Heavy uterine bleeding due to uterine arteriovenous malformations

Abstract

Heavy uterine bleeding without cervical trauma, uterine perforation, atony and refractory to conventional therapies is highly suspicious arising from uterine arteriovenous malformations. Injuries of uterine artery malformations are rare but life-threatening conditions (1–4), which are confirmed with an angiography and treated by a definitive hysterectomy. The patient was a 39-year-old woman, gravida 8, para 1: status postelective dilatation and curettage (D&C) due to a missed abortion at a clinic. On the fifth postoperative day, the patient presented with complaints of intermittently profuse vaginal bleeding with blood clots. Repeat suction curettage was carried out and a foley catheter tamponade was inserted with no obvious affect. She was then transferred to our hospital on the tenth day. Pelvic sonogram showed hematometra over the lower segment of the uterus. Uterine perforation was thought unlikely. The uterus felt firm, and uterotonic agents (prostaglandin E1 and oxytocin) had already been administered. Suction curettage was performed carefully, but heavy bleeding continued from the uterus and the amount of blood loss was approximately 1400 ml within seconds. A balloon tamponade was immediately inserted into the uterus. The patient experienced profuse vaginal bleeding that did not subside. She was hemodynamically unstable, and her hemoglobin dropped to 5.4 gm/dl (hematocrit: 17%) from 11.4 g/dl (hematocrit: 34.3%) after 4 h of the procedure. No gestational production was found during the histologic findings. Coagulation studies were within normal limits. Prompt hemodynamic resuscitation was with intravenous fluids and 4 units of packed red blood cells. It was then decided to intervene with a transarterial embolization. A pelvic arteriogram showed the arteriovenous malformations characterized by dilatation of branches of the uterine artery associated with fast venous filling, hypervascularity and extravasation from bilateral uterine artery malformations (Fig. 1a, b). Bilateral access to the uterine arteries was subsequently obtained, and the arteries were embolized with the use of a coil, with cessation of the bleeding (Fig. 2a, b). After the procedure, the patient's hemodynamics were stable (hemoglobin: 9.1 g/dl, hematocrit: 26.6%). After 2 days, the balloon tamponade was removed without active vaginal bleeding. The patient experienced defervescence and, after remaining afebrile for 48 h on a regimen of antibiotics, was discharged being hemodynamically stable with no active vaginal bleeding on day 3. Pelvic angiograms clearly show that pelvic hypervascularity and contrast extravasations showed the irregular, tortuous vascular nidus (arrow head) with early draining vein (arrow) on arterial phase, consistent with arteriovenous malformations, right (a) and left (b). Pelvic angiograms obtained after the embolic procedure showing complete embolization of the uterine arteries, right (a) and left (b). Unfortunately, she returned to our hospital on postembolized day 36 because of intractable lower abdominal pain and massive vaginal bleeding. A laparoscopically assisted vaginal hysterectomy was performed. The histology showed dilated and tortuous vessels. Finally the patient was discharge from the hospital on the 3th postoperative day in good condition. Uterine artery malformations are defined as having a dysplastic vascular origin with large feeding arteries causing decreased vascular resistance. They are rare but life-threatening conditions. The most common uterine vascular malformations are arteriovenous (1–4). This article described that no retained products of conception were found on repeat aspiration. The uterus felt firm, so uterine perforation was thought unlikely. A balloon tamponade failed to control the hemorrhage. The heavy hemorrhage refractory to treatment was proved to result from the laceration of bilateral uterine arteriovenous malformations by the pelvic angiography. Although finally a hysterectomy was necessitated, prompt diagnosis with pelvic angiography and treatment with embolization could be undertaken before resorting to emergency surgery. Our experience in this instance suggests that a history of abrupt, heavy, intractable uterine hemorrhage without another bleeding source (retained gestational products, traumatic cervix and uterus, atony, etc.) should indicate a uterine vascular malformations injury. A balloon tamponade and angiographic embolization may be useful for either complete ambulatory management or temporizing while awaiting the opportunity to perform definitive surgery such as a hysterectomy. It is possible that not only do uterine arteries feed the uterus but the arteries from the hypogastric artery and other extensive collateral arteries also contribute to uterine flow. The failure of embolization might be due to abundant collateral circulation and revascularization. Attempts to embolization of hypogastric arteries or ovarian vessels might be an effective means of controlling pelvic hemorrhage (5). However, the pati- ent refused to receive any further procedures. Surgical management is possibly an inevitable choice in the cessation of heavy uterine bleeding due to uterine arteriovenous malformations.