Intramyometrial Injection of Vasopressin Resulting in Severe Bradycardia During Myomectomy

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Intramyometrial Injection of Vasopressin Resulting in Severe Bradycardia During Myomectomy

Uterine leiomyomas, commonly known as fibroids, are benign tumors that frequently necessitate surgical intervention. Myomectomy, the surgical removal of these tumors, is a critical procedure for preserving fertility and managing symptoms such as abnormal bleeding or pelvic pressure. To minimize intraoperative blood loss, intramyometrial injection of vasopressin has become a widely adopted adjunct during these surgeries. While vasopressin is effective in reducing hemorrhage, its systemic absorption can precipitate rare but severe cardiovascular complications. This article presents two cases of sudden, life-threatening bradycardia following intramyometrial vasopressin administration during myomectomy, highlighting the mechanisms, clinical implications, and management strategies for such events.

Case Presentations

Case 1
A 36-year-old woman with multiple uterine leiomyomas underwent laparoscopically assisted myomectomy under general anesthesia. Preoperative evaluations, including electrocardiography, chest radiography, and laboratory tests, were unremarkable. Following anesthesia induction and endotracheal intubation, the procedure commenced with pneumoperitoneum at 12 mmHg and Trendelenburg positioning. After trocar placement, multiple fibroids were visualized across the uterine surface. A 16-gauge needle was used to inject 10 mL of diluted vasopressin (0.6 U/mL) into the myometrium after negative aspiration to prevent intravascular injection.

Approximately two minutes post-injection, the patient developed abrupt severe bradycardia. Her heart rate (HR) dropped sequentially from 68 to 47 and then to 25 beats per minute (bpm). Immediate interventions included discontinuation of surgery and anesthesia, repositioning to the supine posture, and administration of intravenous atropine (0.5 mg). Despite transient improvement (HR 55 bpm), her HR plummeted again to 30 bpm within 30 seconds and stabilized at 25 bpm. A second dose of atropine was not required, as her HR gradually normalized to baseline within two minutes. The procedure resumed after ten minutes of observation and concluded without further complications. The patient was discharged four days postoperatively.

Case 2
A 38-year-old woman scheduled for abdominal myomectomy received combined spinal-epidural anesthesia. Intraoperative bleeding during fibroid excision prompted intramyometrial injection of 10 mL diluted vasopressin (0.6 U/mL). Three minutes post-injection, her HR decreased precipitously from 70 to 50 and then to 25 bpm, accompanied by hypotension (70/40 mmHg). Immediate management included intravenous atropine (0.5 mg), supplemental oxygen, and ephedrine (6 mg). The HR rebounded to 108 bpm, and blood pressure normalized to 125/80 mmHg within three minutes. No additional vasoactive agents were needed, and the surgery concluded successfully. The patient recovered uneventfully and was discharged six days later.

Pathophysiological Mechanisms

Vasopressin, a potent vasoconstrictor, exerts its effects primarily via V1a receptors on vascular smooth muscle, increasing systemic vascular resistance and reducing heart rate through baroreceptor-mediated reflexes. Intramyometrial administration aims to localize vasoconstriction to the uterus, but systemic absorption can occur, particularly if inadvertent intravascular injection or rapid diffusion into circulation transpires. Both cases illustrate that even meticulous technique—negative aspiration prior to injection—does not eliminate the risk of systemic effects.

The temporal association between vasopressin administration and bradycardia (2–3 minutes post-injection) suggests rapid absorption into the systemic circulation. The resultant hypertension from vasoconstriction activates carotid baroreceptors, triggering vagally mediated bradycardia as a compensatory response. This mechanism aligns with the observed hemodynamic collapse, where severe bradycardia preceded hypotension in the second case.

Clinical Considerations

  1. Anesthetic Technique and Surgical Approach
    Both cases occurred despite differing anesthetic (general vs. neuraxial) and surgical (laparoscopic vs. open) techniques, underscoring that vasopressin-induced bradycardia is independent of these variables. Laparoscopic procedures, however, may exacerbate hemodynamic instability due to pneumoperitoneum and Trendelenburg positioning, which impair venous return and elevate sympathetic tone.

  2. Dosage and Dilution
    The cases utilized 10 mL of 0.6 U/mL vasopressin (total 6 units), consistent with common protocols. However, no consensus exists on the optimal dose to balance hemostasis and safety. Lower concentrations (e.g., 0.05–0.3 U/mL) have been proposed to mitigate systemic effects, though efficacy in controlling hemorrhage must be preserved.

  3. Timing of Onset
    The rapid onset of bradycardia (2–3 minutes) necessitates continuous hemodynamic monitoring during and after vasopressin injection. Anesthesiologists must anticipate delayed absorption, as vasopressin’s peak systemic effects may occur beyond the immediate post-injection period.

Management Strategies

  1. Immediate Interventions

    • Cessation of Surgery: Halting surgical manipulation reduces further vasopressin release into circulation.
    • Positioning: Supine positioning optimizes venous return, particularly after Trendelenburg posture.
    • Atropine: As the first-line antidote for vagally mediated bradycardia, atropine rapidly restores heart rate by antagonizing muscarinic receptors. Both patients responded to 0.5 mg doses, though higher or repeated doses may be required in refractory cases.
    • Vasopressors: Ephedrine’s alpha- and beta-adrenergic effects counteracted hypotension in the second case, though phenylephrine or epinephrine may be warranted in severe scenarios.

  2. Resuscitation Preparedness
    Progression to pulseless electrical activity or asystole mandates advanced cardiac life support. Early endotracheal intubation and chest compressions should be initiated if bradycardia persists despite pharmacotherapy.

  3. Preventive Measures

    • Alternative Agents: Misoprostol or tranexamic acid may reduce reliance on vasopressin.
    • Ultrasound Guidance: Real-time imaging could enhance injection precision, minimizing intravascular uptake.
    • Gradual Injection: Slow administration may limit peak systemic concentrations.

Conclusion

Intramyometrial vasopressin, while invaluable for hemostasis in myomectomy, carries a risk of severe bradycardia due to systemic absorption. Anesthesiologists must maintain heightened vigilance during and after injection, recognizing that bradycardia may herald cardiovascular collapse. Prompt intervention with atropine and vasopressors, coupled with surgical pause and positioning adjustments, is critical to preventing morbidity. These cases reinforce the need for standardized protocols, dose optimization, and contingency planning to safeguard patient outcomes.

doi.org/10.1097/CM9.0000000000001314

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