cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic damage to the liver (due to alcoholism, hepatitis, or other factors) causes liver cells to die and be replaced by scar tissue in a process called fibrosis. Over time, this scar tissue accumulates, resulting in cirrhosis and impaired liver function.

• Secondary mechanism: The scar tissue disrupts the normal structure and function of the liver, impeding blood flow through the organ. This increases pressure in the portal vein system (portal hypertension), causing complications such as varices and ascites.

• Key complication: The liver's diminished ability to detoxify harmful substances can lead to hepatic encephalopathy. This condition can cause confusion, drowsiness, and tremors, and in severe cases, coma.

Patient Profile

Demographics:

56-year-old male, construction worker

History:

• Diagnosed with Hepatitis C 10 years ago, history of heavy alcohol consumption

• Current medications: Interferon, Ribavirin, multivitamin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Abdominal pain and swelling, fatigue, loss of appetite

• Key symptoms: Jaundice, ascites, spider angiomas, palmar erythema, gynecomastia, mild confusion

• Vital signs: Blood pressure 110/70 mmHg, pulse 85 bpm, temperature 98.6°F, respiratory rate 16 bpm, oxygen saturation 95%

Section 1

Change in Patient Status:

The patient's condition worsened over the next 24 hours. His confusion increased, and he was noted to have subtle hand tremors. His oxygen saturation dropped to 92% on room air, and his respiratory rate increased to 22 bpm. He was drowsy but arousable. His blood pressure remained stable at 110/70 mmHg, but his pulse increased to 96 bpm. The abdominal distension was visibly more pronounced, and the patient complained of increased discomfort. On auscultation, bowel sounds were absent, and hepatomegaly was observed on palpation. The patient's skin and sclera became more jaundiced.

This clinical picture suggested the development of more severe hepatic encephalopathy, possibly precipitated by worsening liver function and the development of spontaneous bacterial peritonitis (SBP). The presence of hepatomegaly, increased abdominal distension, and absent bowel sounds were alarming findings that required immediate attention. The increase in respiratory rate and decrease in oxygen saturation also suggested respiratory distress, possibly due to the pressure of the ascitic fluid or the development of a hepatic hydrothorax.

The worsening of the patient's clinical status required urgent reassessment and intervention, including a diagnostic paracentesis to investigate the possibility of SBP, and further measures to manage hepatic encephalopathy and respiratory distress. This situation demanded a high level of clinical reasoning to prioritize interventions and consider potential complications.

Section 2

New Diagnostic Results:

Following the diagnostic paracentesis, the patient's peritoneal fluid analysis demonstrated a polymorphonuclear leukocyte (PMN) count of 1200 cells/mm3, significantly higher than the 250 cells/mm3 threshold that typically suggests spontaneous bacterial peritonitis. The fluid culture was sent to the lab for identification of the specific causative organism.

In addition, laboratory results showed a significant increase in the patient's serum ammonia level at 120 µmol/L, indicating severe hepatic encephalopathy. His prothrombin time (PT) was prolonged at 18 seconds, suggesting coagulopathy due to impaired liver function. His bilirubin level was also elevated at 4.5 mg/dL, and his albumin level had dropped to 2.2 g/dL.

These new findings confirmed the suspected diagnoses of SBP and hepatic encephalopathy. The elevated PT and low albumin level further suggested more advanced liver disease. The next step would require careful consideration of treatment options to manage these complications and prevent further deterioration of the patient's condition.

Section 3

Change in Patient Status:

Over the next 24 hours, the patient's condition continued to deteriorate. He became increasingly lethargic and disoriented, consistent with the worsening hepatic encephalopathy. His jaundice intensified, and he developed noticeable asterixis, or "liver flap," a tremor of the hands when the wrists are extended. Despite fluid restriction and diuretic therapy, his abdominal distension and discomfort persisted, indicating uncontrolled ascites related to the advanced liver disease and SBP.

In addition, the patient's vitals showed signs of instability. His blood pressure dropped to 90/60 mmHg, and his heart rate increased to 98 beats per minute, raising concerns about possible septic shock secondary to SBP. His respiratory rate also increased to 24 breaths per minute, possibly due to the discomfort from the ascites or the body's attempt to compensate for the metabolic disturbances caused by his liver disease. The gradual but steady decline in the patient's clinical status underscores the urgency of a comprehensive treatment plan and vigilant monitoring.

Section 4

New Diagnostic Results:

The latest lab results showed a significant increase in the patient's serum bilirubin levels to 5.8 mg/dL, up from 3.2 mg/dL, indicating a further decline in liver function. His albumin level dropped to 2.9 g/dL, below the normal range of 3.5-5.5 g/dL, reflecting poor protein synthesis by the liver and contributing to the persistent ascites. Furthermore, the patient's international normalized ratio (INR) was found to be elevated at 1.5, signifying a prolonged clotting time and an increased risk of bleeding due to impaired hepatic synthesis of clotting factors.

Additionally, a repeat paracentesis showed an increased neutrophil count of 3000 cells/microL, suggesting a worsening of the SBP. Blood cultures were sent and a gram stain from the ascitic fluid identified gram-negative bacilli, typically seen in an SBP infection. The worsening lab values and continued deterioration of the patient's clinical status necessitate aggressive and prompt treatment to address the underlying SBP and manage the complications of advanced liver disease.

Section 5

New Complications:

Over the next 24 hours, the patient's condition seemed to further deteriorate, despite the aggressive treatment measures initiated. The patient started complaining of severe abdominal pain, which was noticeably worse than before. Upon examination, the patient's abdomen was found to be more distended and tender to palpation, suggesting an exacerbation of his ascites. His blood pressure also dropped to 90/60 mmHg from a previous reading of 120/80 mmHg, and his heart rate increased to 110 beats per minute, reflecting possible hypovolemic shock secondary to sepsis or gastrointestinal bleeding, both common complications in advanced liver disease.

Furthermore, he became increasingly confused and disoriented, a worrying sign of possible hepatic encephalopathy, a neuropsychiatric syndrome caused by liver failure. His ammonia level was found to be elevated at 120 umol/L, above the normal range of 15-45 umol/L, confirming the suspicion of hepatic encephalopathy. This new development calls for immediate intervention to prevent further progression of the condition, which can lead to coma and death if left untreated. The clinical team must now balance the need to manage these new complications while continuing to address the underlying SBP and liver disease.