ISSN - 0973-0958

Pediatric Oncall Journal

Vomiting in a Tuberculous meningitis

Vomiting in a Tuberculous meningitis

Dr Ira Shah.
Medical Services Department, Pediatric Oncall, Mumbai.

Dr Ira Shah, Medical Sciences Department, Pediatric Oncall, 1, B Saguna, 271, B St. Francis Road, Vile Parle {W}, Mumbai 400056.
Clinical Problem
A 2½ years old boy born of non consanguineous marriage presented with vomiting 4-5 episodes which were non projectile and non bilious. The child was diagnosed as a case of TB meningitis and was on antituberculous therapy {ATT}, steroids {on tapering doses} and diamox for the past 1 month. CT scan done 1 month back had shown basal exudates with minimal hydrocephalus. There was no pain in abdomen, altered sensorium, jaundice or cranial nerve palsy. On examination, there were no signs of raised intracranial tension, no dehydration and no hepatomegaly. Systemic examination was normal.
Investigations showed normal liver transaminases. Fundus examination showed no papilledema. Venous blood gas showed pH of 7.36 with bicarbonate of 13.7 mmol, L. Serum electrolytes were normal.

What is the cause of vomiting in this child__?
When a child with TBM on treatment presents with vomiting, then one must consider the following etiologies:
· Drug induced hepatitis
· Raised intracranial tension due to hydrocephalus {tuberculoma would usually cause focal convulsion}
· Gastritis due to steroids
· Metabolic decompensation due to carbonic anhydrase inhibitor.

In this child, there is no hepatomegaly and liver transaminases are normal ruling out drug induced hepatitis, Hydrocephalus usually presents with spasticity, garbled speech {cocktail speech}, brisk deep tendon reflexes and papilledema on funduscopy. With increasing hydrocephalus, the anterior horns of lateral ventricles are involved first followed later by posterior horns. Thus papilledema due to involvement of optic chiasma will be early sign to develop followed later by involvement of pyramidal tracts due to involvement of posterior horns leading to spasticity and exaggerated deep tendon reflexes. In this child, there are no papilledema or deep tract signs and hence increase in hydrocephalus seems unlikely. Gastritis leads to epigastric pain which was absent in this child. Carbonic anhydrase inhibitor leads to metabolic acidosis which can lead to vomiting. Vomiting leads to metabolic alkalosis due to loss of hydrogen ions in vomitus. In this child, blood gas showed metabolic acidosis suggestive of metabolic decompensation due to carbonic anhydrase inhibitor. Her diamox was stopped and subsequently, her acidosis resolved and vomiting subsided

E-published: January 2009, Vol 6 Issue 1 Art No. 4
Compliance with ethical standards
Funding:  None  
Conflict of Interest:  None
Cite this article as:
Shah I. Vomiting in a Tuberculous Meningitis. Pediatr Oncall J. 2009;6: 17.
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