Buttock Necrosis Following Uterine Artery Embolization: A Case Report

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UAE is a common procedure for the treatment of uterine leiomyoma. These benign fibroid tumors are found in up to 70% of White women and more than 80% of women of African ancestry.¹ Up to 70% of uterine fibroids are asymptomatic; many of the symptomatic cases are medically managed.² Symptoms of these fibroids include increased menstrual bleeding, urinary symptoms, pain, and infertility.¹ UAE is an increasingly commonly performed minimally invasive procedure for treating symptomatic fibroids.³ It is estimated that more than 25 000 patients worldwide undergo UAE annually.⁴ This procedure involves occluding the uterine arteries via endovascular delivery of small particles made of various materials. The embolizing particles are made of polyvinyl acetate, polyethylene glycol, various hydrogels, or trisacryl gelatin. Additionally, the embolizing particles can be different shapes and sizes, ranging from small spheres measuring 40 µm in diameter up to those measuring 1300 µm in diameter.⁵ The various embolizing particles are used to occlude the uterine arteries to reduce blood flow to the fibroids. By reducing the blood flow to the fibroids, they are reduced in size over time.^1,2,6 

Severe complications of UAE are rare and include ischemic injury of the uterus and ovaries.^7,8 Nontarget embolization of skin and subcutaneous tissue is a very rare complication of UAE and can result in full-thickness soft tissue necrosis.⁹ Few instances of buttock and labial soft tissue necrosis have been reported in the literature.^9-12 A recent study reviewed the US Food and Drug Administration device-related adverse event database for UAE-related adverse events.⁷ The review found 193 total reported events between 1998 and 2018 related to UAE. None of these adverse events included nontarget embolization leading to skin necrosis, indicating that this is not a common complication.⁷ Soft tissue necrosis secondary to nontarget embolization after UAE may be underreported in the literature, given that the ulceration can occur weeks after the procedure. 

This report describes a case of full-thickness right buttock necrosis resulting from nontarget embolization during UAE.

A 46-year-old female presented to the wound clinic for evaluation of a large necrotic ulcer to the right buttock, which had been getting progressively larger over several months. The patient had undergone UAE 5 months prior for treatment of symptomatic fibroids. She began experiencing burning and aching in the right buttock immediately after the procedure. After 5 weeks of burning, tingling pain in the right buttock, a diffuse area of necrotic skin appeared and the patient presented to urgent care (Figure 1).

This diffuse area of necrotic skin progressed to an enlarging necrotic ulcer, and the patient later presented to an outside emergency department and was admitted to an outside hospital for 3 days. She was discharged with a referral to wound care and was evaluated in clinic 15 weeks after her UAE procedure. The patient’s past medical history included deafness secondary to childhood meningitis, as well as obesity and fibromyalgia. Pertinent negatives include no prior history of diabetes, limited mobility, vascular disease, or skin ulceration.

At initial evaluation, the right buttock wound measured 12.2 cm × 12.0 cm × 3.0 cm, with a large, moist, well-demarcated eschar over much of the wound. The frank necrotic tissue was debrided in clinic. The remaining wound bed was composed of pink granulation tissue and necrotic yellow adipose tissue. There was moderate seropurulent drainage, and the wound had well-demarcated edges (Figures 2, 3).

A wound culture was positive for mixed skin flora, and no antibiotic therapy was indicated at that time. The patient reported exquisite pain with manipulation of the viable wound tissue. The surrounding tissue was indurated, with no cellulitis or other symptoms of infection present. 

To manage this wound, the necrotic adipose tissue was debrided serially over several visits. During this period the wound was dressed with gauze moistened with Dakin solution for infection control, with superabsorbent secondary dressings to manage drainage. When no necrotic tissue was present in the wound bed, NPWT was initiated to assist in granulation tissue formation. The patient developed wound infection after 1 week of NPWT; a tissue culture grew methicillin-resistant Staphylococcus aureus, Enterococcus, and Pseudomonas. NPWT was stopped for 1 week while the patient was treated with oral antibiotics, and the infection resolved. Six weeks after NPWT was started, substantial wound contraction had occurred and the wound bed was completely filled with granulation tissue. After the wound bed consisted of 100% healthy granulation tissue with no appreciable depth (Figure 4), NPWT was discontinued, and the patient was transitioned to dressings.

Collagen-based primary dressings were used along with secondary dressings of antimicrobial foam for several weeks. As the wound became smaller and drainage became scant, collagen was used, with petrolatum-based fine mesh gauze containing 3% bismuth tribromophenate and silicone foam border dressings. The wound closed by secondary intention 24 weeks after initial evaluation at the wound clinic (Figure 5). 

Nontarget embolization resulting in soft tissue necrosis is a rare complication of UAE, with few case reports describing this wound etiology.^9-12 A proposed mechanism for nontarget embolization and necrosis of the ipsilateral buttock is reflux of the embolizing agent into the internal iliac artery after the uterine artery has been occluded. The embolizing agent can then travel to the inferior gluteal artery or the superior gluteal artery, either of which may supply the skin and subcutaneous tissue over the buttocks and posterior thigh.⁹ There, the embolizing particles occlude arterioles and capillaries of the skin and subcutaneous tissue. An ischemic injury is observed depending on the degree of occlusion and the collateral blood flow to the area. It is possible that normal variations in the anatomy of the uterine and gluteal arteries may play a role in this process.¹³

In the current case, it was not possible to confirm the presence of embolizing particles in the necrotic tissue of the patient’s buttock based on histology due to the timing of the injury and start of care at the authors’ wound center. However, other relevant wound etiologies were excluded. Pressure injuries often occur during surgical procedures. The wound in the current case is unlikely to have occurred due to pressure. The procedure was short, approximately 60 to 90 minutes in total. The procedure was performed under light sedation, not general anesthesia, in an outpatient surgery center. Additionally, the wound did not occur over a bony prominence. According to an international clinical practice guideline, the patient had no known risk factors for developing pressure injuries.¹⁴ Other possible causes that were considered and excluded were burns, trauma, infection, peripheral vascular disease, and autoimmune disease. The patient was cognitively intact and had intact sensation in the affected anatomic areas. She did not report any trauma or burn to this area before or after the procedure. Additionally, no cautery or other equipment that produces intense heat was used in the embolization procedure. The patient experienced pain at the wound site, but no other symptoms of infection during the onset of necrosis. 

The patient in the current case report had no history of vascular disease, and no increased risk of vascular disease based on a risk stratification proposed by the American Heart Association and the American College of Cardiology.¹⁵ She had no history of spontaneous ulceration of the skin and no history of autoimmune disease. The pain in the patient’s right buttock began immediately after the procedure, and the pain was qualitatively consistent with ischemic pain. The pain was constant, nonmechanical, and burning in quality. Other common wound etiologies, such as pressure injuries, do not result in necrosis that progresses for weeks and months after injury. 

Additionally, CT was performed when the patient in the current case report started treatment in the wound clinic and again after 3 months to assess the extent of the injury. The CT scans demonstrated edema and fat stranding in the right buttock adjacent to the skin ulceration. No deeper structures were affected, and no abscesses or fluid collections were identified. The authors of the current report concluded that the wound was caused by nontarget embolization during UAE and was limited to involvement of the skin and subcutaneous tissue. 

The current report has limitations. It was not possible to show direct evidence of embolizing particles in the necrotic soft tissue present in this patient’s wound, due to the timing and setting in which the patient was encountered. Additionally, this case report cannot be generalized, and more research is needed to assess who may be at risk for nontarget embolization after UAE. More research is also needed to assess how frequently nontarget embolization results in ulceration. 

Nontarget embolization is a potential complication of UAE. However, full-thickness necrosis of the skin due to nontarget embolization is very rarely reported. It is possible that such injuries are underreported due to the delay between the procedure and ulceration, which in the current case was greater than 1 month. This case also highlights the importance of investigating wound etiology. Failure to identify the cause of such a large and significant wound may have led to unnecessary medical testing and procedures. This case report seeks to add to the body of literature documenting this rare wound etiology. Additionally, the case demonstrates successful treatment of such a wound in the outpatient setting without the need for further surgery.