cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic liver injury leads to inflammation and fibrosis, where damaged hepatocytes are replaced with scar tissue, disrupting liver architecture and function. This fibrosis impairs blood flow and hepatocyte regeneration.

• Secondary mechanism: Portal hypertension arises from increased resistance to blood flow through the scarred liver. This can lead to collateral circulation, varices, and splenomegaly, further complicating liver function.

• Key complication: Decreased liver function results in reduced detoxification and impaired synthesis of crucial proteins, leading to symptoms like jaundice, coagulopathy, and ascites due to fluid imbalance.

Patient Profile

Demographics:

52-year-old male, construction worker

History:

• Key past medical history: Chronic hepatitis C, diagnosed 10 years ago; alcohol use disorder, currently in remission for 1 year

• Current medications: Lactulose, propranolol, spironolactone

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue and abdominal swelling

• Key symptoms: Jaundice, ascites, peripheral edema, occasional confusion (hepatic encephalopathy), dark urine

• Vital signs: Blood pressure 98/60 mmHg, heart rate 92 bpm, respiratory rate 18 breaths per minute, temperature 99.1°F, oxygen saturation 96% on room air

Section 1

New Complications:

The patient, Mr. Thompson, returns to the clinic two weeks later with worsening symptoms. He reports increased abdominal discomfort and a noticeable increase in abdominal girth despite adherence to prescribed diuretics. On physical examination, Mr. Thompson appears more jaundiced, and his abdominal distension has significantly progressed. There is evidence of shifting dullness upon percussion, indicating a large amount of ascitic fluid. Additionally, the patient exhibits a mild tremor in his hands, known as asterixis, which suggests worsening hepatic encephalopathy.

Recent laboratory tests reveal a further deterioration in liver function: the patient's bilirubin levels have increased to 4.5 mg/dL (previously 3.2 mg/dL), and his albumin level has decreased to 2.5 g/dL (previously 3.0 g/dL), indicating worsening synthetic liver function. His INR is elevated at 1.8, suggesting impaired coagulation. The ascitic fluid analysis shows an elevated white cell count, raising concerns for spontaneous bacterial peritonitis (SBP), a serious complication of cirrhosis. The patient's kidney function tests also show a slight increase in creatinine levels, suggesting the possibility of hepatorenal syndrome, a condition that may occur in advanced liver disease.

In light of these findings, Mr. Thompson's care team is prompted to consider additional interventions. The team discusses the need for paracentesis to relieve the ascites and obtain a culture to confirm SBP. They also explore the possibility of starting antibiotics empirically while awaiting culture results. The altered mental status and asterixis necessitate a review of lactulose dosing to manage hepatic encephalopathy. The patient's worsening renal function could indicate the need for further evaluation and possible adjustments in his medication regimen. The team is also considering early discussions about liver transplantation, given the progression of his liver disease and the emergence of life-threatening complications.

Section 2

Following the decision to perform a paracentesis, Mr. Thompson undergoes the procedure, which relieves some of his abdominal discomfort and provides a sample for analysis. The ascitic fluid culture confirms the presence of bacteria, affirming the diagnosis of spontaneous bacterial peritonitis (SBP). In response, Mr. Thompson is started on broad-spectrum intravenous antibiotics, specifically cefotaxime, to treat the infection while awaiting sensitivity results. Over the next 48 hours, his abdominal discomfort shows slight improvement, and his abdominal girth decreases marginally. However, his liver function tests remain concerning, with bilirubin levels rising further to 5.0 mg/dL and albumin decreasing to 2.3 g/dL.

Despite the antibiotic treatment, Mr. Thompson's cognitive status continues to fluctuate. He experiences episodes of confusion and disorientation, indicative of worsening hepatic encephalopathy. The care team decides to adjust his lactulose regimen, increasing the dose to ensure more frequent bowel movements, aiming to reduce the ammonia levels contributing to his altered mental state. Additionally, the nephrology team is consulted to address his deteriorating renal function. His creatinine level has crept up to 1.6 mg/dL, suggesting the early stages of hepatorenal syndrome. A careful review of his medications is conducted, and diuretics are cautiously adjusted to minimize further kidney impairment while managing fluid overload.

As Mr. Thompson's condition stabilizes slightly with these interventions, the team acknowledges the need for a comprehensive plan moving forward. Discussions regarding liver transplantation are initiated, given the ongoing decline in liver function and the emergence of complications like SBP and potential hepatorenal syndrome. Mr. Thompson and his family are counseled about the severity of his condition and the necessity of considering advanced therapeutic options. These discussions are crucial as they provide an opportunity to explore potential listing for transplantation, which could offer a long-term solution to his multifaceted health issues.

Section 3

In the days following the adjustment of Mr. Thompson's treatment regimen, his clinical status presents mixed developments. While the increased lactulose dose has resulted in more consistent bowel movements, reducing some of the ammonia burden and marginally improving his cognitive state, his overall condition remains precarious. Mr. Thompson's vital signs indicate a temperature of 99.5°F, heart rate of 92 beats per minute, respiratory rate of 20 breaths per minute, and blood pressure of 105/65 mmHg. Despite these stable readings, his laboratory results reveal a concerning trend: his creatinine level has risen to 2.0 mg/dL, indicating a progression towards hepatorenal syndrome, while his sodium level has dropped to 130 mEq/L, suggesting dilutional hyponatremia.

The care team reassesses Mr. Thompson's management plan in light of these developments. Given the rising creatinine and low sodium, the nephrology team recommends cautious volume management to avoid exacerbating renal impairment. A trial of albumin infusion is considered to improve intravascular volume and support renal function. Additionally, the infectious disease specialists review the sensitivity results from the ascitic fluid culture, which indicate susceptibility to cefotaxime, confirming the appropriateness of the current antibiotic therapy. Despite the initial improvement, the persistence of subtle fever and abdominal discomfort prompts consideration of potential secondary infections or complications such as a resistant strain of bacteria.

As Mr. Thompson navigates these challenges, the multidisciplinary team continues to emphasize the importance of monitoring and early intervention. The prospect of liver transplantation becomes increasingly relevant as a viable long-term solution, with the transplant evaluation process expedited in view of his deteriorating hepatic and renal function. Mr. Thompson and his family are engaged in ongoing discussions to ensure they are informed and prepared for the next steps in his care journey, highlighting the need for a seamless transition from current management to potential transplantation candidacy.

Section 4

In the days following the nephrology team's intervention with cautious volume management and albumin infusion, there is a notable change in Mr. Thompson’s status. His blood pressure stabilizes slightly, now reading at 110/70 mmHg, suggesting a mild improvement in intravascular volume. However, his creatinine level continues to hover around 2.0 mg/dL, indicating no significant improvement in renal function despite these efforts. His sodium level remains low at 130 mEq/L, requiring careful monitoring to prevent further dilutional hyponatremia. Clinically, Mr. Thompson reports a slight reduction in abdominal discomfort, but his low-grade fever persists at 99.7°F. This prompts the team to reevaluate the possibility of a secondary infection or a more resistant bacterial strain.

The infectious disease team decides to broaden the diagnostic approach by ordering additional blood cultures and a repeat analysis of ascitic fluid to rule out any resistant organisms or new infectious complications. Meanwhile, hepatology specialists consider the potential benefits and risks of early liver transplantation, given Mr. Thompson’s escalating MELD score, which now stands at 28, reflecting his severe liver dysfunction and increased urgency for transplantation. The transplantation team initiates further compatibility and cross-matching tests to expedite the process, emphasizing the necessity of swift action in light of his declining renal function and overall health.

Throughout this period, the care team diligently updates Mr. Thompson and his family about his condition and the importance of adhering to the current management plan while preparing for the possible transplant. The family is encouraged to consider the implications of transplantation, including the rigorous post-operative care and lifestyle adjustments required. This ongoing dialogue ensures that Mr. Thompson remains at the center of his care decisions, reinforcing the collaborative approach needed to navigate his complex medical challenges effectively.

Section 5

In the following days, Mr. Thompson's condition takes a concerning turn when his temperature spikes to 101.3°F, and he begins to experience increased confusion and disorientation, suggestive of hepatic encephalopathy, a known complication of advanced cirrhosis. The care team promptly initiates a lactulose regimen to decrease ammonia levels and mitigate mental status changes. Despite these efforts, Mr. Thompson remains lethargic, and his family notices a slight yellowing of his eyes, indicating worsening jaundice. His laboratory results reinforce this clinical picture, with a rising bilirubin level now at 4.5 mg/dL and a continued decline in albumin to 2.5 g/dL, underscoring the deterioration in liver synthetic function.

The repeat ascitic fluid analysis reveals an elevated white cell count and the presence of gram-positive cocci, suggesting bacterial peritonitis despite prior antibiotic coverage. The team consults with infectious disease specialists to adjust the antibiotic regimen accordingly, opting for a broader-spectrum antibiotic to address the potential resistant strain. Meanwhile, Mr. Thompson's sodium level drops further to 128 mEq/L, prompting a delicate balance in fluid management to avoid exacerbating his hyponatremia while ensuring adequate circulatory volume.

These developments necessitate intensified monitoring and coordination among the multidisciplinary team members. The hepatology and transplant teams prioritize Mr. Thompson's placement on the liver transplant list, urgently addressing compatibility concerns and pre-operative assessments. This situation highlights the critical need for timely intervention and reassessment of his treatment plan. The team emphasizes the importance of vigilant monitoring for any further signs of deterioration and potential complications, ensuring that Mr. Thompson and his family understand the gravity of his condition and are prepared for the next steps in his care trajectory.