Hepatits C - Nursing Case Study

Pathophysiology

• Primary mechanism: Hepatitis C virus (HCV) primarily invades hepatocytes, triggering an immune-mediated response that leads to chronic inflammation and progressive liver damage. The persistent viral replication and immune cell infiltration result in hepatocyte apoptosis and necrosis.

• Secondary mechanism: Sustained inflammation induces fibrogenesis through the activation of hepatic stellate cells, which deposit extracellular matrix proteins, progressing to liver fibrosis and potentially cirrhosis. This disrupts normal liver architecture and impairs liver function.

• Key complication: Cirrhosis can lead to severe complications such as portal hypertension, hepatic encephalopathy, and an increased risk of hepatocellular carcinoma, significantly impacting patient health and necessitating vigilant nursing care and monitoring.

Patient Profile

Demographics:

52-year-old male, construction worker

History:

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

• Current medications: Sofosbuvir-velpatasvir, insulin, amlodipine, spironolactone

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and confusion

• Key symptoms: Jaundice, ascites, edema in the lower extremities, hematemesis, fatigue

• Vital signs: Blood pressure 88/56 mmHg, heart rate 115 bpm, respiratory rate 24 breaths per minute, temperature 101.3°F, oxygen saturation 89% on room air

Section 1

Following the initial assessment, the patient's condition rapidly deteriorates. The abdominal pain intensifies, and the confusion progresses to altered mental status, indicating possible hepatic encephalopathy. The nursing team performs a focused physical examination, revealing a distended abdomen consistent with severe ascites and pronounced asterixis, suggesting worsening liver function. Laboratory results come back, showing elevated ammonia levels at 125 µmol/L, indicating an impaired ability of the liver to detoxify ammonia. Liver function tests reveal dramatically elevated liver enzymes: ALT 145 U/L, AST 160 U/L, and bilirubin 6.8 mg/dL. Albumin is critically low at 2.1 g/dL, exacerbating the ascites and edema. Coagulation studies reveal an INR of 2.5, heightening concerns of potential bleeding complications.

Given these findings, the medical team suspects acute variceal bleeding as a source of the hematemesis, driven by heightened portal hypertension. An urgent endoscopy is scheduled to confirm the presence of esophageal varices and to attempt hemostasis. The patient's blood pressure continues to trend downward, now at 82/54 mmHg, despite fluid resuscitation efforts, necessitating consideration of vasopressor support. Nursing interventions focus on monitoring for signs of hypovolemia and shock, maintaining airway patency, and providing lactulose to reduce ammonia levels. The interprofessional team discusses the need for a transjugular intrahepatic portosystemic shunt (TIPS) procedure to manage refractory ascites and portal hypertension, while balancing the risk of exacerbating hepatic encephalopathy.

As the patient's condition remains precarious, the team anticipates potential complications, such as acute kidney injury due to hepatorenal syndrome, which could further compromise the patient's status. Close monitoring of renal function, electrolytes, and urine output becomes imperative. The complexity of the case demands advanced clinical reasoning to prioritize interventions, manage complications, and stabilize the patient, as the team prepares for possible escalation to intensive care should his condition worsen.

Section 2

As the situation unfolds, the medical team receives new diagnostic results post-endoscopy, confirming the presence of large esophageal varices with active bleeding. Band ligation is performed successfully, achieving hemostasis. Despite this intervention, the patient's condition remains unstable. The blood pressure continues to hover at critically low levels, now at 78/50 mmHg, even with maximum fluid resuscitation. Vasopressor support is initiated with norepinephrine, titrated to maintain mean arterial pressure above 65 mmHg, but the patient's response is minimal, suggesting a possible progression to septic shock secondary to bacterial translocation from the gastrointestinal tract.

Concurrently, laboratory results reveal a concerning rise in serum creatinine to 2.3 mg/dL from a baseline of 1.1 mg/dL, indicating early signs of acute kidney injury, likely due to hepatorenal syndrome. Urine output has decreased to less than 20 mL/hour, confirming the impaired renal function. Electrolyte imbalances are noted with hyponatremia at 126 mEq/L and hyperkalemia at 5.8 mEq/L, necessitating careful electrolyte management. The nursing team intensifies monitoring, adjusting fluid and medication regimens to support renal perfusion while avoiding further fluid overload due to the existing severe ascites.

The patient's altered mental status shows no improvement despite lactulose administration, with persistent asterixis and confusion. This prompts the team to reassess the risks and benefits of proceeding with the TIPS procedure. They deliberate on the potential for worsening hepatic encephalopathy versus the necessity to control portal hypertension and ascites. As the team navigates these complex decisions, they prepare for the possibility of transferring the patient to the intensive care unit for closer monitoring and advanced supportive measures, recognizing the critical need for comprehensive and well-coordinated care.

Section 3

As the medical team continues to manage the complex case of the patient with Hepatitis C, a new complication emerges. Despite initial successful band ligation of the esophageal varices, the patient's condition deteriorates overnight. The nursing team observes a sudden increase in abdominal distension and tenderness, raising the suspicion of secondary bacterial peritonitis. A diagnostic paracentesis is promptly performed, yielding turbid ascitic fluid with an elevated neutrophil count of 350 cells/mm³, confirming the diagnosis of spontaneous bacterial peritonitis (SBP). Blood cultures are also drawn, and broad-spectrum antibiotics are initiated empirically, leading to a challenging balancing act of managing the infection while maintaining hemodynamic stability.

The patient's vital signs remain concerning, with persistent hypotension, a heart rate of 118 beats per minute, and a respiratory rate of 28 breaths per minute. The norepinephrine infusion is increased, yet the mean arterial pressure struggles to stay above 65 mmHg. Meanwhile, the patient's renal function continues to decline, with serum creatinine now at 3.1 mg/dL and urine output decreasing further to less than 10 mL/hour. This confirms the progression of acute kidney injury, necessitating careful consideration of renal replacement therapy options while avoiding exacerbating the patient's fluid overload.

Clinically, the patient's mental status remains poor, with worsening hepatic encephalopathy despite aggressive medical management. The nursing team, now working closely with the hepatology and critical care specialists, is confronted with the decision to escalate care. The potential benefits of a Transjugular Intrahepatic Portosystemic Shunt (TIPS) to alleviate portal hypertension are weighed against the high risk of exacerbating encephalopathy. As these critical decisions loom, the team prepares to transition the patient to the intensive care unit, recognizing the need for enhanced monitoring, continuous renal replacement therapy, and potential advanced liver support measures. The unfolding scenario demands heightened clinical judgment and a multidisciplinary approach to navigate the patient's increasingly precarious state.

Section 4

As the patient transitions to the intensive care unit, the nursing team conducts a thorough initial assessment, noting several critical changes in the patient's status. The patient's level of consciousness has deteriorated further, with a Glasgow Coma Scale score now reduced to 7, indicating severe encephalopathy. Pupillary response remains sluggish, and the patient exhibits asterixis, reinforcing the need for immediate neurological intervention. Vital signs reveal sustained hypotension despite the increased norepinephrine infusion, with blood pressure readings averaging 82/48 mmHg. The heart rate remains elevated at 122 beats per minute, and the respiratory rate has increased to 32 breaths per minute, suggesting worsening respiratory distress. The oxygen saturation has decreased to 88% on a high-flow nasal cannula, necessitating further respiratory support.

In addition to these concerning clinical findings, new diagnostic results from the laboratory are received. The patient's liver function tests show a marked increase, with an aspartate transaminase (AST) of 210 U/L and alanine transaminase (ALT) of 185 U/L, coupled with a total bilirubin level now elevated to 5.6 mg/dL. These findings indicate significant hepatic compromise. Coagulation studies reveal a prolongation of the prothrombin time (PT) at 22 seconds and an international normalized ratio (INR) of 2.5, highlighting the risk of bleeding complications. Blood cultures confirm the presence of Escherichia coli in both the ascitic fluid and blood, guiding the escalation of targeted antibiotic therapy, while renal function continues to decline with a serum creatinine now at 3.7 mg/dL.

In light of these developments, the multidisciplinary team convenes to evaluate the patient's response to current interventions and to strategize the next steps. Given the critical state and rapid deterioration, the decision is made to initiate continuous renal replacement therapy to manage fluid overload and support declining renal function. Additionally, discussions are underway to consider the initiation of advanced liver support measures, such as extracorporeal liver assist devices, to bridge the patient towards potential liver transplantation candidacy. The team remains vigilant for any new complications while carefully monitoring the patient's hemodynamic and neurological status, recognizing that timely and coordinated intervention is paramount to improving the patient's chances of recovery.

Section 5

The patient's clinical status continues to evolve as the response to interventions is closely monitored. Despite the initiation of continuous renal replacement therapy (CRRT) and escalation of antibiotic therapy, the patient's condition remains precarious. In the hours following these interventions, there is a subtle improvement in renal function, with a slight decrease in serum creatinine to 3.5 mg/dL, suggesting a marginal positive response to CRRT. However, the patient's hemodynamic status remains unstable, with blood pressure persistently low at 78/46 mmHg, despite maximal norepinephrine support. Heart rate remains tachycardic at 118 beats per minute, indicative of underlying cardiovascular strain and possibly exacerbating the patient's metabolic demands.

Neurologically, the patient's Glasgow Coma Scale score remains unchanged at 7, with no significant improvement in consciousness, and the sluggish pupillary response persists. The medical team is concerned about the progression of hepatic encephalopathy and the potential development of intracranial hypertension. An immediate electroencephalogram (EEG) is performed, revealing diffuse slowing consistent with severe encephalopathy, but no seizure activity, ruling out one potential complication. Despite high-flow nasal cannula therapy, the patient's respiratory status deteriorates further, with oxygen saturation dropping to 85%, prompting the decision to escalate respiratory support to non-invasive positive pressure ventilation.

The multidisciplinary team reassesses the treatment plan, recognizing the critical need to address the ongoing hepatic failure and systemic infection. Liver support options, including plasmapheresis and consideration for an extracorporeal liver assist device, are prioritized as potential bridge therapies. Meanwhile, further imaging studies are ordered to evaluate for potential abdominal or cerebral complications, such as spontaneous bacterial peritonitis or cerebral edema. The team's collaborative efforts underscore the complexity of the patient's condition, requiring sophisticated clinical judgment to navigate the intertwined challenges of multi-organ dysfunction and the pressing need for stabilization and potential transplantation evaluation.