cirrhosis - Nursing Case Study
Pathophysiology
• Primary mechanism: Chronic liver injury leads to persistent inflammation and activation of hepatic stellate cells, resulting in excessive deposition of extracellular matrix and fibrosis. This disrupts normal liver architecture and impairs hepatic function.
• Secondary mechanism: Progressive fibrosis causes vascular remodeling and the formation of regenerative nodules, contributing to increased intrahepatic resistance and portal hypertension. This can lead to complications such as variceal hemorrhage and ascites.
• Key complication: Hepatocyte dysfunction and portal hypertension result in impaired detoxification and metabolism, leading to the accumulation of toxins and development of hepatic encephalopathy, characterized by cognitive impairment and altered mental status.
Patient Profile
Demographics:
56-year-old male, retired construction worker
History:
• Key past medical history: Chronic hepatitis C infection, alcohol use disorder (25 years), type 2 diabetes mellitus, hyperlipidemia
• Current medications: Lactulose, spironolactone, furosemide, insulin, atorvastatin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Increased abdominal swelling and confusion
• Key symptoms: Severe ascites, jaundice, hepatic encephalopathy, peripheral edema, gastrointestinal bleeding, fatigue
• Vital signs: Blood pressure 88/54 mmHg, heart rate 122 bpm, respiratory rate 28 breaths per minute, temperature 101.2°F, oxygen saturation 89% on room air
Section 1
In the initial assessment, the care team noted the severity of the patient's hepatic encephalopathy, evidenced by his disorientation to time and place, along with asterixis, or "liver flap," observed in his hands. His abdominal examination revealed tense ascites with prominent distension, and shifting dullness was present. The peripheral edema extended to his thighs, suggesting significant fluid retention. The patient's sclera were icteric, and his skin was jaundiced, consistent with hyperbilirubinemia. Capillary refill was delayed, and his extremities felt cool to the touch, indicating possible hypoperfusion. Despite his respiratory distress, the patient was only mildly responsive to verbal stimuli, raising concerns about his declining mental status.
The team ordered a comprehensive panel of diagnostic tests. Initial lab results showed critically elevated ammonia levels at 145 µmol/L, confirming severe hepatic encephalopathy. Liver function tests were markedly abnormal, with AST at 190 U/L, ALT at 155 U/L, and total bilirubin at 8.7 mg/dL. Coagulation studies revealed an INR of 2.5, indicating impaired synthetic function of the liver. A complete blood count showed thrombocytopenia with platelets at 85,000/mm³ and leukocytosis with a white blood cell count of 15,000/mm³, raising the suspicion of a concurrent infection. Blood cultures were drawn, given the fever and leukocytosis, to rule out spontaneous bacterial peritonitis, a common complication in cirrhotic patients with ascites.
These findings necessitated immediate interventions, including broad-spectrum intravenous antibiotics to address the potential infection, diuretics adjustments, and increased dosing of lactulose to manage the encephalopathy. Meanwhile, the patient's hypotension and hypoxia prompted supplemental oxygen therapy and consideration of intravascular volume expansion, while carefully monitoring for signs of fluid overload due to his compromised cardiac function. The team also scheduled an urgent paracentesis to relieve the tense ascites and obtain fluid for analysis, seeking further clarity on his deteriorating condition. These steps set the stage for the next phase of his management, focusing on stabilizing his vital signs and addressing the underlying causes of his acute decompensation.
Section 2
The patient's condition remained precarious over the subsequent hours, but there were slight improvements noted in his mental status following the administration of increased doses of lactulose. His ammonia levels began to decrease, dropping to 120 µmol/L, and he became more responsive, opening his eyes spontaneously and following simple commands. However, the team remained vigilant as his respiratory distress persisted, with oxygen saturation hovering around 88% on 4 liters of supplemental oxygen. Arterial blood gas analysis revealed a pH of 7.32, PaCO2 of 50 mmHg, and PaO2 of 65 mmHg, indicating respiratory acidosis with hypoxemic features. The team was concerned about potential respiratory failure and considered non-invasive ventilation to improve gas exchange.
Meanwhile, the results of the paracentesis returned, showing an ascitic fluid white cell count of 500 cells/mm³ with 90% neutrophils. This confirmed the presence of spontaneous bacterial peritonitis (SBP), a critical complication requiring aggressive treatment. Despite the initiation of broad-spectrum antibiotics, the patient's fever persisted at 101.8°F, and his blood pressure remained borderline at 95/55 mmHg, with a heart rate of 110 beats per minute. His renal function showed signs of deterioration, with serum creatinine rising to 2.0 mg/dL from a baseline of 1.2 mg/dL, raising concerns for hepatorenal syndrome.
These developments necessitated a reevaluation of the treatment strategy. The care team decided to escalate antibiotic therapy to target SBP aggressively, while also initiating albumin infusions to support renal perfusion and mitigate the risk of hepatorenal syndrome. Continuous monitoring of renal parameters and hemodynamic status was prioritized. Additionally, the team explored the possibility of initiating a trial of terlipressin, given its potential benefits in improving renal function in the context of SBP. These interventions aimed to stabilize the patient further, though the risk of additional complications remained high, demanding ongoing critical assessment and timely adjustments to the care plan.
Section 3
Response to Interventions
Over the next 12 hours, the patient's condition showed mixed responses to the interventions. The initiation of non-invasive ventilation helped improve his oxygenation status modestly, with his oxygen saturation rising to 92% on a BiPAP machine set at 10/5 cmH2O. However, his arterial blood gas analysis showed persistent respiratory acidosis, with a pH of 7.34, PaCO2 of 48 mmHg, and PaO2 of 70 mmHg. This indicated only partial improvement, prompting the team to consider the possibility of intubation if no further progress was made.
Despite aggressive antibiotic therapy and albumin infusions, the patient's fever remained unchanged at 101.5°F, and his blood pressure continued to fluctuate between 90/50 mmHg and 100/55 mmHg. His heart rate remained elevated at 112 beats per minute, suggesting a potential septic picture. Renal function continued to decline, as evidenced by a serum creatinine level that increased to 2.5 mg/dL. This prompted the team to initiate terlipressin, aiming to improve renal perfusion and address the worsening hepatorenal syndrome.
In addition to these challenges, the patient developed new-onset jaundice, with total bilirubin levels rising significantly to 5.2 mg/dL from a previous 2.8 mg/dL. Liver function tests revealed elevated AST and ALT levels, indicating further hepatic decompensation. These developments necessitated a reassessment of the overall management plan, with the care team considering the benefits of early transfer to a specialized liver center for possible liver transplantation evaluation. The situation highlighted the need for ongoing critical assessment and the possibility of escalating care in response to the complex interplay of complications.
Section 4
As the clinical team continued to monitor the patient closely, they noted a significant change in his status over the next few hours. The patient's mental status began to deteriorate, with increasing confusion and episodes of disorientation. His Glasgow Coma Scale (GCS) score dropped to 12, indicating a decrease in neurological function that warranted immediate attention. The possibility of hepatic encephalopathy was suspected, given the underlying cirrhosis and elevated ammonia levels observed at 95 µmol/L. Consequently, lactulose therapy was intensified, and rifaximin was added to the treatment regimen in an attempt to manage his worsening neurological symptoms.
Simultaneously, the patient's hemodynamic status showed further instability. Despite the administration of terlipressin, his mean arterial pressure remained low at 60 mmHg, and his renal function continued to decline, with a serum creatinine level rising to 3.0 mg/dL. The team initiated continuous renal replacement therapy (CRRT) to address the acute kidney injury and maintain fluid and electrolyte balance. Despite these interventions, the patient's overall condition remained precarious, highlighting the need for urgent reassessment of his candidacy for liver transplantation.
In light of these developments, the multidisciplinary team convened to discuss the patient's prognosis and potential transfer to a tertiary care center with liver transplant capabilities. They recognized the need to balance aggressive management of his current complications with the potential benefits and risks of transfer. The decision-making process required careful consideration of the patient's deteriorating hepatic and renal function, the risk of sepsis, and the likelihood of recovery with or without transplant intervention. This complex and dynamic clinical situation necessitated advanced critical thinking and collaboration among the care team, as they navigated the next steps in the patient's challenging medical journey.
Section 5
As the team continued to monitor the patient, they noted further changes in his clinical status that signaled new complications. The patient developed signs of systemic infection, presenting with a fever of 101.8°F, tachycardia at 120 beats per minute, and leukocytosis with a white blood cell count of 16,000/mm³. Blood cultures were drawn, and broad-spectrum antibiotics, including vancomycin and piperacillin-tazobactam, were initiated to cover potential sources of sepsis. Despite the antibiotics, his blood pressure continued to drop, necessitating the initiation of norepinephrine to maintain adequate perfusion. The team suspected that the patient might be progressing towards septic shock, which would further complicate his already critical condition.
In addition to the systemic infection, the patient's respiratory status began to deteriorate. He developed increasing respiratory distress, with a respiratory rate climbing to 28 breaths per minute and an oxygen saturation dropping to 88% on high-flow nasal cannula. A chest X-ray revealed bilateral infiltrates suggestive of acute respiratory distress syndrome (ARDS), likely secondary to the underlying infection and inflammation. This complication required the initiation of non-invasive positive pressure ventilation to support his breathing while minimizing additional stress on his already compromised system.
The emergence of these new complications prompted an urgent reassessment of the patient's care plan. The team faced the challenge of managing the delicate balance between treating the infection aggressively and maintaining stability in his hepatic and renal function. The patient's eligibility for liver transplantation remained a focal point, but the recent developments underscored the complexity of his condition and the need for continuous evaluation and adjustment of his treatment strategy. The multidisciplinary team remained vigilant, aware that any further deterioration could significantly impact his prognosis and the feasibility of a successful transplant intervention.