Spontaneous rectus muscle hematoma following streptokinase therapy for acute myocardial infarction: a case report

Spontaneous rectus muscle hematoma following streptokinase therapy for acute myocardial infarction: a case report

International Journal of Cardiology 84 (2002) 101–103 www.elsevier.com / locate / ijcard Letter to the Editor Spontaneous rectus muscle hematoma fol...

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International Journal of Cardiology 84 (2002) 101–103 www.elsevier.com / locate / ijcard

Letter to the Editor

Spontaneous rectus muscle hematoma following streptokinase therapy for acute myocardial infarction: a case report ¨ ¨ Mehmet Birhan Yilmaz*, Yesim Akin, Umit Guray, Halil Kisacik, Sule Korkmaz ¨ ´ , Ankara, Turkey Yuksek Ihtisas Hospital, Cardiology Clinic, Syhhiye Received 12 January 2002; accepted 23 January 2002

Abstract There is no doubt that appropriate use of thrombolytic drugs improves survival in patients with acute myocardial infarction. Streptokinase, one of the most commonly used thrombolytic drugs in large clinical trials, is not fibrin-specific and brings about a lytic state with potential for bleeding. We report a case of spontaneous rectus muscle hematoma following streptokinase therapy for acute myocardial infarction and review the relevant literature. To our knowledge, this is the first case reported in the literature.  2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Acute myocardial infarction; Streptokinase; Rectus muscle hematoma

1. Introduction Thrombolytic drugs improve survival in patients with acute myocardial infarction (AMI) with ST segment elevation. They have been demonstrated to have a positive impact on mortality in patients with AMI through large prospective, randomized clinical trials since the 1980s [1,2]. Streptokinase, one of the most commonly used thrombolytic drugs in large clinical trials, is not fibrin-specific and brings about a lytic state with potential for bleeding [3]. Thrombolytic therapy has many complications. Bleeding complications are the most common and potentially the most serious. Most of the bleeding episodes occur at the site of vascular punctures [2]. Intracranial hemorrhage is the most serious complicaAbbreviations: AMI, acute myocardial infarction * Corresponding author. SSK Bloklary´ 70 / 7, Demetevler 06200, Ankara, Turkey. Tel.: 190-312-346-9401. E-mail address: [email protected] (M.B. Yilmaz).

tion of thrombolytic therapy. Major bleeding from the genitourinary, gastrointestinal, central nervous systems and retroperitoneum has been reported after thrombolytic therapy for AMI. We report a case with a spontaneous hematoma in the rectus muscle following thrombolytic therapy for AMI and review of the relevant literature. To our knowledge, this is the first case reported in the literature.

2. Case report A 63-year-old woman was admitted to a hospital with acute chest pain, diagnosed acute anteroseptal myocardial infarction and administered streptokinase via a peripheral vein. She was referred to our hospital because of ongoing ischemia and severe abdominal pain of new onset during follow up. At initial physical examination, periumbilical ecchymosis was noticed (Fig. 1). Umbilical and hypogastric regions were painful on

0167-5273 / 02 / $ – see front matter  2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 02 )00039-6

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Fig. 2. A lobulated mass lesion, which originates from anterior abdominal wall extending into peritoneal space and with sharp borders having heterogeneous contrast involvement.

Fig. 1. Periumbilical ecchymosis.

palpation. Neither previous blunt abdominal trauma nor injection of any drug through abdominal wall was noted. Besides, no hematological abnormality was determined. An electrocardiogram showed anteroseptal transmural infarction of subacute phase. The patient was administered standard anti-ischemic therapy with addition of low-molecular-weight heparin, known to have less bleeding complications compared to unfractionated heparin. Initial laboratory data yielded hemoglobin of 8 g / dl, creatine kinase MB of 184 U / l (normal: 0–24 U / l). Following initial stabilization, abdominal ultrasonography was performed and reported as ‘a mass lesion which fills the suprapubic region leading to a defect in the rectus muscle fascia, is thought to take its origin from rectus muscle and be compatible with an image of hyperechoic hematoma having heterogeneous internal

echoes’. Through these findings a conservative strategy was decided. The patient improved well by medical therapy. Then abdominal computed tomography was performed and reported as ‘a lobulated mass lesion, which originates from anterior abdominal wall extending into peritoneal space and is with sharp borders having heterogeneous contrast involvement’ (Fig. 2). The patient was checked for attenuation of the lesion with control visits following discharge, progressive decrease in size and resorption at the end were noted.

3. Discussion Thrombolytic drugs have many complications among which, of course, bleeding complications are the most common and potentially the most hazardous particularly in the setting of intracranial hemorrhage. Thankfully the most devastating one occurs the least frequently. The most common bleeding site following thrombolytic therapy is the site of vascular access, which can easily be managed by local pressure [1]. There are other sites for bleeding including genitourinary, gastrointestinal, rarely retroperitoneal regions, additionally some organs including liver, retina, eye, tongue previously reported in the literature [4–6]. We did a literature search using MEDLINE and to our knowledge spontaneous rectus muscle hematoma

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following streptokinase therapy for acute myocardial infarction was the first case reported in the literature. In summary there is a well-known risk of bleeding following thrombolytic therapy for AMI. Clinicians should be aware of the less frequent sites of bleeding and be alert for the possibility of bleeding into abdominal region when a patient comes with a severe abdominal pain following thrombolytic therapy.

References [1] Antman EM, Braunwald E. Acute myocardial infarction. In: Braunwald E, editor, 5th ed, Heart disease a textbook of cardiovascular medicine, W.B. Saunders, 1997, pp. 1219–20.

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[2] Califf RM, Fortin DF, Tenaglia AN et al. Clinical risks of thrombolytic therapy. Am J Cardiol 1992;69(2):12A–20A. [3] Wong S-MJ, Murphy JG. Thrombolytic trials for acute myocardial infarction. In: Murphy JG, editor, 2nd ed, Mayo Clinic cardiology review, Lippincott Williams and Wilkins, 2000, pp. 175–84. [4] Gersh BJ, Chesebro JH, Clements IP et al. Acute myocardial infarction B: management and complications. In: Giuliani ER, Gersh BJ, McGoon MD, Hayes DL, Schaff HV, editors, 3rd ed, Mayo Clinic practice of cardiology, Mosby-Wolfe Medical Communications, 1996, pp. 1281–3. [5] Willis SM, Bailey SR. Streptokinase induced subcapsular hematoma of the liver. Arch Intern Med 1984;144(10):2084–5. [6] Nam R, Carr MM, Jamieson CG. Delayed rupture of the spleen and streptokinase therapy. Can J Surg 1996;39(2):151–4.