Hepatic Failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Hepatic failure primarily occurs due to extensive liver damage that inhibits the organ’s ability to perform its vital functions. This damage can be a result of various health conditions like hepatitis, cirrhosis, or long-term alcohol abuse, leading to loss of liver cells (hepatocytes) and impaired detoxification.

• Secondary mechanism: The liver plays a critical role in the body's metabolic, synthetic and detoxification processes. In hepatic failure, these functions are compromised. Decreased synthesis of clotting factors and albumin can lead to coagulation abnormalities and fluid imbalances, respectively.

• Key complication: One of the severe complications of hepatic failure is hepatic encephalopathy, a neuropsychiatric syndrome. It results from the liver's inability to detoxify ammonia, leading to its accumulation in the blood, which causes cerebral edema and neurological deterioration.

Patient Profile

Demographics:

55-year-old male, long-time heavy machinery operator.

History:

• Key past medical history: Chronic alcoholism, diagnosed with Non-Alcoholic Fatty Liver Disease (NAFLD) 5 years ago.

• Current medications: Vitamin E, Ursodiol.

• Allergies: No known allergies.

Current Presentation:

• Chief complaint: Persistent fatigue, yellowing of skin and eyes.

• Key symptoms: He reports nausea, loss of appetite, and abdominal swelling. He has also noticed dark urine and light-colored stools. He complains of itchy skin and difficulty in concentration.

• Vital signs: Blood pressure 130/85 mmHg, heart rate 90 bpm, respiratory rate 16 breaths per minute, temperature 37.2°C (98.9°F), oxygen saturation 95%.

Section 1

New Diagnostic Results:

The patient's blood sample was sent to the lab to evaluate liver function and rule out any other possible conditions. The findings from the laboratory tests were as follows: AST (Aspartate Aminotransferase) 120 U/L (normal range 10-40 U/L), ALT (Alanine Aminotransferase) 150 U/L (normal range 7-56 U/L), ALP (Alkaline Phosphatase) 200 U/L (normal range 45-115 U/L), total bilirubin 3.5 mg/dL (normal range 0.1-1.2 mg/dL), and albumin 2.5 g/dL (normal range 3.5-5.5 g/dL). The elevated AST, ALT, ALP and bilirubin levels signify liver damage and impaired liver function. The low albumin level indicates malnutrition and reduced synthetic function of the liver.

A diagnostic paracentesis was also performed due to the patient's abdominal swelling. The ascitic fluid analysis revealed a Serum-Ascites Albumin Gradient (SAAG) of 2.2 g/dL, suggesting the presence of portal hypertension. Additionally, the patient's prothrombin time was prolonged to 16 seconds (normal range 11-13.5 seconds), indicating a potential coagulation abnormality. These findings, combined with his symptoms and history, suggest the patient is progressing towards advanced hepatic failure. This shift in his status necessitates a change in his treatment plan and requires careful monitoring to prevent further complications.

Section 2

A few days later, the patient's condition continued to deteriorate. He started showing signs of encephalopathy, including confusion, slurred speech, and hand tremors. These symptoms suggest the buildup of toxins in the bloodstream due to liver dysfunction. Additionally, his vitals showed a slightly elevated heart rate at 98 bpm (normal range 60-100 bpm) and a low blood pressure of 100/60 mmHg. His temperature was normal at 36.9°C, but his respiratory rate was slightly increased at 22 breaths per minute (normal range 12-20 breaths per minute).

Further diagnostic results showed worsening of his liver function. His AST and ALT levels rose to 200 U/L and 250 U/L respectively, indicating ongoing liver damage. His total bilirubin increased to 5.0 mg/dL, while his albumin fell to 2.0 g/dL, which are also signs of progressive liver failure. His prothrombin time was further prolonged to 18 seconds, heightening concerns about a possible bleeding disorder due to impaired synthesis of clotting factors by the liver. These developments call for urgent interventions to manage the patient's hepatic encephalopathy and coagulopathy, while considering the possible need for a liver transplant.

Section 3

In the subsequent days, the patient's condition took a more critical turn. His symptoms of encephalopathy worsened with increased disorientation, restlessness, and a noticeable development of asterixis, a motor dysfunction characterized by a flapping tremor of the hands. These clinical manifestations suggest the possibility of impending hepatic coma. Additionally, his vitals showed a significant increase in heart rate to 110 bpm, and a further drop in blood pressure to 90/55 mmHg. His respiratory rate also escalated to 25 breaths per minute, indicating possible respiratory distress.

New laboratory results indicated a further decline in liver function. His AST and ALT levels continued to rise to 300 U/L and 350 U/L respectively, suggesting ongoing hepatic cellular damage. His total bilirubin surged to 8.0 mg/dL and his albumin level dwindled to 1.5 g/dL, both indicative of advancing liver failure. His prothrombin time was now at a concerning 25 seconds, raising the risk of spontaneous bleeding. The lab results, combined with his deteriorating clinical state, make it clear that the patient's hepatic failure is advancing rapidly, and that immediate and effective intervention is critical. This may involve treating the underlying cause, managing complications, and considering more aggressive options such as liver transplantation.

Section 4

Following the worsening of the patient's condition, the medical team performed an urgent endoscopic examination to investigate the possible cause of the hepatic failure. The procedure revealed esophageal varices, a complication of liver disease characterized by swollen veins in the esophagus, which presents a risk of rupture and potentially life-threatening bleeding. The varices were graded as grade III, indicating a high risk for hemorrhage.

The patient's worsening symptoms of encephalopathy, coupled with the discovery of esophageal varices, necessitated a change in the treatment plan. The team decided to initiate prophylactic treatment with nonselective beta blockers to reduce portal pressure and the risk of variceal bleeding. Lactulose and rifaximin were also given to reduce the production and absorption of ammonia in the gut, aiming to manage the worsening hepatic encephalopathy. Despite these interventions, the patient's condition remained precarious. His Glasgow Coma Scale (GCS) dropped to 9, and he developed melena, a sign of upper gastrointestinal bleeding, likely related to the esophageal varices.

With the patient's rapidly deteriorating condition and the high risk of variceal hemorrhage coupled with hepatic encephalopathy, the team recognized the need for urgent liver transplantation. However, the patient's eligibility for transplantation would need to be determined, taking into account his overall health status, the severity of his liver disease, and the potential benefits and risks of the procedure. This posed a challenging decision for the team and the patient's family, highlighting the complexity and gravity of managing advanced hepatic failure.

Section 5

The patient's condition further deteriorated over the next 24 hours, marked by a significant decrease in his urine output to less than 0.5 ml/kg/hour and an increase in his serum creatinine from 1.2 mg/dL to 2.1 mg/dL. Blood tests also revealed a marked increase in his international normalized ratio (INR) to 1.8, indicating a significant impairment in his liver's ability to synthesize clotting factors. This development suggested the onset of hepatorenal syndrome, a serious complication of liver disease characterized by rapid deterioration of kidney function.

In response to these alarming signs, the team decided to start the patient on terlipressin and albumin, aiming to improve renal function and decrease portal pressure. Despite these interventions, the patient's condition remained unstable. His blood pressure dropped to 90/60 mmHg and his heart rate increased to 110 beats per minute, indicating a state of shock likely due to variceal bleeding. The team decided to perform an emergency endoscopic variceal ligation, a procedure aimed at stopping the bleeding from the esophageal varices. This critical turn of events underscored the urgency of the patient's need for a liver transplant, while also highlighting the serious challenges posed by his rapidly deteriorating condition.