Cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Liver cell damage – Chronic liver diseases like hepatitis or excessive alcohol consumption cause persistent inflammation, leading to liver cell death. Over time, this initiates a process of scarring or fibrosis, leading to structural changes in the liver.

• Secondary mechanism: Fibrosis to Cirrhosis – As the liver continues to be damaged, fibrosis progresses to cirrhosis. The liver becomes stiff and nodular, disrupting the normal flow of blood and bile. This leads to decreased liver function, including impaired detoxification, protein synthesis and hormone regulation.

• Key complication: Portal Hypertension – Cirrhosis causes resistance to blood flow in the liver, leading to increased pressure in the portal vein (portal hypertension). This can cause complications like varices, ascites and hepatic encephalopathy, which significantly impact patient's quality of life and survival.

Patient Profile

Demographics:

63-year-old male, retired factory worker

History:

• Key past medical history: Chronic Hepatitis C infection, alcohol abuse, diagnosed with mild cirrhosis 5 years ago

• Current medications: Diuretics, Beta-blockers, Multivitamins, Lactulose

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue, abdominal pain, and swelling

• Key symptoms: Jaundice, loss of appetite, weight loss, easy bruising, edema in legs, and mental confusion

• Vital signs: Blood pressure 130/85 mmHg, pulse 92 bpm, temperature 98.2°F, respiratory rate 18/min, oxygen saturation 94% on room air.

Section 1

New Diagnostic Results:

On further examination, laboratory results showed elevated liver enzymes (ALT 120 U/L, AST 145 U/L), increased total bilirubin (2.8 mg/dL), and decreased albumin levels (2.8 g/dL), consistent with deteriorating liver function. The patient's INR was also elevated at 1.8, indicating an increased risk of bleeding. An abdominal ultrasound revealed a coarse liver texture and signs of portal hypertension, including spleen enlargement and ascites.

The most alarming finding was the patient's ammonia level, which was significantly elevated at 95 μmol/L. This, coupled with the patient's reported mental confusion, suggests the likely development of hepatic encephalopathy. These results indicate a progression in the severity of the patient's cirrhosis and highlight the immediate need for intervention to manage the patient's symptoms and prevent further complications. The healthcare team must now decide on the best course of action, considering the patient's worsening condition and the potential risks and benefits of various treatment options.

Section 2

Change in Patient Status:

In the following days, the patient's condition worsened, with increasing confusion and drowsiness, indicating an advancement in hepatic encephalopathy. The patient also developed a low-grade fever (38.2°C), which could suggest an infection. Further complications included worsening ascites, as evidenced by an increase in abdominal girth from 102cm to 108cm over a period of two days, and the onset of mild jaundice. The patient's skin and sclera showed a yellowish discoloration, and the bilirubin level had increased to 3.8 mg/dL.

The patient also reported increasing fatigue and a decreased appetite, with a subsequent weight loss of 2 kg over a week. The patient's blood pressure dropped to 90/60 mmHg, which could be due to the reduced circulating blood volume from the loss of appetite and fluid into the peritoneal cavity. The healthcare team must now reassess the patient's condition and adjust the treatment plan as necessary to manage the new complications effectively while preventing further deterioration. This might involve a combination of medication adjustments, dietary changes, and possibly more invasive interventions.

Section 3

Change in Patient Status:

The patient's status continued to decline over the next few days. Increased lethargy, disorientation, and slight hand tremors were noticed, indicating a progression in hepatic encephalopathy. The patient's fever persisted, now fluctuating around 38.5°C, thereby raising further suspicion for an underlying infection. The ascites also continued to worsen, with the patient's abdominal girth now measuring 112cm, and the patient reported increasing discomfort and shortness of breath, likely due to the pressure on the diaphragm. The jaundice became more pronounced, and the bilirubin level had now risen to 4.2 mg/dL.

The patient's blood pressure remained low at 88/58 mmHg, and the heart rate had increased to 108 beats per minute, possibly a compensatory response to the low blood pressure. Additionally, the patient reported worsening fatigue and had lost another kilogram. Laboratory results showed a decreased hemoglobin level of 10 g/dL, indicating possible anemia, and an elevated white blood cell (WBC) count of 13,000/uL, suggestive of an infection or inflammation. The healthcare team now needs to conduct further investigation to identify the underlying cause of the fever and elevated WBC count, manage the worsening hepatic encephalopathy and ascites, and address the patient's nutritional status and anemia.

Section 4

New Diagnostic Results:

An urgent abdominal ultrasound was ordered to further investigate the worsening ascites and the potential underlying infection. The results revealed an increase in the volume of ascitic fluid, confirming the clinical observation. In addition, septations were observed within the fluid, which is consistent with infected ascites, possibly spontaneous bacterial peritonitis (SBP). Simultaneously, a paracentesis was performed and the ascitic fluid was sent to the lab for analysis. The fluid analysis revealed a high neutrophil count of 500 cells/mm3, confirming the diagnosis of SBP.

The culture sensitivity report of the ascitic fluid indicated the presence of Escherichia coli, which is a common pathogen in SBP. Additionally, blood cultures were sent, which also returned positive for the same organism. Further laboratory investigations showed an elevated prothrombin time (PT) of 18 seconds and international normalized ratio (INR) of 1.7, indicating a potential coagulopathy, which is common in liver disease. These new diagnostic results provide the basis for the next steps in patient management, including the initiation of appropriate antibiotic therapy and measures to manage the coagulopathy and worsening ascites. The healthcare team must also consider the implications of the confirmed SBP on the patient's overall prognosis.

Section 5

After initiating the antibiotic therapy for SBP, the patient was monitored closely for changes in status. Over the next 48 hours, the patient's condition deteriorated. He became increasingly confused and disoriented, a clinical condition known as hepatic encephalopathy. This was likely due to the accumulation of toxins, particularly ammonia, that the cirrhotic liver could not adequately clear. The patient's vital signs also showed significant alterations; his heart rate increased to 120 beats per minute, respiratory rate was 24 breaths per minute, and his blood pressure dropped to 90/60 mmHg, suggesting possible septic shock.

In response to these changes, lactulose was administered to reduce serum ammonia levels and to improve his mental status. Despite these interventions, the patient's condition did not improve significantly. A repeat lab investigation revealed an increase in the patient's serum bilirubin level to 5 mg/dL from a baseline of 2.5 mg/dL, indicating worsening liver function. The patient's international normalized ratio (INR) also increased to 2.0 from 1.7, suggesting further impairment in the liver's ability to produce clotting factors. The healthcare team recognized that these changes indicated a worsening prognosis and the potential need for more aggressive interventions, including a potential liver transplant.