Shock liver otherwise known as ischemic hepatitis is defined as impairment throughout the liver caused by an inadequate blood or oxygen supply. Abnormal heart rhythms, dehydration, heart failure, infection, severe bleeding, blood clot in the main artery to the liver (after surgery or trauma), swelling of blood vessels leading to reduced blood flow (vasculitis), hypotension, respiratory failure, drugs, toxins, and hypoxia can lead to hepatic ischemia. The increase of hepatic enzymes and liver failure is a common characteristic of ischemic hepatitis observed in critically ill patients. At present, this condition is most commonly referred as “hypoxic hepatitis.”
What Are The Symptoms of Shock Liver?
Ischemic hepatitis is often affected in elderly men with mean reported ages between 64 and 70 years-old who suffer from medical co-morbidities with heart failure or chronic respiratory failure. Generally, the signs and symptoms of the underlying condition include
- Ankle edema,
- Hepatojugular reflux
- Shortness of breath as a result of cardiac insufficiency
- Right-upper quadrant abdominal pain
- Hepatomegaly (50% of patients)
- Elevated liver enzyme serum bilirubin >3 mg/dl (36% of patients)
- Sequelae of liver disease, including encephalopathy and hyperammonemia
- Sepsis or hypoxic injury to the brain
- Hypoglycemia and hyperglycemia reported in patients with hypoxic hepatitis.
- In untreated condition, severe fatigue, jaundice (rare), hepatic coma, and loss of function of the liver occur (liver failure).
This condition usually has enlarged liver and may be purplish in congestive heart failure or pale in hypovolemic-traumatic shock. The edges of the liver are rounded and because of the interstitial edema the liver weight is increased. The cut surface of the liver is grayish and pale in pure hypovolemic shock or reveals distended hepatic veins in congestive heart failure. Pale and dry areas of yellow color represent necrotic foci.
Patients always have rapid and short-term rises in serum aminotransferase levels (aspartate and alanine aminotransferase) as well as a dramatic rise in lactate dehydrogenase levels. In hypoxic hepatitis, the severe increase in lactate dehydrogenase can sometimes lead to liver injury as opposed to viral hepatitis. The liver enzymes characteristically present in the high level during the course of the disease and this peak level exists within 24 hours, but after 24 to 72 hours the enzyme levels drop to nearly half of their level and to a normal level usually happens within 1 to 2 weeks.
Reduced prothrombin activity, increases in serum creatinine (>2 mg/dL in 65% of patients), serum bilirubin (>3 mg/dL in 36% of patients), and elevations in the international normalized ratio (INR) can occur in patients characteristically. The international normalized ratio (INR) may increases to a greater level in hypoxic hepatitis i.e. more than 1.5, which supports the diagnosis of acute liver failure.
Many abnormal laboratory outcomes can be found in hypoxic hepatitis patients, but they are non-specific and not considered sufficiently reliable for diagnosis. Severe jaundice develops in approximately 2% of patients with shock resulting from major trauma and may appear within hours. In severely sick individuals progress of jaundice may reflect multiple organ-system failure and poor prognosis.
Ischemic hepatitis is completely different from other types of hepatitis. Most frequently it is referred as “hypoxic hepatitis” because of increase in serum aminotransferase levels. The level of serum aminotransferase is 20 times upper limit of normal is observed in the majority of cases of hypoxic hepatitis. In a recent meta-analysis of 1782 cases, Tapper et al identified the incidence of HH to be 2 in every 1000 patients for all levels of hospital care, but in ICUs alone the pooled incidence is higher, accounting for 2.5 out of every 100 patients.
In ischemic hepatitis, liver cells are damaged or die because the liver does not receive enough blood or oxygen. It often affects elderly men with mean reported ages between 64 and 70 years-old who suffer from medical co-morbidities with heart failure or chronic respiratory failure. Many abnormal laboratory outcomes can be found in hypoxic hepatitis patients, but they are non-specific and not considered sufficiently reliable for diagnosis.
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