolemic shock, hypernatremia with central diabetes insipidus. J Pediatr Crit Care [serial online] 2020 [cited 2020 Nov 30];7:331-5. Available from: http://www.jpcc.org.in/text.asp?2020/7/6/331/300587




  Introduction Top


Central diabetes insipidus (CDI) is a rare endocrine disorder characterized by excessive thirst and polyuria because of the inability to concentrate urine secondary to defect in the synthesis of antidiuretic hormone (ADH).[1] Disseminated tuberculosis (TB) is defined as an infection involving the bloodstream, bone marrow, liver, or two more contiguous sites or miliary TB. The central nervous system (CNS) involvement in children is commoner than adults, can present as hydrocephalous, basilar meningitis, tuberculoma, and infarcts.[2] CDI can happen as part of panhypopituitarism due to isolated sellar or suprasellar TB or isolated tuberculoma involving the hypothalamus-pituitary axis.[3]

Here, we present for 7-year-old girl child admitted with a history of polyuria and polydipsia with pulmonary and CNS TB. Hence, tubercular meningitis (TBM) presenting with CDI, hypovolemic shock with severe hypernatremia, is rare in children.


  Case Report Top


A 7-year-old girl child presented with a history of polyuria, polydipsia with progressive weight loss for 2–3 months, and she was admitted for fever and cough for 2–3 weeks and fast breathing for 3–4 days. The child is born of nonconsanguineous marriage, 3rd child by birth order, developmentally normal up to the age. She had no clinically significant history before this admission. A family history of active pulmonary TB for the past 6 months in the mother was present, who was already on the continuation phase of antitubercular treatment (ATT). The child was completely unimmunized due to a lack of awareness and knowledge.

On admission, the child was lethargic with Glasgow coma scale of 11/15 (E4M4V3), and she was severely dehydrated with sunken eyes and low pulse volume, cold extremities and having hypotension with blood pressure 79/46 mmHg (<5th centile) with narrow pulse pressure, and she had mild respiratory distress with signs of meningeal irritation. Blood investigations suggestive of severe hypernatremia with elevated erythrocyte sedimentation rate (90 mm in 1st h). She was resuscitated for a hypovolemic shock in the form of O2 therapy, intravenous (IV) Isotonic crystalloid fluid bolus of NS 20 ml/kg IV stat, followed full maintenance fluid therapy with deficit water as dehydration correction over >96 h as serum Sodium was 208 meq/L. Her anthropometry on admission was the weight of 14 kg (<3rd percentile, the height of 111.5 cm between 10 and 25th percentiles, and her head circumference of 51 cm (normal for age).

Her chest X-ray showed haziness in the right upper and middle zone, widened subcarinal angle [Figure 1]. She underwent computed tomography thorax with contrast, which showed findings of consolidation changes in the right upper and lower lobes with subtle centrilobular nodules in the apical segment of the right lower lobe represent infective changes with small calcified pretracheal lymph node suggestive of pulmonary Koch's [Figure 2] and [Figure 3], and she was started on anti-tubercular therapy of 2HRZE plus10 HRE. Her cerebrospinal fluid (CSF) analysis showed a total of 5 cells with 100% lymphocytes, sugar 38 mg, protein 124 mg, and CSF for tubercular gene expert test positive. Her gastric aspirate for acid-fast bacilli staining was also positive.
Figure 1: Chest X-ray anterior-posterior view shows haziness in right paracardial and right lower zone

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Figure 2: Mediastinal window (cross-section plane) showing bilateral lower poster basal lung filed consolidation

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Figure 3: Precarinal calcified lymph nodes (cross-section plane)

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As the child had persistent hypernatremia with polyuria, her urine routine and urinary electrolytes showed sodium <20 mel/L, low osmolar diluted urine with a low specific gravity (Specific gravity <1010). Her random blood sugar 109 mg/dl. The child was further evaluated accordingly for suspected DI and serum osmolality of 422 mosm/L, and urine osmolality of <300 mosm/L. The differential diagnosis for polyuria with hypernatremia include nephrogenic DI (NDI), CDI, Osmotic diuresis and psychogenic polydipsia, but the suspicion of CDI was very high as per clinical presentation. She was treated for severe hypernatremic dehydration along with IV vasopressin therapy, she responded to the treatment well, and her serum electrolytes got normalized within the next 96 h. This was a vasopressin clinical challenge test to diagnose the CDI. Magnetic resonance imaging (MRI) brain showed findings of acute cerebral infarcts in bilateral external capsule and chronic lacunar infarcts in the right lentiform nucleus, considered secondary to TBM [Figure 4]. Magnetic resonance angiography or venography was not done due to economic constraints. Her thyroid function test (serum thyroid-stimulating hormone 4.7 mIU/L, FT3 5.2 pmol/L, and FT4 20 pmol/L) was normal and her morning serum cortisol level was 16 mcg/dl, and ACTH level (10 pgm/ml) also were normal, but serum prolactin or growth hormone levels were not done. Moreover, after dehydration correction with hypernatremia, her urine output normalized. After initial IV vasopressin infusion for 3 days, Later, she was started on oral desmopressin with significant improvement. The fluid used was 0.45% DNS, and the child responded well with given antitubercular therapy and oral desmopressin (Tab MINRIN 0.1 mg, half tab tablet 12th h), and the ophthalmological evaluation was normal. Pediatric Neurologist consultation was taken for this child and advised conservative treatment. She was discharged on the same treatment without any neurological deficit with normal sensorium. On subsequent follow-up, the child had adequate weight gain with normalized electrolytes. Her urine output was around 2 ml/kg/h, and serum sodium and potassium were 141 mel/L and 3.8 meq/L, respectively. She required oral desmopressin therapy for about 12 months, along with Antitubercular treatment (ATT). Her weight was 18 kg (between the 10th and 25th percentile for age), and height was 112 cm (between 10th and 25th percentile for age) according to IAP growth charts after 3 months follow-up in outpatient department (OPD).
Figure 4: Magnetic resonance imaging brain showing bilateral acute infarct in external capsule and chronic infarct in the right lentiform nucleus

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  Discussion Top


CNS TB is uncommon nowadays, frequently fatal one with the most debilitating conditions.[1] Tubercular vasculitis-causing infarction, obstructive hydrocephalus, and cranial neuropathies have been noticed as complications of TBM. Other CNS presentations include granulomatous basal meningitis, pachymeningitis, parenchymal TB (included parenchymal tuberculomas, focal tuberculous cerebritis, and encephalopathy, tuberculous abscesses, miliary tuberculomas, etc.), tuberculous hypophysitis, the involvement of the calvarium and the base of the skull, orbital TB, tuberculous otitis media, temporal bone TB, and cold abscess of the spine.[2] Tuberculous ventriculitis is an uncommon disease, with only a few cases reported to date.[3],[4] TBM is the most common cause of death in child hood tuberculosis.[5] Tubercular cerebral vasculitis can be included in the differential diagnosis in complications of any case of tuberculous meningitis. Tuberculomas affecting the hypothalamo-pituitary axis are very rare, and they have been reported in the literature.[3],[6],[7] Disseminated TB involving (CNS, respiratory system) presenting as isolated CDI in our case is comparable to the study done by Chellen et al.[8] except in their case, MRI Brain picked up the pituitary TB and brain parenchyma's tuberculomas. Chellen et al. also used long term oral Desmopressin therapy along with antitubercular therapy for complete recovery.

In our case, the child had acute infarct in bilateral external capsules, and chronic lacunar infarct in the right lentiform nucleus [Figure 4] without tuberculoma/hydrocephalus had presented with encephalopathy, CDI with hypovolemic shock with severe hypernatremia [Table 1]. The clinical presentation will not match with the MRI Brain finding (Normal Pituitaries in MRI Brain in [Figure 5]). but need to treat the child, not the reports. The differential diagnosis for the polyuria with high serum osmolality with hypernatremia could be either DI (Central/Nephrogenic) or Psychogenic Polydipsia. As her blood sugars were within normal limits and without the past history of any medications before the illness rules out the osmotic diuresis. Looking at the background proven CNS TB with high osmolality with severe hypernatremia and decided to do the water deprivation test to confirm DI but parents refused to give the consent in the acute setting. Psychogenic polydipsia is the diagnosis of the exclusion of underlying pathological conditions, so this was an unlikely diagnosis in this child. Our center having 1.5 Tesla MRI machine might not have picked up the lesions in pituitary and hypothalamic areas and small pituitary TB lesions as they are rare and very difficult to pick up the lesions.[6]
Table 1: Her serial sodium levels monitoring

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Figure 5: Magnetic resonance imaging brain with sagittal cuts showing apparently normal pituitary glands

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On literature review on CDI with CNS TB[3],[6],[7],[8] have proven that CDI can happen as part of panhypopituitarism due to isolated sellar or suprasellar TB or isolated tuberculoma involving the hypothalamo-pituitary axis. Some have histologically proven pituitary TB, especially in the AIIMS case series study.[3] CDI can occur at any age, depending on underlying etiology. Most frequently, it is an acquired condition, usually secondary to traumatic injuries. Less common causes are infiltrative lesions such as TB, sarcoidosis, and Langerhans histiocytosis. Here, in this case, scenario, cranial TB involving the cerebral parenchyma with infarcts has led to defective production of ADH/vasopressin resulting in diluted urine in excessive quantity which has presented as CDI. Water deprivation test is the gold standard in differentiating between DI and compulsive water drinking. Dilute urine with an osmolality of <300 mOsm/kg and serum osmolality >300 mOsm/kg is diagnostic for DI.[8],[9] In addition, a 1-deamino-8D-arginine vasopressin challenge test was performed to distinguish between CDI and NDI.[10] We could have done the water deprivation test to differentiate CDI from NDI but not performed. However, clinically, she responded very well to the IV vasopressin initially for 3 days and later, continued on oral vasopressin tablet. She received IV dexamethasone, later oral prednisolone for 4 weeks. She was on oral desmopressin and ATT for 12 months.[11] Oral steroids were tapered and stopped within 6 weeks and on follow-up in OPD after 3 months, her weight was 18 kg (between the 10th and 25th percentile). She was gaining weight, and her polyuria was responding to the treatment without any other neurological deficits. The water deprivation test on the OPD basis was planned after 6 months of treatment, but parents refused for the test as her polyuria responded with urine output around 2 ml/kg/h.


  Conclusions Top


  • CNS TB can present with central diabetes mellitus as a part of disseminated TB
  • Early suspicion, screening, and the treatment of CNS TB can decrease the mortality and morbidity associated with it
  • CDI can present with life-threatening dehydration, hypovolemic shock, and hypernatremia.


Recommendation

The bacillus Calmette Guérin vaccination at birth as a part of UIP to prevent disseminated severe TB in adolescence/adulthood is a must in developing countries like India.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgment

I am thankful to my parents and family.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rock RB, Olin M, Baker CA, Molitor TW, Peterson PK. Central nervous system tuberculosis: Pathogenesis and clinical aspects. Clin Microbiol Rev 2008;21:243-61.  Back to cited text no. 1
    
2.
Story A, Bothamley G, Hayward A. Crack cocaine and infectious tuberculosis. Emerg Infect Dis 2008;14:1466-9.  Back to cited text no. 2
    
3.
Sharma MC, Arora R, Mahapatra AK, Sarat-Chandra P, Gaikwad SB, Sarkar C. Intrasellar tuberculoma – An enigmatic pituitary infection: A series of 18 cases. Clin Neurol Neurosurg 2000;102:72-7.  Back to cited text no. 3
    
4.
Kumar S, Kumar R, Radotra BD, Singh M. Tubercular ventriculitis: An uncommon entity. Indian J Pediatr 2014;81:608-10.  Back to cited text no. 4
    
5.
Aulakh R, Chopra S. Pediatric tubercular meningitis: A review. J Pediatr Neurosci 2018;13:373-82.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Satyarthee GD, Mahapatra AK. Diabetes insipidus in sellar-suprasellar tuberculoma. J Clin Neurosci 2003;10:497-9.  Back to cited text no. 6
    
7.
Jain R, Kumar R. Suprasellar tuberculoma presenting with diabetes insipidus and hypothyroidism – A case report. Neurol India 2001;49:314-6.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Chellen S, Whittaker E, Eisenhut M, Grandjean L. Cerebral tuberculomas in a 6-year-old girl causing central diabetes insipidus. BMJ Case Rep 2018;2018:bcr2018226590.  Back to cited text no. 8
    
9.
Dabrowski E, Kadakia R, Zimmerman D. Diabetes insipidus in infants and children. Best Pract Res Clin Endocrinol Metab 2016;30:317-28.  Back to cited text no. 9
    
10.
Garima M, Chandrashekhar SR. Management of diabetes insipidus in children. Indian J Endocrinol Metab 2011;15 Suppl 3:S180-7.  Back to cited text no. 10
    
11.
Hay WW Jr., Levin MJ, Deterding RR, Abzug MJ. CURRENT Diagnosis and Treatment Paediatrics. 22nd ed. USA: McGrawHill Education; 2014. p. 1063-4.  Back to cited text no. 11
    


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