Case presentation

A healthy, active, nonsmoking 40-year-old man with a history of hypertension and dyslipidemia noted midsternal chest pain while dragging a heavy deer he had just hunted out of the woods and to his car. He stopped to rest, but the pain increased in severity and was associated with diaphoresis. He drove himself to a local hospital’s emergency department, where an electrocardiogram showed sinus tachycardia and ST elevation in the anterior precordial leads. Shortly after the electrocardiogram was obtained, he became unresponsive from ventricular fibrillation and required cardioversion. After administration of 325 mg of aspirin, 5 mg of intravenous metoprolol, an intravenous bolus of unfractionated heparin, and 4 mg of morphine sulfate, he was flown by helicopter to a tertiary care hospital 40 miles away for emergency coronary angiography.

Cardiac catheterization

Angiography confirmed proximal occlusion of the left anterior descending artery (Figure 25-1). The operator successfully restored normal flow in this vessel with balloon angioplasty (2.5 mm diameter by 20 mm long balloon) followed by insertion of a 3.5 mm diameter by 15 mm long bare-metal stent (Figure 25-2). Adjunctive pharmacology included an additional bolus of unfractionated heparin and a bolus and infusion of eptifibatide. The left circumflex and right coronary arteries were angiographically normal. At the end of the procedure, 600 mg of clopidogrel was administered orally. The activated clotting time measured 260 seconds. An angiogram of the right femoral artery performed through the arterial sheath is shown in Figure 25-3 and Video 25-1. The operator successfully achieved access site hemostasis using a closure device (Starclose, Abbott Medical). The patient left the cardiac catheterization laboratory feeling well, with a blood pressure of 110/70 mmHg.

FIGURE 25-1 This is the initial left coronary angiogram demonstrating total occlusion of the proximal left anterior descending coronary artery (arrow).

FIGURE 25-2 Representative left coronary angiogram showing the final angiographic result after balloon angioplasty and stenting.

FIGURE 25-3 This is a right femoral artery angiogram obtained in a right anterior oblique projection. The insertion site of the sheath appears to enter the artery just above the lower border of the inferior epigastric artery (arrow) consistent with a high puncture above the inguinal ligament.

Postprocedural course

Upon arrival to the coronary care unit, he remained free of chest pain but became nauseated and reported right lower abdominal and scrotal pain. His heart rate fell to 51 beats per minute and his blood pressure dropped to 81/56 mmHg. He appeared pale and diaphoretic but denied chest pain. An electrocardiogram confirmed resolution of ST-segment elevation. Examination of the access site did not reveal any abnormalities; however, there was significant tenderness noted in the right lower quadrant, and scrotal swelling was observed. The operator again reviewed the femoral artery angiogram shown in Figure 25-3 and became concerned about the possibility of a retroperitoneal bleed. The infusion of eptifibatide was stopped and manual pressure was applied to the access site for 30 minutes. A bolus of 500 cc of normal saline and 1 mg of atropine restored the blood pressure and heart rate to normal. The hematocrit slowly fell from an immediate postcatheterization value of 36.0% to 27.1%, and increased to 34% after a two unit transfusion of packed red cells. Blood pressure, heart rate, and hematocrit remained stable and right lower abdominal discomfort improved. The right lower abdominal discomfort and scrotal swelling gradually resolved over the subsequent 3 days. He remained symptom-free and was discharged 4 days after admission.

Discussion

Few complications of percutaneous coronary intervention are as insidious as a retroperitoneal bleed. Retroperitoneal bleeds complicate about 0.5% to 0.7% of coronary interventions performed via the femoral artery.^1–3 Although they are relatively rare, they are associated with a high incidence of serious adverse outcomes, including death in 10% to 12% of cases.^2,3 Clearly, the most common cause of a retroperitoneal bleed is from inadvertent puncture of the artery above the inguinal ligament when obtaining femoral artery access. Rarely, a retroperitoneal bleed may be caused by spontaneous hemorrhage from anticoagulation, puncture of a vein, or from perforation of the iliac artery or aorta when advancing guide catheters or sheaths through tortuous vessels. Risk factors for development of retroperitoneal bleed have been well-studied and include female gender, high arterial puncture, chronic renal insufficiency, low body weight, and the use of glycoprotein IIb/IIIa inhibitors.^1–3

The diagnosis of a retroperitoneal bleed may prove challenging, as the initial symptoms are often subtle and mimic other conditions. Often, the only clue to a retroperitoneal bleed is sustained or fluctuating hypotension, present in nearly all cases. The retroperitoneal space is intensely innervated with vagal afferents and thus, symptoms of increased vagal tone such as bradycardia, nausea, diaphoresis, and pallor are very frequently observed. Lower abdominal pain is more common than back pain. Subtle symptoms attributable to other causes may predominate including urinary difficulties, suprapubic discomfort, and symptoms from compression of the femoral nerve. A drop in hematocrit is universally seen but may not be immediately observed, mandating the need for serial assessments when suspecting this complication. Because the bleeding is directed internally, the access site usually appears normal without an associated hematoma.

In most cases, the diagnosis is based on clinical assessment. This complication should be considered in any patient with unexplained hypotension, vagal symptoms, and anemia following the removal of a femoral artery sheath. Computed tomography imaging is diagnostic and confirms the extent of the bleed as well as the precise site of hemorrhage, but this test should be used cautiously as these patients may be too unstable to allow transfer to a radiographic suite.

The patient presented here demonstrated many of the classic manifestations of a postprocedural retroperitoneal bleed. Femoral artery angiography demonstrated a high puncture; additionally, the patient was treated with a glycoprotein IIb/IIIa inhibitor. Symptoms were classic and began soon after sheath removal. Fortunately, this complication was recognized rapidly and aggressive management prevented serious sequelae.

In addition to the high mortality rate, retroperitoneal bleeding is associated with significant morbidity. Many adverse events are related to prolonged hypotension including renal failure, hepatic or acute lung injury, and multisystem failure. Blood transfusion is needed in 60% to 90% of patients.^1,2 Stent thrombosis may arise from hypotension, as well as from abrupt reversal of anticoagulation and transfusion of blood products. Vascular surgical repair may be necessary in 5% to 15% of cases, usually for ongoing bleeding despite conservative measures or for the development of compressive neuropathy or uropathy.^1–4

Although not entirely preventable, this dreaded complication can be minimized by using fluoroscopy to guide femoral artery access. Puncture should be directed no higher than the middle of the femoral head. Femoral artery angiography performed by injecting contrast through the side arm of the femoral sheath confirms the puncture site in most cases. The lower border of the loop created by the inferior epigastric artery defines the lower border of the retroperitoneal space (Figure 25-3); arterial access above this site may lead to a retroperitoneal bleed following sheath removal. Without a firm base formed by the bony mass of the femoral head, application of manual pressure cannot effectively compress the artery. Bleeding is directed internally and, reassured by the absence of bleeding from the incision site or development of a hematoma, the operator falsely assumes hemostasis has been achieved. The role of vascular closure devices in the development of this complication is controversial. Operators are urged to avoid them in the event of high puncture.

Prompt and aggressive management of a retroperitoneal bleed may prevent the serious consequences described above. Initial attention is directed at hemodynamic resuscitation. Infusion of saline followed by transfusion of blood products and pressor support as needed to maintain blood pressure, urine output, and hematocrit represents the mainstay of initial therapy. In most cases, anticoagulants such as heparin and the glycoprotein IIb/IIIa inhibitors should be stopped and their action reversed. The decision to stop clopidogrel and aspirin in a patient with a recently placed stent should be made with great caution; in general, these agents should be continued. Additional manual compression at the site may help staunch the ongoing hemorrhage. While it is prudent to involve vascular surgery early in the management of these patients, surgery is indicated in only 5% to 15% of cases, usually because of ongoing hemodynamic instability or transfusion requirement. Endovascular management includes obtaining access from the contralateral side and placing a covered stent across the puncture site in the vessel to stop the bleeding and eliminate the need for complex surgery.