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Obstetrics & Gynecology:
Original Research

Vaginal Uterine Artery Ligation Avoids High Blood Loss and Puerperal Hysterectomy in Postpartum Hemorrhage

Hebisch, Gundula MD; Huch, Albert MD, FRCOG

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Department of Obstetrics, University Hospital, Zurich, Switzerland.

Address reprint requests to: Gundula Hebisch, MD, University Hospital Zurich, Department of Obstetrics, Frauenklinikstr. 10, Zurich, CH‐8091, Switzerland; E‐mail: gundula. hebisch@fhk.usz.ch.

Received October 16, 2001. Received in revised form March 7, 2002. Accepted April 11, 2002.

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OBJECTIVE: To describe a novel, effective, and minimally invasive surgical technique for avoiding excess blood loss and hysterectomy in intractable postpartum hemorrhage. Previously described techniques—uterine artery ligation at various levels, hypogastric (internal iliac) artery ligation, uterine compression—all require an abdominal approach.

METHODS: This procedure, which is quickly learned, is performable in the delivery room with minimal preparation, with or without bladder retraction. A 2‐cm horizontal incision is made in the anterior cervix 1 cm beneath the estimated vaginocervical fold and the bladder reflected in the natural plane. Firm but gentle downward traction on the uterus to the contralateral side of the intended ligature maximizes cephalad and lateral access, permitting bilateral uterine artery ligation from laterally under direct vision and/or indirect transcervical palpation.

RESULTS: Between November 1997 and June 2001, 13 women with intractable postpartum hemorrhage chose the vaginal route over laparotomy as a uterus‐preserving procedure. Hysterectomy proved necessary in only one case (8%) because of placenta percreta. One woman has since delivered a healthy term infant by cesarean, and uterine vascularization was unimpaired.

CONCLUSION: The vaginal route offers a novel, simple, effective, and minimally invasive technique for treating intractable puerperal hemorrhage by uterine artery ligation. Timely intervention avoids hysterectomy and consumption coagulopathy and preserves reproductive potential.

Major postpartum hemorrhage, defined as blood loss exceeding 1000 mL within 24 hours of delivery, is one of the most frequent causes of maternal mortality and morbidity and, after (pulmonary) embolism and hypertensive disorders, the third most frequent direct cause of maternal death in late pregnancy.1 The main causes are uterine atony and abnormalities of placentation and coagulation. Risk factors include multiple pregnancy, advanced maternal age, operative delivery, and previous postpartum hemorrhage.

Selective uterine or hypogastric (internal iliac) artery ligation and mass uterine artery ligation are surgical options for avoiding hysterectomy in intractable postpartum hemorrhage. The techniques, which all require laparotomy, were described back in the 1950s. One of the largest retrospective series on uterine artery ligation, covering 30 years, was published by O'Leary in 1995 who reported only ten failures in 265 patients.2 However, no literature is available on the use of the vaginal route for uterine artery ligation in intractable obstetric hemorrhage, although the technique is simple, highly effective, and avoids laparotomy.

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The procedure is unsuitable in women known to be infected with the human immunodeficiency virus, who would have been delivered by cesarean anyway, or hepatitis B or C virus. Once consent has been obtained, the procedure is performed without delay after the failure of conventional management (fundal massage, intravenous syntocinon, intramuscular methylergometrine maleate, rectal misoprostol, intramyometrial prostaglandin, etc). Transfer to an operating room is unnecessary and takes time. Intravenous syntocinon is continued during the procedure and regional anesthesia maintained. Local anesthesia, such as pudendal or cervical block, can be administered as required.

The patient is placed in the lithotomy position, swabbed, draped, and catheterized. Birth canal lesions found on vaginal and cervical inspection are repaired. Products retained in utero are removed, clearance confirmed by ultrasound, and uterine integrity checked.

The procedure itself can be performed with or without bladder retraction. The anterior and posterior cervical lips are clamped with sponge holding forceps. A 2‐cm horizontal incision is made in the anterior cervix about 1 cm beneath the estimated vaginocervical fold, and the bladder is reflected in the natural plane using a swab on a stick. Gentle but firm traction is then used to pull the uterus downwards and sideways, towards the contralateral side of the intended ligature, to maximize cephalad and lateral access. From cephalad and behind the bladder, a curved needle is led towards the myometrium under the guidance of the index finger placed in the cervical canal and lower uterine segment. The uterine artery—whose pulsation is readily palpable and sometimes visible from laterally—is then encircled with the vein and a layer of uterine tissue and ligated. Fingertip injury is avoided by retracting the finger after palpation and immediately before applying the stitch. It is very important to pull the uterus gently towards the contralateral side to allow for ample working space and visualization of the vessel bundle. The synthetic absorbable thread (Vicryl, CT2, 2–0, Ethicon, Johnson & Johnson, Spreitenbach, Switzerland) is clamped using Kocher forceps and the vessel bundle pulled caudally. An additional one or two ligatures—or more, depending on the anatomical variations of the uterine artery—are applied cephalad to secure the ligation, using the same technique. The whole procedure is then repeated with the contralateral vessel bundle. The anterior vaginal wall and anterior cervical lip are reunited with a few interrupted stitches (Figure 1).

Figure 1
Figure 1
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Alternatively, if there is massive bleeding and/or limited access to the vessels, mass uterine artery ligation may be performed without preparing the vessel bundles under direct vision. The guiding index finger inside the upper cervical canal/lower uterine segment is then used instead, taking the same precautions against needlestick injury as already described.

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Between November 1, 1997, and June 30, 2001, the procedure was performed on 13 women: 11 within 24 hours of vaginal or cesarean delivery, and two, 14 and 22 days postpartum, for late postpartum hemorrhage and placenta percreta or increta, respectively. All but one woman with hemolysis, elevated liver enzymes and low platelet count syndrome showed uterine atony, and conservative treatment including curettage in ten cases had failed. One or more postpartum hemorrhage risk factors were present in each case. Estimated blood loss from delivery to completed uterine artery ligation totalled a median of 1500 mL (range 1500–5200 mL); blood transfusion requirements were fresh frozen plasma in 12 patients (median 4, range 2–10 units), erythrocyte concentrates in 11 patients (median 4, range 2–10 units), and platelets in two patients (one and two adult doses, respectively).

The women were given the choice between the vaginal and abdominal routes of arterial ligation in an attempt at uterine preservation. All chose the less invasive route, with fall‐back laparotomy. The procedure was successful in preserving the uterus in 12 of 13 (92.3%) cases. One woman with placenta increta and late post‐partum hemorrhage subsequently developed intrauterine adhesions (Asherman syndrome), almost certainly caused by vigorous curettage and not by uterine artery ligation. One woman required hysterectomy for histologic placenta percreta; in her case, the procedure had been performed to minimize blood loss before hysterectomy. Another woman, with massive postpartum hemorrhage caused by placenta accreta and consumption coagulopathy (mild platelet storage pool deficiency), has since delivered a healthy term infant by elective cesarean after an uneventful pregnancy; at operation, the uterine arteries looked normal but were prophylactically ligated.

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If standard conservative management fails to control major postpartum hemorrhage, emergency surgery is required to prevent severe hemorrhage and resulting consumption coagulopathy. The choice of surgery depends greatly on the surgeon's experience. Postpartum vaginal uterine artery ligation, as described by us, involves familiar territory because it resembles the preparation for vaginal hysterectomy, which is part of every gynecologist's training. The descending branches are readily demonstrable, and the immediate hemostatic effect after the first one or two ligatures is substantial, equivalent to that of internal iliac (hypogastric) artery ligation: a pulsating arterial system is changed to one resembling venous flow. As arterial pulsation diminishes, blood clots may form distal to the ligation and remain in situ rather than be dislodged by the pulse pressure.3

Abdominal ligature of the uterine arteries, as first described in 1952, comprised mass ligature of the ascending branches of the uterine artery and vein 2–3 cm below the level of cesarean uterotomy, and included 2–3 cm of myometrium in the suture.4 The method was used with various frequency in the 1960s and came out of fashion with the advent of more potent uterotonic drugs.5 In one of the largest series—a 30‐year review of 265 postcesarean abdominal uterine artery ligatures, but mainly performed prophylactically—the success rate was 95%, and complications (an occasional broad ligament hematoma) were very rare.2 Inadvertent arteriovenous fistula formation has also been described.6

Internal iliac (hypogastric) artery ligation is a similar simple method for controlling postpartum hemorrhage,5,7,8 with the ligature positioned directly below the bifurcation of the common iliac arteries. Only 42% of ligations are successful, probably because of the abundant collateral blood supply of the uterus from the contralateral and iliac vessels.9 The method appears effective for uterine atony and midline perforation, but less so for placenta accreta, and of no use at all for uterine lacerations.5 The immediate risk is inadvertent injury to the adjacent dorsally located common iliac vein. Other side effects are central pelvic ischemia with resulting breakdown of perineal skin and postischemic lower motor neuron damage,5 as well as ureteric lesions. However, normal menstruation and pregnancies after such procedures have been described.2,10

Other abdominal ligation techniques have been described in which the uterus itself is compressed. Cho et al used interrupted circular sutures around the bleeding placental preparation site in placenta previa.11 Compression can also be applied to the upper uterine region.12 In the B‐Lynch brace suture, the whole uterus is compressed from top to bottom and left to right using self‐absorbable stitches fixed at the anterior and posterior lower uterine segments.13 Using this mass occlusion technique, no untoward defects were seen on postpartum magnetic resonance imaging and hysterosalpingography.14

Percutaneous uterine artery embolization or the intra‐uterine insertion of a hydrostatic balloon catheter is less invasive but must be restricted to cases that are cardio‐vascularly stable and to the rare institutions where stand‐by interventional radiology expertise is available.15–17 Embolization is otherwise unpracticable, as the reported interval between diagnosis and definitive hemostasis (60–90 minutes) is in our opinion unacceptable. Packing the uterus with gauze soaked in prostaglandins has been proposed,18 but on the basis of only a handful of cases; the risks are ongoing bleeding and ascending infection.

There are only three situations in which the vaginal technique could fail, but none are specific to the vaginal route: failure to operate in time (allowing coagulopathy to develop); coagulopathy caused by other etiology (infection, preeclampsia, etc); and hemorrhage from the vagina rather than the uterus.

Renal function is checked on the first postoperative day to exclude inadvertent ligation or lesion of a ureter (not observed in our population). Renal ultrasound will exclude or confirm intra‐abdominal urine (fluid) collection or dilatation of the renal pelvis. Inadvertent ureteric occlusion is readily reversed by removing the threads, which are deliberately left long at the end of the procedure for this reason. Another ligature can then be applied if required.

Our preliminary study contains a number of methodologic imperfections. Our characterization of the severity of each postpartum hemorrhage in terms of total blood loss is useful although approximate: in theory, blood loss caused by postpartum hemorrhage could be derived by subtracting blood loss at delivery from total blood loss, but in some cases postpartum hemorrhage began during delivery itself, even before delivery of the placenta. We also did not quantify the efficacy of ligation in terms, for example, of comparing pre‐ versus postprocedure blood loss in mL per minute. Rather, in this preliminary study, we took efficacy to be self‐evident, with ligation being followed by a virtually immediate and substantial reduction in blood loss, confirmed by subsequently stable hemodynamics. Nor did we obtain absolute anatomic confirmation that the arteries we had ligated were indeed the uterine arteries because this would have been impossible without concomitant laparotomy, which would have defeated the primary purpose of the procedure. Appropriate preparation displays the arteries beyond reasonable doubt; their vaginal branches can also be ligated if required. If extensive blood loss had ceased after ligating the cervical branches of the uterine artery (as in a low‐lying placenta or placenta previa), the procedure would still have achieved its aim, making the question as to whether the cervical or abdominal branches of the uterine artery had been ligated essentially academic. Similarly, we did not formally control for the effect of the passage of time on the cessation of bleeding. However, five of our 13 cases were referrals, with a minimum delivery‐procedure interval of 6 hours, compared with the 1–2 hour interval for the eight women who delivered in our unit. The efficacy of the procedure did not differ between these two subgroups, although our sample size was too small for this result to be presented in terms of statistical nonsignificance.

Ideally, the introduction of a new procedure should be justified in terms of the gold standard randomized study design, incorporating in this case a sham ligation arm and blind evaluation of the results. Such a design is applicable to an elective procedure but unsuited to the clinical setting of massive refractory postpartum hemorrhage, a fortunately rare and largely unpredictable emergency, which in our tertiary center occurs approximately once every 2 months. The protracted period required to accumulate a statistically adequate sample while maintaining other factors equal (eg, operator identity), allied to the implausibility—not to mention inhumanity—of requesting informed consent from a frightened and weakened parturient on a concept as unfamiliar to the general public as the randomized clinical trial, often (in our case) in a language not her own, means that we have no plans to confirm our findings along such lines. Given the visually persuasive evidence of a cause‐effect relationship between vessel ligation and cessation of blood loss, we have no wish to seek ethical permission for a randomized study involving sham ligation, even assuming it might be granted. We are instead concerned to maintain the safety of a procedure, which, in our hands at least, has had no detectable adverse effects to date.

Vaginal ligation of the uterine arteries should not be performed in women with known or suspected human immunodeficiency virus and/or hepatitis B or C virus. This procedure is highly effective if performed in time, as shown in this series of 13 women. It is quickly learned as it resembles the preparation for vaginal hysterectomy. Since we introduced it at our regular postgraduate seminars, it has been adopted by a number of obstetricians, even prophylactically in patients at risk (eg, placenta previa, placenta accreta). The procedure can be performed immediately in any delivery room because all the facilities required should be present. Increased obstetrician familiarity with this method would help to reduce the number of hysterectomies performed worldwide, in both the developing and industrialized worlds. In our opinion, the procedure should belong to the standard armamentarium of the practicing obstetrician, especially when treating young primigravids whose obstetric career would otherwise be prematurely and involuntarily ended.

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1. Bonnar J. Massive obstetric haemorrhage. Baillieres Best Pract Res Clin Obstet Gynaecol 2000;14:1–18.

2. O'Leary JA. Uterine artery ligation in the control of post-cesarean hemorrhage. J Reprod Med 1995;40:189–93.

3. Cruikshank SH, Stoelk EM. Surgical control of pelvic hemorrhage: Bilateral hypogastric artery ligation and method of ovarian artery ligation. South Med J 1985;78:539–43.

4. Waters EG. Surgical management of postpartum hemorrhage with particular reference to ligation of uterine arteries. Am J Obstet Gynecol 1952;64:1143–8.

5. Evans S, McShane P. The efficacy of internal iliac artery ligation in obstetric hemorrhage. Surg Gynecol Obstet 1985;160:250–3.

6. Howard LR. Iatrogenic arteriovenous sinus of a uterine artery and vein. Report of a case. Obstet Gynecol 1968; 31:255–7.

7. Burchell RC. Internal iliac artery ligation: Hemodynamics. Obstet Gynecol 1964;24:737–9.

8. Burchell RC, Olson G. Internal iliac artery ligation: Aortograms. Am J Obstet Gynecol 1966;94:117–24.

9. Clark SL, Phelan JP, Yeh SY, Bruce SR, Paul RH. Hypogastric artery ligation for obstetric hemorrhage. Obstet Gynecol 1985;66:353–6.

10. Mengert WF, Burchell RC, Blumstein RW, Daskal JL. Pregnancy after bilateral ligation of the internal iliac and ovarian arteries. Obstet Gynecol 1969;34:664–6.

11. Cho JY, Kim SJ, Cha KY, Kay CW, Kim MI, Cha KS. Interrupted circular suture: Bleeding control during cesarean delivery in placenta previa accreta. Obstet Gynecol 1991;78:876–9.

12. Schnarwyler B, Passweg D, von Castelberg B. Successful treatment of drug refractory uterine atony by fundus compression sutures. Geburtshilfe Frauenheilkd 1996;56:151–3.

13. B-Lynch C, Coker A, Lawal AH, Abu J, Cowen MJ. The B-Lynch surgical technique for the control of massive postpartum haemorrhage: An alternative to hysterectomy? Five cases reported. Br J Obstet Gynaecol 1997; 104:372–5.

14. Ferguson JE, Bourgeois FJ, Underwood PB. B-Lynch suture for postpartum hemorrhage. Obstet Gynecol 2000; 95:1020–2.

15. Merland JJ, Houdart E, Herbreteau D, Trystram D, Ledref O, Aymard A, et al. Place of emergency arterial embolisation in obstetric haemorrhage about 16 personal cases. Eur J Obstet Gynecol Reprod Biol 1996;65:141–3.

16. Vedantham S, Goodwin SC, McLucas B, Mohr G. Uterine artery embolization: An underused method of controlling pelvic hemorrhage. Am J Obstet Gynecol 1997;176:938–48.

17. Johanson R, Kumar M, Obhrai M, Young P. Management of massive postpartum haemorrhage: Use of a hydrostatic balloon catheter to avoid laparotomy. BJOG 2001;108:420–2.

18. Maier RC. Control of postpartum hemorrhage with uterine packing. Am J Obstet Gynecol 1993;169:317–23.

© 2002 The American College of Obstetricians and Gynecologists


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