Hepatitis C - Nursing Case Study

Pathophysiology

• Primary mechanism: Hepatitis C virus (HCV) primarily targets hepatocytes, leading to persistent inflammation. The virus-induced immune response causes hepatocyte apoptosis and necrosis, promoting chronic liver damage.

• Secondary mechanism: Continuous liver injury triggers fibrogenesis, where activated hepatic stellate cells deposit excessive extracellular matrix, leading to fibrosis. Over time, progressive fibrosis can culminate in cirrhosis, characterized by severe architectural distortion and vascular remodeling.

• Key complication: Advanced cirrhosis can progress to hepatocellular carcinoma (HCC) due to genomic instability and increased cellular proliferation, posing significant morbidity and mortality risks.

Patient Profile

Demographics:

52-year-old male, construction worker

History:

• Key past medical history: Chronic Hepatitis C diagnosed 10 years ago, cirrhosis, portal hypertension, type 2 diabetes

• Current medications: Ribavirin, insulin, propranolol, lactulose

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and jaundice

• Key symptoms: Fatigue, confusion, ascites, dark urine, clay-colored stools

• Vital signs: Blood pressure 85/55 mmHg, heart rate 112 bpm, respiratory rate 24 breaths per minute, temperature 38.4°C, oxygen saturation 89% on room air

Section 1

Upon initial assessment, the patient's condition appears to be rapidly deteriorating. His severe abdominal pain and jaundice are accompanied by significant lethargy and worsening confusion, suggestive of hepatic encephalopathy. Physical examination reveals a distended abdomen with positive fluid wave test, indicating worsening ascites. The patient demonstrates asterixis, and his skin and sclera are markedly icteric. His vital signs further underscore the critical status: hypotension with blood pressure at 85/55 mmHg, tachycardia with heart rate at 112 bpm, and hypoxia with oxygen saturation at 89% on room air. He is febrile with a temperature of 38.4°C, raising concerns for a potential infection such as spontaneous bacterial peritonitis (SBP).

Laboratory results reveal several abnormalities: markedly elevated liver enzymes with AST at 290 U/L and ALT at 250 U/L, total bilirubin at 8.5 mg/dL, and an INR of 2.1, indicating significant coagulopathy. Serum ammonia levels are elevated, consistent with encephalopathy, while a complete blood count shows leukocytosis with a WBC count of 16,000/uL, suggesting an infectious process. Additionally, renal function tests show elevated creatinine at 2.5 mg/dL, pointing towards hepatorenal syndrome. Abdominal ultrasound confirms the presence of ascites and reveals splenomegaly, but no focal hepatic lesions are identified at this stage.

The critical nature of the patient's condition demands a multifaceted approach. Immediate interventions include initiating broad-spectrum antibiotics to cover SBP, optimizing lactulose therapy to manage encephalopathy, and careful fluid management to address hypotension and potential renal impairment. The complexity of his presentation requires vigilant monitoring and reassessment to gauge response to treatment and anticipate further complications. This situation necessitates advanced clinical judgment to balance the management of his chronic liver disease with acute complications, ensuring that the care plan adapts to his evolving clinical status. The potential for deterioration into hepatorenal syndrome or the development of variceal bleeding remains a significant concern, necessitating proactive and dynamic clinical management.

Section 2

A few hours after the initial interventions, the patient's condition remains precarious but shows slight improvements in certain parameters. The administration of broad-spectrum antibiotics has led to a modest reduction in fever, with his temperature decreasing to 37.9°C, suggesting a potential response to the treatment for suspected spontaneous bacterial peritonitis. However, his oxygen saturation remains concerning at 90% on supplemental oxygen via nasal cannula at 2 liters per minute. The patient's mental status has shown subtle improvement with more consistent lactulose therapy; his lethargy appears slightly reduced, though he still exhibits confusion and asterixis, indicating persistent hepatic encephalopathy.

Repeat laboratory tests reveal a slight decline in WBC count to 14,800/uL, supporting a possible response to antibiotic therapy, but his liver function tests and coagulopathy remain unchanged. The INR remains elevated at 2.1, and total bilirubin now measures 9.0 mg/dL, indicating ongoing liver dysfunction. His renal function has further deteriorated, with creatinine rising to 3.0 mg/dL, suggestive of progression towards hepatorenal syndrome despite careful fluid management and vasopressor support to maintain blood pressure.

The nursing team is now faced with the challenge of balancing the need for aggressive fluid resuscitation against the risk of worsening ascites and potential variceal bleeding. Additionally, the possibility of initiating renal replacement therapy must be considered if renal function continues to decline. The patient's fragile hemodynamics and risk of further complications require meticulous monitoring and dynamic decision-making. The clinical team must now evaluate the potential benefits of more advanced interventions, such as transjugular intrahepatic portosystemic shunt (TIPS) or liver transplantation assessment, as part of the ongoing care strategy for this complex case.

Section 3

The patient's condition experiences a significant change, as new complications arise that demand immediate attention. Overnight, his respiratory status deteriorates, with oxygen saturation dropping to 85% despite increasing supplemental oxygen to 4 liters per minute via nasal cannula. Auscultation reveals diminished breath sounds at the bases and crackles, suggesting the development of pulmonary edema, likely secondary to fluid overload. This complication necessitates urgent re-evaluation of his fluid management strategy to prevent further respiratory compromise.

Concurrently, the patient's neurological status worsens with increased confusion and the onset of agitation, indicating a potential exacerbation of hepatic encephalopathy. The lactulose therapy is adjusted to increase dosing frequency, but there is concern about the underlying precipitating factors, including electrolyte imbalances. A repeat metabolic panel reveals hyponatremia with sodium levels dropping to 128 mEq/L, which may contribute to the neurological changes and requires careful correction to avoid central pontine myelinolysis.

These developments prompt the clinical team to prioritize interventions to stabilize the patient's respiratory and neurological status while considering the implications on his overall management plan. The possibility of initiating non-invasive ventilation is discussed to support his respiratory function, and a more aggressive approach to correcting electrolyte imbalances is initiated. The team weighs the risks and benefits of renal replacement therapy, given the escalating renal failure and fluid overload, as they continue to explore the feasibility of advanced interventions such as TIPS or prioritizing a liver transplantation assessment. These decisions will be pivotal in guiding the subsequent phases of care for this complex and critically ill patient.

Section 4

As the clinical team addresses the patient's critical condition, they decide to implement non-invasive ventilation to support his respiratory function. This intervention helps improve oxygenation, with oxygen saturation rising to 90%. However, his respiratory rate remains elevated at 28 breaths per minute, and he continues to exhibit accessory muscle use, indicating ongoing respiratory distress. A chest X-ray is ordered, revealing bilateral infiltrates consistent with pulmonary edema, confirming the need for careful fluid management and further respiratory support.

Meanwhile, the patient's neurological status remains a significant concern. Despite increased lactulose dosing, he continues to exhibit confusion and agitation, with a Glasgow Coma Scale score of 12. Laboratory results show a slight improvement in sodium levels to 130 mEq/L after cautious electrolyte correction, but his serum ammonia levels remain elevated at 85 µmol/L. The team hypothesizes that the persistent hepatic encephalopathy may be exacerbated by underlying infection, leading them to obtain blood cultures and consider empirical antibiotic therapy while awaiting results.

The patient's evolving condition highlights the intricate interplay between his respiratory and neurological complications, necessitating a comprehensive and dynamic approach to management. The team deliberates the potential need for renal replacement therapy to address his fluid overload and deteriorating renal function, as his creatinine levels have risen to 2.8 mg/dL. As they continue to monitor and adjust treatment strategies, the possibility of liver transplantation is increasingly prioritized, underscoring the urgency and complexity of his care trajectory.

Section 5

As the team continues to navigate the complexities of the patient's condition, new diagnostic results provide critical insights into his deteriorating status. The blood cultures return positive for Klebsiella pneumoniae, a multidrug-resistant organism, necessitating a shift in antibiotic strategy to target this pathogen effectively. The patient's white blood cell count has increased to 15,000 cells/µL, further supporting the presence of an acute infectious process. Concurrently, his liver function tests demonstrate a worsening trend, with AST and ALT levels rising to 350 U/L and 400 U/L, respectively, suggesting ongoing hepatic injury.

Despite the initiation of targeted antibiotic therapy, the patient's clinical status begins to decline. He develops a fever of 102°F, and his blood pressure drops to 88/56 mmHg, indicating the onset of septic shock. His heart rate surges to 118 beats per minute as compensatory mechanisms struggle to maintain perfusion. The team recognizes the urgent need for aggressive hemodynamic support, prompting the initiation of intravenous vasopressors to stabilize his blood pressure. Additionally, given the risk of further kidney damage from hypotension, renal replacement therapy is expedited to alleviate the accumulating fluid overload and support renal function.

As these complications unfold, the interdisciplinary team is faced with critical decisions regarding the patient's immediate and long-term management. They must weigh the risks and benefits of continuing aggressive supportive measures against the potential for liver transplantation, which is becoming increasingly urgent. The team considers whether advanced therapies, such as extracorporeal liver support systems, might bridge the patient to transplantation while maintaining vital organ function. This juncture demands precise clinical reasoning and swift action to optimize the patient's chances of recovery.