Critical care - Acute liver failure: Nursing

Acute liver, or hepatic, failure is a life-threatening condition characterized by severe damage to the liver that interferes with its ability to function. Causes include infections, like viral hepatitis; toxicity from medications, such as acetaminophen, or from substances like ethanol; hypoperfusion, like with portal vein thrombosis; and metabolic disorders such as Wilson disease. As the nurse, you’ll provide patient-centered care for critically ill patients with acute liver failure.

Now, the liver is located in the upper right quadrant of the abdomen, just below the diaphragm. It performs numerous essential functions including supporting digestion through bile formation and secretion; and production of proteins such as clotting factors necessary for hemostasis, immunoglobulins that are needed to fight infection, and albumin, a protein essential to maintaining intravascular oncotic pressure.

The liver conjugates bilirubin, a by-product of the breakdown of RBCs; regulates glucose metabolism through glycogenesis, or the storing glucose in the form of glycogen; glycogenolysis, or the breaking down of glycogen into glucose; and gluconeogenesis, or the production of glucose from non-carbohydrate sources. It also plays a crucial role in detoxification of medications, hormones, and other substances, and clearing bacteria from the bloodstream through phagocytic cells called Kupffer cells.

In acute liver failure, the liver cells, called hepatocytes, are injured and begin to die. This results in the release of inflammatory mediators, loss of hepatocyte function, and an impaired ability to perform essential functions.

Decreased hepatic bile production and subsequent reduction in bile flow, a condition called cholestasis, leads to a build-up of bile acids in the blood; and impaired glucose regulation results in hypoglycemia. Other problems include impaired hemostasis from lack of clotting factors; and hypoalbuminemia, or decreased albumin in the blood.

On top of that, decreased conjugation of bilirubin leads to hyperbilirubinemia; and loss of the liver’s detoxifying function results in a build-up of toxins in the blood, such as ammonia, lactate, and other substances normally cleared by the liver.

Lastly, reduced Kuffer cell activity increases the risk of infection. In addition, the release of inflammatory mediators triggers systemic vasodilation and impaired renal blood flow. This affects the kidney's ability to regulate fluid and electrolyte balance, like sodium and potassium. If left untreated, acute liver failure can progress to systemic inflammatory response syndrome, multiorgan dysfunction syndrome, and death.

Alright, clinical manifestations are related to the decline in liver function. Initially, signs and symptoms can be non-specific such as right upper quadrant pain, weakness, fatigue, abdominal discomfort, nausea, and vomiting. Elevated serum liver enzymes, like aspartate aminotransferase, or AST; alanine aminotransferase, or ALT; and alkaline phosphatase, or ALP, may also be present. As widespread destruction of hepatocytes occurs, specific and systemic signs and symptoms appear.

As glucose regulation is disrupted, hypoglycemia may develop, along with tremors, sweating, and dizziness. Hyperbilirubinemia can be noted as increased serum bilirubin levels, and jaundice, which is a yellowing of the skin and mucous membranes. Cholestasis can also cause jaundice, along with dark urine and light-colored stools, as well as pruritus, when bile acids leak into the blood.

Impaired hemostasis can manifest as easy bruising and bleeding and is reflected in laboratory studies such as a prolonged prothrombin time, or PT, and increased international normalized ratio, or INR. Hypoalbuminemia and decreased intravascular oncotic pressure promote the leakage of fluid from the capillaries into the interstitial space, causing edema, decreased circulating volume, and hypotension. In addition, the low systemic vascular resistance decreases blood pressure even more.

If the damaged liver becomes fibrotic, portal hypertension can occur, meaning there’s abnormally high pressure in the portal venous system, which is a network of vessels that drain blood from the abdomen into the liver.

As pressure builds and blood backs up in the portal system, hydrostatic pressure increases; however, the decreasing capillary oncotic pressure can’t overcome this increased pressure, so the fluid in blood vessels is pushed into the peritoneal cavity, causing a condition called ascites. Ascites presents as a large, round, protruding abdomen that can also be accompanied by dyspnea, if it’s severe enough to displace the diaphragm up against the lungs.

There are also other problems caused by a build-up of toxins. For example, serum levels of ammonia will increase, which can then cross the blood brain barrier and cause hepatic encephalopathy, a condition that typically presents with neurologic symptoms like lethargy, subtle personality changes, memory loss, irritability, and confusion, along with a tremor called asterixis. Hepatic encephalopathy may also be accompanied by cerebral edema.