Situation: A 68-year-old woman weighing 60 kg is admitted to the intensive care unit (ICU) with fever, flank pain, and confusion from an acute kidney infection. Her temperature is 39.4 °C, heart rate 124/min, respiratory rate 28/min, blood pressure 82/44 mmHg (mean arterial pressure 57 mmHg), and serum lactate 4.8 mmol/L (43 mg/dL). Despite the fluids, her mean arterial pressure (MAP) remains 58 mmHg. Norepinephrine is started through a peripheral intravenous catheter in her forearm while central venous access is arranged. An hour later, the skin around the site is cool, pale, and swollen. The nurse stops the infusion at that site and notifies the provider, who confirms the existing orders. Within minutes her MAP falls to 50 mmHg. Which action should the nurse take NEXT?

All four actions belong to extravasation care, but her MAP has fallen to 50 mmHg without the vasopressor, which threatens every organ. Restoring the norepinephrine through another vein comes first; the local measures (elevating the limb, phentolamine per protocol, marking and documenting the area) follow once perfusion is supported.

Clinical context
This patient is in septic shock with a MAP of 50 mmHg after the norepinephrine infusion was stopped. A MAP below 65 mmHg is the widely accepted threshold for inadequate organ perfusion in septic shock. At 50 mmHg, coronary, cerebral, and renal perfusion are critically compromised, and every minute without vasopressor support increases the risk of irreversible organ injury.

Why the next action is restarting norepinephrine
Norepinephrine is a potent alpha-adrenergic agonist. Its primary action is arterial and venous vasoconstriction, which raises systemic vascular resistance and increases venous return. In distributive shock from infection, the vasculature is pathologically dilated and unresponsive to endogenous catecholamines. Exogenous norepinephrine restores vascular tone and is the first-line vasopressor for septic shock. When the infusion is interrupted, the drug’s half-life is only about 2 to 3 minutes, so the effect dissipates rapidly. The fall in MAP from 58 mmHg to 50 mmHg within minutes is the expected consequence of abrupt norepinephrine withdrawal.

The local extravasation injury is a time-sensitive but nonlethal problem; the systemic loss of perfusion pressure is an immediate threat to life. All four answer choices are legitimate components of extravasation management, but they are not equal in urgency. The priority is to restore the vasopressor through a new, functional intravenous site.

Extravasation care is secondary, not primary
The cool, pale, swollen skin around the peripheral IV site is consistent with norepinephrine extravasation. Norepinephrine causes intense local vasoconstriction, which can lead to tissue ischemia and necrosis if untreated. Standard local measures include:

Intervention	Purpose	Timing relative to restarting the vasopressor
Stop the infusion at the affected site	Prevents further drug delivery into the tissue	Already completed
Restart norepinephrine in a different vein	Restores systemic perfusion pressure	Must occur first
Elevate the affected forearm above heart level	Reduces edema and promotes venous drainage	After perfusion is stabilized
Infiltrate the site with phentolamine	Alpha-adrenergic blockade reverses local vasoconstriction	After perfusion is stabilized
Mark the blanched edge and photograph the site	Documents baseline for monitoring progression	After perfusion is stabilized

Watch out! Phentolamine infiltration is the pharmacologic antidote for norepinephrine extravasation, but it does nothing to restore systemic blood pressure. Giving phentolamine while the MAP is 50 mmHg would address the arm while the brain, heart, and kidneys remain underperfused. The local injury can be treated minutes later without changing the outcome; the same cannot be said for prolonged systemic hypotension.

Peripheral norepinephrine and extravasation risk
The concern about peripheral vasopressor administration has historically centered on extravasation injury. However, recent evidence indicates that peripheral administration through a properly selected vein is relatively safe when protocols are followed. A systematic review found that extravasation events with peripheral vasopressors are uncommon and that severe tissue injury is rare, particularly when the infusion runs for a limited duration and the catheter is placed in a proximal vein such as the antecubital fossa ^[1]. A retrospective review of 202 patients receiving vasopressors through a peripheral venous line similarly reported a low incidence of serious extravasation complications ^[2]. A comprehensive review emphasized that standardized protocols for catheter size, site selection, and monitoring are key to minimizing risk ^[3]. One emergency department protocol recommended peripheral norepinephrine through an 18-gauge or larger catheter at or above the antecubital fossa, with a maximum dose of 20 μg/min ^[4].

These findings do not mean extravasation is harmless. They mean that the systemic benefit of early vasopressor support generally outweighs the local risk, and that extravasation, when it occurs, is manageable with prompt local care. In this scenario, the nurse has already correctly stopped the infusion and notified the provider. The remaining priority is systemic.

In a patient with septic shock, a MAP of 50 mmHg is a perfusion emergency that takes precedence over local tissue care. The nurse should restart the norepinephrine in a different vein as soon as possible, then proceed with the local extravasation measures once the patient’s perfusion pressure is restored.