The nurse evaluates the client's concerns and plans which actions to take.

Select which plan of care recommendations are indicated or not indicated at this time. Each row must only have one response option selected.

Minimal change nephrotic syndrome involves an idiopathic increase in glomerular permeability, specifically targeting the podocytes of the basement membrane. This pathology results in massive protein loss, leading to systemic hypoalbuminemia, which shifts fluid from the intravascular space into the interstitium, causing generalized edema. Early detection of a relapse relies on identifying the recurrence of basement membrane dysfunction before significant clinical symptoms such as severe anasarca or weight gain manifest.

Rationale:

A. Increased thirst is not a recognized early clinical indicator of a recurrence in nephrotic syndrome. While fluid shifts can affect perceived hydration, thirst is more commonly associated with diabetes mellitus or electrolyte imbalances. The primary monitoring focus for MCNS remains the urinary protein status rather than oral intake patterns.

B. Tachypnea may occur in late-stage relapse if pleural effusions or massive ascites develop, causing respiratory compromise. It is considered a secondary complication of severe fluid overload rather than a primary diagnostic sign of early disease activity. Monitoring should focus on the kidneys rather than respiratory rate during the initial stages of relapse.

C. A rounded face, often termed moon face, is a classic side effect of prolonged corticosteroid therapy used to treat the condition. This finding indicates a physiological response to the medication rather than a return of the disease process itself. It can mask the development of edema, making objective laboratory testing more critical.

D. Albuminuria is the most significant and early indicator that the nephrotic process has returned. Parents are often taught to monitor the child's urine daily using dipsticks to detect protein excretion before visible edema occurs. Identifying protein in the urine allows for prompt intervention with steroids to prevent a full-blown clinical relapse.

Brief introduction:

Hepatic encephalopathy is a reversible neuropsychiatric syndrome caused by liver failure and the portosystemic shunting of blood. The primary toxin involved is ammonia, which crosses the blood-brain barrier and causes astrocyte swelling and cerebral edema. Lactulose works by acidifying the colon, converting ammonia into non-absorbable ammonium, which is then excreted via osmotic diarrhea.

Rationale:

A. Blood glucose level monitoring is important in liver disease because of impaired glycogen storage. However, lactulose is not administered to manage glycemic levels, despite being a synthetic sugar. The nurse evaluates the therapeutic efficacy of the drug based on the reduction of nitrogenous waste, not fluctuations in blood sugar.

B. Level of consciousness is the most critical assessment for evaluating therapeutic response. Since lactulose aims to reduce neurotoxic ammonia levels, improvement in mental status, orientation, and the disappearance of asterixis indicate successful treatment. The nurse must monitor for increased alertness and clarity as a sign of decreasing cerebral toxicity.

C. Serum electrolytes must be monitored because lactulose causes frequent osmotic stools, which can lead to dehydration and hypokalemia. While this is an essential safety assessment, it measures a side effect rather than the primary therapeutic goal. The nurse's priority in evaluation is the resolution of the neurological symptoms being treated.

D. Percussion of the abdomen is used to assess for ascites or organomegaly, which are common findings in chronic liver cirrhosis. Although abdominal assessment is part of a comprehensive physical exam, it does not provide data regarding the biochemical clearance of ammonia. The resolution of encephalopathy is measured through neurological function rather than physical abdominal changes.