Bleeding in Hepatic Failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Decreased production of clotting factors - The liver synthesizes most of the body's clotting factors (like fibrinogen, prothrombin, factors V, VII, IX, X). With hepatic failure, the liver's ability to produce these factors decreases, leading to a higher risk of bleeding.

• Secondary mechanism: Thrombocytopenia - Hepatic failure often causes hypersplenism, a condition where the spleen enlarges and sequesters more platelets, reducing their availability for clot formation.

• Key complication: Variceal bleeding - Portal hypertension, common in hepatic failure, leads to the formation of varices, especially in the esophagus and stomach. These varices are prone to rupture, causing potentially life-threatening bleeding.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Chronic Hepatitis C, cirrhosis of the liver, history of alcohol abuse, type 2 diabetes

• Current medications: Metformin, Spironolactone, Propranolol, Multivitamin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Uncontrolled bleeding from the gums and in stool

• Key symptoms: Fatigue, easy bruising, jaundice, swelling in the legs and abdomen, confusion, blood in the stool, bleeding gums

• Vital signs: Blood pressure 90/60 mmHg, pulse 110 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, SpO2 88% on room air

Section 1

Change in Patient Status:

The patient's condition started to deteriorate rapidly. His blood pressure dropped to 80/50 mmHg, pulse increased to 120 bpm, and his respiratory rate rose to 26 breaths per minute. His SpO2 levels also dropped to 85% on room air, indicating that his oxygen saturation was critically low. He became increasingly confused and lethargic, suggesting that hepatic encephalopathy was worsening. The patient also complained of severe abdominal pain, and his abdomen appeared more distended than before, indicating possible ascites or internal bleeding.

Upon further examination, fresh blood was observed in the patient's stool and he started vomiting blood, suggesting that a variceal bleed might have occurred. His gums bled profusely despite attempts to control the bleeding with topical hemostatic agents. The skin and whites of his eyes were noticeably more jaundiced, and the bruising on his skin seemed to be spreading. The patient's lower extremities were markedly edematous, and his urine output had decreased over the last few hours.

These changes in the patient's condition required immediate intervention. The healthcare team needed to work rapidly to stabilize the patient, control his bleeding, and manage his worsening symptoms. The complexity of his condition would require advanced critical thinking and clinical judgment to prioritize interventions and navigate the patient's complex pathophysiology.

Section 2

New Diagnostic Results:

Despite the active bleeding, the medical team proceeded with urgent diagnostic tests to obtain a clearer picture of the patient's condition. The patient's complete blood count (CBC) revealed a decreased hemoglobin level of 6.2 g/dL, a significant drop from his previous level of 9.5 g/dL, indicative of a significant blood loss. His platelet count was also critically low at 40,000/uL, further complicating his bleeding risk. The coagulation profile was alarming with an INR of 3.5 and a PTT of 55 seconds, reflecting a significant coagulation deficiency.

An ultrasound of the abdomen showed an increased amount of free fluid suggestive of ascites and possibly blood, further reinforcing the suspicion of a variceal bleed. His liver function tests (LFTs) showed elevated levels of ALT and AST at 110 U/L and 130 U/L respectively, and his bilirubin level had risen to 15 mg/dL. His ammonia level was critically high at 110 µg/dL, likely contributing to his worsening mental status. These results confirmed the severity of the patient's hepatic failure and the dire need for immediate intervention.

The healthcare team had to rapidly interpret these results, and based on their findings, needed to prioritize the interventions. The patient needed immediate blood transfusions to replace the lost blood and restore his hemoglobin levels. The clotting factors and platelets also needed to be replaced to prevent further bleeding. Further diagnostic tests such as a CT abdomen and a possible endoscopy might be needed once the patient was stable enough to undergo these procedures. The team also needed to address the hepatic encephalopathy and manage the patient's worsening symptoms. This would require advanced critical thinking and clinical judgement, as the patient's pathophysiology was complex and his condition was rapidly deteriorating.

Section 3

Change in Patient Status:

Despite immediate interventions, the patient's condition continued to decline. His blood pressure dropped to 90/50 mmHg and his heart rate increased to 120 beats per minute, indicating possible compensatory tachycardia in response to the hypotension. His oxygen saturation also dropped to 88% on room air, requiring supplemental oxygen therapy. His Glasgow Coma Scale (GCS) score decreased from an initial 15 down to 11, and he exhibited asterixis, indicating a worsening of his hepatic encephalopathy.

The patient also started complaining of increased abdominal pain. On physical examination, the abdomen was distended and tense, with decreased bowel sounds, suggestive of worsening ascites and possible spontaneous bacterial peritonitis, a common complication in hepatic failure patients. The healthcare team had to reassess their approach and consider introducing more aggressive interventions. This could potentially include a paracentesis to both relieve the pressure and get a sample for analysis, or even considering a transjugular intrahepatic portosystemic shunt (TIPS) procedure. The team also needed to balance these interventions with the critical issue of the patient's ongoing coagulopathy and the risks associated with invasive procedures.

Section 4

New Diagnostic Results:

Additional laboratory tests revealed further alarming results. The patient's liver function tests were markedly abnormal, with significantly elevated AST, ALT, and bilirubin levels at 1200 IU/L, 900 IU/L, and 35 mg/dL respectively, along with a decreased albumin level of 2.0 g/dL. The prothrombin time (PT) was prolonged at 22 seconds, and the international normalized ratio (INR) was 2.3, reflecting the patient's worsening coagulopathy related to hepatic failure. The patient's creatinine also increased to 2.5 mg/dL and blood urea nitrogen (BUN) to 45 mg/dL, suggesting possible hepatorenal syndrome.

An abdominal ultrasound revealed a significant amount of free fluid, confirming ascites, along with heterogeneous liver echotexture suggestive of cirrhosis. Given the patient's worsening condition and the ultrasound findings, the team decided to proceed with diagnostic paracentesis despite the coagulation risk. The fluid analysis returned with an elevated white blood cell (WBC) count of 950 cells/mm3, with 60% neutrophils, indicating spontaneous bacterial peritonitis (SBP). These new diagnostic findings prompted a further alteration in the management plan, with the initiation of broad-spectrum antibiotics to manage the SBP, while also considering the possibility of TIPS for management of the refractory ascites and hepatorenal syndrome.

Section 5

In response to the broad-spectrum antibiotics, the patient's fever subsided and the WBC count in the ascitic fluid decreased to 500 cells/mm3. However, the bilirubin level continued to increase to 40 mg/dL and the INR rose to 2.6, indicating worsening hepatic function. Simultaneously, the patient's creatinine rose to 3.0 mg/dL and BUN to 50 mg/dL, further suggesting ongoing hepatorenal syndrome. The patient also reported increased difficulty in breathing and physical examination revealed decreasing oxygen saturation levels, dropping to 88% on room air, indicating possible hepatic hydrothorax.

Given the worsening hepatic and renal function, as well as the new onset of respiratory distress, the management plan was adjusted. In addition to the ongoing antibiotics for SBP, the medical team initiated measures to manage the hepatorenal syndrome, including albumin infusions and terlipressin therapy. A thoracentesis was scheduled for the following day to alleviate the patient's respiratory distress. Concurrently, consultation with the interventional radiology department was scheduled for possible TIPS placement to manage the refractory ascites and ongoing hepatic failure. The critical nature of the patient's condition necessitated careful monitoring and swift action, while the complex interplay of complications required skillful clinical reasoning and judgement.