Chapters:

Introduction0:00–0:32

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 right upper quadrant of the abdomen just below the diaphragm.

Pathophysiology0:32–2:51

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 byproduct of the breakdown of red blood cells regulates glucose metabolism through glycogenesis or 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 cooper 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 buildup 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 buildup of toxins in the blood such as ammonia, lactate and other substances normally cleared by the liver.
Lastly reduced cooper 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 kidneys ability to regulate fluid and electrolyte balance like sodium and potassium. If left untreated, acute liver failure can progress to systemic inflammatory response syndrome, multi organ dysfunction syndrome and death.

Clinical Manifestations2:51–5:50

All right, clinical manifestations are related to the decline in liver function. Initially, signs and symptoms can be nonspecific 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 BP 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 buildup 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. Lastly, a buildup of lactate in the blood which is an acidic byproduct of cellular metabolism can lead to acidosis manifesting as tachypnea, mental status changes and fatigue if left untreated seizures and hepatic coma can develop when caring for your critically ill patient with acute liver failure.

Nursing Considerations5:50–9:16

Your goals of care include providing supportive care, monitoring for and addressing complications and optimizing nutrition.
Begin by assessing your patient's airway breathing and circulation or ABC S and place them on a continuous monitor for any emergent life threating findings activate emergency protocols as needed.
Next. Support your patients, BP and fluid and electrolyte balance by administering the prescribed IV fluids and albumin as indicated if they don't respond adequately to fluid resuscitation, administer the prescribed vasopressor at the same time.
Be sure to routinely monitor your patient's labs such as creatinine and bun urine output and weight to evaluate their fluid status.
Once your patient's BP is normalized, administer the prescribed diuretics to address the acidic fluid. If your patient requires a paracentesis to remove the fluid work with the interdisciplinary team to prepare your patient for the procedure and be sure to monitor them closely afterwards following your facility's protocol, then to address elevated ammonia levels, administer the prescribed lactulose or antibiotics to destroy ammonia, producing bacteria in the intestines.
Lastly monitor your patient's arterial blood gasses as needed. Assess your patient for bleeding such as unusual bruising hematomas or bleeding from IV sites to prevent injury, pad the side rails of your patients bed and assist them with activities.
You can also take steps to limit venipunctures and other needle sticks, monitor your patient's coagulation studies closely and administer blood products as prescribed.
Also ensure you have ready access to Vitamin K fresh frozen plasma or platelets if active bleeding does occur. Also monitor your patient for signs and symptoms of infection, like fever, cough and sputum production and collect urine, blood and sputum for cultures.
As ordered, regularly, assess your patients pain level and administer the prescribed analgesics to promote comfort. Keep in mind since the liver metabolizes many of these medications, you should closely monitor for signs of toxicity.
If opioids are given watch closely for respiratory depression, in particular, you can also offer nonpharmacologic techniques to promote comfort like listening to music or guided meditation.
If your patient is able to eat and drink by mouth, offer small frequent nutritious snacks. Be sure to follow the prescribed diet.
If your patient is unable to tolerate oral intake, insert a nasogastric tube for enteral feedings and collaborate with the dietician to formulate a nutritional plan regardless of how your patient is taking in nutrition.
Be sure to check their blood glucose routinely and as needed if they develop signs or symptoms, suggestive of hypoglycemia.
Keep a close eye on your patient's bilirubin levels. And liver function test results to assess the effectiveness of treatment and to detect if any worsening of liver damage has occurred.
Finally, assist the healthcare team to address the underlying cause of your patient's liver failure. All right.

Review9:16–9:36

As a quick recap, acute liver failure is a condition characterized by damage to the liver that interferes with its ability to function as the nurse caring for a critically ill patient with acute liver failure.
Goals of care include providing supportive care, monitoring and addressing complications and optimizing nutrition.