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Updated: Mar 24, 2026
Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
Published on: August 4, 2012
[Analysis of clinical characteristics of hypoxic hepatitis in children]
Huabo Cai1, Baoxing Huang, Zhongsheng Zhu
1Department of Gastroenterology, Shenzhen Children's Hospital, Shenzhen 518038, China.
Insights
Hypoxic hepatitis (HH) in children is primarily caused by severe conditions like heart failure and shock. Laboratory tests show a significant rise in liver enzymes, which normalize once the underlying illness is treated.
Area of Science:
- Pediatric Hepatology
- Critical Care Medicine
- Pediatric Gastroenterology
Background:
- Hypoxic hepatitis (HH) is a form of liver injury resulting from insufficient oxygen supply to the liver.
- Understanding the causes and clinical presentation of HH in children is crucial for timely diagnosis and management.
Purpose of the Study:
- To investigate the etiological factors and clinical characteristics of hypoxic hepatitis in a pediatric population.
- To identify the key laboratory findings associated with HH in children.
Main Methods:
- Retrospective review of clinical data from 7 pediatric patients diagnosed with HH.
- Analysis of patient demographics, primary diagnoses, laboratory results, and outcomes.
Main Results:
- HH occurred in 0.32% of pediatric intensive care unit patients, with primary causes including respiratory failure and cardiac shock from severe hand-foot-and-mouth disease and fulminant myocarditis.
- All patients exhibited significantly elevated alanine aminotransferase (ALT) levels (≥20 times the upper limit of normal), with rapid normalization after treatment of the primary condition.
- No viral hepatitis markers (Hepatitis B, C, Epstein-Barr, Cytomegalovirus) were detected.
Conclusions:
- Severe conditions such as heart failure, hypoxemia, and shock are the primary drivers of HH in children.
- A marked elevation in ALT, aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) is characteristic of HH and typically resolves with treatment of the underlying disease.
- Reversible changes in blood urea nitrogen (BUN) or creatine kinase (CK) may also be observed in some cases.
Objective:
To explore the etiology and clinical characteristics of hypoxic hepatitis (HH) in children.
Method:
Clinical data of 7 patients with HH in Shenzhen Children's Hospital from January 2011 to March 2014 were retrospectively reviewed.
Result:
Seven cases diagnosed as HH, age from 4 months to 11 years, were admitted to pediatric intensive care unit (PICU), and accounted for 0.32% of patients in PICU during the same period. The primary causes of HH were respiratory failure and cardiac shock caused by severe hand-foot-and-mouth disease, fulminant myocarditis, infant muggy syndrome . Serologic tests for hepatitis B virus, hepatitis C virus, as well as serum antibody and DNA for Epstein-Barr virus and cytomegalovirus were all negative. There was an increase of alanine aminotransferase (ALT) (≥20 time supper limit of normal (ULN), the highest ALT was more than 130 times ULN in all the patients, which was decreased to 2 times ULN from peak within 10 days. There was a significant relationship between ALT and aspartate aminotransferase(AST)in 3 cases(r=1.000, 1.000, and 0.833, respectively, P<0.05), ALT and lactate dehydrogenase (LDH)in 2 cases(r=1.000 and 0.886, respectively, P<0.05), ALT and blood urea nitrogen(BUN)in 1 case(r=1.000, P<0.05), and ALT and creatine kinase(CK)in 1 case(r=0.964, P<0.05). The ALT, AST and LDH returned to normal soon after the primary diseases were controlled.
Conclusion:
Severe heart failure, hypoxemia, shock, etc. are the leading primary diseases causing HH. The sharp increase in ALT, AST and LDH is the typical laboratory manifestion in HH after the onset, which may decline to normal shortly after the treatment, sometimes complicated with reversible change in BUN or CK.
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