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Spontaneous Hemopericardium Leading to Cardiac Tamponade in a Patient with Essential Thrombocythemia

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Spontaneous Hemopericardium Leading to Cardiac Tamponade in a Patient with Essential Thrombocythemia SAGE-Hindawi Access to Research Cardiology Research and Practice Volume 2011, Article ID 247814, 3 pages doi:10.4061/2011/247814 Case Report Spontaneous Hemopericardium Leading to Cardiac Tamponade in a Patient with Essential Thrombocythemia Anand Deshmukh,1, 2 Shanmuga P. Subbiah,3 Sakshi Malhotra,4 Pooja Deshmukh,4 Suman Pasupuleti,1 and Syed Mohiuddin1, 4 1 Department of Cardiovascular Medicine, Creighton University Medical Center, Omaha, NE 68131, USA 2 Creighton Cardiac Center, 3006 Webster Street, Omaha, NE 68131, USA 3 Department of Hematology and Oncology, Creighton University Medical Center, Omaha, NE 68131, USA 4 Department of Internal Medicine, Creighton University Medical Center, Omaha, NE 68131, USA Correspondence should be addressed to Anand Deshmukh, [email protected] Received 30 October 2010; Accepted 29 December 2010 Academic Editor: Syed Wamique Yusuf Copyright © 2011 Anand Deshmukh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Acute cardiac tamponade requires urgent diagnosis and treatment. Spontaneous hemopericardium leading to cardiac tamponade as an initial manifestation of essential thrombocythemia (ET) has never been reported in the literature. We report a case of a 72-year-old Caucasian female who presented with spontaneous hemopericardium and tamponade requiring emergent pericardiocentesis. The patient was subsequently diagnosed to have ET. ET is characterized by elevated platelet counts that can lead to thrombosis but paradoxically it can also lead to a bleeding diathesis. Physicians should be aware of this complication so that timely life-saving measures can be taken if this complication arises. 1. Introduction anti-inflammatory drugs (NSAIDs) for her pain. A week later, she presented to the emergency department (ED) with Pericardial diseases principally manifest as pericarditis or episodes of chest pressure, worsening shortness of breath, pericardial effusion. Pericardial effusions resulting in cardiac and orthopnea. The patient had no known chronic medical tamponade can occur from a number of causes, including illnesses in the past and was not on any other prescription pericarditis, malignancy, acute myocardial infarction, end- medications. She had a 50-pack year history of smoking. stage renal disease, congestive heart failure, collagen vascular On physical examination, her heart rate was 115 beats/ disease, and viral and bacterial infections. Hemopericardium minute and blood pressure was 123/44 mm of Hg. Other vital and resulting tamponade can result from any form of chest signs were within normal limits. She had jugular venous dis- trauma, free wall rupture following myocardial infarction, tension on neck examination. Cardiovascular examination retrograde bleeding into the pericardial sac following aortic revealed tachycardia and positive pulsus paradoxus. Chest root (type A aortic) dissection, as a complication of any inva- examination was unremarkable. sive cardiac procedure, anticoagulation, and acute leukemias. Laboratory data showed normal electrolytes and renal In this paper, we describe a case of cardiac tamponade functions. Her white count was elevated at 12,900 cells/mic- resulting from hemopericardium as an initial manifestation roliter, hemoglobin was marginally low at 11.2 g/dl, and of essential thrombocythemia (ET). platelet count was elevated at 745,000 cells/microliter. Cell differential was within normal limits. Cardiac biomarkers 2. Case Presentation were within normal limits. TSH level was 3.57 mIU/L. Electrocardiogram (ECG) showed normal sinus rhythm and A 72-year-old Caucasian female presented to her primary left atrial enlargement. There were no electrical alternans or care physician for ear pain. She was prescribed nonsteroidal changes of pericarditis on the ECG. 2 Cardiology Research and Practice Chest X-ray showed cardiomegaly and small left sided MI: 1.5 ff S3 pleural e usion. Computed tomography (CT) scan of the 04 AUG 09 chest in the ED showed a moderate-sized pericardial effusion 14 : 07: 51 ff 2/1/D/H5 and a small left pleural e usion. Cardiology consultation was Creighton univ. obtained due to the presence of pericardial effusion. Cardiac center CU echo A transthoracic echocardiogram confirmed pericardial effusion with evidence of tamponade physiology (Figure 1). Gain 67 Comp 54 The patient was taken to cardiac catheterization laboratory 102 BPM and pericardiocentesis was done. A total of 300 mL of 24 cm hemorrhagic fluid was drained during the initial procedure. 40 Hz Drainage of pericardial fluid resulted in immediate improve- T ment of patient’s symptoms. A pigtail catheter was left in P R place and the patient was transferred to coronary care unit. 1.6 3.2 Over next two days, additional 310 mL of hemorrhagic fluid was drained and subsequently pigtail catheter was removed. Pericardial fluid examination was unremarkable for Figure 1: Subcostal view of hemorrhagic pericardial effusion. any evidence of malignancy or infection. The etiology of (There is a collapse of the right ventricular free wall during diastole.) hemorrhagic pericardial effusion was unclear even after extensive evaluation for malignancy, infection, autoimmune disease, or any other obvious systemic disease. Bleeding diathesis leading to spontaneous hemopericardium The patient continued to have elevated platelet count secondary to congenital coagulation defect has been sparsely throughout the hospital stay with the highest platelet count reported in the literature [2–4]. being 855,000 cells/microliter. She denied any history of prior ET is currently classified among the bcr/abl negative, thrombotic or bleeding episodes. The elevation in platelet “Classic” myeloproliferative disorders (MPDs), which also count was thought to be due to reactive thrombocytosis. include polycythemia vera (PV) and primary myelofibrosis The patient was discharged on fourth hospital day. She was (PMF) [5, 6]. Each of these MPDs represents a stem cell instructed to followup with her primary care physician in derived clonal myeloproliferation. ET is characterized by two weeks with complete blood count to ensure resolution megakaryocyte expansion leading to increased platelets. ET of thromobycytosis. is an uncommon disease with prevalence of 2-3 cases per At followup, the patient continued to have elevated million. Median age at diagnosis is usually between 65– platelet counts. She was referred for hematology evaluation. 75 years with female preponderance. The life expectancy of A peripheral blood smear, bone marrow aspiration, and ET patients is generally long and similar to that of an age- core biopsy were done for further evaluation of throm- matched normal population [7]. Many patients with ET bocytosis. Peripheral blood smear showed occasional giant are asymptomatic, but a large number of them manifest platelets with no platelet aggregates. There were no immature symptoms or signs of bleeding, usually as ecchymoses or myeloid forms. Bone marrow aspirate showed prominent mucosal hemorrhage, or microvascular thrombosis, usually megaloblastoid change and increased number of megakary- as erythromelalgia, digital ischemia, or transient ischemic ocytes. Core biopsy also showed increased number of attack [8, 9]. The risk of thrombohemorrhagic complications megakaryocytes. The megakaryocytes exhibited large hyper- remains unpredictable in individuals. The initial presen- segmented nuclei with occasional megakaryocytic mitoses. tation in our patient was spontaneous hemopericardium Flow Cytometry was negative for any immunophenotypic that required emergency pericardiocentesis. Bleeding in ET abnormalities. Fluorescence in situ hybridization (FISH) is thought to be secondary to Acquired Von Willebrand for BCR-ABL translocation was negative arguing strongly disease (AVWD) and due to qualitative platelet defects. against chronic myeloid leukemia. JAK 2 real-time PCR The main sites affected are skin, mucous membranes, assay was negative for JAK2 V617 mutation. Thus, bone and gastrointestinal tract. Severe bleeding is rare but fatal marrow biopsy showed megakaryocytic hyperplasia with intracranial bleeding has been reported. AVWD in ET dysmegakaryopoiesis consistent with ET. patients is characterized by the loss of large von Willebrand factor (VWF) multimers that results in a functional defect 3. Discussion of the VWF, with increasing platelet counts (usually >1.5 million). Normalization of the platelet count results in Pericardial effusions can be serous or hemorrhagic. The normal plasma VWF multimeric distribution and regression etiology of pericardial effusion is often influenced by the of the hemorrhagic tendency [10]. Serious hemorrhages geographical region and patient-related factors. Hemor- maybetriggeredbysimultaneousantithrombotictherapy rhagic pericardial effusions often have different etiologies with anticoagulants, antiplatelet therapy, and NSAIDs. We than serous effusions. In a retrospective study done by Atar believe that hemorrhagic conversion of pericardial effusion et al., the most common cause of hemorrhagic effusions in our patient was triggered by NSAID therapy. However, was found to be iatrogenic (31%) namely, secondary to we cannot exclude the possibility of viral syndrome resulting invasive cardiac procedures followed by malignancies [1]. in pericarditis with subsequent conversion to hemorrhagic Cardiology Research and Practice 3 pericardial effusion
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