Dae-Yeon Won, et al. potheses have been suggested, including forceful muscular strain, diffuse small vessel arteriosclerosis, heparin-induced immune microangiopathy, and unrecognized minor trau- ma.7-9 As the indications for anticoagulation increase, the associated hemorrhagic complication will also likely in- crease. The clinical presentation of SRH may show a wide range of symptoms from leg-hip pain or paresis to abdominal/ flank/back pain or a catastrophic shock. One third of the pa- tient with retroperitoneal hematoma have presented with severe pain, shock and a palpable mass, which is referred to as Lenk’s triad, as with our case.10 Massive bleeding into the retroperitoneum represents a problem not only because of the loss of intravascular volume, but also because an in- creased IAP. The femoral nerve is subject to compressive neuropathy secondary to compartment syndrome because of its location. The two main mechanisms for developing FN are ischemia and pressure-related nerve damage.11 An abnormal, sudden increase in the volume of any component of the intra-peritoneal or retroperitoneal space can cause in- tra-abdominal hypertension. Measurement using a Foley catheter placed in the bladder has become the gold standard for determining the IAP.12 A sustained IAP > 20 mmHg and a IAPP < 60 mmHg that occur in association with new or- gan dysfunction or failure describes ACS.12 The manifesta- tions of ACS, both systemic and clinical, are closely related to the consequences of intra-abdominal hypetension (IAH) at the organ level. Elevated IAP causes expansion of the ab- dominal cavity, which in turn results in cephalad displace- ment of the diaphragm, with a consequential reduction in dynamic pulmonary compliance and an increase in intra- thoracic pressure. The cycle consisting of impaired outflow, decreased capillary perfusion and increased pressure also results in decreased renal and hepatosplanchnic flow, inferi- or vena cava (IVC) compression, and decreased venous re- turn with a consequential decrease in cardiac output.13 The mortality rate varies from 29% to 62%, and death is usually due to multiple organ failure and sepsis.14,15 To prevent end- organ failure and to decrease mortality, frequent IAP moni- toring and timely surgical decompression are mandatory. Although there have been some reports about ACS com- bined with anticoagulation-related SRH,2,16,17 our current case is only the second reported case of ACS due to warfa- rin-related SRH.18 There are various types of approaches for the treatment of this relatively uncommon complication, such as conser- vative management, TAE, or surgical intervention. Conser- vative management for warfarin-related SRH consists of discontinuation of the drug, administration of vitamin-K and fresh frozen plasma, volume resuscitation and transfu- sion. Surgery or radiologic intervention should be per- formed, if the patient does not respond to supportive thera- py. The surgical treatment of SRH is limited by the inability to localize or control the bleeding vessel and the risk of worsening the bleeding due to releasing the tamponade.19 When compared with surgical management, TAE is safe, fast and less invasive. The main drawback of TAE is that it cannot alleviate the mass effect of the hematoma. Ultra- sound-guided decompression has been shown to alleviate neuropathy. Merrick, et al.20 reported that when even a small volume is aspirated, symptoms may improve. But when this procedure is done, there is the risk of a significant delay in definitive treatment. With regards to our current case, a nonoperative ap- proach to the retroperitoneal bleeding was first attempted. However, after successful bleeding control by TAE, the pa- tient’s general status deteriorated and she presented a clini- cal picture of ACS, which led to a straightforward decision to perform a laparotomy. The result of this case suggests that a sequential approach, that is, TAE followed by surgi- cal decompression, is a safe, effective method to treat SRH complicated with femoral neuropathy or ACS. REFERENCES 1. Pode D, Caine M. Spontaneous retroperitoneal hemorrhage. J Urol 1992;147:311-8. 2. Chan-Tack KM. Fatal spontaneous retroperitoneal hematoma sec- ondary to enoxaparin. South Med J 2003;96:58-60. 3. Curry PV, Bacon PA. Retroperitoneal haemorrhage and neuropa- thy complicating anticoagulant therapy. Postgrad Med J 1974;50: 37-40. 4. Hodin E, Dass T. Spontaneous retroperitoneal hemorrhage com- plicating anticoagulant therapy. Ann Surg 1969;170:848-51. 5. Bhasin HK, Dana CL. Spontaneous retroperitoneal hemorrhage in chronically hemodialyzed patients. Nephron 1978;22:322-7. 6. 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 Relat Res 1996; (328):19-24. 7. Heim M, Horoszowski H, Seligsohn U, Martinowitz U, Strauss S. Ilio-psoas hematoma--its detection, and treatment with special ref- erence to hemophilia. Arch Orthop Trauma Surg 1982;99:195-7. 8. Torres GM, Cernigliaro JG, Abbitt PL, Mergo PJ, Hellein VF, Fernandez S, et al. Iliopsoas compartment: normal anatomy and pathologic processes. Radiographics 1995;15:1285-97. 9. McCort JJ. Intraperitoneal and retroperitoneal hemorrhage. Radiol Clin North Am 1976;14:391-405. 360 Yonsei Med J http://www.eymj.org Volume 52 Number 2 March 2011