DOCSLIB.ORG

Protruding Left Ventricular Thrombus Formation Following Blunt Chest Trauma

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read 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. Clin light of our findings, we propose that SACE elevation could Chem 1981:27:1114-B. 11. Milledge JS, Catley DM. Renin, aldosterone and converting reflect acute endothelial vascular damage (both in general enzyme during exercise and acute hypoxia in humans. J Appl and in particular in the cardiac vasculature) in subjects Physiol 1982;52:3‘20-3. with clinical and ECG signs of myocardial ischemia during stress testing (regardless of the duration of exercise). Protruding left ventricular thrombus REFERENCES formation following blunt chest trauma 1. Erdos EG. The angiotensin I converting enzyme. Fed Proc 1977;36:1760-5. Eldad Rechavia, MD, Shula Imbar, 2. Soffer RL. Angiotensin-converting enzyme and the regulation Yochai Birnbaum, MD, Boris Strasberg, MD, and of vasoactive peptides. Ann Rev Biochem 1976;45:73-94. 3. Skeggs TL, Kahn JR, Shumway NP. The preparation and Samuel Sclarovsky, MD function of the angiotensin-converting enzyme. J Exp Med Petah-Tiqva and Tel-Aviv, Israel 1956;103:295-9. 4. Caldwell PRB, Seegal BG, Hsu RC, Das M, Sofl’er RL. Angiotensin converting enzyme vascular endothelial localiza- tion. Science 1976;191:1050-1. 5I Ryan JW, Ryan US. Correlation of pulmonary structure with From the Cardiovascular Division and Coronary Care Unit. Beilinson Med- pharmacokinetic function. Agents Actions 1976;4:510-4. ical Center, Petah-Tiqva; and the Tel-Aviv University Sackler School of 6. Studdy PR, Lapworth R, Bird R. Angiotensin-converting en- Medicine. zyme and its clinical significance: a review. J Clin Path01 198X36:938-47. Reprint requests: Eldad Rechavia, MD, Cardiovascular Division. Beilinson Medical Center, Petah-Tiqva, 49100 Israel. 7. Wigger HS, Stalcup SA. Distribution and development of an- giotensin-converting enzyme in the fetal and newborn rabbit. AM HEART J 1993;125:893-896. An immunofluorescence study. Lab Invest 1978:38:581-X Copyright 1993 by Moshy-Year Book. Inc. 8. dohnson AR, Erdos EG. Angiotensin I converting enzyme 000’.8703/93/WXl+ .lO 4/4/43467 March 1993 Amencan Heart Journai Fig. 1. ECG showing QS complex in the precordial leads and a right h\lnrl!e branch I)!ock-left anterior hemiblock pattern. Following myocardial contusion, attention has been tradi- 120/80 mm Hg and the pulse rate was 64 beats/min. On ex- tionally directed toward the hemodynamic derangement amination. there was tenderness over t.he left precordium that it produces as well as life-threatening ventricular ar- and a fourth heart sound was audible. As the possibility 01 rhythmias. I,? Little attention has been devoted to the pos- chest trauma was considered, careful anamnesis elicited sible formation of thrambus and the potential thromboem- that the patient had probably sutfered bruising of the left bolic hazards thus evoked. A case is presented of a young anterior chest wali. A chest x-ray film was normal. Contin- patient with normal coronary arteries in whom an unnoted uous monitoring revealed frequent ventricular premature blunt trauma to the chest gave rise to septoapical dyskine- beats and short. runs of ventricular tachycardia. Cardiac sia and protruding left ventricular (LV) thrombus forma- enzyme levels including creatine kinase MB fraction were tion. indicative of infarction. Two-dimensiona echocardiogra- A 35year-old man with no history of heart disease or phy performed the next day showed septoapical dyskine- cardiac risk factors was referred to a surgical department sia and an LV mass protruding into the chamber cavity of our hospital following maxillofacial trauma. He was with marked mobility (Fig. 2). The mass length from apex pushed from a one-story structure, falling on a slanted sur- to the mobile end reached 1.2 cm. Cardiac catheterization face scattered with fairly large poles. An open fracture of demonstrated patent coronary arteries. Ventriculography the left zygomatic bone was accompanied with swelling and was not performed for fear of dislodging the thrombus. The the appearance of hematoma around the lateral aspect of patient was treated by continuous intravenous heparin in- his left eye. Apart from pain at the site of trauma, the pa- fusion (1000 units per hour), followed by warfarin treat- tient complained of blurred vision and troublesome irrita- ment. Follow-up echocardiographic examinat.ion at 1 week, tion in his eye. At the time of admission, no history or ev- 2 weeks, and 1 month later showed gradual regression of the idence of chest trauma was obtained. Three days later, in t.hrombus dimensions, with diminished protrusion and the operating room and just before surgical repair and re- mobility. At a X-month follow-up, echocardiographic find- positioning of the zygomatic fracture, he complained of ings were compatible with mural nonprotruding apical sharp precordial pain on deep inspiration, radiating to his thrombus. No seyuelae of embolization or further ECG left arm. An electrocardiogram (ECG) performed in the changes were noted during the 4-month follow-up period. operating room showed a right bundle branch block-left Ventricular thrombus, logically expected in the setting of anterior hemiblock pattern and QS complex in the precor- myocardial contusion, is surprisingly a relatively rare dial leads (Fig. 1). At this stage, surgery was postponed, and echocardiographic finding. In three prospective echocar- the patient was transferred to the coronary care unit. When diographic studies involving 2’79 individuals, thromhus was seen For the first time in the unit, his blood pressure was documented in none of the patients suff’ering myocardial Volume 125, Number 3 Rechauia et al. 895 American Heart Journal Fig. 2. Two-dimensional two-chamber apical view showing a protruding thrombus in the dyskinetic sep- toapical area of the left ventricle. contusion.“.” However, there is more than anecdotal evi- configuration. Anticoagulation proved to be efficient, de- dence to suggest that in those patients demonstrating wall creasing the size of the thrombus and presumably reducing motion abnormalities related to cardiac contusion, a high the potential risk for embolization. Thrombus formation index of suspicion should be maintained to ensure that no following myocardial contusion may be related either to clinical sequelae of ventricular thrombus may occur. In direct myocardial insult or to compression of a coronary this context, it has been recently concluded by Wisner et artery, resembling myocardial infarction. The first seems al.’ that most of the patients who are prone to life-threat- the more plausible explanation in our patient, who was ening cardiac complications from blunt cardiac injury can thought to have myocardial contusion based on elevation be identified soon after the traumatic event in an emer- of serum cardiac enzymes, electrical instability, mechani- gency room setting. However, one should bear in mind that cal dysfunction, and a normal coronary angiogram. We thrombus could easily be missed if echocardiography is have been able to find in the literature only two reported performed immediately after blunt contusion. As in myo- cases of ventricular protruding thrombus induced by blunt cardial infarction, it is not inconceivable that ventricular chest trauma.*, “’ thrombus, either mural or protruding, will be seen 2 or 3 Cardiac injury is a common and frequently unsuspected days following myocardial contusion, giving rise to a visceral injury. r’ Patients may be free of any cardiac delayed embolic complications As thrombus formation is symptoms or may have transient complaints. In the present promoted by severe wall motion abnormality, echocardio- case, chest trauma was probably masked by the major graphic follow-up is strongly recommended in this subset maxillofacial injury. As we noted, even “innocent” trauma of patients demonstrating early wall motion abnormalities. may result in protruding thrombus formation, and had the Embolic complications in patients with thrombus-re- patient not complained of chest pain, the thrombus could lated myocardial contusion have been sparse.H-12 It remains have gone undetected, with the patient exposed to both debatable whether an echocardiographic finding of a mu- operative and a major delayed embolic risk.” ral thrombus warrants prophylactic anticoagulation.“’ The therapeutic approach might be entirely different when REFERENCES protruding thrombus is apparent, mainly because of its higher propensity (up to 60’, of cases) toward emboliza- 1. Traumatic injury of the heart. Lancet 1990;336:1287-9. 2. Tenser ML. The spectrum of myocardial contusion: a review, tion.‘.l, ” Although anticoagulation has questionable ben- .J Trauma 1985;25:620-7.
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]
  • Severe Disseminated Intravascular Coagulation Associated with Massive Ventricular Mural Thrombus Following Acute Myocardial Infarction
    Postgrad Med J: first published as 10.1136/pgmj.64.756.791 on 1 October 1988. Downloaded from Postgraduate Medical Journal (1988) 64, 791-795 Severe disseminated intravascular coagulation associated with massive ventricular mural thrombus following acute myocardial infarction S.A. Solomon, D.W.K. Cotton, F.E. Preston and L.E. Ramsay University Departments of Haematology, Pathology and Therapeutics, Royal Hallamshire Hospital, Sheffield S1O 2JF, UK Summary: We describe three patients who developed severe disseminated intravascular coagula- tion associated with large ventricular mural thrombi shortly after presenting with acute myocardial infarction. To our knowledge this association has not been reported before. Introduction Disseminated intravascular coagulation (DIC) has episode of ventricular fibrillation, which was cor- been reported in a wide variety of disorders, with rected promptly by defibrillation, followed by epi- infection, malignancy, trauma and surgery account- sodes of supraventricular and broad-complex ing for most cases.1 Modest increases in fibrin tachycardia. She was well on day 2, but developed by copyright. degradation products have been reported in mild left ventricular failure and right lower lobe patients with severe myocardial infarction but overt consolidation on the third day. Streptococcus pneu- DIC is rare.2 We describe three patients who moniae was cultured from sputum, but blood cul- developed severe DIC associated with large ventri- tures were sterile. The heart failure and pneumonia cular thrombi shortly after presenting with acute responded to diuretic and antibiotic treatment. myocardial infarction. Large intravascular thrombi Progress was then uncomplicated until the 12th arising from intra- or extracardiac sites have been hospital day, when she developed spontaneous reported to cause DIC."",2 We propose that the bleeding from venepuncture sites and purpura.
    [Show full text]