liver cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic liver injury leads to hepatocyte death, triggering inflammation and activation of hepatic stellate cells. These cells transform into myofibroblasts, producing excess collagen and extracellular matrix, resulting in fibrosis and nodule formation.

• Secondary mechanism: The distorted architecture increases intrahepatic vascular resistance, causing portal hypertension. This disrupts normal blood flow through the liver and contributes to the development of varices and ascites.

• Key complication: Portal hypertension can lead to life-threatening complications such as variceal bleeding and hepatorenal syndrome, emphasizing the need for early detection and management in clinical settings.

Patient Profile

Demographics:

52-year-old male, construction worker

History:

• Key past medical history: Chronic hepatitis C infection, alcohol use disorder (20-year history, currently abstinent for 6 months), hypertension

• Current medications: Enalapril, propranolol, lactulose, spironolactone

• Allergies: No known drug allergies

Current Presentation:

• Chief complaint: Increased abdominal girth and discomfort

• Key symptoms: Fatigue, jaundice, peripheral edema, occasional confusion

• Vital signs: Blood pressure 138/88 mmHg, heart rate 96 bpm, respiratory rate 18 breaths per minute, temperature 37.2°C, oxygen saturation 94% on room air

Section 1

New Diagnostic Results:

Following the initial assessment, the healthcare team decided to perform a series of diagnostic tests to further evaluate the extent of the patient's liver cirrhosis and related complications. The abdominal ultrasound revealed significant ascites, and Doppler studies indicated increased portal vein pressures consistent with portal hypertension. Laboratory tests showed worsening liver function, with elevated bilirubin levels at 4.5 mg/dL, indicating increased jaundice, and an international normalized ratio (INR) of 1.8, suggesting impaired coagulation. The albumin level was low at 2.8 g/dL, which correlates with the patient's peripheral edema and ascites. A complete blood count revealed thrombocytopenia, with platelets at 85,000/µL, a common finding in cirrhotic patients due to splenic sequestration.

An upper endoscopy was performed to assess for variceal bleeding risk. The procedure identified the presence of large esophageal varices, which are a significant concern in this patient with a history of portal hypertension. Given these findings, the healthcare team initiated a plan to manage the varices proactively, including the potential use of non-selective beta-blockers, such as propranolol, which the patient was already taking, to reduce portal pressures.

These diagnostic results highlight the complexity of the patient's condition and underscore the need for comprehensive management to prevent further complications. The team will monitor the patient closely for signs of variceal bleeding or hepatic encephalopathy, given his occasional confusion, and may consider further interventions such as paracentesis for symptomatic relief of ascites or adjustments in medication to optimize liver function. This step in the patient's journey emphasizes the interconnected nature of cirrhosis complications and the critical role of early detection and intervention in improving outcomes.

Section 2

Change in Patient Status:

Several days after the initial interventions, the patient's condition began to evolve, warranting a reassessment of his status. During a routine evaluation, the patient was noted to have increased confusion and disorientation, struggling with simple tasks and exhibiting asterixis, a flapping tremor indicative of hepatic encephalopathy. Vital signs were stable with a blood pressure of 110/70 mmHg, heart rate of 82 bpm, respiratory rate of 18 breaths per minute, and oxygen saturation of 97% on room air. However, the patient's mental status changes prompted an immediate review of his medication regimen and ammonia levels, which were found to be elevated at 80 µmol/L, reinforcing the suspicion of hepatic encephalopathy.

In response to these findings, the healthcare team initiated treatment with lactulose to reduce ammonia levels and prevent further neurological deterioration. The patient was also educated on the importance of adhering to a low-protein diet to decrease ammonia production. Concurrently, a repeat abdominal ultrasound was performed, which showed an increase in ascites despite the current treatment plan. Given the patient's increasing abdominal discomfort and respiratory distress from the fluid accumulation, a therapeutic paracentesis was conducted, yielding 2 liters of straw-colored fluid, which provided immediate symptomatic relief.

These developments underscore the intricate interplay between liver dysfunction and its systemic effects, demanding careful adjustment of therapeutic strategies. The patient's response to lactulose and paracentesis will be closely monitored, with attention to potential electrolyte imbalances or infection risks associated with ascites. The team plans for ongoing surveillance of the patient's cognitive function and fluid status, while also evaluating the need for additional interventions, such as the possible initiation of rifaximin to further manage hepatic encephalopathy, setting the stage for the next phase of his treatment journey.

Section 3

Response to Interventions:

Following the initiation of lactulose and the therapeutic paracentesis, the healthcare team closely monitored the patient for changes in his clinical status. Over the next 48 hours, there was a noticeable improvement in the patient's mental alertness and orientation. The asterixis diminished significantly, suggesting a positive response to the lactulose therapy aimed at reducing ammonia levels. However, blood work revealed mild hyponatremia, with sodium levels dropping to 130 mmol/L, likely due to the lactulose and the removal of ascitic fluid. The team decided to adjust the lactulose dosage carefully and initiate a fluid management plan to address the electrolyte imbalance, while still achieving the goal of reducing ammonia production.

Despite these improvements in neurological status, the patient began to exhibit signs of worsening jaundice, with total bilirubin levels increasing to 4.5 mg/dL. This rise in bilirubin indicated a progression in liver dysfunction, prompting the team to reassess the patient's overall hepatic function. Further diagnostic tests, including liver function tests and a repeat ultrasound, were ordered to evaluate the liver's structural changes and check for any possible complications such as portal vein thrombosis or further liver deterioration.

The team remains vigilant for signs of spontaneous bacterial peritonitis (SBP), a serious complication in patients with ascites, by regularly monitoring the patient's temperature and obtaining ascitic fluid cultures during the paracentesis. The patient was started on a prophylactic antibiotic regimen to prevent SBP, due to his high risk. These developments highlight the complexity of managing liver cirrhosis, requiring a dynamic and multifaceted approach to treatment, and set the stage for potential adjustments in the patient's therapeutic regimen to address the evolving clinical picture. The next steps involve continuous monitoring and collaboration among the multidisciplinary team to optimize the patient's liver function and overall health status.

Section 4

New Complications:

In the following days, the patient's clinical course took an unexpected turn as he developed a low-grade fever and abdominal tenderness, raising concerns for spontaneous bacterial peritonitis (SBP) despite the prophylactic antibiotic regimen. A repeat paracentesis was promptly performed, and analysis of the ascitic fluid revealed an elevated white blood cell count with a predominance of neutrophils, confirming the diagnosis of SBP. The patient was immediately started on a targeted antibiotic therapy, and his fluid intake was adjusted to maintain hemodynamic stability and address the ongoing risk of hyponatremia.

Concurrently, the patient's renal function began to deteriorate, evidenced by an increase in serum creatinine to 1.8 mg/dL from a baseline of 1.1 mg/dL, indicating the possible onset of hepatorenal syndrome (HRS). The healthcare team initiated albumin infusions and continued to monitor renal parameters closely while considering additional pharmacological interventions to support renal perfusion. This development necessitated a reevaluation of the patient's medication regimen, particularly the use of diuretics, which were temporarily held to prevent further renal compromise.

These complications underscore the delicate balance required in managing advanced liver disease, where interventions to address one issue may inadvertently exacerbate another. The team is now focused on stabilizing the patient's condition through vigilant monitoring and timely adjustments to the treatment plan, aiming to mitigate the impact of these complications on the patient's overall prognosis. The next steps involve reassessing the patient's nutritional status and exploring potential liver transplantation options, given the progression of his liver dysfunction and associated complications.

Section 5

As the healthcare team continued to monitor the patient, they observed a notable change in his status. The patient's mental status began to fluctuate, with episodes of confusion and disorientation, suggesting the development of hepatic encephalopathy. His ammonia levels were found to be elevated at 86 μmol/L, significantly above the normal range, correlating with his neurological symptoms. The team promptly initiated lactulose therapy to reduce ammonia absorption from the gut, adjusting the dosage to achieve two to three soft stools per day, and considered adding rifaximin for additional ammonia-lowering effect.

Simultaneously, a new diagnostic ultrasound was performed to assess the patient's abdominal vasculature and liver anatomy due to the ongoing concern for portal hypertension. The ultrasound revealed a further increase in portal vein diameter and signs of splenomegaly, indicating worsening vascular congestion. Esophageal varices were suspected, prompting an urgent endoscopic evaluation to assess the risk of variceal bleeding, a potentially life-threatening complication. Beta-blocker therapy was initiated to reduce portal pressure and prevent variceal rupture.

These developments highlight the interconnected challenges in managing advanced liver disease, where complications such as hepatic encephalopathy and portal hypertension require careful consideration of therapeutic priorities. The team is now focused on optimizing the patient's neurological status while preventing further vascular complications, ensuring a comprehensive approach to his complex medical needs. The possibility of liver transplantation remains a critical consideration as the patient's condition evolves, underscoring the urgency of multidisciplinary collaboration in his ongoing care.