liver failure - Nursing Case Study
Pathophysiology
• Primary mechanism: Hepatocyte injury and necrosis lead to loss of liver function, resulting in impaired protein synthesis, detoxification, and metabolism. This causes accumulation of toxins like ammonia, leading to hepatic encephalopathy.
• Secondary mechanism: Portal hypertension arises from increased resistance to blood flow in the liver due to fibrosis and regenerative nodules, causing complications such as varices and ascites.
• Key complication: Impaired bile production and excretion result in cholestasis, causing jaundice and further contributing to systemic toxin buildup.
Patient Profile
Demographics:
56-year-old male, construction worker
History:
• Key past medical history: Chronic hepatitis C, alcohol use disorder
• Current medications: Lactulose, spironolactone, propranolol
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Increasing abdominal pain and swelling
• Key symptoms: Jaundice, fatigue, confusion, easy bruising, ascites
• Vital signs: Blood pressure 100/60 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 37.8°C, oxygen saturation 94% on room air
Section 1
New Diagnostic Results:
The medical team ordered a comprehensive metabolic panel, complete blood count, liver function tests, and coagulation profile to assess the patient's current liver status and related complications. The results highlighted several concerning findings. The liver function tests revealed significantly elevated bilirubin levels at 5.6 mg/dL, indicating worsening jaundice and impaired bile excretion. Serum ammonia was markedly elevated at 180 µmol/L, correlating with the patient's confusion and increasing severity of hepatic encephalopathy. Albumin levels were notably low at 2.5 g/dL, contributing to the patient's ascites and generalized edema.
Additionally, the coagulation profile showed a prolonged prothrombin time (PT) of 19 seconds and an INR of 2.1, suggesting impaired synthetic function of the liver and a heightened risk for bleeding. The complete blood count indicated thrombocytopenia with a platelet count of 90,000/mm³, further increasing the bleeding risk. These lab results, combined with the patient's clinical presentation, suggest an acute exacerbation of chronic liver failure, likely precipitated by ongoing alcohol use and advanced hepatitis C-related liver damage.
These findings necessitate prompt intervention to manage the complications and prevent further deterioration. The healthcare team must consider adjusting the patient's medication regimen, including optimizing doses of lactulose to reduce ammonia levels and considering potential diuretics for ascites management. Close monitoring of mental status, hemodynamic stability, and potential bleeding is crucial. The results also underscore the need for patient education and support to address the underlying alcohol use disorder, a critical step in preventing further liver damage and improving overall prognosis.
Section 2
As the healthcare team began implementing interventions to address the patient's acute exacerbation of chronic liver failure, they closely monitored the patient's response. The initial focus was on controlling the elevated serum ammonia levels by adjusting the dose of lactulose. Within 24 hours, the patient showed a slight improvement in mental status; however, the confusion persisted, suggesting only partial effectiveness of the intervention. The medical team decided to add rifaximin to the regimen to further target the ammonia-producing bacteria in the gut.
Concurrently, the patient's ascites was managed with a low-sodium diet and the cautious use of diuretics. Furosemide and spironolactone were initiated, leading to a gradual reduction in abdominal girth and a slight improvement in respiratory effort, as evidenced by a decrease in respiratory rate from 24 to 20 breaths per minute. Despite these improvements, the patient experienced a new complication: a sudden onset of hematemesis, indicating a potential upper gastrointestinal bleed. The patient's blood pressure dropped to 88/54 mmHg with a heart rate of 112 beats per minute, triggering an immediate concern for hypovolemic shock.
The team quickly halted diuretics and initiated fluid resuscitation with intravenous crystalloids while preparing for an urgent upper endoscopy to identify and potentially control the source of bleeding. This development highlighted the delicate balance required in managing liver failure, where interventions for one complication could exacerbate another. The healthcare team recognized the need for vigilant monitoring and rapid response to stabilize the patient and prevent further deterioration, reinforcing the complexity of liver failure management and the interconnection of systemic complications.
Section 3
As the healthcare team proceeded with the urgent upper endoscopy, they encountered esophageal varices, a common complication in patients with chronic liver failure due to portal hypertension. The procedure revealed multiple varices, one of which had ruptured, leading to the hematemesis. The endoscopist successfully performed band ligation to control the bleeding, a critical intervention to stabilize the patient. Meanwhile, the critical care nurse closely monitored the patient's vital signs, noting a gradual improvement in blood pressure to 98/62 mmHg and a decrease in heart rate to 100 beats per minute following fluid resuscitation and stabilization of the bleed.
Lab results from the arterial blood gas analysis showed a partially compensated metabolic acidosis, likely due to the acute blood loss and hypoperfusion. Hemoglobin levels had dropped to 7.4 g/dL, necessitating the administration of packed red blood cells to address the significant anemia and support oxygen delivery. The patient's liver function tests revealed worsening of the liver profile, with elevated bilirubin and transaminase levels, indicating a potential progression of liver dysfunction.
As the immediate crisis of the gastrointestinal bleed was managed, the team recognized the need to reevaluate the patient's overall treatment plan. They deliberated on the potential benefits of a transjugular intrahepatic portosystemic shunt (TIPS) procedure to alleviate portal hypertension and reduce the risk of future variceal bleeds. This consideration underscored the complexity of balancing immediate interventions with long-term management strategies, as the team aimed to stabilize the patient while minimizing the risk of further complications. The patient's journey now hinged on a delicate interplay between acute management and the strategic prevention of future episodes, emphasizing the need for continuous assessment and adaptive clinical reasoning.
Section 4
As the patient stabilized post-endoscopy, the healthcare team continued to monitor for potential complications. Within 24 hours, the patient's condition began to show new signs of deterioration. The nurse noted that the patient's mental status had altered significantly; he was now increasingly lethargic and had difficulty maintaining a coherent conversation. Suspecting hepatic encephalopathy, a common complication of liver failure characterized by a decline in brain function due to the liver's inability to remove toxins from the blood, the team promptly assessed ammonia levels, which returned elevated at 85 µmol/L (normal range: 15-45 µmol/L).
In response to this new development, the team adjusted the treatment regimen to include lactulose, aiming to reduce the systemic ammonia levels and mitigate the effects of encephalopathy. Despite this intervention, the patient also began to exhibit signs of ascites, with noticeable abdominal distension and shifting dullness upon physical examination. An abdominal ultrasound confirmed significant fluid accumulation, prompting discussion among the team about the need for a therapeutic paracentesis to relieve discomfort and prevent further complications such as spontaneous bacterial peritonitis (SBP).
As the patient grappled with these evolving complications, the team faced a critical juncture. The decision to pursue a TIPS procedure became more pressing, given the dual benefits of addressing portal hypertension and potentially alleviating both variceal bleeding and ascites. This decision required careful weighing of the risks, particularly the potential exacerbation of encephalopathy following TIPS. The interdisciplinary team, including hepatology, gastroenterology, and critical care specialists, engaged in a thorough discussion with the patient's family to consider the procedure's implications and align on the best course of action. This phase of the patient's journey highlighted the complexity of managing advanced liver disease and underscored the importance of a tailored, dynamic approach to treatment.
Section 5
As the healthcare team continued to monitor the patient's condition, they observed a change in his respiratory status. The patient began to exhibit mild tachypnea, with a respiratory rate of 24 breaths per minute, and his oxygen saturation decreased to 92% on room air. Concerned about potential respiratory compromise due to ascites, the team performed an arterial blood gas analysis, revealing mild respiratory alkalosis with a pH of 7.47, PaCO2 of 33 mmHg, and PaO2 of 78 mmHg. These findings suggested that the increasing abdominal pressure from ascites might be impairing the patient's diaphragmatic function, leading to his altered respiratory status.
In addition to respiratory changes, the patient's laboratory results revealed worsening coagulopathy, with an international normalized ratio (INR) of 2.5 and a platelet count of 90,000/µL, indicating a heightened risk for bleeding. This raised further concerns about performing invasive procedures such as paracentesis or TIPS, as the risk of bleeding complications could potentially outweigh the benefits. Nonetheless, the patient's discomfort from ascites was becoming more pronounced, and the risk of spontaneous bacterial peritonitis remained a significant concern.
These developments necessitated a reassessment of the patient's treatment plan. The healthcare team discussed the potential need for fresh frozen plasma or platelet transfusions to correct the coagulopathy before any invasive procedures. Additionally, they considered the possibility of initiating diuretic therapy with spironolactone and furosemide to manage the ascites conservatively. The team also re-evaluated the patient's medication regimen to ensure that nephrotoxic drugs were minimized, aiming to preserve kidney function and prevent hepatorenal syndrome. As they navigated these challenges, the team remained committed to providing comprehensive care, balancing the risks and benefits of each intervention while keeping the patient's family informed and involved in the decision-making process.