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Table of Contents
Year : 2013  |  Volume : 29  |  Issue : 1  |  Page : 135-136

Intramyometrial vasopressin: Anesthesiologists' nightmare

Department of Anesthesiology (MAMBS), MAX Superspeciality Hospital, Saket, New Delhi, India

Date of Web Publication10-Jan-2013

Correspondence Address:
Lakshmi Jayaraman
H 426 , Palam Vihar, Gurgaon, Haryana 122017
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-9185.105832

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How to cite this article:
Jayaraman L, Sinha A, Punhani D. Intramyometrial vasopressin: Anesthesiologists' nightmare. J Anaesthesiol Clin Pharmacol 2013;29:135-6

How to cite this URL:
Jayaraman L, Sinha A, Punhani D. Intramyometrial vasopressin: Anesthesiologists' nightmare. J Anaesthesiol Clin Pharmacol [serial online] 2013 [cited 2021 Jun 24];29:135-6. Available from:


Vasopressin, a hormone naturally secreted by the posterior pituitary, acts on V1 and V2 receptors present in blood vessels and kidney. Anesthesiologists are familiar with the widespread clinical applications of vasopressin, like in cardiopulmonary resuscitation, diabetes insipidus, etc., Intramyometrial vasopressin, a potent vasoconstrictor, has found a new role in the surgical management of uterine myomas.

We report our observation in few patients administered intramyometrial vasopressin.

  • All the patients were American Society of Anesthesiologists grade 1 and 2, young women posted for laparoscopic myomectomy. Standard balanced general anesthesia was given in all patients with propofol, sevoflurane, and muscle relaxant. Standard monitoring techniques were followed. After 25-30 min of induction of anesthesia, the surgeon injected 20 units of vasopressin intramyometrially diluted in 200 ml normal saline after negative aspiration of blood. Two to three minutes later, there was a decrease in the amplitude to complete absence of waveforms and readings in the pulse oximetry, along with a significant drop in the mean arterial pressures. During this period, the radial artery was not palpable but the carotid artery was palpable with a good volume. However, there was no change in the electrocardiogram (ECG) or the end-tidal carbon dioxide (EtCO 2 ) waveform and its values [Figure 1]. The changes reverted back to baseline in 15-25 min time.
Figure 1: Disappearance of Pulse oximetry waveforms and readings with hypotension but with regular electrocardiogram and steady end-tidal carbon dioxide

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The two possible reasons for this were global hypotension and severe vasospasm. [1] Global hypotension is always accompanied by a significant drop in the EtCO 2 and requires the advanced cardiac life support protocols to be followed. In our cases, the stable EtCO 2 , steady ECG, and palpable good volume carotid pulses ruled out global hypotension, and we concluded that it was a case of severe vasospasm. Severe vasospasm may have been identified if a radial artery cannulation had been done, wherein a dampening to disappearance of waveforms would be seen. In severe vasospasm, a central arterial catheter (axillary or femoral) will continuously measure the correct central blood pressure, while the non-invasive blood pressure measurement will show lower pressure and pulse oximetry may show disappearance of waveforms and fallacious values.

An ultrasound machine can be used to measure the basal diameter of the radial artery before and after the vasopressin injection. In our patients, the radial artery which was initially measured by ultrasound almost became invisible after vasopressin administration. The flow was re-established by approximately 15-25 min, which corresponds to the pharmacokinetics of vasopressin. This corresponded with the reappearance of the pulse oximetry waveform.

We report these cases to alert the anesthesiologists [2],[3],[4],[5] and the anesthesia faculty so that guidelines can be framed regarding the dose, concentration and the continued use of vasopressin and if there are any other alternatives to vasopressin available.

  References Top

1.Riess ML, Ulris JG, Pagel PS, Woehlck HJ. Severe vasospasm mimics hypotension after high dose intrauterine vasopressin. Anesth Analg 2011;113:1103-5.  Back to cited text no. 1
2.Hobo R, Netsu S, Koyasu Y, Tsutsumi O. Bradycardia and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted myomectomy. Obstet Gynecol 2009;113:484-6.  Back to cited text no. 2
3.Nehzat F, Admon D, Nehzat CH, Dicorpo JE, Nezhat C. Life threatening hypotension after vasopressin injection during operative laparoscopy, followed by uneventful repeat laparoscopy. J Am Assoc Gynecol Laparosc 1994;2:83-6.  Back to cited text no. 3
4.Aparna AA, Nerurkar VV, Laheri DW, Mohite SN. Bradycardia, absent radial pulse and convulsions following intramyometrial vasopressin. J Anaesth Clin Pharmacol 2010;26:109-10.  Back to cited text no. 4
5.Kim SY, Lee JH, Bang EC, Lee HS, Kang YI, Cho KS, et al. Pulmonary edema following intramyometrial injection and paracervical infiltration of vasopressin during laparoscopic myomectomy and LAVH (Laparoscopic abdominal vaginal hysterectomy): A report of 2 cases. Anesth Pain Med 2010;5:333-7.  Back to cited text no. 5


  [Figure 1]

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