cirrhosis - Nursing Case Study
Pathophysiology
• Primary mechanism: Chronic liver injury leads to persistent inflammation, which stimulates fibrogenesis. This process involves the activation of hepatic stellate cells that deposit excess collagen, causing fibrosis and architectural distortion of the liver.
• Secondary mechanism: The progression of fibrosis results in the formation of regenerative nodules, disrupting normal blood flow and liver function. This leads to increased portal pressure and impaired liver regeneration.
• Key complication: Portal hypertension from increased resistance to portal blood flow can result in ascites, variceal bleeding, and splenomegaly, significantly impacting patient health and requiring careful management.
Patient Profile
Demographics:
56 years old, male, construction worker
History:
• Key past medical history: Chronic Hepatitis C infection, alcohol use disorder (20 years, abstinent for 1 year), type 2 diabetes mellitus
• Current medications: Metformin 500 mg twice daily, Lisinopril 10 mg once daily, Lactulose 30 mL twice daily, Propranolol 20 mg twice daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Increasing abdominal swelling and discomfort
• Key symptoms: Fatigue, jaundice, increasing abdominal girth, mild confusion, leg edema
• Vital signs: Blood pressure 110/70 mmHg, heart rate 98 bpm, respiratory rate 20 breaths per minute, temperature 37.8°C, oxygen saturation 94% on room air
Section 1
As the medical team conducts an initial assessment of the 56-year-old male with a history of cirrhosis, several significant findings emerge that require careful clinical reasoning. On physical examination, his abdomen is distended with positive fluid wave, indicating the presence of ascites. The patient's sclerae are icteric, and there is notable spider angioma on his upper chest. His lower extremities show pitting edema, especially around the ankles, which aligns with fluid retention. A mental status examination reveals mild confusion and disorientation to time, suggestive of hepatic encephalopathy, likely exacerbated by the buildup of ammonia due to impaired liver detoxification.
Laboratory results further illustrate the extent of liver dysfunction. The patient's serum albumin is low at 2.5 g/dL, contributing to the oncotic pressure imbalance and subsequent fluid accumulation. His total bilirubin is elevated at 4.0 mg/dL, correlating with his jaundice. Additionally, the prothrombin time is prolonged, indicating a decreased synthesis of clotting factors by the liver. An abdominal ultrasound confirms the presence of ascites and shows signs of splenomegaly, consistent with portal hypertension. The portal vein diameter is increased, further supporting the diagnosis.
These findings necessitate the implementation of a comprehensive care plan targeting his complications. Adjustments to his current medications are considered to better manage his hepatic encephalopathy and ascites. Diuretics may be introduced to promote fluid excretion, and the dosage of lactulose could be titrated to optimize ammonia clearance. The healthcare team also contemplates the need for a paracentesis to relieve abdominal pressure and improve breathing. Ongoing monitoring for signs of variceal bleeding remains critical, given the elevated risk associated with portal hypertension. These strategies aim to stabilize the patient's condition and prevent further deterioration as the team prepares for the next phase of his management journey.
Section 2
Two days following the initial interventions, the medical team observes a change in the patient's status, prompting a reassessment of both his clinical condition and the effectiveness of the current treatment plan. The patient appears more lethargic, with his mild confusion progressing to moderate disorientation; he now struggles to recognize familiar faces and places. Despite an initial titration of lactulose aimed at enhancing ammonia clearance, these neurological symptoms suggest a worsening hepatic encephalopathy. A follow-up ammonia level is obtained, revealing an increase to 150 µmol/L, up from the previous 100 µmol/L, indicating inadequate control of the metabolic derangement.
Simultaneously, the patient reports increased abdominal discomfort and difficulty breathing, which the team attributes to the ascites. A repeat ultrasound shows further ascites accumulation despite the introduction of diuretics. His blood pressure has dropped to 98/60 mmHg, and his heart rate has increased to 105 bpm, raising concerns about effective circulating volume and potential hemodynamic instability. Laboratory evaluations reveal a further decline in serum albumin to 2.1 g/dL, exacerbating the fluid imbalance. Moreover, his hemoglobin level has decreased to 9.0 g/dL from 11.0 g/dL, necessitating an investigation for potential gastrointestinal bleeding, a possible complication of portal hypertension.
These developments necessitate immediate clinical reasoning and adjustments to his care plan. The team considers increasing the frequency and dosage of lactulose, alongside exploring alternative ammonia-lowering therapies such as rifaximin. Given the ineffective diuresis, a paracentesis is scheduled to alleviate ascites and improve respiratory function. The decrease in hemoglobin and the risk of variceal bleeding prompt an urgent endoscopic evaluation to identify and manage any bleeding sources. These strategic interventions aim to stabilize the patient, mitigate complications, and reassess the overall trajectory of his liver disease management.
Section 3
As the medical team implements the revised care plan, the patient undergoes a scheduled paracentesis, which successfully drains approximately 4 liters of ascitic fluid. Post-procedure, the patient reports a noticeable reduction in abdominal discomfort and an improvement in his ability to breathe more comfortably. However, despite these initial positive outcomes, the healthcare providers remain vigilant, aware that the removal of such a significant volume of fluid could potentially lead to hypovolemia and electrolyte imbalances. To counteract this, albumin infusion is administered to support vascular volume and prevent circulatory dysfunction.
Subsequent lab results show a slight improvement in ammonia levels, which have decreased to 120 µmol/L following the adjustment in lactulose dosing and the initiation of rifaximin therapy. However, the patient's mental status remains a concern; although slightly improved, he continues to exhibit moderate disorientation, suggesting the need for continuous monitoring and possible further adjustments in treatment. Meanwhile, the endoscopic evaluation reveals esophageal varices, though fortunately, no active bleeding is detected at this time. Prophylactic measures, including beta-blocker therapy, are initiated to reduce the risk of future variceal hemorrhage.
Despite these interventions, the patient's overall condition underscores the complexity of managing advanced cirrhosis with multiple complications. The medical team recognizes the importance of a multidisciplinary approach, involving hepatologists, nutritionists, and nursing specialists to optimize care. As they continue to monitor the patient's response to treatment and assess his nutritional status, the emphasis remains on preventing further deterioration, managing symptoms, and supporting his quality of life. The next steps in the patient's care will involve ongoing assessment for potential new complications, adjustment of the therapeutic regimen, and planning for long-term management strategies, including discussions around potential liver transplantation candidacy.
Section 4
As the multidisciplinary team continues to monitor the patient, a change in his status becomes apparent, prompting a reevaluation of the care plan. Over the next 48 hours, the patient develops mild jaundice, and his sclerae appear slightly icteric, indicating a potential exacerbation of his liver dysfunction. His vital signs show a blood pressure of 100/65 mmHg, with a heart rate of 95 beats per minute, both of which suggest a possible compensatory response to reduced circulatory volume following the paracentesis. His respiratory rate remains stable at 18 breaths per minute, and his oxygen saturation is 96% on room air. However, the nursing team notes increased fatigue and lethargy, with the patient spending more time in bed and requiring assistance with activities of daily living.
Concurrent lab work reveals a concerning elevation in his bilirubin levels, now at 3.5 mg/dL, up from 2.8 mg/dL prior to the paracentesis. His liver function tests show further compromise, with an AST of 85 U/L and an ALT of 78 U/L, highlighting the ongoing hepatic strain. Moreover, his INR is slightly elevated at 1.5, indicating impaired synthetic function and heightened bleeding risk. Despite the initial improvement in ammonia levels, the patient’s persistent disorientation necessitates the continuation of lactulose and rifaximin, along with careful electrolyte monitoring to prevent further complications.
In light of these developments, the medical team decides to intensify the supportive measures, with a focus on optimizing the patient's nutrition and addressing potential dehydration. A tailored nutritional plan is devised by the dietitian, emphasizing easy-to-digest, protein-rich meals to support hepatic function while monitoring for signs of hepatic encephalopathy. The hepatologist discusses the possibility of incorporating additional pharmacotherapy to manage cholestasis and improve bile flow. The ongoing evaluation of the patient's condition will guide further interventions, with an emphasis on stabilizing his current status and considering long-term options such as liver transplantation eligibility, while ensuring that he receives comprehensive care addressing both his physical and psychosocial needs.
Section 5
Two days later, the patient's condition exhibits further changes that necessitate immediate attention. He begins to exhibit signs of increasing abdominal distension and discomfort, despite the recent paracentesis, suggesting rapid reaccumulation of ascitic fluid. The nursing staff measures his abdominal girth, noting an increase of 4 centimeters since the last measurement. His blood pressure has decreased to 95/60 mmHg, with a heart rate now elevated to 105 beats per minute, indicating a potential hypovolemic state or worsening portal hypertension. Additionally, the patient complains of mild dyspnea, and his oxygen saturation has decreased slightly to 92% on room air, prompting consideration of fluid overload or compromised respiratory function due to ascites.
A repeat ultrasound of the abdomen confirms significant ascitic fluid reaccumulation. The patient's laboratory results show a further increase in bilirubin, now at 4.0 mg/dL, and a slight drop in albumin levels to 2.8 g/dL, suggesting worsening liver function and decreased oncotic pressure contributing to fluid shift. His renal function tests reveal a serum creatinine of 1.5 mg/dL, up from 1.2 mg/dL, indicating possible hepatorenal syndrome or acute kidney injury secondary to liver dysfunction. The elevated INR persists at 1.6, increasing concerns about coagulopathy and bleeding risk.
In response to these developments, the medical team decides to initiate diuretic therapy cautiously to manage ascites while monitoring renal function closely. They also consider the introduction of midodrine to address potential hepatorenal syndrome, alongside continued albumin infusion to support circulatory volume. The hepatologist emphasizes the need for frequent monitoring of electrolytes, renal function, and hemodynamic status to prevent further complications. As the team evaluates the patient's eligibility for liver transplantation, they also explore the need for advanced care planning and potential palliative measures to address the patient's quality of life and comfort.