|Year : 2017 | Volume
| Issue : 6 | Page : 609-610
Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children
Shefali Parikh, Ira Shah
Department of Pediatric GI and Hepatology, B. J. Wadia Hospital for Children, Mumbai, Maharashtra, India
|Date of Web Publication||17-Jan-2018|
Dr. Ira Shah
1/B Saguna, 271/B St. Francis Road, Vile Parle (W), Mumbai - 400 056, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Parikh S, Shah I. Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children. Med J DY Patil Univ 2017;10:609-10
|How to cite this URL:|
Parikh S, Shah I. Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children. Med J DY Patil Univ [serial online] 2017 [cited 2020 Sep 19];10:609-10. Available from: http://www.mjdrdypu.org/text.asp?2017/10/6/609/223355
We would like to thank the reader for the insightful comments in response to our article “Uncommon associations of Hepatitis A in children: Acute respiratory distress syndrome and erosive gastritis.”
The author has raised a number of relevant points. The second case describes a 5-year-old boy who presented with sequential symptoms of fever, abdominal pain, vomiting, puffiness of the face, and breathlessness. This young boy first presented at another center where he was treated for 2 days including management with intravenous antibiotics and fresh frozen plasma (FFP) before transfer to our tertiary center. Prothrombin time before the FFP was 36 s with international normalized ratio of 3.1. His serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) at first presentation, before transfer, were 1120 IU/L and 1080 IU/L, respectively. Baseline investigations at our center included an albumin level of 2.8 g/dL and bilirubin level of 1.8 mg/dL. These clinical and biochemical findings are consistent with a presentation of acute liver injury. Interestingly, his liver enzyme levels significantly dropped to SGOT 83 IU/L and SGPT 29 IU/L in the next 48–72 h. We suspect that this can be explained by development of acute liver failure and significant hepatic necrosis, despite the absence of objective hepatic encephalopathy which can often be very difficult to assess in children.
The clinical signs of edema, ascites, and pleural effusion are known complications of acute liver injury., Pathophysiologically, the acute systemic inflammatory response and hypoalbuminemia would both contribute to these clinical manifestations. Nevertheless, acute respiratory distress syndrome (ARDS) remains a diagnosis of exclusion, and we agree that cardiogenic pulmonary edema is an important differential. However, echocardiography at the time of presentation showed ejection fraction of 52% with mild diastolic dysfunction which is not consistent with acute biventricular failure or acute myocarditis.
In addition, symptoms and signs of infectious febrile diseases in children can often be nonspecific. Clinical clues such as a delayed presentation of breathlessness and absence of early upper and lower respiratory tract symptoms make atypical pneumonia less likely though chest X-ray findings of bilateral ground-glass changes cannot differentiate ARDS from atypical pneumonia. Similarly, the absence of eschar, rash, tender lymphadenopathy, and a negative Weil-Felix test make rickettsial disease unlikely.
Serum investigations included a positive anti-HAV IgM. HIV ELISA, hepatitis B surface antigen, hepatitis C ELISA, Dengue IgM, Leptospira IgM/IgG, Weil-Felix test, and Rapid malaria tests were all negative. Blood cultures were negative. We were unable to do tests for cytomegalovirus and Epstein–Barr virus in our patient.
Given the positive serology with evidence of early abdominal symptoms, coagulopathy, mildly raised bilirubin, and raised hepatic enzymes at first presentation - a diagnosis of acute liver failure secondary to hepatitis A infection, complicated by ARDS, seems most consistent with all clinical evidence.
We welcome and agree with the author comments on the importance of a drug history in a setting of suspected gastritis as a complication of an acute infection. Though no such offending medications were identified in our case, this is indeed a very relevant clinical point.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Parikh S, Shah I, Bhatnagar S. Uncommon associations of hepatitis A in children: Acute respiratory distress syndrome and erosive gastritis. Medical J Dr D Y Patil Univ 2017;10:284-6.
Pandit A, Mathew LG, Bavdekar A, Mehta S, Ramakrishnan G, Datta S, et al.
Hepatotropic viruses as etiological agents of acute liver failure and related-outcomes among children in India: A retrospective hospital-based study. BMC Res Notes 2015;8:381.
Squires RH Jr., Shneider BL, Bucuvalas J, Alonso E, Sokol RJ, Narkewicz MR, et al.
Acute liver failure in children: The first 348 patients in the pediatric acute liver failure study group. J Pediatr 2006;148:652-8.
Gugig R, Rosenthal P. Fulminant hepatic failure in children. Therapy 2008;5:451-63.
Kumar Bhat N, Dhar M, Mittal G, Shirazi N, Rawat A, Prakash Kalra B, et al.
Scrub typhus in children at a tertiary hospital in North India: Clinical profile and complications. Iran J Pediatr 2014;24:387-92.