DOCSLIB.ORG

Case of the Disappearing Heat-Induced Thrombus Causing Pulmonary Embolism During Ultrasound Evaluation

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Case of the Disappearing Heat-Induced Thrombus Causing Pulmonary Embolism During Ultrasound Evaluation Case of the disappearing heat-induced thrombus causing pulmonary embolism during ultrasound evaluation Shekeeb Sufian, MD, Alejandro Arnez, MD, and Sanjiv Lakhanpal, MD, Glenn Dale, Md We report a case of a 58-year-old male patient who underwent successful endovenous radiofrequency ablation of the left great saphenous vein for CEAP class 4a venous disease. On the third postoperative day, he had a duplex ultrasound scan for evaluation which showed successful occlusion of the great saphenous vein (GSV) with class 2 endovenous heat- induced thrombus (EHIT) that disappeared during the evaluation and caused a pulmonary embolism. To our knowledge, no case of pulmonary embolism has been reported to occur during postoperative follow-up duplex scanning. Relevant literature is reviewed and a possible mechanism for thrombus dislodgement is entertained. (J Vasc Surg 2012;55: 529-31.) Endovenous thermal ablation of the saphenous veins blood pressure was 110 over 68, his pulse rate was 82/minute, and using radiofrequency ablation (RFA) or endovenous laser his respiratory rate was 16/minute. The general physical examina- ablation has become the most common method of treat- tion was essentially negative. The right leg had no evidence of ment for varicose veins and symptomatic venous reflux varicose veins or stigmata of venous insufficiency. On the left leg, disease, and is getting wide acceptance.1,2 Minor compli- there was an area of skin hyperpigmentation in the distal medial cations such as skin bruising/hematoma, bleeding, tran- calf. There were also obvious varicosities in the medial and poste- sient paresthesias, and skin burns have been reported in 3% rior calf regions. His CEAP class was 4a and the Venous Clinical to 20% of patients.3 Major complications which include Severity Score was 6. The patient used compression stockings in deep venous thrombosis (DVT) and pulmonary embolism the past for about 3 months without significant improvement. (PE) are rare. Extension of thrombus from the saphenous Duplex ultrasound scan evaluation was performed in our to the femoral or popliteal veins have been reported to Intersocietal Commission for the Accreditation of Vascular Labo- occur in 0% to 6% of patients.4 The term endovenous ratories which showed reflux in the left great saphenous vein (GSV) heat-induced thrombus (EHIT) was introduced by Kab- with a maximum reflux of 3.5 seconds near the confluence of the nick4 who also classified the level of thrombus from 1 to 4 saphenous vein. The maximum diameter of the GSV was 11 mm classes.4 Hingorani et al5 reported extension of thrombus above the knee and 5 mm below the knee. The deep veins were all in 16% of limbs treated with RFA, and raised caution about normal. The patient underwent RFA of the left GSV using Clo- the procedure and recommended early postoperative du- sureFAST (VNUS MEDICAL Technologies Inc, San Jose, Calif) plex scan evaluation. Most of these thrombi retract or in a standard technique, with the head down position using tumes- absorb, but they theoretically can also detach and cause cent anesthesia totaling 290 mL. The vein was accessed below the a PE. knee. The catheter tip was 2.8 cm from the saphenofemoral junction and 2.3 cm from the superficial epigastic vein. No pro- CASE REPORT phylactic anticoagulation or aspirin was given to the patient. Post- A 58-year-old man was referred to our office by his primary operatively, the patient was active and walking, and used elastic physician with symptoms of left calf pain and progressive edema stockings. The patient was re-evaluated 3 days later in our vascular which had gradually gotten worse over the previous 3 months. The laboratory, and the GSV was noted to be completely occluded. symptoms were more prominent at the end of the day. There was There was EHIT class 2 in the left saphenofemoral junction. The no family history of thrombophilia and his medical history was common femoral vein was compressible and had flow but there was negative. He had no history of DVT and no history of smoking. He thrombus protruding into the lumen filling Ͻ50% of the lumen was taking no medications. On examination, his weight was 134 (Fig 1). There was no loose tail or floating thrombus. The evalu- pounds, height was 5=6Љ, with a body mass index of 21.63. His ation was done in a routine fashion and no excessive compression was used. When the saphenofemoral region was re-evaluated after From the Center for Vein Restoration. the compression test, the thrombus, which was protruding into the Competition of interest: none. femoral vein, disappeared (Fig 2). The patient was immediately Reprint requests: Shekeeb Sufian, MD, Center for Vein Restoration, 12200 Annapolis Road, Suite 225, Glenn Dale, MD 20769 (e-mail: shekeeb. referred to the hospital for PE workup. A computed tomography sufi[email protected]). (CT) scan of the chest with contrast was obtained. This was The editors and reviewers of this article have no relevant financial relationships positive for acute bilateral small segmental pulmonary emboli (Fig to disclose per the JVS policy that requires reviewers to decline review of any 3). The patient had no symptoms of cough, chest pain, or shortness manuscript for which they may have a competition of interest. of breath. His vital signs were normal except for a heart rate of 116. 0741-5214/$36.00 Copyright © 2012 by the Society for Vascular Surgery. The pulse oximetry was 100% on room air. He was admitted to the doi:10.1016/j.jvs.2011.07.070 hospital and treated with enoxaparin sodium (lovenox) 1 mg/kg 529 JOURNAL OF VASCULAR SURGERY 530 Sufian et al February 2012 Fig 3. Computed tomography (CT) of the chest showing acute bilateral small segmental pulmonary emboli. until the international normalized ratio (INR) was therapeutic. He was discharged from the hospital after 3 days on 7.5 mg of warfarin Fig 1. Duplex ultrasound scan of the left saphenofemoral junc- daily by mouth and followed as an out-patient. Follow-up duplex tion (SFJ) with thrombus protruding from the great saphenous scans done after 1 week, 1 month, 2 months, and 6 months showed vein (GSV) into the common femoral vein (CFV) (endovenous no evidence of DVT and the GSV remained occluded. The oral heat-induced thrombus [EHIT] class 2). anticoagulation was discontinued after 4 months. The Venous Clinical Severity Score improved from 6 to 4. DISCUSSION DVT and PE are rare complication of EHIT. Kabnick4 introduced the term EHIT and noted that this is more benign than the spontaneously occurring thrombosis, in that it is stable and usually regresses or shows complete resolution. He also made the observation that EHIT dis- plays a different sonographic echogenicity and becomes echogenic in Ͻ24 hours. The EHIT in our case does show increased echogenicity. He classified EHIT from class 1 to class 4. Another classification system was recently intro- duced by Lawrence et al6 from level 1 to 6. The Interna- tional Endovascular Working Group registry shows that DVT/EHIT occurred in 0.27% (10 of 3696 cases) and PE occurred in 0.023% (1 of 3696) after endovenous laser ablation.4 In a review of 11 articles, Mozes et al7 reported 21 case of DVT and 2 cases of PE after the VNUS Closure (VNUS MEDICAL Technologies Inc) procedure.7 At the Arizona Heart Institute, with Ͼ1000 cases of venous abla- tion, only 1 case of pulmonary embolism was reported.8 To decrease the risk of EHIT formation, several suggestions have been offered: the position of the catheter tip should be Fig 2. Duplex ultrasound scan of the saphenofemoral junction (SFJ) at least 2 cm from the saphenofemoral or saphenopopliteal after compression, showing disappearance of thrombus from the com- junction, reduce the thrombus load by elevation of the leg mon femoral vein (CFV) and distal great saphenous vein (GSV). during ablation, and also by using adequate tumescent anesthesia.7 A recent article showed that a GSV diameter of Ͼ8 mm and history of DVT were associated with EHIT subcutaneously twice a day and then converted to warfarin. The class 2 or greater.6 But another study which evaluated the admission was made necessary because he could not be treated as influence of procedural factors concluded that there was no an outpatient over the weekend. The enoxaparin was continued difference in catheter tip position or mean diameter of the JOURNAL OF VASCULAR SURGERY Volume 55, Number 2 Sufian et al 531 treated vein between the EHIT and non-EHIT groups.9 blinded, randomized study (RECOVERY Study). J Vasc Interv Radiol There is no report on association of EHIT with hyperco- 2009;20:752-9. agulable states. 2. Lurie F, Creton D, Eklof B, Kabnick LS, Kistner RL, Pichot O, et al. Prospective randomised study of endovenous radiofrequency oblitera- Our patient had no history of DVT or family history of tion (closure) versus ligation and vein stripping (EVOLVeS): two-year thrombophilia, and the catheter tip was definitely identified follow-up. Eur J Vasc Endovasc Surg 2005;29:67-73. at 2.8 cm from the saphenofemoral junction and 2.3 cm 3. Merchant RF, Pichot O, Closure Study Group. Long-term outcomes of from the superficial epigastic vein. The diameter of his GSV endovenous radiofrequency obliteration of saphenous reflux as a treat- ment for superficial venous insufficiency. J Vasc Surg 2005;42:502-9; was 11 mm, which may have contributed to the EHIT. We discussion 509. hypothesize that the standard technique of compression of 4. Kabnick LS. Complications of endovenous therapies: statistics and the superficial and deep veins10 used to evaluate for DVT at treatment. Vascular 2006;14:S31-32.
Load more

Recommended publications
  • Disseminated Intravascular Coagulation (DIC) and Thrombosis: the Critical Role of the Lab Paul Riley, Phd, MBA, Diagnostica Stago, Inc
    Generate Knowledge Disseminated Intravascular Coagulation (DIC) and Thrombosis: The Critical Role of the Lab Paul Riley, PhD, MBA, Diagnostica Stago, Inc. Learning Objectives Describe the basic pathophysiology of DIC Demonstrate a diagnostic and management approach for DIC Compare markers of thrombin & plasmin generation in DIC, including D-Dimer, fibrin monomers (FM; aka soluble fibrin monomers, SFM), and fibrin degradation products (FDPs; aka fibrin split products, FSPs) Correlate DIC theory and testing to specific clinical cases DIC = Death is Coming What is Hemostasis? Blood Circulation Occurs through blood vessels ARTERIES The heart pumps the blood Arteries carry oxygenated blood away from the heart under high pressure VEINS Veins carry de-oxygenated blood back to the heart under low pressure Hemostasis The mechanism that maintains blood fluidity Keeps a balance between bleeding and clotting 2 major roles Stop bleeding by repairing holes in blood vessels Clean up the inside of blood vessels Removes temporary clot that stopped bleeding Sweeps off needless deposits that may cause blood flow blockages Two Major Diseases Linked to Hemostatic Abnormalities Bleeding = Hemorrhage Blood clot = Thrombosis Physiology of Hemostasis Wound Sealing break in vesselEFFRAC PRIMARY PLASMATIC HEMOSTASIS COAGULATION strong clot wound sealing blood FIBRINOLYSIS flow ± stopped clot destruction The Three Steps of Hemostasis Primary Hemostasis Interaction between vessel wall, platelets and adhesive proteins platelet clot Coagulation Consolidation
    [Show full text]
  • Heart – Thrombus
    Heart – Thrombus Figure Legend: Figure 1 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A thrombus is present in the right atrium (arrow). Figure 2 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 1). Multiple layers of fibrin, erythrocytes, and scattered inflammatory cells (arrows) comprise this right atrial thrombus. Figure 3 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A large thrombus with two foci of mineral fills the left atrium (arrow). Figure 4 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 3). This thrombus in the left atrium (arrows) has two dark, basophilic areas of mineral (arrowheads). 1 Heart – Thrombus Comment: Although thrombi can be seen in the right (Figure 1 and Figure 2) or left (Figure 3 and Figure 4) atrium, the most common site of spontaneously occurring and chemically induced thrombi is the left atrium. In acute situations, the lumen is distended by a mass of laminated fibrin layers, leukocytes, and red blood cells. In more chronic cases, there is more organization of the thrombus (e.g., presence of vascularized fibrous connective tissue, inflammation, and/or cartilage metaplasia), with potential attachment to the atrial wall. Spontaneous rates of cardiac thrombi were determined for control Fischer 344 rats and B6C3F1 mice: in 90-day studies, 0% in rats and mice; in 2-year studies, 0.7% in both genders of mice, 4% in male rats, and 1% in female rats.
    [Show full text]
  • Thrombotic Thrombocytopenic Purpura
    Thrombotic thrombocytopenic Purpura Flora Peyvandi Angelo Bianchi Bonomi Hemophilia and Thrombosis Center IRCCS Ca’ Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Disclosures Research Support/P.I. No relevant conflicts of interest to declare Employee No relevant conflicts of interest to declare Consultant Kedrion, Octapharma Major Stockholder No relevant conflicts of interest to declare Speakers Bureau Shire, Alnylam Honoraria No relevant conflicts of interest to declare Scientific Advisory Ablynx, Shire, Roche Board Objectives • Advances in understanding the pathogenetic mechanisms and the resulting clinical implications in TTP • Which tests need to be done for diagnosis of congenital and acquired TTP • Standard and novel therapies for congenital and acquired TTP • Potential predictive markers of relapse and implications on patient management during remission Thrombotic Thrombocytopenic Purpura (TTP) First described in 1924 by Moschcowitz, TTP is a thrombotic microangiopathy characterized by: • Disseminated formation of platelet- rich thrombi in the microvasculature → Tissue ischemia with neurological, myocardial, renal signs & symptoms • Platelets consumption → Severe thrombocytopenia • Red blood cell fragmentation → Hemolytic anemia TTP epidemiology • Acute onset • Rare: 5-11 cases / million people / year • Two forms: congenital (<5%), acquired (>95%) • M:F ratio 1:3 • Peak of incidence: III-IV decades • Mortality reduced from 90% to 10-20% with appropriate therapy • Risk of recurrence: 30-35% Peyvandi et al, Haematologica 2010 TTP clinical features Bleeding 33 patients with ≥ 3 acute episodes + Thrombosis “Old” diagnostic pentad: • Microangiopathic hemolytic anemia • Thrombocytopenia • Fluctuating neurologic signs • Fever • Renal impairment ScullyLotta et et al, al, BJH BJH 20122010 TTP pathophysiology • Caused by ADAMTS13 deficiency (A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, member 13) • ADAMTS13 cleaves the VWF subunit at the Tyr1605–Met1606 peptide bond in the A2 domain Furlan M, et al.
    [Show full text]
  • 32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies
    32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies Introduction Antiphospholipid antibodies (aPL) are related to thrombosis in the antiphospho- lipid syndrome (APS) [1, 2] and numerous pathophysiological mechanisms have been suggested involving cellular effects, plasma coagulation regulatory proteins, and fibrinolysis [3, 4]: aPL may act as blocking agents directly inhibiting antigen enzymatic or co-factor function of hemostasis; may bind fluid-phase antigens of hemostasis involved proteins and then decrease plasma antigen levels by clearance of immune complexes; may form immune complexes with their antigens that may be deposited in blood vessels causing inflammation and tissue injury; may cause dysregulation of antigen–phospholipid binding due to cross-linking of membrane bound antigens; and may trigger cell mediated events by cross-linking of antigen bound to cell surfaces or cell surface receptors [3, 4]. Moreover, several characteris- tics of the aPL, such as the concentration, class/subclass, affinity or charge, and several characteristics of the antigens, as the concentration, size, location or charge, may influence which of the theoretical autoantibody actions will occur in vivo [3]. Among the cellular mechanisms supposed to be involved, platelets have been considered as one of the most promising potential target for circulating aPL that may cause antibody mediated thrombosis as a part of the clinical spectrum of the autoimmune disorder of the APS. In the present chapter we will focus on the inter- actions that involve aPL binding to platelet membrane or platelet membrane bound antigens. Platelets as Target for aPL Platelets play a central role in primary hemostasis involving platelet adhesion to the injured blood vessel wall, followed by platelet activation, granule release, shape change, and rearrangement of the outer membrane phospholipids and proteins, transforming them into a highly efficient procoagulant surface [5].
    [Show full text]
  • Thrombosis and Embolism After Injury J Clin Pathol: First Published As 10.1136/Jcp.S3-4.1.86 on 1 January 1970
    J. clin. Path., 23, Suppl. (Roy. Coll. Path.), 4, 86-101 Thrombosis and embolism after injury J Clin Pathol: first published as 10.1136/jcp.s3-4.1.86 on 1 January 1970. Downloaded from S. SEVITT From the Birmingham Accident Hospital Thrombosis is frequent in injured patients. It classified as follows, namely, local thrombosis, takes different forms, and at least one of them, deep vein thrombosis, pulmonary microem- deep vein thrombosis in the lower limbs, is a bolism, glomerular microthrombosis, allied to common cause of morbidity and death through the Schwartzman reaction, occasional cases of embolic detachment. The different kinds may be arterial thrombosis, and rarely, abacterial vege- tative endocarditis. Thrombi form in flowing blood and are layered structures, unlike blood clots which form copyright. in static blood. They contain platelets, fibrin, red cells, and leucocytes, or a variable mixture, the differences depending on size, genesis, age, and venous or arterial location; but whatever the origin, the building blocks of enlarging thrombi are closely packed clumps of platelets with narrow fibrin borders (Fig. 1). Two main pro- http://jcp.bmj.com/ cesses are involved, namely, coagulation and platelet aggregation. These are interlinked and local release of thrombin is probably the key factor; thrombin promotes platelet clumping at a low concentration and fibrin formation at a higher concentration. Further, the release of substances from platelets can set in motion the coagulation on September 30, 2021 by guest. Protected process. Local Thrombosis and Haemostasis Thrombosis is frequent as a direct response to injury. In burned skin, for example, small venous thrombi may become prominent in the subdermis and subcutaneous tissue.
    [Show full text]
  • Zebrafish Depends on Von Willebrand Factor
    Hemostasis ARTICLE Histone-induced thrombotic thrombocytopenic Ferrata Storti Foundation purpura in adamts13-/- zebrafish depends on von Willebrand factor Liang Zheng,1 Mohammad S. Abdelgawwad,1 Di Zhang,1 Leimeng Xu,1 Shi Wei,2 Wenjing Cao1 and X. Long Zheng1 Divisions of 1Laboratory Medicine and 2Anatomic Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA ABSTRACT Haematologica 2020 Volume 105(4):1107-1119 hrombotic thrombocytopenic purpura (TTP) is caused by severe deficiency of ADAMTS13 (A13), a plasma metalloprotease that Tcleaves endothelium-derived von Willebrand factor (VWF). However, severe A13 deficiency alone is often not sufficient to cause an acute TTP; additional factors may be required to trigger the disease. Using CRISPR/Cas9, we created and characterized several novel zebrafish lines carrying a null mutation in a13-/-, vwf, and both. We fur- ther used these zebrafish lines to test the hypothesis that inflammation that results in neutrophil activation and release of histone/DNA com- plexes may trigger TTP. As shown, a13-/- zebrafish exhibit increased lev- els of plasma VWF antigen, multimer size, and ability of thrombocytes to adhere to a fibrillar collagen-coated surface under flow. The a13-/- zebrafish also show an increased rate of occlusive thrombus formation in -/- the caudal venules after FeCl3 injury. More interestingly, a13 zebrafish exhibit ~30% reduction in the number of total, immature, and mature thrombocytes with increased fragmentation of erythrocytes. Administration of a lysine-rich histone results in more severe and persist- Correspondence: ent thrombocytopenia and a significantly increased mortality rate in a13-/- zebrafish than in wildtype (wt) ones. However, both spontaneous and X.
    [Show full text]
  • Surgical Treatment of Cardiogenic Shock Due to Huge Right Atrial Thrombus
    Türk Kareliyol Dem Arş 2000; 28:458-460 CASEREPORT Surgical Treatment of Cardiogenic Shock Due to Huge Right Atrial Thrombus Ahmet BALT ALARLI MD, Bekir Hayrettin Ş İRİN MD, Asuman KAFTAN MD* Pamukkale Universty Medical Faculty Deparimenis o.fCardiovascular Surgery and Cardiology, Denizli DEV SAG ATRİYAL TROMBÜS NEDENiYLE and sero-sanguineous in charactcr. The story of a blunt GELiŞEN KARDiYOJENiK ŞOK VE CERRAHi chest ı rauma due to a ıraffic accidcnt 20 days ago w itlıout TEDAVİSİ any lung complication was obtained from the hospital's transfer note. ÖZET The patient was conscious and oriented. The systolic blood Kardiyojenik şok ve mu/tip/ pulmoner mikroemboliye prcssure was 65 mmHg, the pulse was regular at 130 per neden olan bir sağ atriya/ tromboemboli olgusu, nadir minute, and the respiratory rate was 20 breat lı per minutc. o lması sebebiyle bildirilmiştir. Sağ atriyumda serbestçe His neck veins were distended. The li ver was not enlarged dolaşan, diyasro/ sırasında trikiispit kapaktan sağ but tender. He had a vague calf tenderness on the right, ventrikiile prolabe olan ve sağ ventrikül g iriş (inj7ow) ve and H onıan's sign was considered positive. No pe riplı eral çıkı şmda ( outflow) tıkamklığa yol açan dii:ensiz geniş bir cdema was present. kitle iki boyutlu ekokardiyografi ile tespit edilmiş tir. Acil The ECG s lı owcd sin us tachycardia witlı T wavc invcrsion operasyona alınarak kardiyopulmoner baypasa girilmed­ in leads lll and V t-3.T lı e clıes t x-ray film sh o wed minimal en, tromboembolik materyal sağ atriyumdan başarıyla pleural cffusion at right sin us.
    [Show full text]
  • Upper-Extremity Deep Venous Thrombosis After Whole Blood Donation: Report of Three Cases from a Single Blood Center
    BLOOD DONORS AND BLOOD COLLECTION Upper-extremity deep venous thrombosis after whole blood donation: report of three cases from a single blood center Bruce Newman,1 Madhvi Rajpurkar,2 Bulent Ozgonenel,2 Anup Lal,3 and Philip Kuriakose4 pper-extremity deep venous thrombosis BACKGROUND: There are two upper-extremity deep (UEDVT) after whole blood donation is rarely venous thrombosis (UEDVT) cases after whole blood reported. There are two reported cases in the donation reported in the English medical literature. English medical literature.1-3 Our institution Three additional UEDVT cases after whole blood Uhad three UEDVT cases after whole blood donation within donation were reported to our blood center within a a 13-month period. We report the three cases and also 13-month period. review the two cases reported in the literature. In addition, STUDY DESIGN AND METHODS: A case study was we are aware of 20 more cases reported in a recent done for each case in collaboration with a clinical abstract from 4.2 million whole blood donations in Aus- physician. A description of the donation event, donor tralia,4 and we report on the abstract. demographics, risk factors for thrombosis, treatment, and outcome were described. RESULTS: A 33-year-old woman and two 17-year-old, MATERIALS AND METHODS first-time-donating men presented with arm pain, Three donation events were reported to American Red swelling, and bruising within hours to 3 days after Cross, SE Michigan Region, by the donors, donors’ rela- donation. Two had distal UEDVTs in the basilic or tives, or patients’ physician.
    [Show full text]
  • Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management
    Journal of Clinical Medicine Review Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management Senthil Sukumar 1 , Bernhard Lämmle 2,3,4 and Spero R. Cataland 1,* 1 Division of Hematology, Department of Medicine, The Ohio State University, Columbus, OH 43210, USA; [email protected] 2 Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, CH 3010 Bern, Switzerland; [email protected] 3 Center for Thrombosis and Hemostasis, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany 4 Haemostasis Research Unit, University College London, London WC1E 6BT, UK * Correspondence: [email protected] Abstract: Thrombotic thrombocytopenic purpura (TTP) is a rare thrombotic microangiopathy charac- terized by microangiopathic hemolytic anemia, severe thrombocytopenia, and ischemic end organ injury due to microvascular platelet-rich thrombi. TTP results from a severe deficiency of the specific von Willebrand factor (VWF)-cleaving protease, ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13). ADAMTS13 deficiency is most commonly acquired due to anti-ADAMTS13 autoantibodies. It can also be inherited in the congenital form as a result of biallelic mutations in the ADAMTS13 gene. In adults, the condition is most often immune-mediated (iTTP) whereas congenital TTP (cTTP) is often detected in childhood or during pregnancy. iTTP occurs more often in women and is potentially lethal without prompt recognition and treatment. Front-line therapy includes daily plasma exchange with fresh frozen plasma replacement and im- munosuppression with corticosteroids. Immunosuppression targeting ADAMTS13 autoantibodies Citation: Sukumar, S.; Lämmle, B.; with the humanized anti-CD20 monoclonal antibody rituximab is frequently added to the initial ther- Cataland, S.R.
    [Show full text]
  • Platelet and Thrombophilia-Related Risk Factors of Retinal Vein Occlusion
    Journal of Clinical Medicine Review Platelet and Thrombophilia-Related Risk Factors of Retinal Vein Occlusion Adrianna Marcinkowska 1,2, Slawomir Cisiecki 2 and Marcin Rozalski 1,* 1 Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland; [email protected] 2 Department of Ophthalmology, Karol Jonscher’s Municipal Medical Center, 93-113 Lodz, Poland; [email protected] * Correspondence: [email protected] Abstract: Retinal vein occlusion (RVO) is a heterogenous disorder in which the formation of a thrombus results in the retinal venous system narrowing and obstructing venous return from the retinal circulation. The pathogenesis of RVO remains uncertain, but it is believed to be multifactorial and to depend on both local and systemic factors, which can be divided into vascular, platelet, and hypercoagulable factors. The vascular factors include dyslipidaemia, high blood pressure, and diabetes mellitus. Regarding the platelet factors, platelet function, mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (PLCR) play key roles in the diagnosis of retinal vein occlusion and should be monitored. Nevertheless, the role of a hypercoagulable state in retinal vein occlusion remains unclear and requires further studies. Therefore, the following article will present the risk factors of RVO associated with coagulation disorders, as well as the acquired and genetic risk factors of thrombophilia. According to Virchow’s triad, all factors mentioned above lead Citation: Marcinkowska, A.; Cisiecki, to thrombus formation, which causes pathophysiological changes inside venous vessels in the fundus S.; Rozalski, M. Platelet and of the eye, which in turn results in the vessel occlusion.
    [Show full text]
  • Protocol for the Prevention of Venous Thromboembolism at the Ivo Pitanguy Institute: Efficacy and Safety in 1351 Patients
    ARTIGO ORIGINAL Protocolo de prevenção de tromboembolismoVendraminFranco T FSet al.et venoso al. no Instituto Ivo Pitanguy Protocolo de prevenção de tromboembolismo venoso no Instituto Ivo Pitanguy: eficácia e segurança em 1.351 pacientes Protocol for the prevention of venous thromboembolism at the Ivo Pitanguy Institute: efficacy and safety in 1351 patients RITA A. PAIVA1 RESUMO JIHED CHADRAOUI2 Introdução: Eventos tromboembólicos causam grande preocupação, em decorrência das BArbARA B. MACHADO3 altas taxas de morbidade e mortalidade existentes e da possibilidade de apresentação clínica NATALE F. GONTIJO DE com sintomas escassos e, muitas vezes, inespecíficos. A prevenção é a maneira mais eficaz AMORIM3 de lidar com esse tipo de evento, que, uma vez estabelecido, pode levar rapidamente à HAZEL FISCHDICK4 morte. Método: Foi realizado estudo retrospectivo, no período entre maio de 2009 e maio IVO PITAngUY5 de 2010, com pacientes submetidos a cirurgia plástica no Instituto Ivo Pitanguy. Todos os pacientes foram submetidos ao protocolo de prevenção de tromboembolismo venoso, após serem avaliados quanto aos fatores predisponentes e de risco. A soma desses fatores gerou uma pontuação, que determinou a profilaxia a ser adotada. Resultados: Foram avaliados 1.351 pacientes durante o período de um ano. Não houve incidência de tromboem bolismo venoso. Foram observados 16 casos de hematoma, 9 (56,25%) deles ocorreram após profi- laxia com heparina e 7 (43,75%) sem o uso de quimioprofilaxia. Conclusões: O protocolo para prevenção de tromboembolismo venoso no Instituto Ivo Pitanguy foi eficaz, sem ocor- rência de eventos tromboembólicos e com incidência de hematomas abaixo da encontrada na literatura médica. Descritores: Tromboembolia venosa/prevenção & controle.
    [Show full text]
  • Protruding Left Ventricular Thrombus Formation Following Blunt Chest Trauma
    Volume 125, Number 3 American Heart Journal Rechavia et aE. 893 * P c 0.01 vs baseline values A P e 0.005 vs recovery values of nMI r* ; E 40. recovery F maximum ’ 30. MI 5 5 20 nMI I -10 recovery g baseline maximum a ul Rest 0 1 1.5 5 9 minutes Fig. 1. SACE levels in ischemic (IMI) and nonischemic (nMII subjects during exercise test. Table II. SACE activity during the exercise test SACE (nmol/ml/mini Groups -10 0 Maximum Recovery Ischemic (n = 9) "0.78 t 1.99 22.06 f 2.17 ‘25.18 t xv*I I 28.95 t 5.09*i Nonischemic (n = 9) 21.80 c X.70 21.50 k 4.80 2::.30 +- ,'3.10 22.00 k 3.40 *p < 0.01 versus baseline values. tp < 0.005 versus nonischemic at recovery in the event of myocardial ischemia, SACE increases (kininase II) in human endoehelial cells in culture. Adv Exp markedly at maximum effort as well as during recovery. Med Biol 1978;120B:287-90. Our data on SACE activity in nonischemic subjects support 9. Hayes LW, Goguen CA, Ching SF, Slakey LL. Angiotensin- converting enzyme: accumulation in medium from cultured similar results obtained by Milledge and Catley,” who endothelial cells. Biochem Biophys Commun 1978;82:1147-9. found SACE to remain unchanged during extended stress 10. Kasahara Y, Ashihara Y, Harada T. The method for determi- testing (up to 60 minutes) in normal healthy subjects. In nation of angiotensin I converting enzyme (ACE) activity.
    [Show full text]