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Posted On : 14 Sep 2025

A 28-day-old neonate weighing 3 kg at present came with a history of seizures on 22 day of his life with bruising and petechial rash over the body. There was hepatomegaly, but the consistency was soft. The neonate was dull and lethargic with poor neonatal reflexes. Ser sodium was 132 and pott was 5.2, LFT was normal except for the raised GGT to 2000. The CECT was normal except for the leptomeningeal enhancement.CSF showed a raised protein of 300 and low sugar of 28{blood sugar -80} and a few degenerated cells{had received antibiotics for 6 days outside}.IV antibiotics were started in meningitic doses. The neonate has started improving. Platelets have improved. required a blood transfusion in view of low Hb of 7 gm percent. Serum Albumin was low. Urea and creatinine were within normal range. Electrolytes are presently within normal range. Presently on Phenobarbitone and IV antibiotics and feeds are going and; neurologically, the neonate has improved.
But the concern is that the neonate does not pass adequate urine and does so only after he is given Lasix. Would it be wise to give Lasix, although renal parameters and electrolytes are normal?
What could be the reason for raised GGT?

Expert Answer :

Answer Discussion :

N

Noel Neil

0

If Ceftriaxone was used, Ceftriaxone can cause temporary biliary sludge (biliary pseudolithiasis) in infants, particularly with higher doses or longer treatment durations, due to the drug's calcium-binding properties.

5 Days ago

W

Wonder Apetorgbor

2

Possible causes:

1. Biliary tract involvement: Cholestasis (biliary atresia, neonatal hepatitis). But LFT otherwise normal and hepatomegaly soft makes BA less likely, though early cholestasis can present this way.

2. Drug induced: Phenobarbitone and antibiotics (esp. cephalosporins, aminoglycosides) can markedly raise GGT by inducing hepatic microsomal enzymes.

3. Sepsis-related cholestasis: Neonatal sepsis/meningitis can cause sepsis-associated cholestasis ? often with high GGT, even if bilirubin not very raised yet.

4. Total parenteral nutrition (TPN) cholestasis (not mentioned here).

5. Hemolysis/liver immaturity less likely to give this degree of elevation.

In this baby, the most likely cause is sepsis-induced cholestasis, possibly aggravated by phenobarbitone therapy.

6 Days ago

T

TASHLIM ARIF

0

meningitis

6 Days ago

S

ShubhraDaniel Sarkar

3

In this baby , GGT is markedly elevated, but bilirubin and transaminases are not significantly abnormal.
The most likely causes are
1. Sepsis-associated cholestasis .

2. Phenobarbitone therapy (enzyme induction effect, phenobarbitone, which is well known to raise GGT by inducing hepatic microsomal enzymes ).
Lasix is only a symptomatic measure, not treating the cause. In a neonate with normal renal parameters and electrolytes, routine Lasix use is not justified unless there is fluid overload / pulmonary edema / congestive signs.Giving Lasix chronically could worsen electrolyte disturbances, cause volume contraction, and mask underlying pathology.

7 Days ago

A

Ako Shenl

0

gall bladder involvement

7 Days ago

Answer 1

This seems to be a case of late-onset Neonatal sepsis with CNS involvement.
Regular Furosemide is not recommended for any condition except in the acute stage of documented Acute Renal Failure. As such, Furosemide is a nephrotoxic drug. It is essential to calculate the 24-hour urine output accurately so as to document whether the baby really has oliguria or not. If there is oliguria, it is necessary to see the trend, if it is improving or static. Documented oliguria could be a sign of SIADH (Syndrome of Inappropriate ADH secretion), which is a known and not uncommon complication in neonatal meningitis. Usually, this is indicated by an unusually increasing body weight, edema, and hyponatremia. In most cases, it is self-limiting and resolves in 7 - 10 days if the etiology was not very severe.
Raised GGT usually indicates intrahepatic biliary obstruction. In this case, it is possibly due to sepsis and circulating toxins. I think it should be repeated once the sepsis is well under control. If the hepatic function is normal as assessed by coagulation profile, S. Albumin, hepatic enzymes, and biliary conjugation and excretory function, I think the GGT would normalize spontaneously.
A raised GGT in an otherwise normal child could be an indicator of Progressive Familial Intrahepatic Cholestasis (PFIC).

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