الفهرس 
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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.