“Oxytocin Hand”: Extravasation and Vascular Compromise after Obstetrical Pitocin

Sir: Oxytocin [produced commercially as oxytocin (Pitocin; Allscripts Healthcare Solutions, Chicago, Ill.) and Syntocinon (Sandoz Pharmaceuticals Corp., East Hanover, N.J.)] and vasopressin are well known for their effects on human reproduction (tetanic uterine contraction) and on sodium excretion (an antidiuretic effect), respectively.1 More recently, these homologous hormones have been considered to be potent cardiovascular hormones, with oxytocin most often provoking vasodilatation and decreased cardiac rate and force of contraction, whereas vasopressin triggers vasoconstriction (a vasopressor effect).2–4 As such, vasopressin is now an emerging drug of choice for vasodilatory shock states.3 Whether vasopressin and oxytocin cause vasoconstriction or vasodilatation depends on four variables, according to Holmes et al.3: (1) the vascular bed and model studied, (2) receptor population (receptor density), (3) dose of hormone, and (4) duration of exposure. We would now add a fifth variable based on recent experience: space-confinement, favoring intense drug exposure and receptor activation. A 24-year-old woman with a history of one normal delivery and one stillbirth presented at 15 weeks’ gestation with uncontrolled vaginal bleeding. Hemorrhage responded to the infusion of saline and 2 units of packed red blood cells through a port in the dorsum of the right hand, dilatation, and curettage, and then 3 units of Pitocin. Within 30 minutes of the last infusion of Pitocin, the hand became edematous and cyanotic (Fig. 1). Extravasation was apparent, and the port was removed. The patient complained of aching of the hand and was noted to have an increased heart rate and elevated blood pressure.Fig. 1.: Early vascular compromise of the right hand, soon after onset, as photographed by the patient’s family.On arrival at our institution, she denied Raynaud phenomenon, cigarette consumption, diabetes mellitus, or side effects from prior infusions of Pitocin. The soft tissue of the hand was not under tension, and discoloration was diffuse (Fig. 2). Neither radial nor ulnar pulses could be palpated, the hand was cool to touch, and capillary refill was delayed. Doppler sounds were faint over the ulnar and radial arteries. Function was intact. The extremity was elevated in a foam support (Carter Block) above heart level, and heat was applied (Bair Hugger; Augustine Medical, Inc., Eden Prairie, Minn.). The hand improved over the ensuing hours, and increased flow through both arteries was suggested by more audible Doppler pulsations, such that the patient refused a stellate ganglion block. Function remained intact. An Allen test was negative. The patient was discharged without surgery, stellate ganglion block, or other intervention. A final hematocrit value was 26.5 percent. Coagulopathy profile was unremarkable, as was follow-up examination (Fig. 3).Fig. 2.: Vascular compromise as depicted in photographs on presentation to Chandler Medical Center.Fig. 3.: Follow-up evaluation 3 weeks after discharge.An algorithm of probable cause follows: extravasation at the site of the infusion port plus high tissue concentrations of oxytocin in a confined space (hand and wrist), which led to vasopressin receptor (V1R) activation, after the vasodilatory oxytocin receptors were overwhelmed, which led to vasoconstriction of radial and ulnar arteries, which led to transient vascular compromise and ischemia. Antagonists to oxytocin (vaptans) are currently used to suppress premature labor, and it may be that atosiban (Tractocile; Ferring Pharmaceuticals, Parsippany, N.J.) and other drugs that occupy oxytocin receptors should be considered in future cases of extravasation of oxytocin unresponsive to conservative measures. Research into the pathophysiologic roles of vasopressin, oxytocin, and their antagonists is underway at several centers.5 Richard A. Pollock, M.D. Jennifer R. Olges, M.P.H. Daniel H. Stewart, M.D. Division of Plastic Surgery University of Kentucky Lexington, Ky. ACKNOWLEDGMENT The authors gratefully acknowledge active discussions with Cheryl L. Holmes, M.D., Medical Director of Critical Care (Department of Medicine), Kelowna General Hospital, Kelowna, British Columbia, Canada, regarding this report and her research. DISCLOSURE None of the authors has any financial disclosures to declare.

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