Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE)
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Clinical Case: Post-Procedure Thrombophlebitis
Clinical Case: Post-procedure Thrombophlebitis A 46 year old female presented with long-standing history of right lower limb fatigue and aching with prolonged standing. Symptoms –Aching, cramping, heavy, tired right lower limb –Tenderness over bulging veins –Symptoms get worse at end of the day –She feels better with lower limb elevation and application of elastic compression stockings (ECS) History Medical and Surgical history: Sjogren syndrome, mixed connective tissue disease, GERD, IBS G2P2 with C-section x2, left breast biopsy No history of venous thrombosis Social history: non-smoker Family history: HTN, CAD Allergies: None Current medications: Pantoprazole Physical exam Both lower limbs were warm and well perfused Palpable distal pulses Motor and sensory were intact Prominent varicosities Right proximal posterior-lateral thigh and medial thigh No ulcers No edema Duplex ultrasound right lower limb GSV diameter was 6.4mm and had reflux from the SFJ to the distal thigh No deep venous reflux No deep vein thrombosis Duplex ultrasound right lower limb GSV tributary diameter 4.6mm Anterior thigh varicose veins diameter 1.5mm-2.6mm with reflux No superficial vein thrombosis What is the next step? –Conservative treatment – Phlebectomies –Sclerotherapy –Thermal ablation –Thermal ablation, phlebectomies and sclerotherapy Treatment Right GSV radiofrequency ablation Right leg ultrasound guided foam sclerotherapy with 0.5% sodium tetradecyl sulfate (STS) Right leg ambulatory phlebectomies x19 A compression dressing and ECS were applied to the right lower limb after the procedure. Follow-up 1 week post-procedure –The right limb was warm and well perfused –There was mild bruising, no infection and signs of mild thrombophlebitis –Right limb venous duplex revealed no deep vein thrombosis and the GSV was occluded 2 weeks post-procedure –Tender palpable cord was found in the right thigh extending into the calf with overlying hyperpigmentation. -
Pulmonary Veno-Occlusive Disease
Arch Dis Child: first published as 10.1136/adc.42.223.322 on 1 June 1967. Downloaded from Arch. Dis. Childh., 1967, 42, 322. Pulmonary Veno-occlusive Disease K. WEISSER, F. WYLER, and F. GLOOR From the Departments of Paediatrics and Pathology, University of Basle, Switzerland Pulmonary venous congestion with or without time. She gradually became more dyspnoeic, with 'reactive' or 'protective' pulmonary arterial hyper- increasing weakness and fatigue, and her weight fell. tension (Wood, 1954; Wood, Besterman, Towers, In October 1961 she developed jaundice with acholic and McIlroy, 1957) is most commonly caused by stools and dark urine. Infective hepatitis was diagnosed, and she was put on a diet and, 2 weeks later, on corti- left heart disease. The obstruction to blood flow costeroids. She had had no known contact with a case may, however, also be located upstream to the left of hepatitis. Again, except for her dyspnoea, no cardiac atrium. Among the known causes of such obstruc- or pulmonary abnormality was found. The icterus tion are compression of the pulmonary veins by a decreased very slowly, but never disappeared entirely. mediastinal mass (Edwards and Burchell, 1951; In the following months her general condition deteriora- Andrews, 1957; Evans, 1959); congenital stenosis of ted and she was breathless even at rest. On two occasions the pulmonary veins at the veno-atrial junction she had syncopal attacks lasting a few minutes. She lost (Lucas, Woolfrey, Anderson, Lester, and Edwards, 12 kg. within one year. In January 1962 the parents finally consented to her being admitted to hospital. 1962); or thrombus formation in the pulmonary On admission she was obviously ill, wasted, jaundiced, veins due to greatly reduced blood flow associated cyanotic, and severely dyspnoeic and orthopnoeic. -
Pleural Effusion and Ventilation/Perfusion Scan Interpretation for Acute Pulmonary Embolus
ventricular function by radionuclide angiography during exercise in normal subjects 33. Verani MS. Myocardial perfusion imaging versus two-dimensional echocardiography: and patients with chronic coronary heart disease. J Am Coll Cardiol 1983;1:1518- comparative value in the diagnosis of coronary artery disease. J NucÃCardiol 1529. 1994;1:399-414. 29. Adam WE. Tarkowska A, Bitter F, Stauch M, Geffers H. Equilibrium (gated) 34. Foster T, McNeill AJ, Salustri A, et al. Simultaneous dobutamine stress echocardiog radionuclide ventriculography. Cardiovasc Radial 1979;2:161-173. raphy and technetium-99m SPECT in patients with suspected coronary artery disease. 30. Hurwitz RA, TrêvesS, Kuroc A. Right ventricular and left ventricular ejection fraction J Am Coll Cardiol I993;21:1591-I596. in pediatrie patients with normal hearts: first pass radionuclide angiography. Am 35. Marwick TH, D'Hondt AM, Mairesse GH, Baudhuin T, Wijins W, Detry JM, Meiin Heart J 1984;107:726-732. 31. Freeman ML, Palac R, Mason J, et al. A comparison of dobutamine infusion and JA. Comparative ability of dobutamine and exercise stress in inducing myocardial ischemia in active patients. Br Heart J 1994:72:31-38. supine bicycle exercise for radionuclide cardiac stress testing. Clin NucÃMed 1984:9:251-255. 36. Senior R, Sridhara BS, Anagnostou E, Handler C, Raftery EB, Lahiri A. Synergistic 32. Cohen JL, Greene TO, Ottenweller J, Binebaum SZ, Wilchfort SD, Kim CS. value of simultaneous stress dobutamine sestamibi single-photon-emission computer Dobutamine digital echocardiography for detecting coronary artery disease. Am J ized tomography and echocardiography in the detection of coronary artery disease. -
Deep Vein Thrombosis in Behcet's Disease
BRIEF PAPER Clinical and Experimental Rheumatology 2001; 19 (Suppl. 24): S48-S50. Deep vein thrombosis ABSTRACT stitute the most frequent vascular mani- Objective festation seen in 6.2 to 33 % cases of in Behcet’s disease We aimed to describe the epidemiologi - BD (1, 2). We carried out this study to cal and clinical aspects of deep vein d e t e rmine the fre q u e n cy, the cl i n i c a l M.H. Houman1 thrombosis (DVT) in Behçet’s disease characteristics and course of deep vein 1 (BD) and to determine the patients at thrombosis (DVT) in BD patients and I. Ben Ghorbel high risk for this complication. to define a subgroup of patients at high I. Khiari Ben Salah1 Methods risk for this complication. M. Lamloum1 Among 113 patients with BD according 2 to the international criteria for classifi - Patients and methods M. Ben Ahmed cation of BD, those with DVT were ret - The medical records of one hundred M. Miled1 rospectively studied.The diagnosis of and thirteen patients with BD were re- DVT was made in all cases using con - viewed in order to investigate the pa- 1Department of Internal Medicine. La ventional venous angiography, venous tient’s medical history, the clinical ma- Rabta Hospital, 2Department of Immuno- ultrasonography and/or thoracic or ab - nifestations and outcome of the disease logy, Institute Pasteur. Tunis, Tunisia. dominal computed tomograp hy. Pa - as well as the treatment prescribed.The Houman M Habib, MD; Ben Ghorbel tients were divided in two subgroups diagnosis of BD was made based on the Imed, MD; Khiari Ben Salah Imen; a c c o rding to the occurrence of DV T criteria established by the international Lamloum Mounir, MD; Ben Ahmed other than cereb ral thromboses. -
Lower Extremity Deep Venous Thrombosis
SECTION 5 Vascular System CHAPTER 34 Lower Extremity Deep Venous Thrombosis Ariel L. Shiloh KEY POINTS • Providers can accurately detect lower extremity deep venous thrombosis with point-of- care ultrasound after limited training. • Compression ultrasound exams are as accurate as traditional duplex and triplex vascular ultrasound exams. • Compression ultrasound exam at only two sites, the common femoral vein and popliteal vein, permits rapid and accurate assessment of deep venous thrombosis. Background care providers can perform lower extremity compression ultrasonography exams rapidly Venous thromboembolic disease (VTE) is a and with high diagnostic accuracy to detect common cause of morbidity and mortality in DVT. 7–13 A meta-analysis of 16 studies showed hospitalized patients and is especially preva- that point-of-care ultrasound can accurately lent in critically ill patients.1–3 Approximately diagnose lower extremity DVTs with a pooled 70% to 90% of patients with an identified source sensitivity of 96% and specificity of 97%.14 of pulmonary embolism (PE) have a proxi- Traditional vascular studies, the duplex mal lower extremity deep venous thrombosis and triplex exams, use a combination of (DVT). Conversely, 40% to 50% of patients two-dimensional (2D) imaging with compres- with a proximal DVT have a concurrent pul- sion along with the use of color and/or spectral monary embolism at presentation, and simi- Doppler ultrasound. More recent studies have larly, in only 50% of patients presenting with a demonstrated that 2D compression ultrasound PE can a DVT be found.4–6 exams alone yield similar accuracy as tradi- Point-of-care ultrasound is readily available tional duplex or triplex vascular studies.9,11,15–17 as a diagnostic tool for VTE. -
Diagnosing Pulmonary Embolism M Riedel
309 Postgrad Med J: first published as 10.1136/pgmj.2003.007955 on 10 June 2004. Downloaded from REVIEW Diagnosing pulmonary embolism M Riedel ............................................................................................................................... Postgrad Med J 2004;80:309–319. doi: 10.1136/pgmj.2003.007955 Objective testing for pulmonary embolism is necessary, embolism have a low long term risk of subse- quent VTE.2 5–7 because clinical assessment alone is unreliable and the consequences of misdiagnosis are serious. No single test RISK FACTORS AND RISK has ideal properties (100% sensitivity and specificity, no STRATIFICATION risk, low cost). Pulmonary angiography is regarded as the The factors predisposing to VTE broadly fit Virchow’s triad of venous stasis, injury to the final arbiter but is ill suited for diagnosing a disease vein wall, and enhanced coagulability of the present in only a third of patients in whom it is suspected. blood (box 1). The identification of risk factors Some tests are good for confirmation and some for aids clinical diagnosis of VTE and guides decisions about repeat testing in borderline exclusion of embolism; others are able to do both but are cases. Primary ‘‘thrombophilic’’ abnormalities often non-diagnostic. For optimal efficiency, choice of the need to interact with acquired risk factors before initial test should be guided by clinical assessment of the thrombosis occurs; they are usually discovered after the thromboembolic event. Therefore, the likelihood of embolism and by patient characteristics that risk of VTE is best assessed by recognising the may influence test accuracy. Standardised clinical presence of known ‘‘clinical’’ risk factors. estimates can be used to give a pre-test probability to However, investigations for thrombophilic dis- orders at follow up should be considered in those assess, after appropriate objective testing, the post-test without another apparent explanation. -
Difference Between Vein and Venule Key Difference - Vein Vs Venule
Difference Between Vein and Venule www.differencebetween.com Key Difference - Vein vs Venule The veins are the blood vessels that carry blood towards the heart. It always has a low blood pressure. Except the pulmonary and the umbilical veins, all the remaining veins carry the deoxygenated blood. On the contrary, the arteries carry blood away from the heart. The veins have valves in them to prevent the black flow of blood and to maintain unidirectional blood flow. They are less muscular, larger and are located closer to the skin. Venules are very smaller veins. They are the ones that collect blood from the capillaries. The collected blood will be directed to the larger and medium veins where the blood is transported towards the heart again. Many venules unite to form larger veins. The key difference between Vein and Venule is, the vein is a larger blood vessel that carries blood towards the heart while, the venule is a smaller minute blood vessel that drains blood from capillaries to the veins. What is a Vein? The veins are larger blood vessels present in throughout the body. The main function of veins is to carry oxygen-poor blood back into the heart. Veins are classified into some categories such as, superficial veins, pulmonary veins, deep veins, perforator veins, communicating veins and systematic veins. The wall of the vein is thinner and less elastic than the wall of an artery. The walls of the veins consist three layers of tissues which are named as tunica externa, tunica media, and tunica intima. Veins also have larger and irregular lumen. -
An Interesting Case of Undiagnosed Pleural Effusion Case Report
Amit Panjwani, Thuraya Zaid [email protected] Pulmonary Medicine, Salmaniya Medical Complex, Manama, Bahrain. An interesting case of undiagnosed pleural effusion Case report Pleural effusions are commonly encountered in the Investigations revealed a haemoglobin level Cite as: Panjwani A, Zaid T. clinical practise of both respiratory and nonrespiratory of 16.4 g⋅dL−1, and total leukocyte count of An interesting case of specialists. An estimated 1–1.5 million new cases in 8870 cells⋅mm−3 with a differential count of 62% undiagnosed pleural effusion. the USA and 200 000–250 000 new cases of pleural neutrophils, 28% lymphocytes, 7% monocytes, 2% Breathe 2017; 13: e46–e52. effusions are reported from the UK each year [1]. eosinophils and 1% basophils. The platelet count Analysis of the relevant clinical history, physical was 160 000 cells⋅mm−3. Creatinine, electrolytes examination, chest radiography and diagnostic and liver function tests were normal. The ECG was thoracentesis is useful in identifying the cause of unremarkable and cardiac enzymes were within pleural effusion in majority of the cases [2]. In a few normal limits. Chest radiograph (figure 1) showed a cases, the aetiology may be unclear after the initial mild, right-sided pleural effusion, blunting of the left assessment. The list of diseases that may account for costophrenic angle, no shift of mediastinal position a persistent undiagnosed pleural effusion is long [3]. and no lung parenchymal opacities. We present an interesting case of undiagnosed pleural effusion that was encountered in our hospital. R Case presentation A 33-year-old male presented to our hospital with a history of sudden-onset, pleuritic, right-sided chest pain of 2 days’ duration. -
Diagnosis of Chronic Thromboembolic Pulmonary Hypertension After Acute Pulmonary Embolism
Early View Review Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism Fredrikus A. Klok, Francis Couturaud, Marion Delcroix, Marc Humbert Please cite this article as: Klok FA, Couturaud F, Delcroix M, et al. Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism. Eur Respir J 2020; in press (https://doi.org/10.1183/13993003.00189-2020). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2020 Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism Fredrikus A. Klok, Francis Couturaud F2, Marion Delcroix M3, Marc Humbert4-6 1 Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands 2 Département de Médecine Interne et Pneumologie, Centre Hospitalo-Universitaire de Brest, Univ Brest, EA 3878, CIC INSERM1412, Brest, France 3 Department of Respiratory Diseases, University Hospitals and Respiratory Division, Department of Chronic Diseases, Metabolism & Aging, KU Leuven – University of Leuven, Leuven, Belgium 4 Université Paris-Saclay, Faculté de Médecine, Le Kremlin-Bicêtre, France 5 Service de Pneumologie et Soins Intensifs Respiratoires, Hôpital Bicêtre, AP-HP, Le Kremlin-Bicêtre, France 6 INSERM UMR S 999, Hôpital Marie Lannelongue, Le Plessis Robinson, France Corresponding author: Frederikus A. Klok, MD, FESC; Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands; Albinusdreef 2, 2300RC, Leiden, the Netherlands; Phone: +31- 715269111; E-mail: [email protected] Abstract Chronic thromboembolic pulmonary hypertension (CTEPH) is the most severe long-term complication of acute pulmonary embolism (PE). -
Peripheral Vascular Disease (PVD) Fact Sheet
FACT SHEET FOR PATIENTS AND FAMILIES Peripheral Vascular Disease (PVD) What is peripheral vascular disease? Vascular disease is disease of the blood vessels (arteries and veins). Peripheral vascular disease (PVD) affects The heart receives blood, the areas that are “peripheral,” or outside your heart. sends it to The most common types of PVD are: the lungs to get oxygen, • Carotid artery disease affects the arteries and pumps that carry blood to your brain. It occurs when it back out. one or more arteries are narrowed or blocked by plaque, a fatty substance that builds up inside artery walls. Carotid artery disease can increase Veins carry Arteries carry your risk of stroke. It can also cause transient blood to your oxygen-rich [TRANZ-ee-ent] ischemic [iss-KEE-mik] attacks (TIAs). heart to pick blood from up oxygen. your heart TIAs are temporary changes in brain function to the rest of that are sometimes called “mini-strokes.” your body. • Peripheral arterial disease (PAD) often affects the arteries to your legs and feet. It is also caused by Healthy blood vessels provide oxygen plaque buildup, and can for every part of your body. cause pain that feels like a dull cramp or heavy tiredness in your hips or legs when • Venous insufficiency affects the veins, usually you exercise or climb stairs. in your legs or feet. Your veins have valves that This pain is sometimes Damaged Healthy keepvalve blood fromvalve flowing backward as it moves called claudication. If PAD toward your heart. If the valves stop working, blood worsens, it can cause cold Plaque can build backs up in your body, usually in your legs. -
Anatomy of the Large Blood Vessels-Veins
Anatomy of the large blood vessels-Veins Cardiovascular Block - Lecture 4 Color index: !"#$%&'(& !( "')*+, ,)-.*, $()/ Don’t forget to check the Editing File !( 0*"')*+, ,)-.*, $()/ 1$ ($&*, 23&%' -(0$%"'&-$(4 *3#)'('&-$( Objectives: ● Define veins, and understand the general principles of venous system. ● Describe the superior & inferior Vena Cava and their tributaries. ● List major veins and their tributaries in the body. ● Describe the Portal Vein. ● Describe the Portocaval Anastomosis Veins ◇ Veins are blood vessels that bring blood back to the heart. ◇ All veins carry deoxygenated blood. with the exception of the pulmonary veins(to the left atrium) and umbilical vein(umbilical vein during fetal development). Vein can be classified in two ways based on Location Circulation ◇ Superficial veins: close to the surface of the body ◇ Veins of the systemic circulation: NO corresponding arteries Superior and Inferior vena cava with their tributaries ◇ Deep veins: found deeper in the body ◇ Veins of the portal circulation: With corresponding arteries Portal vein Superior Vena Cava ◇Formed by the union of the right and left Brachiocephalic veins. ◇Brachiocephalic veins are formed by the union of internal jugular and subclavian veins. Drains venous blood from : ◇ Head & neck ◇ Thoracic wall ◇ Upper limbs It Passes downward and enter the right atrium. Receives azygos vein on its posterior aspect just before it enters the heart. Veins of Head & Neck Superficial veins Deep vein External jugular vein Anterior Jugular Vein Internal Jugular Vein Begins just behind the angle of mandible It begins in the upper part of the neck by - It descends in the neck along with the by union of posterior auricular vein the union of the submental veins. -
Incidence of Deep Venous Thrombosis and Stratification of Risk Groups in A
ORIGINAL ARTICLE Incidence of deep venous thrombosis and stratification of risk groups in a university hospital vascular surgery unit Incidência de trombose venosa profunda e estratificação dos grupos de risco em serviço de cirurgia vascular de hospital universitário 1 1 1 2 Alberto Okuhara *, Túlio Pinho Navarro , Ricardo Jayme Procópio , José Oyama Moura de Leite Abstract Background: There is a knowledge gap with relation to the true incidence of deep vein thrombosis among patients undergoing vascular surgery procedures in Brazil. This study is designed to support the implementation of a surveillance system to control the quality of venous thromboembolism prophylaxis in our country. Investigations in specific institutions have determined the true incidence of deep vein thrombosis and identified risk groups, to enable measures to be taken to ensure adequate prophylaxis and treatment to prevent the condition. Objective: To study the incidence of deep venous thrombosis in patients admitted to hospital for non-venous vascular surgery procedures and stratify them into risk groups. Method: This was a cross-sectional observational study that evaluated 202 patients from a university hospital vascular surgery clinic between March 2011 and July 2012. The incidence of deep venous thrombosis was determined using vascular ultrasound examinations and the Caprini scale. Results: The mean incidence of deep venous thrombosis in vascular surgery patients was 8.5%. The frequency distribution of patients by venous thromboembolism risk groups was as follows: 8.4% were considered low risk, 17.3% moderate risk, 29.7% high risk and 44.6% were classified as very high risk. Conclusion: The incidence of deep venous thrombosis in vascular surgery patients was 8.5%, which is similar to figures reported in the international literature.