Cardiovascular Disease: Cardiothoracic Disorders |

A 62-Year-Old Woman With Pulmonary Tuberculosis Complicating Left Ventricular Thrombus and Splenic Infarction FREE TO VIEW

Hairong Bao, MMSc; Xiaoju Liu, PhD; Enli Tan, MMSc; Yi Zhang, MMSc
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The First Hospital of Lanzhou University, Lanzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A65. doi:10.1016/j.chest.2016.02.069
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SESSION TITLE: Cardiothoracic Disorders

SESSION TYPE: Case Report Slide

PRESENTED ON: Saturday, April 16, 2016 at 04:00 PM - 05:00 PM

INTRODUCTION: Tuberculosis is a common respiratory disease, and its diagnosis and treatment methods have been known to the majority of physicians. But its cause of coagulation disorders can easily be overlooked. We report a case of pulmonary tuberculosis induced coagulation disorders, which resulted left ventricular thrombus and splenic infarction.

CASE PRESENTATION: A 62-year old woman was hospitalized because of intermittent cough and dyspnea for 8 months, aggravating with fever for 4 days. The symptoms relieved intermittently by anti-infection treatment. On presentation, her admission temperature was 38.1℃ and D-dimer level was 5.86ug/ml. Chest CT scan revealed a multiple patched and nodal image with hilus pulmonis and mediastina lymph nodes enlargement, part of which had been calcified (Figs 1A-C). The patient received standard 4-drug antituberculous therapy and anti-infection treatment. On hospital day 13, dyspnea aggravated with heart palpitation. Electrocardiogram has shown atrial flutter (Fig 2A). After cedilanid 0.2mg by intravenous injection, atrial flutter changed to sinus rhythm (Fig 2B). On hospital day 16, a sudden epigastric pain occurred. Echocardiography and enhancement CT confirmed left ventricular thrombus and splenic infarction (Figs 1D, 2C). After 3-day-treatment of low molecular heparin and warfarin, when INR rose from 1.46 to 2.81, molecular heparin was discontinued. Antituberculous therapy was going on. On hospital day 28, her fever dropped to normal and her left ventricle thrombosis disappeared (Fig 2D). Results of CT-guided percutaneous needle lung biopsy confirmed tuberculosis (Figs 2E, 2F).

DISCUSSION: Mycobacterium tuberculosis could release endotoxin, tubercle bacillus metabolic product and decomposition product which activate the complement. Then the inflammatory cells gather together and release enzyme and peroxide, which damage the blood capillary and vascular endothelial cell. The increased amount of D-dimmer shows that the organism may be in a hypercoagulable state. Her admission D-dimmer obviously increases, considering she has been in a hypercoagulable state. The endothelial cells dysfunction caused by tuberculosis promote an endothelial injury and hypercoagulable state of the blood, then leading to the formation of the left ventricular thrombus. The fall off thrombosis causes a splenic infarction.

CONCLUSIONS: For tuberculosis patients in a poor general condition, especially of wide range of diseases, physicians should pay attention to guard against the occurrence of coagulopathy.

Reference #1: Peng LM, Deng CQ. Modern Laboratory Technology and Its Application in Thrombosis and Hemostasis. Beijing: People's Medical Publishing House, 2005.

Reference #2: Liu DB, Liu JF, Liu Q, et al. Diagnosis and Treatment of Splenic Infarction (Report of 7 cases). Chin J Bases Clin General Surg, 2011,18(2):200-201.

Reference #3: Jiang YX, Jia YH. Research Status of Left Ventricular Thrombus in Acute Myocardial Infarction. Adv Cardiovasc Dis, 2013,34(6):756-760.

DISCLOSURE: The following authors have nothing to disclose: Hairong Bao, Xiaoju Liu, Enli Tan, Yi Zhang

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