Retroperitoneal bleed

When Should You Become Aggressive in a Patient With a Retroperitoneal Bleed?

Morton J. Kern, MD, Clinical Editor; Chief Cardiology, Long Beach Veterans Administration Health Care System, Long Beach, California; Associate Chief Cardiology, Professor of Medicine, University of California Irvine, Orange, California

Morton J. Kern, MD, Clinical Editor; Chief Cardiology, Long Beach Veterans Administration Health Care System, Long Beach, California; Associate Chief Cardiology, Professor of Medicine, University of California Irvine, Orange, California

You are called to the recovery room 2 hours after a routine femoral approach diagnostic catheterization. Your patient had 20 minutes with a blood pressure (BP) of 80/60. What should we be thinking and doing for this patient? This common scenario occurs every day in every lab around the world. Most of the time, it requires little more than saline and observation. However, one can never know with certainty whether the hypotension is a harbinger of disaster, namely an impeding or ongoing retroperitoneal bleed or hematoma (RPH) leading to exsanguination and death. Every year, 1 or 2 patients die from RPH.1,2  

Incidence and risk factors of RPH after PCI

From Trimarchi et al2, in PCI patients, RPH occurred in 482 (0.4%) in over 110,000 patients reviewed. Of these, 92% were treated medically and 8% underwent surgical repair. Female sex, body surface area <1.8 m2, emergency procedure, history of chronic obstructive pulmonary disease, cardiogenic shock, pre-procedural intravenous heparin, pre-procedural glycoprotein IIb/IIIa inhibitors, adoption of sheath size ≥8 French, and use of vascular closure devices were independent predictors of RPH, whereas the use of bivalirudin was associated with a lower risk. The development of RPH was associated with a higher frequency of post-procedure myocardial infarction (6% vs. 2%, P<0.0001), infection and/or sepsis (17% vs. 3%, P<0.0001), and heart failure (8% vs. 2%, p<0.0001). In-hospital mortality was significantly higher in patients who developed RPH than in patients who did not (7% vs. 1%, P<0.0001). Among patients with RPH, independent predictors of death were history of myocardial infarction, cardiogenic shock, pre-procedural creatinine ≥1.5mg/dl, and left ventricular ejection fraction <50%.

Causes and treatment of hypotension after cath

Hypotension is defined as systolic (S) BP <90mmHg or SBP 30mmHg lower than the patient’s entrance SBP. For example, if the patient enters the lab with a SBP of 150mmHg and after sedation, has a SBP of 125mmHg that in the recovery room drops to 95mmHg, this would be considered hypotension needing evaluation and possibly treatment. Any SBP <90 mmHg, in my book, needs attention, regardless of the starting point.  

The most common cause of hypotension after cath is a vagal episode due to a combination of back pain (pre-existing or possibly new) related to the required recumbent positioning during and after the procedure, and groin puncture site pain (sometimes from the compression). The treatment is to give a saline infusion 250-500cc NS over 20-30 minutes, atropine (0.5mg IV) and maybe some mild analgesia, like low-dose fentanyl, 12.5mcg IV. This treatment should restore SBP and heart rate (if bradycardic). (Recall that a vagal reaction in the elderly may not manifest with bradycardia, but only vasomotor dilation and hypotension.) Restoration of the SBP should validate that this initial episode of hypotension was likely vagal.  

However, the next most common cause of hypotension would be that of volume loss, i.e. bleeding. Bleeding from the vascular access site is responsible over 90% of the time, but spontaneous bleeding away from the access site can also rarely occur. Other rare causes of hypotension after cath include ischemia, infarction, tamponade, new mitral regurgitation, persistent arrhythmias, or inability to accurately record a correct BP due to equipment or body type. These uncommon causes are always associated with evident signs and symptoms suggesting their origins, but in some cases, require emergency echocardiography to make the diagnosis, especially tamponade.  

Treatment for hypotension should begin with management of the most common problems. We should presume there is blood loss if the SBP does not return to normal levels after fluid bolus and atropine as above. The further treatment for presumed femoral access site bleeding is renewed femoral site compression [application of a Femostop device (St. Jude Medical) may be helpful] and cessation of any anticoagulation. Draw blood and send the sample for a type-and-cross match for possible transfusion. Most femoral access site bleeding, even if there is some degree of retroperitoneal blood accumulation, usually is controlled by the conservative approach of supporting blood pressure and manual compression.

Signs of RP bleeding include new severe back and groin pain, emerging bruising over the abdomen or flank with blood tracking into the inguinal soft tissues, low BP, and increasing heart rate. When these signs are present, a RP bleed is presumed to be the cause. You do not need a computed tomography (CT) scan to prove it. In fact, in some cases, the CT may delay the appropriate treatment in the hypotensive patient.

Now for the hard part. When should your team call for help in dealing with a hypotensive patient with RP bleed? There is no general consensus as to the best management plan for patients with RPH. Since most RP bleeds are controlled without surgery or intervention, many operators are reluctant to activate the teams needed for percutaneous intervention or surgery. Experience suggests that when the SBP continues to drift downward, bleeding is continuing at a rate exceeding that of saline and transfusion volume replacement. This is the time to take aggressive action.

Interventions for RP bleeds

There are two approaches to aggressively managing RP bleeding: 

1) Percutaneous intervention with balloon tamponade of the bleeding site, followed by stenting, covered stenting or if needed vascular surgery;

2) Vascular surgery after angiographic documentation of bleeding site.  

My preference is the first option. Return the patient to the cath lab, perform contralateral femoral access, cross over the iliac artery to perform angiography, identify the bleeding site and then follow with balloon tamponade, stent, and covered stent as indicated by the vascular response. If the balloon/stent approach fails or is not possible, then at least the bleeding site has been identified so that the vascular surgeon can do his or her job.

The patient with hypotension post cath should be rapidly stabilized, and if not stabilized, then rapidly diagnosed and treated for the cause of hypotension. If RP bleeding is the cause and BP still cannot be maintained after fluid challenge, then intervention for RP bleeding must proceed in rapid order. Failure to do this may result in a catastrophic outcome.

Case illustration

We recently had an elderly man with aortic stenosis and dyspnea on minimal exertion. Femoral access was selected over radial because we wanted to get an optimal and quick hemodynamic study for his aortic stenosis. He was 5’3” tall and weighed 220 lbs. Femoral access was difficult because of his body shape. Ultrasound imaging was requested in order to make a more accurate puncture, but was not immediately available to guide us. Fortunately, after femoral angiography, we found that the blind puncture was adequate and above the common bifurcation (Figure 1). The venous access was also difficult, requiring several attempts. The procedure ultimately succeeded smoothly, without evident problems. However, after the procedure and just before the sheath pull, a large superficial hematoma above the groin was noted.  Because of suspected bleeding due to a kinked sheath (a steep angle of entry to the artery), I requested our best femoral compression person to take over. Our holding person did a good job and the patient was taken to the recovery room. One hour later, the patient’s SBP was 70mmHg. Fluids were opened and the SBP increased to 95mmHg for 20 minutes, but the hematoma was enlarging visibly. We brought the patient back to the cath lab and performed left femoral access, crossover right iliofemoral angiography, and found active bleeding at the site of the right femoral puncture (Figure 2). Using a 7 mm x 3 cm balloon (Figure 3), repeated prolonged balloon compressions sealed the leaking site (Figure 4). No stent or surgery was required. His post procedure hematoma was extensive (Figure 5). The patient did well in follow-up and went on to aortic valve replacement.  

Bottom line for managing RP bleeding

In a patient with post procedure hypotension and suspected RPH, treat for a vagal reaction first with saline, then atropine. If the SBP is not completely responding to conservative measures, you should become more aggressive. Get blood ready to transfuse. Use the cath lab to find, then control, the bleeding site.  

One more thing for us to think about in preventing RPH — I should have followed my own advice, and gone “radial first.” I really wish I had in this case.

Disclosure: Dr. Kern reports that he is a speaker for Volcano Therapeutics and St. Jude Medical, and is a consultant for Merit Medical.

References

  1. Chan YC, Morales JP, Reidy JF, Taylor PR. Management of spontaneous and iatrogenic retroperitoneal hemorrhage: conservative management, endovascular intervention or open surgery? Int J Clin Pract. 2008 Oct;62(10):1604-1613.
  2. Trimarchi S, Smith DE, Share, D et al. Retroperitoneal hematoma after percutaneous coronary intervention: prevalence, risk factors, management, outcomes, and predictors of mortality. A report from the BMC2 (Blue Cross Blue Shield of Michigan Cardiovascular Consortium) registry. J Am Coll Cardiol Intv. 2010;3(8):845-850.