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Difficulty: Very hardPharmacological and Parenteral Therapies

A critical care nurse is evaluating a client who has been receiving a continuous intravenous infusion of sodium nitroprusside at 3 mcg/kg/min3\text{ mcg/kg/min} for the management of a hypertensive emergency. The client's renal function has deteriorated over the last 4848 hours, evidenced by a urine output of 15 mL/hr15\text{ mL/hr} and a serum creatinine level of 3.1 mg/dL3.1\text{ mg/dL}. The client now presents with profound confusion, muscle twitching, and a mixed venous oxygen saturation (SvO2SvO_2) of 88%88\% (normal range: 60%−80%60\% - 80\%). Based on these assessment data, which of the following pharmacological interventions should the nurse anticipate immediately?

  1. A
    Decrease the sodium nitroprusside infusion rate to 1.5 mcg/kg/min1.5\text{ mcg/kg/min} and assess the client for signs of early shock.
  2. B
    Administer intravenous sodium thiosulfate via a secondary Y-site connection while maintaining the sodium nitroprusside infusion.
  3. Discontinue the sodium nitroprusside and administer intravenous sodium thiosulfate.Answer
  4. D
    Maintain the sodium nitroprusside infusion and administer intravenous sodium bicarbonate to correct the metabolic state.

Answer

Discontinue the sodium nitroprusside and administer intravenous sodium thiosulfate.
The client's presentation of altered mental status, muscle twitching, and an elevated SvO2SvO_2 in the setting of prolonged sodium nitroprusside use and renal failure indicates cyanide toxicity. The definitive treatment requires immediately discontinuing the nitroprusside and administering sodium thiosulfate, which converts the cyanide into thiocyanate to be safely excreted.

Step-by-Step Solution

1
Analyze the client's current clinical presentation and medication history.
The client is receiving sodium nitroprusside, has acute kidney injury (oliguria, elevated creatinine), and presents with neurotoxicity alongside an abnormally high SvO2SvO_2.
Identifying the correlation between the continuous infusion, compromised renal clearance, and specific toxic symptoms is the first critical step in clinical reasoning.
2
Differentiate the physiological cause of the abnormally high SvO2SvO_2 and neurological symptoms.
Sodium nitroprusside metabolizes into cyanide and thiocyanate, which require renal excretion. The high SvO2SvO_2 indicates cells are unable to extract oxygen from the blood.
Cyanide toxicity inhibits cytochrome c oxidase in the cellular electron transport chain, halting aerobic respiration and causing oxygen to bypass the tissues entirely.
3
Determine the highest priority pharmacological intervention based on the identified toxicity.
The offending medication must be stopped immediately, and the specific antidote (sodium thiosulfate) must be administered.
Sodium thiosulfate acts as a sulfur donor, accelerating the conversion of toxic cyanide into less toxic thiocyanate for eventual elimination.

Key Concept

Sodium nitroprusside-induced cyanide toxicity and pharmacological antidotes
Estimated Time:2m 30s
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Topics

Pharmacological and Parenteral Therapies

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