The primary cause of abdominal ascites in a patient with cirrhosis of the liver is?

AIIMS Bhatinda NO - 2019

Medical & Surgical Nursing

Medium

Appeared in: AIIMS Bhatinda NO - 2019

Explanation

In liver cirrhosis, the damaged liver is unable to synthesize sufficient amounts of albumin, a crucial protein for maintaining blood volume.
A low level of serum albumin (hypoalbuminemia) leads to a decrease in plasma colloid oncotic pressure.
Oncotic pressure is the 'pulling' force that holds fluid inside blood vessels. When this pressure drops, fluid leaks out into surrounding tissues, including the abdominal (peritoneal) cavity.
This fluid shift, combined with increased pressure in the portal vein (portal hypertension), is the fundamental cause of ascites.

Option A: An increased vasopressin (antidiuretic hormone) level is a secondary response to systemic vasodilation and perceived low blood volume in cirrhosis. It causes water retention, which contributes to ascites but is not the primary initiating cause.
Option B: Patients with advanced cirrhosis and ascites typically have dilutional hyponatremia (low serum sodium), not an increased level. This is due to the disproportionate retention of free water compared to sodium.
Option C: The renin-angiotensin-aldosterone system is activated in cirrhosis, leading to hyperaldosteronism (an increased level of aldosterone), not a decreased level. This promotes sodium and water retention.

Clinical Relevance

Nursing practice connection: Use the key finding related to Pathophysiology of ascites in liver cirrhosis to guide bedside assessment, documentation, and the next nursing action.
Nurses play a vital role in managing ascites by monitoring daily weights, abdominal girth, intake/output, and respiratory status, as large amounts of fluid can compromise breathing.
Monitoring serum albumin levels is crucial. A low level indicates poor nutritional status and a higher risk for fluid shifts, edema, and ascites.
Patient education on a low-sodium diet (typically less than 2g/day) is a cornerstone of ascites management to prevent further fluid retention.

How to Approach the Question

First, identify the core concept of the question: the pathophysiology of ascites in liver cirrhosis.
Analyze the function of the liver and how cirrhosis impairs it. Key impairments include protein synthesis (albumin) and blood flow (portal hypertension).
Evaluate each option based on the known physiological changes in cirrhosis.
Option D (decreased albumin): Recall that the liver makes albumin and that albumin maintains oncotic pressure. This is a direct consequence of liver failure.
Option C (decreased aldosterone): Recall that cirrhosis activates the RAAS, which increases aldosterone. This option is the opposite of what happens.
Option A (increased vasopressin): Recognize this as a compensatory, secondary mechanism, not a primary cause.

Concept Tested & Keywords

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