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Case Reports
. 2017 Oct 28;23(40):7337-7342.
doi: 10.3748/wjg.v23.i40.7337.

Rescue case of low birth weight infant with acute hepatic failure

Affiliations
Case Reports

Rescue case of low birth weight infant with acute hepatic failure

Noriki Okada et al. World J Gastroenterol. .

Abstract

We report a case involving a rescued low birth weight infant (LBWI) with acute liver failure.

Case: The patient was 1594 g and 323/7 gestational wk at birth. At the age of 11 d, she developed acute liver failure due to gestational alloimmune liver disease. Exchange transfusion and high-dose gamma globulin therapy were initiated, and body weight increased with enteral nutrition. Exchange transfusion was performed a total of 33 times prior to living donor liver transplantation (LDLT). Her liver dysfunction could not be treated by medications alone. At 55 d old and a body weight of 2946 g, she underwent LDLT using an S2 monosegment graft from her mother. Three years have passed with no reports of intellectual disability or liver dysfunction. LBWIs with acute liver failure may be rescued by LDLT after body weight has increased to over 2500 g.

Keywords: Acute liver failure; Liver transplantation; Low birth weight infant; Monosegment graft; Transplantable body weight.

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Conflict of interest statement

Conflict-of-interest statement: The authors have no competing interests to disclose.

Figures

Figure 1
Figure 1
The preoperative treatment and changes in body weight and total bilirubin. The patient was able to gain weight due to the use of internal medication and enteral nutrition.
Figure 2
Figure 2
Images. A: The S2 monosegment graft (107 g) on the back table; B: An image obtained after reperfusion, the graft was too large to close the abdominal fascia; C: The abdominal fascia could not be closed at the time of living donor liver transplantation (LDLT), excess water was removed by continuous hemodiafiltration after LDLT; D: Secondary skin closure was performed on postoperative day 5; E: The resected liver was 78 g; F: Hematoxylin and eosin staining revealed a marked lack of hepatocytes and the presence of multinucleated hepatocytes; G: Azan staining revealed widespread fibrosis around Glisson’s sheath and the parenchymal area (F3-4).

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