Abdominal tuberculosis has been widely reported as a
cause for chylous ascites in adults and children [1]; though, not in
neonates and young infants. We report an extreme preterm infant, who
presented at 2.5 month of age with chylous ascites caused by perinatal
tuberculosis.
A 2.5-month-old girl presented with fever, excessive
crying and grunting. The infant was first of twins born at 27 weeks with
birthweight of 870 g. Both twins had received surfactant therapy, and
ventilation of 48 hours followed by continuous positive airway pressure
(CPAP) for five weeks. The second twin girl had birthweight of 1090 g.
She had enterobacter sepsis in the third week of nursery stay from which
she recovered after receiving intravenous antibiotics. She had also
received packed cell transfusion for anemia. The first twin did not
require any transfusion. Both infants were fed initially with
pasteurized donor milk (PDHM) followed by mother’s own milk. They gained
weight along the 10th centile for preterm Fenton growth chart. At the
time of discharge, the first and second twin weighed 1.58 kg and 1.6 kg,
respectively. Both twins received iron, calcium and vitamin D
supplements at discharge at corrected gestational age of 35 weeks. Their
mother received antibiotics for fever and cesarian section wound
dehiscence in the second post-partum week.
At the time of re-admission, the infant was febrile
and her systemic examination was normal. The investigations showed
leukocytosis (28.9×109/L) with raised C-reactive protein (CRP, 97.5
mg/L). The infant was started on intravenous fluids and antibiotics. The
fever spikes reduced and CRP showed declining trend over the next week.
Blood and urine cultures were reported sterile. In the second week of
admission, the infant started developing abdominal distention. Her
abdominal ultrasound showed moderate ascites with multiple necrotic
abdominal lymph nodes. An abdominal paracentesis showed milky ascitic
fluid. Ascitic fluid microscopy showed high leukocytes count (3.6×109/L)
with lymphocyte predominance (95%). Triglycerides in ascitic fluid were
high (836 mg/dL), suggestive of chylous ascites. The infant was started
on octreotide infusion and medium chain triglyceride (MCT)- based
formula feeds. The ascitic fluid was negative for acid fast bacilli,
bacterial culture and polymerase chain reaction (PCR) for
cytomegalovirus and Epstein Barr virus. GeneXpert for tuberculosis was
reported as positive. A tuberculin skin test was negative after 72
hours. A computerized tomography (CT) scan of abdomen and chest revealed
multiple necrotic lymph nodes in gastro-hepatic, celiac, periportal and
retroperitoneal areas with necrotic lesions in spleen, and moderate
ascites. A repeat ascitic fluid and gastric lavage sample for GeneXpert
was also reported positive.
The infant was started on anti-tuberculosis therapy
(isoniazid, rifampicin, pyrazinamide and ethambutol). Repeat abdominal
paracentesis days later showed reduced triglycerides content (230
mg/dL). Octreotide infusion was stopped after seven days. Over the next
four weeks, the abdominal circumference returned back to normal on
MCT-based formula feeds. Family screening for tuberculosis was advised
but got delayed due to coronavirus disease (COVID-19) related lockdown,
and non-availability of non-emergency laboratory services.
At five months of age, the second twin was noted to
have cervical lymphadenopathy. An excisional biopsy of lymph node showed
caseating granuloma with Mycobacterium tuberculosis grown on
Bactec MGIT system. The mother’s sputum tested positive for tuberculosis
on GeneXpert. The second twin and the mother were also started on four
drug anti-tuberculosis treat-ment. The twin girl with chylous ascites
was gradually shifted from MCT-based formula to term formula after 12
weeks. The infant had no ascites and was gaining weight at four months
of follow up.
In addition to the known etiological factors such as
congenital lymphatic malformations or surgical injury to the lymphatic
system and infections, in a large number of cases the cause for chylous
ascites remains unidentified [2]. The presence of necrotic lymph nodes
in the ultrasound (and later in the CT scan) prompted us to investigate
for tuberculosis as the cause of chylous ascites. We used
GeneXpert for the diagnosis of tuberculosis in this child as gene-based
tests have been shown to increase the diagnostic yield in infantile and
childhood tuberculosis [3].
In spite of widely reported criteria for
differentiation between congenital and postnatal onset of tuberculosis
and its subsequent modification, tuberculosis infection in utero can be
indistinguishable from perinatal or early post-partum infection [4,5].
Therefore, we have used the term ‘perinatal tuberculosis’ for both the
twins. As such, the differentiation is only of epidemiological
importance and their mode of presentation, treatment, and immediate
prognosis do not differ [6]. In our case, the mother had fever during
post-partum period, the cause for which was attributed to the wound
dehiscence. However, it is likely that the mother could have contracted
tuberculosis infection during this period. Women in early postpartum
period are twice as likely to develop tuberculosis as nonpregnant women.
In our case, both twins did not have any evidence of tuberculosis at
birth as well as during their prolonged nursery stay. The identification
of tuberculosis bacilli in mother itself indicates her being the source
of TB leading to affection of both infants.
We wish to sensitize the readers about the need to
also consider tuberculosis as a cause of chylous ascites in infants,
especially in high disease burden countries.
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