A nurse is planning care for a client who had a lumbar laminectomy. Which of the following interventions should the nurse include in the plan of care?

Rationale:
A. Stop the blood transfusion immediately: There is no need to stop the transfusion, as type B negative blood is compatible with AB positive recipients. AB positive individuals are universal recipients and can safely receive red blood cells from any ABO and Rh-negative or Rh-positive blood type.

B. Prepare to administer antipyretics: Antipyretics are not required unless the client shows signs of a febrile reaction. There is no indication from the question that the client is experiencing such symptoms.

C. Monitor the client for any adverse reactions: This is the appropriate action. Although the blood type is compatible, it is standard protocol to closely monitor all clients during transfusion for signs of adverse reactions, especially within the first 15 minutes.

D. Transfuse the blood over 6 hr: Blood transfusions should be completed within 4 hours to reduce the risk of bacterial growth and hemolysis. Extending the transfusion to 6 hours violates safety guidelines.

Rationale:

• Hepatic encephalopathy: This is caused by the buildup of neurotoxins, particularly ammonia, due to impaired liver function. The client’s elevated ammonia level and history of chronic alcohol use and jaundice support this diagnosis. Early signs may include confusion and lethargy, progressing to coma if untreated.
• Uremic encephalopathy: This condition is caused by accumulation of urea and toxins due to kidney failure. There is no evidence in the case of renal impairment, such as elevated BUN or creatinine levels, making this diagnosis unlikely in the current context.
• Hypoglycemia: Low blood glucose can cause confusion or altered mental status, but this client’s symptoms and labs do not indicate hypoglycemia. There is no mention of a low glucose level, and the focus of concern is more aligned with liver failure than endocrine causes.

• Abdominal pain: Although abdominal pain is a relevant symptom in liver disease, it is nonspecific and not directly responsible for hepatic encephalopathy. It reflects general liver inflammation or ascites but does not cause neurologic symptoms on its own.
• Albumin 3.0 g/dL: Low albumin indicates reduced liver synthetic function and contributes to fluid shifts like ascites, but it is not neurotoxic. It does not directly cause hepatic encephalopathy or altered mental status.
• Ammonia 150 mcg/dL: This is a critically elevated value, more than double the normal upper limit. High ammonia levels are the most direct biochemical cause of hepatic encephalopathy and require immediate treatment to prevent worsening neurological decline.
• Total Bilirubin 2.0 mg/dL: While elevated bilirubin suggests cholestasis and impaired liver clearance, it leads to jaundice rather than mental status changes. It reflects liver dysfunction but is not the key factor in encephalopathy development.