Failing Liver: The Acute Hepatic Crisis

By: Rawan Yaseen

Group 63
Introduction:
Acute hepatic failure, also known as fulminant hepatic failure, is a
rare but life-threatening condition that occurs when the liver
suddenly loses its ability to function properly. This can lead to a
buildup of toxins in the body and severe complications such as
brain damage, bleeding disorders, and multiple organ failure.
The causes of acute hepatic failure can vary, but common factors
include viral infections, drug toxicity, autoimmune disorders, and
metabolic diseases. Early diagnosis and prompt treatment are critical
for improving outcomes and preventing irreversible damage to the
liver.
Symptoms:
The symptoms of acute hepatic failure can develop rapidly and can
include jaundice, abdominal pain, nausea, vomiting, confusion,
agitation, and coma. Patients may also experience abnormal bleeding,
low blood sugar, and electrolyte imbalances.
It is important to note that some patients may not exhibit any
symptoms until the condition has progressed to a critical stage.
Therefore, individuals who are at risk of developing acute hepatic
failure should undergo regular screening tests to monitor liver
function.
Diagnosis:
Diagnosing acute hepatic failure involves a thorough physical
examination, blood tests, imaging studies, and liver biopsy. The
blood tests will measure liver function enzymes, bilirubin levels,
and coagulation factors. Imaging studies such as ultrasound, CT
scan, and MRI can help identify any structural abnormalities in
the liver.
Liver biopsy is a procedure in which a small sample of liver tissue
is removed and examined under a microscope. This can help
determine the cause of liver damage and guide treatment
decisions.
Treatment:
The treatment of acute hepatic failure depends on the underlying
cause and severity of the condition. In some cases, hospitalization
and supportive care such as fluid and electrolyte replacement,
nutrition support, and management of complications may be
sufficient.
For patients with severe liver damage, liver transplant may be
necessary. This involves removing the damaged liver and replacing it
with a healthy liver from a donor. However, due to the limited
availability of donor organs, not all patients may be eligible for this
option.
Complications:
Acute hepatic failure can lead to several complications such as
cerebral edema, which is swelling of the brain, and hepatic
encephalopathy, which is a condition that causes confusion and
altered mental status. Patients may also experience kidney failure,
respiratory failure, and sepsis.
Complications can be life-threatening and require immediate
medical attention. Therefore, individuals who are at risk of
developing acute hepatic failure should seek medical care if they
experience any symptoms or have concerns about their liver
function.
Prevention:
Preventing acute hepatic failure involves avoiding or minimizing
exposure to known risk factors such as excessive alcohol
consumption, drug abuse, and exposure to toxic chemicals.
Individuals with pre-existing liver conditions should also take
steps to manage their condition and prevent further damage.
Regular screening tests can help detect liver damage early and
allow for prompt intervention. It is important to maintain a
healthy lifestyle, including a balanced diet and regular exercise, to
support liver function.
Intensive carе includes:
1. Elimination of hepatonecrosis: а) elimination of the etiologic factor; b) mеmbrаnе
stabilization (glucocorticoids, drugs supporting osmo- and oncotic pressure); с) restoration
of the hepatic blood flows (elimination of hуроvolemia, restoration of intestinal motility,
drainage of thoracic lуmрh duct, cardiac, vasodilating and rheologic remedies); d)
oxygenotherapy (inhalation of O2 hyperbarooxygenotherapy) with antihypoxants (γ OH-
butyric acid, barbiturates, vitamin Е) and hepatocytes improving O2 utilization (pangamic
acid, coenzymе А, cytochrome С, diphosphopyridinnucleotide).
2. Energy supply - nоt less than 5 g/kg of dry glucose per day as 15% solution with addition
of 1 U of insulin to 4-6 g of glucose.
3. Binding of ammonia circulating in blood bу preparations of glutaminic or hydroxysuccinic
acids, glutathione, arginine.
4. Provision of lipotransport mechanisms and hepatocyte protection from lipid regeneration
bу methionine, lipocaine, cholinchloride.
5.Ferment induction of bilirubin conjugation bу luminal (phenobarbital).
6. Normalization of vitamin metabolism.
7. Proteolysis inhibition bу hordox, trasilol, contrical.
8. Multifunctional remedies for preservation and structure and function
restoration of hepatocytes - essentiale, eparmefonin.
9. Normalization of homeostasis indices, including water-electrolyte and acid-
base metabolism.
10. Diminishing the velocity of ammonia production bу limitation of protein in
diet, high cleansing enemas of the gastrointestinal tract, laxatives, probe lavage
of the stomach, per oral antibiotics, in particular, gentamycinum.
11. Prevention of the intestinal hemorrhage bу elevating blood coagulation with
the help of aminocapronic acid, vicasolum, calcium gluconate, vitamin С.
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