Rectus Sheath Hematoma as a Complication of Ablation of Atrial Fibrillation
VASCULAR DISEASE MANAGEMENT 2010;7:E230-E232
Abstract
A rectus sheath hematoma is an uncommon condition and, to the best of our knowledge, no case has been reported in the literature as a complication of radiofrequency ablation of atrial fibrillation. Along with review of the pathophysiology and anatomy of this entity we report a case of a rectus sheath hematoma complicating an atrial fibrillation ablation procedure and propose methods for treatment and prevention.
Introduction
Atrial fibrillation ablation procedures have become a common electrophysiologic procedure, but continue to have a significant complication rate. Peripheral vascular complications are the most common complication seen after this procedure.1,2 While retroperitoneal bleeding, groin hematomas, and arteriovenous fistulae are more common vascular complications, rectus sheath hematomas have not been reported. We report a case of rectus sheath hematoma complicating an atrial fibrillation ablation procedure, review the literature and anatomy of this entity, and propose methods for treatment and prevention.
Case Presentation
A 63-year-old female with paroxysmal atrial fibrillation was referred for radiofrequency ablation. Low-molecular-weight heparin (LMWH) was prescribed for anticoagulation prior to the procedure and oral anticoagulation was discontinued. Her coagulation profile on the day of the procedure revealed a prothrombin time of 19.8 seconds (international normalized ratio, 1.7). The patient reported some bruising at the injection sites of LMWH. Venous access was obtained via both femoral veins. There was no apparent inguinal hemorrhage or hematoma formation throughout the procedure. Pulmonary vein isolation was performed via a transseptal route and all four pulmonary veins (PV) were electrically isolated. Heparin sodium was used intravenously throughout the procedure to maintain adequate anticoagulation. The patient was hemodynamically stable throughout the intervention. Three hours after the procedure, the patient reported persistent urinary urgency; her Foley catheter was irrigated without evidence of catheter obstruction. She subsequently became progressively hypotensive with a normal heart rate in sinus rhythm. Physical examination revealed a normal cardiovascular system. An abdominal examination was significant for a large ecchymosis and a palpable mass adjacent to the injection site of the LMWH. Transthoracic echocardiography (TTE) showed no evidence of pericardial effusion. Computed tomography (CT) of the abdomen revealed hemorrhage in the right rectus sheath and extension of the hemorrhage into the pelvis. Doppler ultrasound examination of the abdomen showed active bleeding of the inferior epigastric vein in the posterior aspect of the rectus sheath. Anticoagulation was discontinued. Due to a progressive decline in the patient’s hemoglobin level, she received 2 units of erythrocyte transfusion. A CT of the abdomen showed reduction of the hematoma on the following day. Surgical consultation recommended conservative management in view of patient’s hemodynamic stability. The patient’s condition remained stable and required no further blood transfusions. Oral anticoagulation was resumed 4 days after the procedure in the hospital and she was discharged home on postoperative day 6 in stable condition.
Discussion
Rectus sheath hematoma as a result of abdominal trauma was first described by the Greeks, Hippocrates and Galen, as early as the fifth century B.C.3 It may be caused by bleeding into the rectus sheath from injury to the superior or inferior epigastric artery or vein or from a direct tear of the rectus muscle.
Anatomic features. The rectus sheath consists of the rectus abdominis muscles, a fascial sheath, and their blood supply via the epigastric arteries and veins. The arcuate line located about 5 cm below the umbilicus functionally separates the rectus sheath into superior and inferior portions. The arterial supply to the rectus sheath is derived from the superior and inferior epigastric arteries which form rich anastomoses near the level of the umbilicus. Hematomas below the arcuate line are caused by damage to the inferior epigastric vein or artery. They may protrude posteriorly and dissect extensively because of the absence of a posterior sheath wall to tamponade the bleeding. Dissection of the hematoma inferiorly into the prevesicular space of Retzius may result in tenesmus, as seen in the patient in this case. Hematomas near the peritoneum can result in peritoneal irritation.4 The severity of rectus sheath hematoma may be categorized on the basis of the appearance on CT scan and clinical features.5 CT imaging is superior to ultrasound in localization and evaluation of the size of the hematoma.6 Anticoagulation is the most frequent predisposing factor for rectus sheath hematoma. Recent case series indicate an increasing prevalence largely due to the increased use of anticoagulant medication.7 Anticoagulation can be a predisposing factor, or it can directly cause rectus sheath hematoma by accidental intramuscular injection of LMWHs.8 It is 2–3 times more common in females than in males due to the smaller muscle mass in women.9 In addition to LMWH injection, rectus sheath hematoma has also been reported secondary to subcutaneous insulin injections.10 Vascular conditions such as hypertension and collagen vascular disease as well as blood dyscrasias are associated with rectus sheath hematoma.
Physical findings and signs. Rectus sheath hematoma often presents with abdominal pain, with or without a mass. On abdominal examination, these patients may exhibit a positive Fothergill’s or Carnett’s sign. The Fothergill sign is positive when the hematoma within the rectus sheath produces a mass that does not cross the midline and remains palpable when the patient tenses his or her rectus muscle.11 The Carnett’s sign is an exacerbation of the abdominal pain and tenderness over the hematoma by contraction of the rectus muscle.12 The Cullen sign of periumbilical ecchymosis is associated with retroperitoneal or abdominal wall hemorrhage. In rectus sheath hematoma, ecchymosis appears after 2–5 days.13
Treatment and prevention of rectus sheath hematoma. Conservative treatment is the mainstay of management in hemodynamically stable patients with a non-expanding hematoma.14 In cases of failure of conservative therapy, a surgical approach or coil embolization can be an alternative management strategy.15 The frequency of injection-site hematomas with enoxaparin was reported to be greater than 10% in a large series.16 Adequate education of patients self-administering enoxaparin should be an important step toward prevention of rectus sheath hematoma. Altering the administration technique and syringe size were shown to affect the size of the hematoma associated with subcutaneously administered heparin.17,18 A less traumatic injection technique would involve a shallow entry of the needle into a skinfold beyond the umbilicus to avoid direct damage to the underlying large vessels. Recent data indicate that pulmonary vein ablation under the therapeutic effect of warfarin may be a safe alternative to bridging anticoagulation with enoxaparin in the periprocedural period.19 With this approach, a very low incidence of 0.66% of groin hematomas was reported, which may be due to multiple factors including the absence of LMWH after the ablation. Our laboratory has recently adopted this strategy for left atrial ablation procedures.
Conclusion
To the best of our knowledge, this is the first report of a rectus sheath hematoma complicating catheter ablation of atrial fibrillation. It may be added to the list of reported complications associated with this invasive procedure.20 Prevention of this complication may be achieved with the avoidance of LMWH in the periprocedural period or with adequate education of patients in the self-administration of enoxaparin before and after ablation of atrial fibrillation.
From the Division of Cardiology, Caritas St. Elizabeth’s Medical Center, Boston, Massachusetts.
Disclosure: The authors report no financial relationships or conflicts of interest regarding the content herein.
Manuscript submitted June 17, 2010, provisional acceptance given June 29, 2010, final version accepted June 29, 2010.
Address for correspondence: John V. Wylie, MD, St. Elizabeth’s Medical Center, Tufts University School of Medicine, 736 Cambridge Street, Boston, MA. E-mail: john.wylie@caritaschristi.org
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