الفهرس | Only 14 pages are availabe for public view |
Abstract Acute liver failure is a complex, uncommon illness which can rapidly progress to multisystem organ failure and death. It is characterized by acute hepatocellular injury or death, leading to rapid loss of hepatocellular function resulting in multisystem involvement and eventually, failure. It can be defined as biochemical evidence of acute liver injury in a child with unknown evidence of chronic liver disease along with INR > 1.5, not corrected with vitamin K supplementation, with encephalopathy or INR > 2.0, not corrected with vitamin K supplementation, without encephalopathy. Hepatic encephalopathy is a progressive but potentially reversible neuropsychiatric syndrome that occurs as a complication of liver failure. The clinical features of HE can range from subtle cognitive or motor deficits to irritability to overt cerebral edema leading to coma. Pathogenesis of hepatic encephalopathy is not completely understood. Hyperammonemia, increased cerebral blood flow, and augmented inflammatory response are pivotal in causing the increased ICP. Intracranial hypertension secondary to CE is one of the complications and causes of mortality in patients with ALF. Invasive monitoring (intracranial bolts) is the gold standard method for measurement of ICP, but it is associated with complications, especially in ALF because of inherent coagulation abnormalities. Computed tomography scan and MRI of head have been used also as non‐invasive tools for the detection of ICP but shifting of critically sick patients to radiology suites is often difficult, time-consuming, costly and usually require patient transportation. The changes of ONSD have been used to assess changes of the ICP for 20 years in adults. Thus, ultrasound assessments of ONSD could be a better option because of the low cost and rapid bedside operation without the need for radiation exposure, especially for cases that are unstable and require real-time monitoring of ICP in the intensive care unit. Study population: This prospective observational study was conducted on a total of 38 children with ALF (ALF group) admitted to the ICU in the Pediatric Hepatology Department, NLI, Menoufia University recruited from 2021-2023. A second group of 38 apparently healthy children were enrolled as a control group. All diseased children recruited consecutively, according to fulfilment of the inclusion and exclusion criteria. Inclusion criteria: Patient age (infants with closed anterior fontanel) 1.5- 18 years For ALF: - Biochemical and/or clinical evidence of severe liver dysfunction: hepatic-based coagulopathy, with a prothrombin time (PT) ≥20s or international normalized ratio (INR) ≥2.0, that is not corrected by parenteral vitamin K and/or hepatic encephalopathy (must be present if the PT is 15.0–19.9s or INR 1.5–1.9, but not if PT ≥20s or INR≥2.0). Exclusion criteria: Patients with history of ocular trauma Vitreous haemorrhage. Central nervous system infection like meningitis. Hydrocephalus. Previous neurosurgery including ventriculoperitoneal shunt. |