The main purpose for administering blood to the massively hemorrhaging client is to

A. Decreased seizure activity: Mannitol does not have anticonvulsant properties. Seizure activity is managed with antiepileptic medications, not osmotic diuretics. Monitoring for seizure reduction is not a therapeutic goal of mannitol.

B. Decreased urinary output: Mannitol is an osmotic diuretic, which increases urine output to remove fluid from tissues, including the brain. A decrease in urine output would indicate a problem with the drug’s effectiveness or renal function.

C. Decreased cerebral metabolism: Mannitol does not directly reduce cerebral metabolic rate. Its primary action is fluid removal, not altering neuronal metabolism or oxygen consumption.

D. Decreased cerebral edema: Mannitol reduces intracranial pressure by drawing water out of edematous brain tissue into the intravascular space. This decrease in cerebral edema is the expected therapeutic effect and is monitored through neurologic assessments and ICP measurements.

A. Hyperkalemia and hypernatremia: During the diuretic phase, the kidneys excrete large volumes of urine, leading to loss of potassium and sodium. Hyperkalemia and hypernatremia are more characteristic of the oliguric phase of AKI.

B. Hypokalemia and hypernatremia: Although potassium is lost, sodium loss also occurs during the diuretic phase, making hypernatremia unlikely. Sodium depletion can result from excessive urinary losses.

C. Hyperkalemia and hyponatremia: Hyperkalemia is typically seen in the oliguric phase. In the diuretic phase, potassium is excreted in large amounts, making hypokalemia more common.

D. Hypokalemia and hyponatremia: The diuretic phase causes high urine output with excessive loss of electrolytes. Both potassium and sodium are depleted, putting the client at risk for hypokalemia and hyponatremia. Monitoring and replacement are essential.