cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic liver injury from factors like alcohol or hepatitis leads to persistent inflammation, causing hepatocyte death and regeneration, which disrupts normal liver architecture and forms fibrous scar tissue.

• Secondary mechanism: The buildup of scar tissue impairs blood flow through the liver, increasing pressure in the portal vein (portal hypertension), which can cause varices and ascites.

• Key complication: Impaired liver function due to extensive fibrosis results in decreased synthesis of essential proteins and detoxification processes, leading to complications such as coagulopathy and hepatic encephalopathy.

Patient Profile

Demographics:

58-year-old male, retired construction worker

History:

• Key past medical history: Chronic hepatitis C infection, alcohol use disorder (20 years, ceased 1 year ago), hypertension

• Current medications: Lisinopril, spironolactone, propranolol, lactulose

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing abdominal distension and discomfort

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

• Vital signs: Blood pressure 100/60 mmHg, heart rate 96 bpm, respiratory rate 18 breaths per minute, temperature 37.3°C, oxygen saturation 94% on room air

Section 1

As the healthcare team continues to monitor the patient, they observe a change in his status. The patient develops increased confusion, becoming disoriented to time and place. His family reports that he is increasingly forgetful and has difficulty maintaining conversations. Upon examination, the nurse notes asterixis, a characteristic flapping tremor of the hands, indicating worsening hepatic encephalopathy. The patient's vital signs show a blood pressure of 94/58 mmHg and heart rate of 102 bpm, suggesting hemodynamic instability likely due to worsening portal hypertension and possible hypovolemia from third-spacing of fluids.

Concurrent laboratory results reveal elevated ammonia levels at 112 µmol/L (normal range: 11-32 µmol/L), confirming the clinical suspicion of hepatic encephalopathy. Additionally, there is a decrease in serum albumin to 2.5 g/dL (normal range: 3.5-5.0 g/dL), which correlates with his worsening peripheral edema and ascites. This hypoalbuminemia further complicates his fluid balance, emphasizing the need for meticulous management of ascites and potential adjustment of diuretics to prevent further electrolyte imbalances or renal impairment.

In response to these findings, the medical team considers adjustments to the patient's lactulose regimen to enhance ammonia clearance, closely monitors his fluid status, and evaluates the need for potential escalation to more advanced therapies such as rifaximin. Additionally, discussions regarding the potential need for paracentesis to relieve abdominal discomfort and prevent further respiratory compromise begin to take place. These changes in the patient's condition prompt the team to reassess his overall management plan and engage in multidisciplinary discussions to optimize his care and address the evolving complications associated with his cirrhosis.

Section 2

As the team continues to monitor the patient, an unexpected change in his status is observed. Over the next 48 hours, the patient's abdominal distension becomes more pronounced, and he reports increased discomfort and difficulty breathing. A focused physical assessment reveals decreased breath sounds at the lung bases and dullness to percussion, consistent with fluid accumulation. His respiratory rate has increased to 24 breaths per minute. Despite ongoing management with diuretics, his weight has increased by 3.5 kg, further indicating fluid retention and the likely need for a therapeutic paracentesis.

Repeat laboratory tests reveal further declines in serum sodium, now at 128 mmol/L (normal range: 135-145 mmol/L), suggesting worsening dilutional hyponatremia. The patient's renal function tests show an increase in serum creatinine to 1.8 mg/dL from a previous level of 1.4 mg/dL, raising concerns about hepatorenal syndrome. The multidisciplinary team discusses the need for careful fluid management, balancing the reduction of ascites with maintaining renal perfusion, and considers the initiation of albumin infusions to support intravascular volume.

In response to these developments, the team prioritizes the scheduling of a prompt paracentesis to alleviate the patient's respiratory distress and abdominal discomfort, while planning to initiate rifaximin to synergize with lactulose in managing hepatic encephalopathy. The ongoing clinical reasoning involves evaluating the risks and benefits of each intervention, considering the potential impact on kidney function and electrolyte balance, and adjusting the care plan to align with the dynamic nature of the patient's cirrhosis complications. This coordinated approach aims to stabilize the patient's condition and prevent further deterioration.

Section 3

As the team proceeds with the planned interventions, the patient undergoes a therapeutic paracentesis. The procedure successfully drains approximately 4 liters of ascitic fluid, providing immediate relief from abdominal distension and significantly improving his respiratory status. Post-paracentesis, his respiratory rate decreases to 18 breaths per minute, and he reports feeling less breathless. However, the team remains vigilant for potential complications, including fluid shifts and electrolyte imbalances. Continuous monitoring is initiated to observe any signs of hypotension or changes in mental status, which could indicate worsening hepatic encephalopathy or other complications.

Subsequent laboratory tests reveal a slight improvement in serum sodium, now at 130 mmol/L, which suggests some stabilization of his hyponatremia. However, the serum creatinine remains elevated at 1.9 mg/dL, raising persistent concerns about renal function and the possibility of hepatorenal syndrome. The patient's blood pressure has decreased slightly to 110/70 mmHg, necessitating further evaluation of intravascular volume status. In response, the team carefully administers albumin infusions to support circulatory volume without overloading the kidneys, while adjusting diuretic therapy to optimize fluid balance.

Despite these efforts, the patient begins to exhibit new signs of hepatic encephalopathy, characterized by increased confusion and asterixis during the neurological assessment. The team responds by titrating the dose of lactulose and initiating rifaximin, aiming to reduce ammonia levels and prevent further cognitive decline. These developments underscore the complexity of managing cirrhosis with multi-organ involvement and highlight the need for ongoing clinical reasoning to adapt the treatment plan. With each intervention, the team's goal is to stabilize the patient's condition, mitigate complications, and improve his overall prognosis. The next steps will focus on close monitoring of his neurological status, renal function, and electrolyte levels to guide further therapeutic decisions.

Section 4

As the team continues to monitor the patient, new diagnostic results bring attention to changes in his renal function and liver status. A repeat assessment of renal function reveals that serum creatinine has risen to 2.3 mg/dL, indicating a worsening of renal impairment. This change heightens the concern for hepatorenal syndrome, necessitating a reevaluation of the patient's fluid management strategy and prompting consideration for nephrology consultation. Concurrently, liver enzyme tests show a slight elevation in ALT and AST levels, suggesting ongoing hepatic inflammation or injury. These findings necessitate a closer look at potential underlying causes, such as medication effects or evolving liver pathology, and prompt adjustments in the patient's medication regimen to minimize hepatotoxic risks.

In addition to the laboratory results, the patient's neurological status presents new challenges. Despite the intensified lactulose and rifaximin therapy, the patient exhibits fluctuating levels of consciousness, with periods of somnolence interspersed with moments of agitation. His Glasgow Coma Scale score drops to 12, raising concerns about the progression of hepatic encephalopathy. The team prioritizes continuous monitoring of ammonia levels, which are found to be elevated, reinforcing the need for aggressive management of his encephalopathy. The patient's family is updated on the situation, and discussions regarding potential escalation of care, including the possibility of liver transplantation evaluation, are initiated.

These developments underscore the intricate balance required in managing cirrhosis with multi-organ involvement. The team remains focused on stabilizing the patient's condition through careful titration of medications, vigilant monitoring, and timely interventions. The next steps involve a comprehensive approach to address the renal and hepatic deterioration, enhance the patient's neurological status, and evaluate the broader implications for his long-term management and prognosis. As the team plans for the subsequent phase of care, they are reminded of the importance of interdisciplinary collaboration and adaptive clinical reasoning to navigate the complexities of this case.

Section 5

New Complications

As the clinical team continues to manage the patient's cirrhosis and associated complications, they encounter a new challenge: the development of ascites, which becomes increasingly pronounced. The patient's abdominal girth has visibly expanded, and he reports a sensation of bloating and discomfort. A focused abdominal assessment reveals shifting dullness and a positive fluid wave test, confirming the presence of ascites. Laboratory analysis of the ascitic fluid, obtained via paracentesis, indicates a serum-ascites albumin gradient (SAAG) of greater than 1.1 g/dL, consistent with portal hypertension due to cirrhosis. The ascitic fluid cell count shows no evidence of spontaneous bacterial peritonitis, yet the team remains vigilant for potential infectious complications.

In response to the worsening ascites, the team initiates a diuretic regimen, cautiously balancing the need for fluid removal with the risk of exacerbating the patient's renal impairment. Spironolactone and furosemide are prescribed in a ratio aimed at optimizing diuresis while maintaining electrolyte balance. The patient's vital signs are monitored closely, with particular attention to blood pressure and heart rate, as his mean arterial pressure trends downward to 65 mmHg, raising concerns about hypotension. Electrolyte panels are checked frequently to track sodium and potassium levels, ensuring that diuretic therapy does not lead to severe electrolyte imbalances.

While addressing these new complications, the healthcare team recognizes the need for a multidisciplinary approach to manage the patient's complex condition effectively. The nephrology and hepatology teams collaborate to refine the treatment plan, considering adjustments in diuretic dosing and exploring options such as albumin infusions to support intravascular volume and renal perfusion. The patient's response to these interventions will be crucial in determining the next steps in his care, with the possibility of requiring more advanced therapies or consideration for liver transplantation evaluation depending on his progress. The team remains committed to adapting their strategies based on the patient's evolving clinical picture, ensuring proactive management of his cirrhosis and related complications.