A client with chronic cirrhosis has esophageal varices.
It is most important for the nurse to monitor the client for the onset of which problem?

Drinking plenty of water whenever thirsty is not the most appropriate action for a patient with hypernatremia. While it's important to stay hydrated, excessive water intake can potentially worsen hypernatremia by diluting blood sodium levels further. This is because the body tries to balance sodium levels by either retaining water or excreting it through urine. In hypernatremia, the body is already short on water relative to sodium, so consuming too much water can exacerbate the imbalance.

Choice B rationale:

Reviewing food labels for sodium content is crucial for managing hypernatremia. It empowers patients to make informed choices and limit their sodium intake.

Sodium is a major contributor to hypernatremia, and reducing dietary sodium intake is a key strategy to lower blood sodium levels.

By carefully reading food labels and selecting low-sodium options, patients can effectively manage their sodium intake and promote a gradual return to normal sodium levels.

This approach addresses the root cause of hypernatremia and promotes long-term control of blood sodium levels.

Choice C rationale:

Monitoring daily urine output volume can be helpful in tracking fluid status, but it's not the primary action for managing hypernatremia.

While urine output can provide insights into fluid balance, it doesn't directly address the underlying issue of excessive sodium. Focusing on dietary sodium intake is a more direct and effective approach to correcting hypernatremia.

Choice D rationale:

Using salt tablets after strenuous exercise is not recommended for patients with hypernatremia.

Salt tablets are intended to replenish electrolytes lost through sweating, but they can worsen hypernatremia by further increasing sodium levels.

Patients with hypernatremia should focus on reducing sodium intake, not increasing it.

Choice A rationale:

Lactulose is a non-absorbable disaccharide that is metabolized by bacteria in the colon to produce lactic acid and acetic acid. These acids acidify the colon, which traps ammonia (NH3) in the colon and converts it to ammonium (NH4+). Ammonium is not absorbed by the colon and is excreted in the stool. This ammonia-lowering effect is the primary mechanism by which lactulose improves mental status in patients with hepatic encephalopathy.

Hepatic encephalopathy is a neuropsychiatric syndrome that occurs in patients with severe liver disease. It is caused by the buildup of ammonia in the blood, which can cross the blood-brain barrier and cause cerebral edema and impaired brain function.

The clinical manifestations of hepatic encephalopathy range from mild confusion and personality changes to coma. Improved mental status is a key therapeutic goal in the treatment of hepatic encephalopathy.

Studies have shown that lactulose can improve mental status in patients with hepatic encephalopathy. A meta-analysis of 11 randomized controlled trials found that lactulose was associated with a significant improvement in mental status compared to placebo.

The improvement in mental status is typically seen within 24 to 48 hours of starting lactulose therapy.

Choice B rationale:

Increased urine output is not a direct therapeutic effect of lactulose. Lactulose can cause diarrhea, which can lead to increased urine output due to fluid loss. However, this is not the primary mechanism by which lactulose improves mental status in patients with hepatic encephalopathy.

Choice C rationale:

Reduction in the number of liquid stools is a common side effect of lactulose. However, it is not a therapeutic goal in the treatment of hepatic encephalopathy. The goal of lactulose therapy is to improve mental status by lowering ammonia levels in the blood.

Choice D rationale:

Ability to ambulate independently is not a direct therapeutic effect of lactulose. Lactulose can improve mental status, which may indirectly lead to improved ambulation in some patients. However, this is not the primary mechanism by which lactulose works.