A patient with liver cirrhosis presents with severe abdominal distension, confusion, jaundice, and fever. Laboratory findings indicate low serum albumin, elevated INR, high serum ammonia, and increased creatinine. The nurse suspects spontaneous bacterial peritonitis (SBP) and initiates empirical antibiotic therapy. Which intervention should the nurse prioritize to address the patient's respiratory compromise due to ascites?

C) Prepare the patient for a therapeutic paracentesis to relieve abdominal pressure

A) Administer supplemental oxygen to maintain adequate oxygen saturation

B) Position the patient in a high Fowler's position to facilitate diaphragmatic movement

C) Prepare the patient for a therapeutic paracentesis to relieve abdominal pressure

D) Encourage deep breathing exercises and incentive spirometry to improve lung expansion

A patient with advanced liver cirrhosis presents with signs of hepatic encephalopathy, ascites, and suspected spontaneous bacterial peritonitis (SBP). The nurse is preparing to administer the prescribed empirical antibiotic therapy. Which intervention should the nurse prioritize to ensure patient safety and maximize therapeutic effectiveness?

B) Assess the patient's allergy history prior to administering antibiotics.

A) Administer a diuretic to reduce ascites before starting antibiotics.

B) Assess the patient's allergy history prior to administering antibiotics.

C) Monitor the patient's blood glucose levels closely during antibiotic therapy.

D) Initiate a fluid restriction protocol to manage peripheral edema.

A patient with spontaneous bacterial peritonitis and worsening hepatic encephalopathy develops respiratory distress with bilateral pleural effusions and type 1 hepatorenal syndrome. Which nursing intervention is the highest priority to stabilize the patient's condition?

B) Initiate vasopressor support to maintain adequate mean arterial pressure.

A) Administer lactulose to reduce ammonia levels and improve mental status.

B) Initiate vasopressor support to maintain adequate mean arterial pressure.

C) Provide supplemental oxygen to maintain oxygen saturation above 92%.

D) Administer intravenous albumin to support renal perfusion and intravascular volume.

A patient diagnosed with spontaneous bacterial peritonitis (SBP) and hepatic encephalopathy is experiencing respiratory decline with bilateral pleural effusions and renal impairment. Given the patient's complex condition, which nursing intervention is most critical to prioritize to stabilize the patient and address the multi-organ involvement?

C) Administering intravenous albumin and initiating vasopressor support to maintain hemodynamic stability.

A) Administering lactulose to reduce ammonia levels and prevent further hepatic encephalopathy.

B) Initiating supplemental oxygen and ensuring adequate ventilation to improve respiratory status.

C) Administering intravenous albumin and initiating vasopressor support to maintain hemodynamic stability.

D) Consulting with nephrology to initiate renal replacement therapy for deteriorating renal function.

A patient with hepatic encephalopathy, respiratory distress, and hemodynamic instability is being managed in the ICU. Despite intensified lactulose therapy and rifaximin, the patient's mental status and respiratory function continue to decline. Which nursing intervention is most critical to implement immediately?

B) Initiate non-invasive ventilation to improve oxygenation and reduce work of breathing.

A) Increase the frequency of lactulose administration to reduce ammonia levels.

B) Initiate non-invasive ventilation to improve oxygenation and reduce work of breathing.

C) Administer an additional dose of vasopressors to stabilize blood pressure.

D) Prepare for continuous renal replacement therapy to manage worsening renal function.

A patient with refractory hepatic encephalopathy and deteriorating respiratory and hemodynamic status is being managed in the ICU. Based on the current clinical presentation, what is the priority nursing intervention to address his compromised respiratory status?

B) Prepare for possible intubation and mechanical ventilation to secure the airway and support oxygenation.

A) Increase the rate of lactulose administration to reduce ammonia levels.

B) Prepare for possible intubation and mechanical ventilation to secure the airway and support oxygenation.

C) Initiate continuous renal replacement therapy to address metabolic acidosis and support renal function.

D) Administer additional vasopressors to stabilize blood pressure and improve perfusion.

A patient with decompensated cirrhosis develops significant coagulopathy and is at risk for bleeding due to invasive procedures. Which nursing intervention is most appropriate to prioritize in this situation?

B) Prepare for a plasma transfusion to mitigate bleeding risk.

A) Administer vitamin K to the patient to correct coagulopathy.

B) Prepare for a plasma transfusion to mitigate bleeding risk.

C) Monitor for signs of volume overload due to potential transfusion.

D) Evaluate the need for additional vasopressors to manage hemodynamic instability.

A patient with decompensated cirrhosis is experiencing multiple complications, including coagulopathy, spontaneous bacterial peritonitis (SBP), and hemodynamic instability. The medical team is considering various interventions. As the nurse, what is the priority nursing intervention to address the immediate risk to the patient’s safety?

C) Monitoring and adjusting vasopressor therapy to stabilize the patient's blood pressure.

A) Administering intravenous broad-spectrum antibiotics to treat the suspected infection.

B) Preparing for a plasma transfusion to correct the coagulopathy and reduce bleeding risk.

C) Monitoring and adjusting vasopressor therapy to stabilize the patient's blood pressure.

D) Initiating continuous renal replacement therapy to manage metabolic derangements.

A 65-year-old male with a history of liver cirrhosis is being treated for spontaneous bacterial peritonitis. Despite treatment, the patient shows signs of declining respiratory and neurological status. Which nursing intervention is the most critical to implement immediately to address the patient's current condition?

B) Escalate respiratory support to BiPAP to improve oxygenation.

A) Initiate continuous renal replacement therapy to manage lactic acidosis.

B) Escalate respiratory support to BiPAP to improve oxygenation.

C) Administer vasopressors to stabilize blood pressure.

D) Re-evaluate the antibiotic regimen based on culture sensitivities.

A patient with spontaneous bacterial peritonitis is experiencing a rapid decline in condition, presenting with fever, hypotension, tachycardia, tachypnea, hypoxemia, and confusion. The nurse needs to prioritize interventions to stabilize the patient. Which of the following should be the nurse's immediate priority action?

C) Administer IV fluids and vasopressors to address hypotension and tissue perfusion.

A) Increase the supplemental oxygen flow rate to improve oxygen saturation.

B) Prepare for endotracheal intubation due to declining respiratory status.

C) Administer IV fluids and vasopressors to address hypotension and tissue perfusion.

D) Initiate continuous renal replacement therapy to manage lactic acidosis and renal impairment.

cirrhosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic liver injury, often due to chronic alcohol use or hepatitis, leads to persistent inflammation and hepatocyte necrosis, triggering fibrogenesis. Activated hepatic stellate cells deposit collagen, replacing normal liver tissue with fibrotic scar tissue, disrupting liver architecture and function.

• Secondary mechanism: Progressive fibrosis and regenerative nodules cause increased intrahepatic resistance, leading to portal hypertension. This increased pressure in the portal venous system results in the development of collateral circulation and varices, contributing to potential life-threatening bleeding.

• Key complication: Portal hypertension and impaired synthetic liver function lead to ascites, hepatorenal syndrome, and hepatic encephalopathy, severely impacting patient morbidity and mortality by causing fluid retention, renal dysfunction, and neurological impairment due to toxin accumulation.

Patient Profile

Demographics:

56-year-old male, former construction worker

History:

• Key past medical history: Alcoholic liver disease, Hepatitis C, Type 2 Diabetes, Hypertension

• Current medications: Furosemide, Spironolactone, Lactulose, Metformin, Enalapril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and swelling, confusion

• Key symptoms: Jaundice, ascites, esophageal varices, hepatic encephalopathy, peripheral edema

• Vital signs: Blood pressure 92/58 mmHg, heart rate 118 bpm, respiratory rate 24 breaths per minute, temperature 101.3°F, oxygen saturation 88% on room air

Section 1

Upon initial assessment, the patient presents with severe abdominal distension and tenderness, particularly in the right upper quadrant. His confusion is evident, with disorientation to time and place, indicating a progression of hepatic encephalopathy. The patient exhibits significant jaundice, and his skin is cool and clammy. Peripheral edema is noted bilaterally in the lower extremities, extending to the mid-calf. The abdominal exam reveals positive shifting dullness, confirming the presence of ascites. Auscultation of the lungs indicates decreased breath sounds at the bases, suggestive of possible pleural effusion secondary to ascites.

Laboratory results reveal a critically low serum albumin level of 2.1 g/dL, exacerbating the ascitic fluid accumulation due to reduced oncotic pressure. The patient's INR is elevated at 2.5, indicating impaired synthetic function of the liver and increased bleeding risk. Serum ammonia levels are significantly raised at 85 µmol/L, correlating with his encephalopathy symptoms. Renal function tests show a concerning rise in creatinine to 2.2 mg/dL, suggesting the onset of hepatorenal syndrome. Arterial blood gas analysis indicates a partially compensated respiratory alkalosis, with a pH of 7.47, PaCO2 of 30 mmHg, and PaO2 of 60 mmHg, reflecting compromised respiratory function likely due to ascites-related diaphragmatic elevation.

The patient's unstable hemodynamic status, with persistent hypotension and tachycardia, coupled with the signs of systemic infection, necessitates immediate intervention. The fever and elevated white blood cell count of 15,000/mm³ raise suspicion for spontaneous bacterial peritonitis (SBP), a severe complication in patients with cirrhotic ascites. Empirical antibiotic therapy is initiated, and a diagnostic paracentesis is performed to confirm the presence of SBP. These findings require advanced clinical reasoning to prioritize interventions, address potential multi-organ failure, and prepare for possible escalation to intensive care management.

Section 2

Following the initiation of empirical antibiotic therapy and diagnostic paracentesis, the patient's condition remains precarious. The paracentesis confirms spontaneous bacterial peritonitis, with elevated polymorphonuclear leukocytes in the ascitic fluid. Despite the early administration of antibiotics, the patient develops new complications overnight. His mental status deteriorates further, progressing from confusion to somnolence, indicative of worsening hepatic encephalopathy. The ammonia levels rise to 105 µmol/L, necessitating urgent measures to reduce neurotoxic burden. Lactulose therapy is intensified to facilitate ammonia clearance, while rifaximin is added to the regimen to target gut flora contributing to ammonia production.

In the midst of managing hepatic complications, the patient's respiratory status declines. The decreased breath sounds at the lung bases progress to audible crackles, and his oxygen saturation drops to 88% on room air. A chest X-ray reveals bilateral pleural effusions, more pronounced on the right side, and bilateral basilar infiltrates suggestive of infection or atelectasis. The patient's respiratory rate climbs to 28 breaths per minute, and he requires supplemental oxygen via nasal cannula to maintain adequate oxygenation.

The renal function further deteriorates, with creatinine rising to 3.0 mg/dL, confirming the progression to type 1 hepatorenal syndrome. Urgent nephrology consultation is sought for potential renal replacement therapy, while intravenous albumin is administered to support intravascular volume and renal perfusion. The patient's hypotension persists despite fluid resuscitation, necessitating the initiation of vasopressor support to maintain mean arterial pressure. The complexity of multi-organ involvement requires a coordinated, multidisciplinary approach to stabilize the patient and prevent further decompensation. As the team prepares for potential transfer to the intensive care unit, they must prioritize interventions that address the interconnected pathophysiological processes and anticipate further complications.

Section 3

Change in Patient Status:

As the medical team continues to manage the patient's complex condition, a noticeable change in his status occurs. Despite intensified lactulose therapy and the addition of rifaximin, the patient's mental status fails to improve. He becomes increasingly unresponsive, with a Glasgow Coma Scale score dropping to 9, prompting concerns about his airway protection. The elevated ammonia levels remain a significant challenge, and the team considers the possibility of a more refractory hepatic encephalopathy, potentially necessitating additional interventions such as extracorporeal liver support systems.

The patient's respiratory status also deteriorates further. Despite supplemental oxygen, his oxygen saturation fluctuates between 85-88%, and his respiratory rate remains elevated at 32 breaths per minute. The increased work of breathing and persistent hypoxemia suggest a progression of pulmonary complications, possibly evolving into acute respiratory distress syndrome (ARDS). Serial arterial blood gases show a rising PaCO2 and a pH edging towards acidosis, even with oxygen support. These developments prompt an urgent reassessment of his respiratory support needs, potentially requiring non-invasive ventilation or mechanical ventilation for stabilization.

Concurrently, the patient's hemodynamic instability poses additional challenges. Despite vasopressor support, his blood pressure remains labile, with mean arterial pressures hovering around 60-65 mmHg. The nephrology team, evaluating the worsening renal function, considers commencing renal replacement therapy, as the patient's urine output dwindles, and metabolic acidosis worsens. The multidisciplinary team must now balance the immediate need to stabilize the patient's failing systems with the long-term goal of addressing the underlying liver pathology, all while preparing for potential ICU transfer to manage the escalating complexity of his condition.

Section 4

New Complications:

As the medical team continues to grapple with the patient's deteriorating condition, new complications arise, further challenging their management strategies. The patient develops significant coagulopathy, evidenced by an international normalized ratio (INR) of 2.5 and a platelet count that has fallen to 45,000/µL. This raises concerns about the risk of bleeding, particularly in the setting of potential invasive interventions needed. The team cautiously considers the use of plasma transfusions or prothrombin complex concentrates to mitigate the bleeding risk, all while balancing the potential for volume overload, given the patient's tenuous respiratory status.

Additionally, abdominal distention increases notably, raising the suspicion of spontaneous bacterial peritonitis (SBP), a common complication in patients with decompensated cirrhosis. Paracentesis is performed, revealing an ascitic fluid white blood cell count of 350 cells/µL with a predominance of neutrophils, confirming the diagnosis. Broad-spectrum antibiotics are initiated promptly, but the added infection exacerbates the patient's hemodynamic instability. This development necessitates a reevaluation of the current vasopressor regimen and consideration of additional agents to support circulatory demands.

The combination of refractory hepatic encephalopathy, progressive respiratory failure, and now the added burden of coagulopathy and infection, calls for an urgent multidisciplinary meeting. The team must reassess their approach, potentially prioritizing interventions that could provide rapid stabilization, such as initiating continuous renal replacement therapy to address metabolic derangements and pursuing extracorporeal liver support as a bridge to transplantation evaluation. Each decision is critical, carrying significant implications for the patient's already fragile state, and requires careful, collaborative clinical reasoning to navigate the complex interplay of his organ dysfunctions.

Section 5

Change in Patient Status:

Over the next 24 hours, the patient's condition takes a precarious turn. Despite the initiation of broad-spectrum antibiotics for spontaneous bacterial peritonitis, his fever spikes to 39.5°C (103.1°F), and his blood pressure becomes increasingly labile, fluctuating between 85/50 mmHg and 110/70 mmHg. His heart rate remains elevated at 115 beats per minute, and his respiratory rate increases to 28 breaths per minute, with oxygen saturation dipping to 88% on 6 liters of supplemental oxygen via nasal cannula. The patient exhibits worsening confusion, with a Glasgow Coma Scale score dropping to 10, indicating a decline in neurological status.

Laboratory results reveal further deterioration: his bilirubin rises to 18 mg/dL, and lactate levels increase to 5 mmol/L, suggesting worsening liver dysfunction and tissue hypoperfusion. Arterial blood gases indicate a mixed metabolic acidosis with a pH of 7.28, HCO3 at 18 mEq/L, and PaCO2 at 38 mmHg. These findings highlight the urgent need for more aggressive circulatory and respiratory support. The decision is made to escalate to bi-level positive airway pressure (BiPAP) ventilation to optimize oxygenation while minimizing the risk of aspiration in the setting of his encephalopathy.

Given the critical state, the team convenes to discuss the feasibility of initiating continuous renal replacement therapy to address the lactic acidosis and potential renal impairment, as his creatinine has climbed to 2.4 mg/dL. Meanwhile, the infectious disease specialist recommends adjusting the antibiotic regimen based on culture sensitivities, with particular attention to covering resistant organisms. As the patient teeters on the brink of multi-organ failure, each intervention requires precise coordination and rapid response to any further changes in his clinical trajectory.