A patient with liver dysfunction presents with confusion and an elevated ammonia level. Which nursing intervention should the nurse prioritize to address the underlying cause of the patient's altered mental status?

A) Administer lactulose as prescribed to reduce ammonia levels.

B) Increase dietary protein intake to promote liver regeneration.

C) Administer intravenous fluids to manage dehydration.

D) Provide supplemental oxygen to improve cerebral perfusion.

A patient with liver dysfunction presents with elevated ammonia levels, ascites, and confusion. Which nursing intervention should be prioritized to address the hepatic encephalopathy?

A) Administering lactulose to reduce ammonia levels.

B) Initiating a low-protein diet to decrease ammonia production.

C) Preparing the patient for paracentesis to relieve ascites.

D) Monitoring vital signs closely for signs of variceal bleeding.

A patient with worsening ascites and suspected hepatorenal syndrome has just undergone a therapeutic paracentesis. Which nursing intervention is most appropriate to prioritize immediately after the procedure?

A) Monitor the patient's blood pressure and heart rate for signs of hypovolemia.

B) Encourage the patient to ambulate to prevent venous thromboembolism.

C) Administer a high-protein diet to address low serum albumin levels.

D) Place the patient in a supine position to promote fluid redistribution.

A patient with worsening ascites and a recent therapeutic paracentesis is being monitored. Which nursing intervention is most appropriate to prevent complications related to the procedure?

B) Monitor for signs of infection such as fever or abdominal pain

A) Encourage the patient to ambulate immediately after the procedure

B) Monitor for signs of infection such as fever or abdominal pain

C) Increase oral fluid intake to compensate for fluid removal

D) Position the patient flat on their back to prevent hypotension

After a therapeutic paracentesis in a patient with cirrhosis and ascites, the patient shows signs of intravascular volume depletion and potential renal dysfunction. What is the most appropriate nursing intervention to prioritize in this situation?

B) Administer an albumin infusion to support intravascular volume.

A) Administer a diuretic to manage fluid overload.

B) Administer an albumin infusion to support intravascular volume.

C) Increase oral fluid intake to improve renal perfusion.

D) Prepare the patient for emergent dialysis to address renal failure.

A patient who recently underwent therapeutic paracentesis is showing signs of intravascular volume depletion, including elevated heart rate, decreased blood pressure, and reduced urine output. Which nursing intervention should be prioritized to address the patient's current clinical status?

C) Infuse intravenous albumin to support intravascular volume.

A) Administer diuretics to further reduce ascitic fluid.

B) Initiate a fluid restriction to prevent fluid overload.

C) Infuse intravenous albumin to support intravascular volume.

D) Increase oral fluid intake to enhance renal perfusion.

A patient with advanced cirrhosis is experiencing hemodynamic instability and signs of hepatic encephalopathy. Which nursing intervention should be prioritized to address this patient's current condition?

B) Administer lactulose to reduce ammonia levels

A) Initiate a high-protein diet to promote liver regeneration

B) Administer lactulose to reduce ammonia levels

C) Discontinue supplemental oxygen to avoid further respiratory distress

D) Increase intravenous fluids to stabilize blood pressure

A patient with advanced cirrhosis is experiencing increasing lethargy, confusion, and respiratory distress. The healthcare team has initiated interventions including supplemental oxygen and considering lactulose administration. What is the most appropriate nursing action to prioritize in this situation?

D) Reassess vital signs and monitor for signs of shock.

A) Administer lactulose to manage potential hepatic encephalopathy.

B) Increase the oxygen flow rate to improve oxygen saturation.

C) Notify the healthcare provider about the patient's deteriorating mental status.

D) Reassess vital signs and monitor for signs of shock.

A patient with worsening hepatic injury presents with moderate ascites, elevated serum ammonia levels, and altered mental status. Which nursing intervention should be prioritized to address the patient's critical needs?

A) Administer lactulose to decrease serum ammonia levels.

B) Prepare the patient for therapeutic paracentesis to relieve ascites.

C) Monitor the patient's electrolyte levels to prevent imbalances.

D) Educate the patient on dietary modifications to reduce liver workload.

A patient with a known history of liver cirrhosis presents with elevated bilirubin, ALT, and ammonia levels. The patient is also experiencing moderate ascites and partially compensated metabolic acidosis. Which nursing intervention should be prioritized to address the patient's immediate needs?

B) Prepare the patient for therapeutic paracentesis to relieve respiratory distress caused by ascites.

A) Administer lactulose to reduce serum ammonia levels and prevent hepatic encephalopathy.

B) Prepare the patient for therapeutic paracentesis to relieve respiratory distress caused by ascites.

C) Initiate intravenous bicarbonate therapy to correct metabolic acidosis.

D) Monitor vital signs and oxygen saturation continuously to detect early signs of respiratory failure.

Cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic liver injury, often from alcohol abuse or viral hepatitis, leads to repeated cycles of liver cell damage and inflammation. This triggers fibrosis, where excess collagen and connective tissue replace normal liver tissue, disrupting its architecture and function.

• Secondary mechanism: Progressive fibrosis results in the formation of regenerative nodules. These nodules further distort liver structure, impairing blood flow through the liver, which increases pressure in the portal vein (portal hypertension).

• Key complication: Portal hypertension causes blood to bypass the liver, leading to varices, ascites, and splenomegaly. Additionally, impaired liver function reduces detoxification and protein synthesis, contributing to hepatic encephalopathy and coagulopathy.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

• Key past medical history: Alcohol use disorder, Hepatitis C

• Current medications: Lactulose, Spironolactone, Propranolol

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing abdominal discomfort and swelling

• Key symptoms: Ascites, fatigue, jaundice, confusion

• Vital signs: Blood pressure 110/70 mmHg, heart rate 98 bpm, respiratory rate 20 breaths/min, temperature 98.6°F, oxygen saturation 94% on room air

Section 1

New Diagnostic Results:

During the initial assessment, the healthcare team decided to conduct a series of diagnostic tests to better understand the extent of the patient's liver dysfunction and the associated complications. A complete blood count (CBC) revealed thrombocytopenia with a platelet count of 85,000/µL, indicating possible hypersplenism secondary to portal hypertension. Liver function tests showed an elevated bilirubin level of 3.2 mg/dL and a prolonged prothrombin time (PT) of 18 seconds, suggesting impaired liver synthetic function. Serum albumin was low at 2.8 g/dL, correlating with the presence of ascites and edema due to decreased oncotic pressure.

An abdominal ultrasound confirmed moderate ascites and splenomegaly, with a small yet significant amount of fluid present in the peritoneal cavity. The portal vein appeared dilated, reinforcing the diagnosis of portal hypertension. These findings, combined with the patient's confusion and altered mental status, prompted further evaluation for hepatic encephalopathy. An ammonia level was drawn and returned elevated at 78 µmol/L, supporting the suspicion of encephalopathy as a contributing factor to the patient's confusion.

Given these diagnostic results, the healthcare team needs to prioritize interventions that address portal hypertension and hepatic encephalopathy, while carefully monitoring the patient's hemodynamic status and risk of bleeding. This includes managing ascites through diuretics adjustment, considering paracentesis if necessary, and optimizing lactulose therapy to reduce ammonia levels. The team must also evaluate the need for further imaging or endoscopic assessment of potential varices to prevent variceal bleeding, a serious complication of portal hypertension.

Section 2

Change in Patient Status:

Following the initial interventions, the patient exhibited a mixed response. While the use of lactulose resulted in a modest improvement in mental clarity, reducing the frequency of confusion episodes, new concerns emerged. The patient began to complain of increased abdominal discomfort and shortness of breath, particularly when lying flat, suggesting worsening ascites. Upon examination, the patient's abdomen was found to be more distended and tense compared to the initial assessment, and shifting dullness was pronounced, indicating increased fluid accumulation.

Vital signs showed a blood pressure of 100/68 mmHg, a heart rate of 112 beats per minute, respirations at 22 breaths per minute, and oxygen saturation at 92% on room air. These changes, coupled with a further drop in serum albumin to 2.5 g/dL, highlighted the progression of fluid retention and possible hypovolemia. The team also noted a mild increase in serum creatinine to 1.4 mg/dL from a baseline of 1.0 mg/dL, raising concerns for renal perfusion issues possibly linked to hepatorenal syndrome.

Given these developments, the healthcare team decided to perform a therapeutic paracentesis to relieve the symptoms of ascites, while also adjusting the diuretic regimen to prevent further renal compromise. Continuous monitoring was required to assess hemodynamic stability and to address the risk of variceal bleeding, considering the potential for further portal hypertension exacerbation. This evolving clinical picture necessitates ongoing vigilance and timely intervention to prevent the progression of hepatic decompensation and its associated complications.

Section 3

Following the therapeutic paracentesis, the patient initially reported significant relief from abdominal discomfort and an improved ability to breathe while lying flat. However, within 24 hours, the patient’s clinical status shifted again. The healthcare team observed that the patient's heart rate remained elevated at 110 beats per minute, and blood pressure decreased further to 94/60 mmHg. Respiratory rate increased to 24 breaths per minute, and oxygen saturation dropped to 90% on room air. These signs pointed to possible intravascular volume depletion despite the relief of ascitic pressure.

Laboratory results revealed further deterioration. The serum creatinine level had increased to 1.7 mg/dL, suggesting worsening renal function. Urine output decreased, with the patient producing less than 400 mL over the previous 24 hours, signaling potential acute kidney injury. Additionally, the patient’s INR had risen to 1.8, highlighting a decline in synthetic liver function and increased risk of bleeding. A repeat ultrasound of the abdomen showed no significant variceal bleeding but confirmed substantial collateral circulation indicative of severe portal hypertension.

The healthcare team faced the challenge of managing these complications while balancing fluid management and renal perfusion. A cautious approach to diuretic therapy was considered, alongside possible albumin infusion to support intravascular volume without exacerbating ascites. The team also discussed the potential need for more frequent monitoring of renal function and coagulation profiles. This complex clinical scenario required careful prioritization of interventions, aimed at stabilizing renal function and preventing further hepatic decompensation, while closely watching for any signs of variceal bleeding or infection, such as spontaneous bacterial peritonitis.

Section 4

Change in Patient Status:

As the healthcare team initiated interventions, including cautious diuretic therapy and albumin infusion, the patient's condition continued to evolve. Despite initial efforts to stabilize intravascular volume, the patient's heart rate increased further to 120 beats per minute, and blood pressure dropped to 88/55 mmHg, indicating persistent hemodynamic instability. Respiratory distress became more pronounced, with the patient exhibiting labored breathing and an increased respiratory rate of 28 breaths per minute. Oxygen saturation remained concerning at 88% on room air, prompting the team to administer supplemental oxygen to maintain adequate oxygenation.

In addition to hemodynamic challenges, the patient's mental status began to deteriorate. The patient became increasingly lethargic and confused, raising concerns about hepatic encephalopathy, a complication often associated with liver failure. The healthcare team initiated a thorough assessment to evaluate the patient's neurological status and considered the administration of lactulose to help reduce ammonia levels in the bloodstream. These developments required prompt attention to prevent further decompensation and to address both the hemodynamic and neurological aspects of the patient's clinical picture.

In light of these changes, the team prioritized continuous monitoring of vital signs, mental status, and renal function. The need for vigilant observation and timely intervention became paramount, as the patient's condition was precariously balanced between stabilization and potential deterioration. This complex scenario underscored the necessity for a multidisciplinary approach, with collaboration between hepatology, nephrology, and critical care specialists to navigate the intricate challenges posed by advanced cirrhosis and its complications.

Section 5

New Diagnostic Results:

As the healthcare team continued to address the patient's deteriorating condition, additional diagnostic tests were performed to provide further insights into the underlying issues and guide the treatment plan. A comprehensive metabolic panel revealed further derangements in liver function tests, with significantly elevated bilirubin levels at 5.4 mg/dL and an increase in alanine aminotransferase (ALT) to 145 U/L, indicating worsening hepatic injury. Additionally, the patient's serum ammonia levels were markedly elevated at 98 µmol/L, corroborating the suspicion of hepatic encephalopathy as the cause of the patient's altered mental status.

Further imaging studies, including an abdominal ultrasound, were conducted to evaluate for potential complications such as ascites or portal vein thrombosis. The ultrasound confirmed moderate ascites, which was contributing to the patient's respiratory distress by increasing abdominal pressure and reducing diaphragmatic excursion. No evidence of portal vein thrombosis was noted, which provided some relief in terms of potential vascular complications. However, the presence of ascites necessitated consideration of therapeutic paracentesis to alleviate the pressure and improve respiratory mechanics.

The patient also underwent an arterial blood gas analysis, which showed a partially compensated metabolic acidosis, with a pH of 7.32, bicarbonate level of 18 mEq/L, and a PaCO2 of 32 mmHg. This finding was consistent with the increased respiratory effort and reflected the body's attempt to compensate for the metabolic derangements. The healthcare team recognized the need for immediate intervention to address the fluid overload and stabilize the patient's acid-base balance, while concurrently managing the neurological symptoms with lactulose therapy. This complex interplay of diagnostic results required coordinated efforts to prioritize interventions and mitigate the risk of further decompensation.