Retroperitoneal hemorrhage (RPH) is a potentially fatal complication and is most often related to invasive cardiac procedures using the femoral artery access route. RPH rarely occurs spontaneously. For cardiac cath procedures, RPH is more often related to a cranially positioned (high) arterial puncture, a location which cannot be determined with certainly beforehand since femoral anatomy is variable and the puncture technique is performed in a blind manner (i.e. no ultrasound guidance).

RPH is most commonly seen in association with patients with anticoagulation therapy, bleeding abnormalities and hemodialysis. The incidence of retroperitoneal hematoma has been reported at 0.6-6.6% of patients undergoing therapeutic anticoagulation. Warfarin, unfractionated and low-molecular weight heparins have all been associated with RPH. Interestingly, the risk of bleeding during unfractionated heparin therapy has been estimated to be two- to five-fold greater than that with warfarin.

As an aside, some patients may have spontaneous RPH unrelated to the vascular access. Spontaneous retroperitoneal bleeding is a distinctive clinical entity, occurring without specific underlying pathology or trauma. Rare case reports include spontaneous hemorrhage into a pre-existing masses, cysts or arterial structures. Spontaneous RPH can occur in patients with factor IX or factor X deficiency, in patients with von Willebrand disease, antiphospholipid syndrome or rarely, on potent antiplatelet agents (e.g. clopidogrel).

The clinical presentation of RPH may not be immediately apparent after the cath procedure. However, RPH should be considered if patients complain of back pain, have a drop in blood pressure or develop unexplained tachycardia. This symptom complex should be presumed to be RPH, and if not recognized and treated promptly, may ultimately cause death from hypoperfusion.

For patients undergoing coronary interventions, an interesting controversy exists with regard to whether vascular closure devices increase the potential for retroperitoneal hematoma.1-4

A recent study by K. A. Tiroch et al5 reviewed the risk predictors of retroperitoneal hemorrhage following percutaneous coronary intervention and provides us with some insight into the potential role of vascular closure devices and RPH. In their study, Tiroch and colleagues looked at 3,482 percutaneous coronary interventions (PCIs) at the Brigham and Women’s Hospital between 2005 and 2007. The patients were divided into groups with (n=17) and without (n=3465) retroperitoneal hematoma. Patients were characterized by the presence of renal failure, emergent or elective procedures, size of arterial sheath, use of glycoprotein blockers, and a number of other important clinical features. The “high stick” femoral artery location was defined as the upper third of the femoral head on fluoroscopy. Vascular closure devices were not used if there was ≥ 50% artery narrowing, artery diameter < 4 mm, or calcific plaque in the target femoral artery. Vascular closure devices in the study included Angio-Seal (St. Jude Medical, Minnetonka, MN), StarClose (Abbott Vascular, Redwood City, CA) and Perclose (Abbott Vascular). Standard manual compression was used for patients ineligible for vascular closure devices. Standard PCI anticoagulation regiments were used and sheaths were removed when activated clotting times were < 160 sec.

The results indicated that of the 17 patients with retroperitoneal hematoma, there was a statistically higher incidence of renal insufficiency (29 versus 6% with creatinine of 2.11 vs1.7), INR >1.8 (24 versus 2%) and greater use of glycoprotein IIb/IIIa blockers (77 versus 42%). The presence of high puncture near or above the external iliac artery occurred in 29% of the RPH group versus 2% of those without retroperitoneal hematoma.

Vascular closure devices were used in 82% of patients in both groups. Sixty-three patients had unsuccessful vascular closure device deployment, distributed similarly between groups. A vascular closure device was not an independent predictor of retroperitoneal hematoma as opposed to the presence of renal insufficiency, glycoprotein use, or a high stick, all statistically significant risks by uni- and multi-variate analysis.

How can we use this information in our labs today? A review of literature indicates that although some vascular closure devices may be associated with more retroperitoneal hematomas, this fact does not appear in this particular large, single-center database report. The comfort, ease of use, and security of hemostasis with vascular closure devices has proven their worth in most clinical practices. A meta-analysis of 37 trials with 4,000 patients showed no difference regarding efficacy and safety of the closure devices as compared to manual compression.6 It is unclear why patients with chronic renal insufficiency should have a higher incidence of retroperitoneal hematoma. One can speculate that the impaired platelet function, increased small vessel vascular disease and perhaps abnormal coagulation responses might predispose to this association. Additional RPH risk factors, including female gender, longer procedure times, and emergency admissions with urgent puncture, should be considered. The placement of venous sheaths with possible change in arterial reference point may also increase the likelihood of a high femoral puncture site. Importantly, physicians from Brigham and Women’s Hospital note that in their experience with over 20,000 vascular closure deployments, routine femoral angiograms and weight-based anticoagulation regimens contribute to a reduced complication rate when using vascular closure devices.

While this study is probably not the last word on the subject, it does direct our attention toward retroperitoneal hematoma being a function of an accurate stick location, critical in the diabetic or renal patients who are anticipated to be on intense anticoagulant regimens. Pre-puncture assessment of the precise access location should be routinely emphasized to reduce the potential retroperitoneal hematoma as a complication of cardiac catheterization.