The curious case of an H1N1 positive child.




This incident happened when I was posted at PICU for the first time. I got a call from one of my colleague to inform me that they were planning to shift a 4 years old child from ward to PICU as the child had deranged liver function. As a pleasant surprise, my colleague arrived with a well looking child who could walk and talk which was in contrast with my expectation that the child would be sick looking as her liver was apparently not working well. I was informed that the liver enzymes AST and ALT levels were in thousands (IU/ml) and they have sent all the other relevant investigation which included viral markers and PT/INR.


As a routine in PICU, I examined the child and made confirmed that she doesn’t need any emergency interventions. Her vitals were stable and she was indeed communicating well with her mother. Minutes later, Gastroenterologist came who was called for an emergency consultation for the same child. He, suspecting toxic hepatitis, advised a battery of tests. Once he left, I started to take a detailed history of the case.

She was a developmentally normal and immunized for age baby who had no significant history of any diseases. Her illness started 7 days back when he developed cough. Two days later, she developed fever which was intermittent low grade in nature. A day later, she started to have multiple episodes of abdominal pain with vomiting. While asking about any recent drug intake, mother told us that she had given the child Paracetamol syrup and Mephenamic acid syrup. We asked in detail about the dose of each medication and we found out that each medication was in higher dose but not at the toxic dose. Paracetamol can cause hepatic injury and Mephenamic acid can affect kidneys. There were no clinical signs suggestive of hepatic encephalopathy.

Keeping toxic injury in mind, we probed about having food from hotels or street vendors but we didn’t get any suggestive history. Leptospirosis is notorious to cause hepatitis therefore we asked leading question about any history of contact with water bodies but the mother denied. On clinical examination, we noticed crepitations on chest auscultation even though there was no respiratory distress. On abdomen examination, we found out that there is hepatomegaly without splenomegaly. There was no pallor, rash or icterus. At the end of the examination, our inference was that the condition that the child had involved two systems in the body, respiratory system and hepatobiliary system.

Couple of hours later, her investigation results came. Her serum creatinine was 1.5 mg/dl, INR was 1.4, serum urea was 72 mg/dl. AST and ALT were 7000 IU/ml and 3000 IU/ml respectively. Alkaline phosphatase was in the normal range, ruling out an obstructive cause in the hepatobiliary system. Serum bilirubin level was mildly raised (1.1). Analyzing the test reports, it was evident that child also had renal system involvement. Her urine output was at the normal range at that point of time. So, the disease involved three systems of the body.

We explained the situation to the parents and counseled them about the possible complications. We catheterized the patient to monitor the urine output as the child had AKI. Child was given one shot of vitamin K as INR was slightly elevated. Child was started on Cefotaxime and Crystalline Penicillin. Oseltamivir was added as there were multiple cases of viral pneumonia getting admitted at PICU during that month and our patient had signs suggestive of respiratory infection. Tablet Doxycycline was added a day later. Rifaximin and Ursodeoxycholic acid were added as hepato-protective measures. Child was maintaining normal glucose levels throughout the course of illness.

Hepatotrophic (HAV, HBV, HCV) and non-hepatotrophic viruses (EBV, CMV, HSV), Plasmodium, Dengue and Leptospira were the posiible infectious agents which were possible in the clinical scenario. Relevant investigations were sent to find if there was any presence of any of those agents and the entire tests were negative. Throat swab was sent for H1N1, Influenza A&B. We monitored liver function, renal function and blood counts daily and the trends were quite interesting. Liver enzymes were coming down but the creatinine was going up. Along with that, on day 2 of admission, child developed hematuria. To find out the cause, we sent urine culture and urine microscopy. There were plenty of RBCs in urine according to microscopy report but at the same time urine had elevated levels of myoglobin. Creatinine became 2.5 on day 4 of admission and child started to develop anemia. LDH was raised, but peripheral smear had no evidence of hemolysis. We sent a repeat LDH 2 days later revealed a decreasing trend.

Oral bicarbonate syrup administration started in view of urine myoglobin to alkalinize the urine. Her hemoglobin dipped to 5.6 g/dl from 10.1 g/dl in 6 days and she was given one unit of PRC. Autoimmune workup came positive for Anti-dsDNA (weakly positive) but ANA was negative which is actually more sensitive.
Surprisingly, H1N1 test came positive. The child’s respiratory complaints weren’t severe and she never required any respiratory support. Her renal function parameters started to improve after 5 days. Urine color became normal after 2 days. Child was shifted back to ward after around 10 days of stay. Parents were advised to repeat autoimmune work up again and bring the reports of the same.

Discussion
H1N1 infection usually doesn’t involve other systems in the initial stage. Here, what is interesting was, her primary complaint was gastrointestinal (abdominal pain and vomiting) and she then developed hematuria. Even though she had cough, it was never debilitating. H1N1 infection with rhabdomyolysis & AKI and H1N1 infection with altered liver function has been reported but in our case, the child had both. Nevertheless, child survived and she didn’t develop any complication or sequelae.

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