Spontaneous Extraperitoneal Hemorrhage with Hemodynamic Collapse in Patients Undergoing Anticoagulation: Management with Selective Arterial Embolization

Spontaneous Extraperitoneal Hemorrhage with Hemodynamic Collapse in Patients Undergoing Anticoagulation: Management with Selective Arterial Embolization Melhem J. Sharafuddin, MD, Kelli J. Andresen, MD, Shiliang Sun, MD, Elvira Lang, MD,1 Michael S. Stecker, MD,2 and Lucy A. Wibbenmeyer, MD The authors report their experience with management of unstable spontaneous extraperitoneal hemorrhage (SEH) with selective transcatheter embolization. Five consecutive patients underwent angiographic evaluation for SEH complicated by hemodynamic collapse while undergoing anticoagulation therapy. Bleeding occurred via one or two lumbar arteries in psoas hematomas. Two abdominal wall hematomas were supplied by the inferior epigastric artery, with additional supply via the deep circumflex iliac artery in one. Microcoil embolization successfully controlled extravasation in all patients, with stabilization of hemodynamic parameters. Four of the five patients survived the immediate postprocedural interval. Selective transcatheter embolization may be a viable life-saving option in SEHassociated hemodynamic collapse. Index terms:

Anticoagulants

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Embolization

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Spontaneous extraperitoneal hemorrhage

J Vasc Interv Radiol 2001; 12:1231–1234 Abbreviation:

SEH ⫽ spontaneous extraperitoneal hemorrhage

SPONTANEOUS extraperitoneal hemorrhage (SEH) is a distinct clinical entity that can present in the absence of specific underlying pathology or trauma and is typically associated with anticoagulation therapy (1). Transcatheter embolization is a well-recognized treatment modality in life-threatening extraperitoneal hemorrhage secondary to trauma (2) or other underlying hemorrhagic retroperitoneal abnormalities (3,4). HowFrom the Departments of Radiology (M.J.S., K.J.A., S.S., E.L., M.S.S.) and Surgery (L.A.W.), University of Iowa College of Medicine, Iowa City, Iowa. Received March 19, 2001; revision requested May 4; final revision received and accepted June 8. From the 2000 SCVIR Annual Meeting. Address correspondence to M.J.S., Department of Radiology, 3889 JPP, University of Iowa Hospitals and Clinics, 200 Hawkins Dr., Iowa City, IA 52242-1077; E-mail: [email protected] 1 Current address: Beth Israel Deaconess Medical Center, Harvard School of Medicine, Boston, Massachusetts. 2 Current address: Department of Radiology, Indiana University Medical Center, Indianapolis, Indiana. © SCVIR, 2001

ever, reports on the angiographic findings or management in SEH are very scarce (5). In this article, we describe our single institutional experience with angiography in five consecutive patients who presented with massive SEH that caused hemodynamic collapse and the percutaneous management of SEH with use of transcatheter microcoil embolization.

MATERIALS AND METHODS Retrospective review of our Section’s case logs identified five consecutive patients who, between November 1997 and August 1999, were referred with hemodynamic collapse caused by SEH and underwent angiography to localize a source of bleeding. All patients had been undergoing anticoagulation therapy when bleeding occurred. SEH was defined as extraperitoneal hemorrhage without preceding trauma or underlying pathology on crosssectional imaging. Findings on contrastenhanced computed tomography (CT) were noted, including signs of active bleeding and anatomic localization of the

bleeding, in addition to exclusion of underlying retroperitoneal pathology. Indication for angiography included persistent bleeding and hemodynamic instability despite reversal of anticoagulation. Anticoagulation/coagulopathy was appropriately managed by fresh frozen plasma and/or platelet transfusions in all patients before angiography. The transfemoral angiography route was used in all patients. Digital subtraction angiography of the aorta and/or pelvic arteries was performed first to localize the site of bleeding. Selective catheterization was subsequently used to better characterize the site(s) of extravasation. Therapeutic embolization was performed with use of microcoils (Boston Scientific/Meditech, Natick, MA) through a microcatheter system (Tracker-18; Boston Scientific/Medi-tech). CT and angiographic findings including the location and source(s) of bleeding, and embolization technique were recorded. Need for transfusion as well as hemodynamic parameters were all compared before and after

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Summary of Five Patients with Primary Spontaneous Retroperitoneal Hemorrhage Treated with Embolization Age (y)/ Sex 1

35/M

2

Anticoagulation Therapy (indications)

CT Findings

Tranfusions

Bleeding Source

Heparin IV: 36 h (septic emboli)

Large right psoas hematoma with Hct level

77/F

Lovenox SC: 6 d (DVT prophylaxis)

Large right psoas Right fifth lumbar hematoma, with Hct level (multifocal)

3

73/F

4

45/F

5

78/F

Large right iliopsoas Heparin IV: 4 mo, hematoma with prior warfarin PO: 18 y intraperitoneal rupture (valve replacement) Contrast extravasation, no Hct level Large left retroperitoneal Heparin IV: 9 d, hematoma, smaller left prior warfarin PO: 8 y pelvic hematoma ⫹ (valve replacement) hematocrit level Warfarin PO: 1 y Large left rectus sheath (atrial fibrillation) hematoma Pelvic hematomas, hematocrit levels

Pre

Right third lumbar (monofocal)

5 PRBC 2 FFP (1 d) 12 PRBC 9 FFP (1 d) 6 PRBC 6 FFP (1 d)

Right second lumbar (monofocal)

Left inferior epigastric Deep circumflex iliac Superficial circumflex iliac (multifocal) Left inferior epigastric (monofocal)

4 PRBC 2 FFP (1 d)

Post

Outcome

6 PRBC Survival (3 d) 2 PRBC Death (1 d) (care withdrawn) 4 PRBC Survival (3 d)

8 PRBC Survival (4 d)

10 PRBC 3 PRBC Survival 1 FF 7 FFP (1 d) (1 d)

Note.—IV ⫽ intravenously; SC ⫽ subcutaneously; PO ⫽ orally; Hct ⫽ hematocrit; PRBC ⫽ packed red blood cells; FFP ⫽ fresh frozen plasma; PTT ⫽ activated partial thrombin time; INR ⫽ international normalized ratio; SBP ⫽ systolic blood pressure (mm Hg); HR ⫽ heart rate.

intervention. Patients typically underwent transfusion to a hematocrit level of 30% after the procedure. Statistical comparison of transfusions requirement was performed with use of the Student t-test.

RESULTS The demographic features, angiographic findings, interventions, and clinical course of the five reported patients are summarized in the Table. Nonselective aortic and/or pelvic digital subtraction angiography demonstrated active bleeding in all patients. In all cases, bleeding location on angiography correlated closely with CT (Figs 1,2). A single lumbar artery was identified as the primary source of bleeding in all three patients with iliopsoas hematomas. The inferior epigastric artery was the primary source of bleeding in one patient with a rectus sheath hematoma, whereas multiple arteries (inferior epigastric, deep circumflex iliac, and superficial circumflex iliac arteries) supplied the bleed in another patient with flank and rectus sheath hematomas. Multifocal bleeding (multiple, small foci) was noted in the territory of the feeding vessel in three patients (Fig 2). Secondary col-

lateral supply from a neighboring vessel was noted in two of three patients with lumbar artery bleeding (via an adjacent lumbar artery) and in one patient with a flank hematoma (via collateral communication between the deep and superficial circumflex iliac arteries). A microcoil-packing technique of the segment supplying the bleed in addition to any segments supplying collateral communications was used. In one patient (case 4), after initially successful embolization, a second episode of bleeding 3 days later required repeat embolization to control recurrent bleeding via a new collateral supply. Nontarget embolization of one 2-mm ⫻ 3-mm coil into a small medial femoral circumflex branch of the profunda femoris complicated one procedure (patient 4). This was believed to be of little consequence and was therefore not retrieved. No other complications occurred. In all patients, stabilization of hemodynamic parameters (blood pressure and heart rate) occurred shortly after embolization, with a decrease in transfusion requirements. Additional transfusion (2– 8 U packed red blood cells) was required in the first two

postprocedural days. Transfusion requirement decreased over a mean of 2.4 ⫾ 1.3 days (preembolization: 7.4 U ⫾ 3.4 [range, 4 –12 U], postembolization: 4.6 U ⫾ 2.4 [range, 2– 8 U]. Transfusion requirement per day decreased significantly from 6.2 U/d ⫾ 2.3 to 2.1 U/d ⫾ 0.35 (P ⬍ .005). Four of the five patients survived the postprocedural interval. Despite stabilization of hemodynamic and hematologic parameters following embolization, one patient (case 2) died 1 day after the procedure from multiple organ system failure after her family chose to withdraw care.

DISCUSSION Extraperitoneal hemorrhage is most frequently seen after femoral artery catheterization or pelvic and lumbar trauma (2,6,7). In the absence of trauma, extraperitoneal hemorrhage most frequently results from a ruptured abdominal aortic aneurysm or bleeding from underlying condition in the kidneys or adrenal glands. SEH denotes bleeding without known inciting trauma or underlying retroperitoneal pathology. SEH is uncommon and is almost exclusively seen in association with anticoagulation states,

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Figure 1. (a) CT image demonstrating a large retroperitoneal hematoma with heterogeneous high attenuation foci (arrows) suggestive of active bleeding. Note is also made of peritoneal fluid collection (arrowhead) indicative of intraperitoneal rupture (clearly shown on other images). (b) Early and late phases of selective injection of the right 2nd lumbar artery demonstrating active extravasation from a muscular branch (arrows). (c) Selective injection of the right 2nd lumbar artery after superselective microcoil embolization of a long segment of the muscular branch. (d) Termination aortic flush angiogram demonstrating cessation of bleeding and lack of collateral supply.

coagulopathies, and hemodialysis (8 –11). Little is known about the pathophysiology of SEH. It has been hypothesized to be caused by diffuse small vessel arteriosclerosis (12), whereas others have suggested a heparin-induced immune microangiopathy. Unrecognized minor trauma in the microcirculation in the presence of coagulopathy has also been suggested (13). Occult vasculopathy involving the adrenal gland has also been proposed (10,14). Although the term

“spontaneous” indicates the lack of observable injury, the possibility of minor trauma, such as that sustained during patient transport or forced passive joint motion, in initiating bleeding that continues unabated in the presence of coagulopathy cannot be excluded. In fact, such minor trauma is a recognized inciting factor in hemophilia-related SEH (10,11). It had been our belief that SEH is an angiographically occult diffuse microvascular condition for which angiog-

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raphy had no diagnostic nor therapeutic role. The mainstay management currently continues to consist of withdrawal of anticoagulation therapy, correction of the anticoagulation state, volume resuscitation, and supportive measures (9,15). Surgical intervention has been considered the only option in uncontrollable hemodynamic collapse (16), although it is severely limited by the inability to localize or control the bleeding vessel(s) and the risk that releasing the tamponade may further worsen bleeding (17). Embolization therapy in retroperitoneal hemorrhage secondary to trauma is widely accepted (2). Underlying hemorrhagic retroperitoneal abnormalities may also be amenable to embolization (3,4). However, reports of transcatheter embolization in SEH are very scarce (5,18). This is likely because the common belief is that this entity is caused by diffuse microvascular pathology. Hence, angiography is seldom requested. Indications for angiography in the setting of trauma include continued hemodynamic instability despite four or more units of blood transfusion within 24 hours or six or more units of blood transfusion within 48 hours (2). Our patients’ transfusion requirements were greater, which was likely a reflection of the traditional conservative management initially adopted in these patients. Our patients typically underwent arteriography within 18 hours of diagnosis by CT. Unlike traumatic lumbar artery injury, in which hemorrhage can be controlled by gelatin sponge pledget embolization (7), SEH is often multifocal and involves complex collateral pathways. We therefore prefer to pack the entire length of the major supplying vessel(s) with coils to prevent retrograde filling from collaterals. In additions, coils offer the advantage of radiopacity, accuracy, and safer deployment. Our study is hindered by a number of obvious drawbacks. Although all our patients had angiographically demonstrable bleeding, they represent a preselected group because they also all had evidence of active bleeding on CT. The number of patients in this study is too small to derive any meaningful statistical comparison and limits our series to a descriptive report of a limited clinical experience. Also, our patients represent a heterogeneous

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Figure 2. (a) Pelvic CT image demonstrating a large abdominal wall hematoma with a hematocrit level. (b) Recurrent bleeding occurred 3 days after initial successful microcoil embolization of the inferior epigastric artery (arrowheads), which supplied a large monofocal bleed. Late-phase digital subtraction angiogram of the deep lateral circumflex iliac artery demonstrates multifocal bleeding supplied by both medial and lateral branches (arrows). Retrograde filling of collateral supply from the superficial circumflex iliac artery is also identified (concave arrowhead). (c) Pelvic arteriogram after microcoil embolization of the additional bleeding feeders (short and long arrows) demonstrate cessation of the bleed with no further collateral filling.

group of patients, with various types of anticoagulation agents, for various durations, and with various anticoagulation levels. In conclusion, SEH is a relatively uncommon complication of anticoagulation therapy. In the event of failure of conservative management and development of hypovolemic shock, and when signs of localized active bleeding are present on CT, angiographic evaluation may be helpful for localization of the bleed and percutaneous embolization. Prompt improvement in hemodynamic status and decline in transfusion requirement can be expected when successful angiographic outcome is achieved. References 1. Pode D, Caine M. Spontaneous retroperitoneal hemorrhage. J Urol 1992; 147:311–318. 2. Panetta T, Sclafani SJ, Goldstein AS, Phillips TF, Shaftan GW. Percutaneous transcatheter embolization for massive bleeding from pelvic fractures. J Trauma 1985; 25:1021–1029. 3. Friedberg EB, Stock JR, Husted JW, Westby GR. Transcatheter embolization for retroperitoneal hemorrhage secondary to acquired cystic kidney disease. J Vasc Interv Radiol 1996; 7:291–294.

4. Jonsson E, Sueoka BL, Spiegel PK, Richardson JR Jr, Heaney JA. Angiographic management of retroperitoneal hemorrhage from renal angiomyolipoma in polycystic kidney disease. J Urol 1991; 145:1248 –1250. 5. Kalinowski EA, Trerotola SO. Postcatheterization retroperitoneal hematoma due to spontaneous lumbar arterial hemorrhage. Cardiovasc Intervent Radiol 1998; 21:337–339. 6. Illescas FF, Baker ME, McCann R, Cohan RH, Silverman PM, Dunnick NR. CT evaluation of retroperitoneal hemorrhage associated with femoral arteriography. AJR. Am J Roentgenol 1986; 146:1289 –1292. 7. Sclafani SJ, Florence LO, Phillips TF, et al. Lumbar arterial injury: radiologic diagnosis and management. Radiology 1987; 165:709 –714. 8. Bhasin HK, Dana CL. Spontaneous retroperitoneal hemorrhage in chronically hemodialyzed patients. Nephron 1978; 22:322–327. 9. Sasson Z, Mangat I, Peckham KA. Spontaneous iliopsoas hematoma in patients with unstable coronary syndromes receiving intravenous heparin in therapeutic doses. Can J Cardiol 1996; 12:490 – 494. 10. Heim M, Horoszowski H, Seligsohn U, Martinowitz U, Strauss S. Ilio-psoas hematoma—its detection, and treatment with special reference to hemo-

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philia. Arch Orthop Traumatic Surg 1982; 99:195–197. Fernandez-Palazzi F, Hernandez SR, De Bosch NB, De Saez AR. Hematomas within the iliopsoas muscles in hemophilic patients: the Latin American experience. Clin Orthop 1996; 328:19 – 24. Torres GM, Cernigliaro JG, Abbitt PL, et al. Iliopsoas compartment: normal anatomy and pathologic processes. Radiographics 1995; 15:1285–1297. McCort JJ. Intraperitoneal and retroperitoneal hemorrhage. Radiol Clin North Am 1976; 14:391– 405. Di Rosa C, Venora S, Monterosso N, La Spada NM, Viola S. [Retroperitoneal hematoma during heparin therapy: comments on 3 cases. Minerva Chir 1997; 52(4):493– 497. Sherer DM, Dayal AK, Schwartz BM, Oren R, Abulafia O. Extensive spontaneous retroperitoneal hemorrhage: an unusual complication of heparin anticoagulation during pregnancy. J Matern Fetal Med 1999; 8:196 –199. Baker BH, Baker MS. Indications for exploring the retroperitoneal space. South Med J 1980; 73:969 –970. Grimm MR, Vrahas MS, Thomas KA. Pressure-volume characteristics of the intact and disrupted pelvic retroperitoneum. J Trauma 1998; 44:454 – 459. Kastan DJ, Burke TH. Images in clinical medicine: retroperitoneal hemorrhage. N Engl J Med 2000; 9:702.