A nurse is administering desmopressin to a client who has diabetes insipidus. The nurse should monitor the client for which of the following adverse effects?

Stop the infusion.

Disconnect the IV tubing from the IV hub.

Aspirate the medication from the IV catheter.

Elevate the affected extremity.

Brief Introduction:

Extravasationis a severe clinical complication where a vesicantmedication leaks from the intravascular space into the surrounding dermal or subcutaneous tissue. Vesicants, such as certain chemotherapeutic agents, cause cellular necrosis, tissue sloughing, and permanent nerve damage upon contact with extravascular structures. Emergency management focuses on immediate cessation of the insult and the removal of as much residual toxin as possible to mitigate localized destruction.

Rationale:

A. Disconnecting the IV tubingfrom the IV hub is the second priority action. Once the pump is deactivated, the tubing must be removed while leaving the catheter in place to serve as a conduit for further intervention. This step prepares the site for aspirationand prevents any further residual medication within the line from being accidentally flushed into the compromised tissue.

B. Elevating the affected extremityis the final step in the immediate response sequence. Elevation utilizes gravity to promote venous returnand lymphatic drainage, which helps reduce localized edema and limits the spread of the vesicant within the interstitial spaces. This maneuver is part of supportive care and should only be performed after the chemical threat has been physically addressed.

C. Stop the infusionis the absolute first action the nurse must perform the moment extravasation is suspected. Continued administration of a vesicant exponentially increases the volume of tissue exposed to the toxin, leading to wider areas of necrosis. Halting the flow immediately limits the scope of the injury and is the highest priority for limb preservation and safety.

D. Aspirate the medicationfrom the client's IV catheter is performed after the tubing is disconnected but before the catheter is removed. Using a syringe to pull back on the hub allows the nurse to extract residual vesicant still sitting in the catheter and the immediate extravasation pocket. This critical step reduces the total concentration of the drug remaining in the tissue, potentially decreasing the severity of the subsequent chemical burn.

Digoxinis a cardiac glycoside that exerts a positive inotropic and negative chronotropic effect by inhibiting the sodium-potassium ATPasepump. This mechanism increases intracellular calcium, enhancing myocardial contractility while slowing the heart rate to improve cardiac outputin heart failure. Therapeutic monitoring is essential because a narrow therapeutic index exists, and electrolyte imbalances, particularly hypokalemia, significantly increase the risk of digitalis toxicity and life-threatening dysrhythmias.

Rationale:

The current potassium levelof 3.2 mEq/L is unexpectedand clinically significant as it falls below the physiological range of 3.5 to 5.0 mEq/L. While digoxin itself does not typically cause potassium loss, it competes with potassium for binding sites on the ATPase pump. Low serum potassium levels sensitize the myocardium to the drug, dramatically increasing the risk of digoxin toxicityeven when the drug level remains within the therapeutic range.

The digoxin levelof 0.8 ng/mL is expectedas it sits at the lower end of the standard therapeutic window of 0.8 to 2.0 ng/mL. This concentration indicates that the medication has reached a steady state in the plasma without exceeding safety thresholds. Maintaining this therapeutic levelis crucial for managing heart failure symptoms effectively while preventing the gastrointestinal and neurological complications associated with excessive cardiac glycoside accumulation.

The reported urinary concernregarding increased output is an expectedtherapeutic outcome of improved cardiac performance. As digoxin increases the force of myocardial contraction, renal perfusion is enhanced, which stimulates the kidneys to increase glomerular filtrationand urine production. This natural diuresis helps the body mobilize and excrete excess fluid volume that had previously accumulated in the tissues due to pump failure.

The current heart rateof 82/min is expectedand demonstrates a positive response to the negative chronotropic effects of cardiac glycoside therapy. Digoxin slows the conduction through the atrioventricular nodeand increases vagal tone, which effectively lowers the heart rate from the initial tachycardic state of 102/min. A resting heart rate between 60 and 100/min indicates that the medication is successfully reducing myocardial workload.

The reported current leg findingsof decreased swelling are expectedbecause they indicate a reduction in peripheral edema. By improving the heart's ability to circulate blood efficiently, digoxin reduces the venous hydrostatic pressure that causes fluid to leak into the interstitial spaces of the lower extremities. This clinical improvement correlates with the client's report of easier breathing and reflects successful management of congestive symptoms.