When Blood Is Gushing Out Again What Does That Mean

West J Emerg Med. 2013 Sep; 14(v): 411–414.

Uterine Arteriovenous Malformation with Sudden Heavy Vaginal Hemmorhage

Received 2012 Jul 24; Revised 2012 November 16; Accepted 2012 Dec 12.

Abstract

Dysfunctional uterine bleeding (DUB) is a common presentation in the emergency section and has a broad differential. Almost presentations of DUB are in hemodynamically stable patients and can be evaluated as an outpatient. Uterine arteriovenous malformation (AVM) is one presentation that tin can result in a life-threatening medical emergency with unexpected sudden and massive vaginal bleeding. We depict a case of a 24-year-old female with sudden heavy vaginal haemorrhage requiring a blood transfusion, ultrasound bear witness of uterine AVM, and a treatment method of expectant management using an intrauterine device in an attempt to preserve fertility.

CASE REPORT

A 24-year-onetime female, G3P0030 with a history of low presented to the emergency department (ED) for evaluation of abrupt heavy vaginal bleeding. The patient noticed a sudden gush of blood between her thighs, prompting her visit to the ED. She had 2 days of light spotting preceding this sudden heavy bleeding, also as irregular catamenia ever since a missed abortion iv months prior. She had 2 constituent terminations of pregnancies in the preceding year secondary to severe hyperemesis gravidarum. During this episode of sudden heavy vaginal haemorrhage, she also complained of balmy suprapubic cramping, simply no associated nausea, vomiting, dizziness, chest pain, or shortness of breath.

Upon presentation to the ED, approximately 30 minutes after the bleeding began, the patient's triage vital signs showed a blood pressure of 123/81 mmHg, pulse of 102, respiratory rate of twenty, pulse oximetry of 100% on room air, oral temperature of 98.7°F, and a negative rapid urine pregnancy. Intravenous admission was obtained and blood was drawn for laboratory analysis. Upon evaluation, she was awake, alarm and oriented ×3, and she was neither pale nor diaphoretic. She was haemorrhage through her sanitary napkins onto her apparel, just walked with ease to the test table without any shortness of breath. Her abdomen had normoactive bowel sounds and was soft and non-tender. She had normal external genitalia with no signs of trauma. Her vaginal exam revealed copious dark blood and clots, with no trauma noted. There was approximately 300 mL of blood on the exam room flooring. Her cervix had no lesions and clots were noted in the bone. On bimanual exam, she had a closed cervical bone, no cervical move tenderness, and no adnexal tenderness.

Her laboratory studies, including a complete blood count (CBC), electrolyte console, coagulation studies, and thyroid function tests ,were unremarkable. She had a hemoglobin (Hgb) of 12.i thou/dL and hematocrit (Hct) of 37.1%. A signal-of-care ED transvaginal ultrasound showed an enlarged endometrial cavity containing irregularities with an area of pulsatile menstruum via Doppler, no free fluid, and normal ovaries. Despite receiving an initial 2-liter bolus of intravenous crystalloid, the patient developed symptoms of postural hypotension with average blood pressures at approximately 100/sixty mmHg. Her heart rate remained in the nineties; however, she continued to accept persistent heavy vaginal bleeding. The conclusion was made to admit the patient to the gynecology service for possible surgical intervention of massive dysfunctional uterine bleeding, and farther evaluation of an enlarged endometrial cavity.

During her access, and 9 hours afterwards presentation, a repeat CBC due to heavy vaginal bleeding showed a 3-point drop in Hgb to eight.eight g/dL and Hct to 26.half-dozen%. She was transfused 4 units of packed red blood cells. On hospital day 2, her formal sonogram showed an enlarged endometrial cavity measuring 26 mm transversely with multiple hypertrophied vessels within the myometrium at the endometrial junction showing low resistance arterial period, but no active catamenia within the endometrial crenel, suggesting a diagnosis of uterine arteriovenous malformation (AVM) (Figures 1 and ​ 2). A magnetic resonance imaging angiogram (MRI/A) of the pelvis showed an amorphous drove of vessels arising from the pelvic arterial branches confirming the ultrasound diagnosis of multiple parametrial AVM or pseudoaneurysms (Figure 3).

Ultrasonography of uterus in long axis showing enlarged endometrial cavity (2.65 cm) with irregular clot.

Ultrasonography of uterus in transverse centrality with color doppler menstruum showing pulsatile flow inside the endometrial cavity.

Magnetic resonance imaging of uterus in transverse centrality demonstrating amorphous collection of vessels with fluid in the endometrial cavity.

On hospital 24-hour interval 3, she had minimal vaginal bleeding, normal vitals, and stable blood counts (Hgb 9 g/dL and Hct 27%). Subsequently a multidisiciplinary give-and-take involving gynecology and interventional radiology, the patient declined surgical intervention, including uterine embolization of the AVM, and preferred to try medical direction in an endeavour to preserve her fertility. A hormonal intrauterine device (IUD) was placed and the patient was discharged with strict instructions on when to return to the infirmary if the bleeding returned.

Discussion

Uterine AVMs are a rare cause of uterine bleeding with fewer than 100 cases reported.¹ The true incidence is unknown, but with increased use of ultrasound to evaluate abnormal vaginal bleeding, O'Brien et al² propose a crude predicted incidence of 4.5%. AVMs consist of an abnormal growth and connection between arteries and veins without a capillary bed, creating areas of high and depression flow, which are frail and prone to bleeding. ⁱⁱⁱ Uterine AVMs near commonly nowadays with sudden heavy vaginal bleeding and tin can be built or acquired. Built AVMs form through disturbances in angiogenic development creating multiple connections between arteries and veins that tend to be deeper in surrounding tissue. Acquired AVMs form smaller arteriovenous fistulas that occur every bit a complication of uterine surgery or curettage, gestational trophoblast illness, choriocarcinoma, and infection.⁴

In a patient with massive vaginal bleeding, especially in the presence of hemodynamic instability, it is of import to initiate aggressive resuscitation with intravenous fluids and early use of claret products.⁵ Temporizing measures, such equally intrauterine tamponade with a foley catheter, can be performed in the ED to treat life-threatening vaginal hemorrhage.⁶ In the unstable patient, the treatment regimens include dilation and curretage (D&C), intravenous estrogen, uterine artery embolization, and hysterectomy.^seven Uterine AVMs oftentimes cause sudden massive bleeding, and in an unstable patient appropriate diagnosis is important because emergent handling with D&C can worsen the underlying status, leading to profuse uterine hemorrhage, shock, and potentially hysterectomy.²

Traditionally, uterine AVMs were diagnosed after hysterectomy with histopathologic evidence of the arteriovenous fistulas.ⁱⁱⁱ In the nowadays 24-hour interval, angiography has become the gold standard for diagnosis of uterine AVMs with the added do good of the ability to deliver handling through embolization.⁸ Ultrasonography, computed tomography (CT) and MRI are being used more frequently as initial diagnostic modalities.⁸ Ultrasonography is becoming the preferred method for diagnosing AVMs, reserving angiography for planned therapeutic embolization or prior to surgical intervention.

Every bit ultrasonography is becoming more than readily available in the ED, bedside ultrasonography by the emergency physician or consulting gynecologist can assist in the initial diagnosis of uterine AVMs. Gray scale ultrasonography will oftentimes show nonspecific heterogenous or anechoic tortuous spaces in the myometrium.⁹ Color and spectral Doppler ultrasonography shows further detailing of a tangle of vessels producing a "color mosaic" pattern with multidirectional high and low velocity menstruum.^{2 , 10} Ultrasonography has also been used to demonstrate the efficacy of treatment by evaluating for resolution of AVMs within 24 hours of embolization.²

Treatment of uterine AVMs remains controversial, often with great business organization for fertility. Hysterectomy remains the definitive treatment, particularly in a symptomatic patient without desired fertility.^iv A minimally invasive arroyo through angiographic embolization of the AVM, which has potential to preserve fertility, is currently the preferred treatment. In 1997, ten years after the first successful uterine AVM embolization, there were only five pregnancies documented.^iv A review of electric current literature to 2004 shows slightly more successful pregnancies following embolization at a mere x pregnancies; however, this still does not demonstrate acceptable fertility preservation.⁸ Congenital AVMs tend to be treated with hysterectomy or embolization as they pose a college risk of recurrent menorrhagia. And finally, in the right clinical setting, bourgeois management is another treatment modality, typically offered to cases of acquired AVMs. Patients with ane episode of bleeding and hemodynamic stability can be offered treatment with combined oral contraceptive pills (OCP).¹¹ Timmerman et al¹² report 8 cases of spontaneous resolution of acquired AVMs following OCP utilize or expectant management, improving the chances of preserved fertility. Fifty-fifty more example reports in the current literature show resolution of AVMs and successful pregnancies after conservative management.^thirteen

In this case report, a fertile female presented with sudden heavy vaginal bleeding in the setting of two contempo D&Cs. The abrupt nature and volume of bleeding indicated the need to closely monitor for signs of hemorrhagic daze, and farther evaluate for acquired uterine AVMs. The indicate-of-intendance ED ultrasound demonstrated a pulsatile mass in the endometrial cavity, prompting further workup for potentially life-threatening haemorrhage from a uterine AVM. One time hemodynamically stable, the patient opted for conservative medical management with an IUD to provide the highest probability of preserved fertility. IUDs have non been shown to reduce the size or risk of rupture of uterine AVMs, and there are no information to suggest that insertion is contraindicated. The patient was advised that her uterine AVM was probable acquired from her prior D&Cs and they could regress spontaneously or rupture again, perhaps complicating time to come pregnancy. Her futurity might involve AVM embolization or hysterectomy as a last resort.

CONCLUSION

Dysfunctional uterine bleeding is a mutual complaint in the ED, and in the right clinical setting, can be life threatening. When faced with a patient with sudden and massive vaginal bleeding and a history of prior uterine instrumentation, the diagnosis of uterine arteriovenous malformation should be considered. Colour or spectral Doppler ultrasonography should be used to ostend the diagnosis and provide the most accurate information to the consulting gynecologist.

Footnotes

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources and financial or management relationships that could exist perceived as potential sources of bias. The authors disclosed none.

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3789894/

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