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CASE REPORT |
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Year : 2016 | Volume
: 9
| Issue : 6 | Page : 750-752 |
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A rare case of tuberculous meningitis with pancreatitis
Drishti Chandru Tolani, Ira Shah
Department of Pediatrics, Pediatric Tuberculosis Clinic, B. J. Wadia Hospital for Children, Mumbai, Maharashtra, India
Date of Web Publication | 16-Nov-2016 |
Correspondence Address: Ira Shah 1/B Saguna, 271/B St. Francis Road, Vile Parle (W), Mumbai - 400 056, Maharashtra India
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/0975-2870.194210
Tuberculous meningitis (TBM) is the most common form of central nervous system manifestation of tuberculosis. However, tuberculous pancreatitis is rarely reported. We present an 8-year-old female child with TBM who had intractable vomiting that persisted even after fever and meningeal signs had decreased after starting antituberculous therapy and did not respond to antacids. She was subsequently detected to have elevated serum amylase and lipase suggestive of pancreatitis. She responded to conservative management. Keywords: Pancreatitis, tuberculosis, tuberculous meningitis
How to cite this article: Tolani DC, Shah I. A rare case of tuberculous meningitis with pancreatitis. Med J DY Patil Univ 2016;9:750-2 |
Introduction | | |
One of the most common extrapulmonary manifestations of tuberculosis (TB) is tuberculous meningitis (TBM). Any part of the body can be affected by TB although it rarely affects the heart, skeletal muscles, or pancreas. [1] Cases involving primary pancreatic TB have been increasingly reported perhaps because of evolutionary changes in the biology of the mycobacterium, drug resistance, and new population of immunocompromised patients. [2],[3],[4] However, TBM with pancreatic involvement has been reported rarely. [5] We present an 8-year-old female child with TBM who presented persistent vomiting likely due to pancreatitis.
Case Report | | |
An 8-year-old female child presented with fever, headache, and drowsiness for 8 days. She also had neck stiffness and nonprojectile, nonbilious vomiting. There was no history of contact with a TB patient. Her weight was 24 kg (normal weight for age). Other than being febrile, her vital parameters were normal. She was arousable and the Glasgow Coma Scale was 13/15. Fundoscopy revealed no papilledema. No additional neurological manifestations were found. Her hemoglobin was 9.9 g/dl (normal: 11.5-16.5 g/dl) and white blood cell count was 6300/mm 3 . Differential leukocyte count showed 36% neutrophils and 63% lymphocytes. The Mantoux tuberculin test was negative. Chest radiograph was normal. Cerebrospinal fluid (CSF) analysis revealed 380 cells/mm 3 of which 90% were lymphocytes and 10% were polymorphs, CSF glucose (52 mg/dl) versus blood glucose (109 mg/dl) ratio was <50% of blood glucose, and CSF proteins were 149 mg% (normal = 20-50 mg%). Computed tomography revealed a moderate hydrocephalus with basal exudates suggestive of TBM. CSF TB polymerase chain reaction and culture was not done due to nonaffordability. The patient was started on four-drug antituberculous therapy (ATT) consisting of isoniazid (H), rifampicin (R), pyrazinamide (Z), and streptomycin (S) along with steroids and acetazolamide. Her fever and meningeal signs decreased, but vomiting persisted. She had no other signs of raised intracranial pressure and no abdominal pain. She was started on antacids and ranitidine but with no improvement. Ultrasound of the abdomen was normal. Serum glutamic pyruvic transaminase was 21 IU/L (normal: 7-56 IU/L). Her serum lipase was 824 U/L (normal: 0-160 U/L) and serum amylase was 2280 IU/L (normal: 23-85 IU/L). HIV ELISA was negative. Her vomiting gradually subsided and lipase and amylase returned to normal after 21 days of ATT. Steroids were omitted after 2 months of ATT, and the patient was continued on HR after 2 months of intensive phase. Magnetic resonance imaging of the brain after 6 months of therapy was normal and ATT was stopped after 1 year of therapy. On follow-up 3 months after stopping ATT, the child was asymptomatic.
Discussion | | |
Acute pancreatitis in children is predominantly caused by multisystem diseases, such as viral, sepsis, shock, and hemolytic-uremic syndrome in 33%, blunt trauma in 15%, acquired or congenital structural defects in 10%, metabolic diseases in 10%, and drug toxicity in 3%. [6] In up to 25% of children with acute pancreatitis, no identifiable etiology can be found. [6] Pancreatitis may be caused by a number of viruses, most notably mumps, coxsackie B, cytomegalovirus, varicella zoster, and hepatitis B viruses. Other viral diseases, including hepatitis A and HIV infection, have been more weakly associated with pancreatic injury. Bacteria such as Salmonella and Mycoplasma have been implicated in a few cases of pancreatitis. [7] Pancreatitis caused by infections usually subsides once the infections have resolved. [7] Although pancreatic involvement in TB is very rare, it is possible for TB to spread hematogenously to the pancreas. [7] Pancreatitis can also be induced by isoniazid or corticosteroids. [8] In cases of pancreatitis recorded due to isoniazid, the pancreatitis subsided on withdrawal of isoniazid therapy. [8] In our patient, the lipase and amylase normalized after 21 days of ATT without requiring modification of treatment; therefore, pancreatitis was likely not drug induced and more likely caused by TB or any other infection. On reviewing the literature; we found a single case report which reported pancreatic involvement in a case of TBM. [5]
Pancreatitis usually presents with abdominal pain, persistent vomiting, fever, and irritability. Most of these symptoms in this patient were masked by the common symptoms of TBM. Our patient did not suffer from any abdominal pain but had only vomiting as presenting symptom of pancreatitis. It has also been found that young patients have lesser complaints of abdominal pain with pancreatitis. [9] There is no one specific test to diagnose pancreatitis. Serum lipase and amylase levels are most common and reliable. Twenty percent of children with acute pancreatitis have normal imaging studies. [10] TB of the pancreas usually shows findings in imaging studies such as hypodense collections [11] or cystic masses [10] within the pancreas with peripancreatic lymphadenopathy. [11] None of these findings were seen in our patient.
The treatment of acute pancreatitis in children involves supportive care which includes fluid resuscitation, pain medication, and attention to nutritional needs. [12] No single medication or treatment is available for pancreatitis. The child can be started on a low-fat elemental diet which may decrease the need for total parenteral nutrition without aggravating pancreatitis. [13] Meperidine (Demerol) is preferred to morphine for pain control because it is less likely to cause spasm of the sphincter of Oddi (which could worsen pancreatitis). [14] If vomiting persists, nasogastric suctioning is useful. [12] Since our patient did not complain of any pain and the vomiting subsided with ATT, after 21 days she did not require any specific supportive therapy. A limitation to this case is that we could not confirm the diagnosis of meningitis or pancreatitis due to nonaffordability to run tests that would help identify the organism.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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