Prognosis of Patients with Retinal Embolism
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Review Cutaneous Patterns Are Often the Only Clue to a a R T I C L E Complex Underlying Vascular Pathology
pp11 - 46 ABstract Review Cutaneous patterns are often the only clue to a A R T I C L E complex underlying vascular pathology. Reticulate pattern is probably one of the most important DERMATOLOGICAL dermatological signs of venous or arterial pathology involving the cutaneous microvasculature and its MANIFESTATIONS OF VENOUS presence may be the only sign of an important underlying pathology. Vascular malformations such DISEASE. PART II: Reticulate as cutis marmorata congenita telangiectasia, benign forms of livedo reticularis, and sinister conditions eruptions such as Sneddon’s syndrome can all present with a reticulate eruption. The literature dealing with this KUROSH PARSI MBBS, MSc (Med), FACP, FACD subject is confusing and full of inaccuracies. Terms Departments of Dermatology, St. Vincent’s Hospital & such as livedo reticularis, livedo racemosa, cutis Sydney Children’s Hospital, Sydney, Australia marmorata and retiform purpura have all been used to describe the same or entirely different conditions. To our knowledge, there are no published systematic reviews of reticulate eruptions in the medical Introduction literature. he reticulate pattern is probably one of the most This article is the second in a series of papers important dermatological signs that signifies the describing the dermatological manifestations of involvement of the underlying vascular networks venous disease. Given the wide scope of phlebology T and its overlap with many other specialties, this review and the cutaneous vasculature. It is seen in benign forms was divided into multiple instalments. We dedicated of livedo reticularis and in more sinister conditions such this instalment to demystifying the reticulate as Sneddon’s syndrome. There is considerable confusion pattern. -
Presented: February 2, 2017 Thru February 4, 2017
2017 ACP Colorado Chapter Meeting February 2, 2017 thru February 4,2017 Broadmoor Hotel, Colorado Springs, Colorado Resident Abstracts Presented: February 2, 2017 thru February 4, 2017 2017 ACP Colorado Chapter Meeting – February 2, 2017 thru February 4, 2017 – Broadmoor Hotel – Colorado Springs, Colorado Name: Angela Burgin, MD Presentation Type: Oral Presentation Residency Program: University of Colorado School of Medicine Additional Authors: Winthrop Lockwood MS3, Katarzyna Mastalerz, MD Abstract Title: Use Clean Needles, Boil you Cotton: Advice for the Modern Drug User Abstract Information: Introduction: Fever in an intravenous drug abuser results in a wide differential diagnosis for the physician to consider, ranging from simple soft tissue infections to endocarditis or epidural abscess. This large breadth of possibilities often leads to dilemmas on which studies to order first, usually resulting in an expensive evaluation. We present one more option to add to the differential diagnosis in an IV drug user who presents with fever, with the hopes of increasing awareness of this condition to the medical community. Case Description: A 31 year old female with a history significant for IV drug abuse presented with dyspnea, chest pain, severe abdominal pain, right arm swelling, and generalized weakness for several days. She worked for a home health company and admitted to recently injecting hydromorphone and other opiates into her veins. Physical exam on admission was notable for a high fever, tachycardia, and right forearm edema, erythema, and induration, with a benign chest and abdominal exam. Ancillary studies revealed a urine toxicology positive for opiates, methadone, and cocaine, as well as a white blood cell count of 13. -
Pulmonary Embolism
JAMA PATIENT PAGE The Journal of the American Medical Association VASCULAR DISEASE Pulmonary Embolism How pulmonary embolism occurs Pulmonary 3 The embolus obstructs artery a vessel in the lung and Lung pulmonary embolism (PE) is a blood clot that deprives tissue of blood. blocks the blood vessels supplying the lungs. The clot (embolus) most often comes from the leg veins A Embolus and travels through the heart to the lungs. When the blood clot lodges in the blood vessels of the lung, it may limit the Heart heart’s ability to deliver blood to the lungs, causing shortness of breath and chest pain, and, in serious cases, death. The US surgeon general estimates that 100 000 to 180 000 deaths occur from PE each year in the United States and identifies PE 2 The embolus travels through as the most preventable cause of death among hospitalized bloodstream and heart into patients. The January 9, 2013, issue of JAMA contains an Inferior the vessels of the lung. vena cava article about management of PE. TO 1 A blood clot forms in HEART RISK FACTORS a vein and breaks free from the vessel wall. • Genetic and acquired tendencies to develop blood clots • Free blood clot Pregnancy; use of birth control pills or hormone therapy Femoral Vein (embolus) • Obesity vein • Smoking Blood clot • Cancer • Medical illnesses including heart disease, lung disease, and kidney disease Valve • Older age • Recent surgery, trauma, hospitalization, or prolonged bed rest SIGNS AND SYMPTOMS FOR MORE INFORMATION • Shortness of breath • Palpitations • American Venous Forum • Chest discomfort • Dizziness and fainting www.veinforum.org • Coughing up blood • Leg swelling and discomfort • North American Thrombosis Forum www.NATFonline.org TREATMENT INFORM YOURSELF Anticoagulants (commonly called blood thinners) are the main treatment for pulmonary embolism and work by preventing new blood clots from forming while the To find this and previous JAMA body breaks down the pulmonary embolism. -
The Cholesterol Emboli Syndrome in Atherosclerosis
Curr Atheroscler Rep (2013) 15:315 DOI 10.1007/s11883-013-0315-y CORONARY HEART DISEASE (JA FARMER, SECTION EDITOR) The Cholesterol Emboli Syndrome in Atherosclerosis Adriana Quinones & Muhamed Saric # Springer Science+Business Media New York 2013 Abstract Cholesterol emboli syndrome is a relatively rare, artery (typically the aorta) embolize to small or medium caliber but potentially devastating, manifestation of atherosclerotic arteries, which then results in end-organ damage secondary to disease. Cholesterol emboli syndrome is characterized by either mechanical obstruction and/or inflammatory response waves of arterio-arterial embolization of cholesterol crystals [1•]. This syndrome has also been referred as atheroembolism, and atheroma debris from atherosclerotic plaques in the atheromatous embolization syndrome, cholesterol crystal em- aorta or its large branches to small or medium caliber bolization and cholesterol embolization syndrome [2]. arteries (100–200 μm in diameter) that frequently occur It is important to emphasize that CES is a separate entity after invasive arterial procedures. End-organ damage is from a more common phenomenon of another arterio- due to mechanical occlusion and inflammatory response in arterial embolization syndrome, namely arterio-arterial the destination arteries. Clinical manifestations may include thromboembolism, in which a thrombus overlying an ather- renal failure, blue toe syndrome, global neurologic deficits omatous plaque breaks loose and travels distally to occlude and a variety of gastrointestinal, ocular and constitutional large-caliber downstream arteries [3]. In arterio-arterial signs and symptoms. There is no specific therapy for cho- thromboembolism, there is typically a sudden release of lesterol emboli syndrome. Supportive measures include thrombi, resulting in acute ischemia of a target organ. -
Unprotected Carotid Artery Stenting in Symptomatic Patients with High-Grade Stenosis: Results and Long-Term Follow-Up in a Single- ORIGINAL RESEARCH Center Experience
Published March 15, 2012 as 10.3174/ajnr.A2951 Unprotected Carotid Artery Stenting in Symptomatic Patients with High-Grade Stenosis: Results and Long-Term Follow-Up in a Single- ORIGINAL RESEARCH Center Experience R. Oteros BACKGROUND AND PURPOSE: The use of cerebral protection during CAS is an extended practice. E. Jimenez-Gomez Paradoxically it is open to question because it can lead to potential embolic complications. The aim of this study was to evaluate the safety and efficacy of CASWPD in patients with severe symptomatic F. Bravo-Rodriguez carotid artery stenosis. J.J. Ochoa R. Guerrero MATERIALS AND METHODS: A prospective study was performed including 210 consecutive patients (201 symptomatic and 9 asymptomatic) with carotid artery stenosis Ͼ70%. All patients were treated F. Delgado by CASWPD. Angiographic results and neurologic complications were recorded during the procedure and within 30 days after it. All patients underwent clinical evaluation and Doppler sonography follow-up at 3, 6, and 12 months after the procedure. RESULTS: Two hundred twenty carotid arteries were treated. The average degree of stenosis was 88.9%. The procedure was successfully completed in 212 (96.4%) arteries. After stent placement, 98.6% of arteries showed no residual stenosis or Ͻ30%. Balloon angioplasty dilation before stent placement was performed in 16% of cases. During the 30-day periprocedural period, there were 3 major complications (1.4%), including 1 disabling ischemic stroke, 1 acute stent thrombosis, and 1 MI. The last 2 patients died from these complications. At 1-year follow-up 24 (12.8%) restenoses, 2 new ipsilateral strokes, 1 contralateral stroke, and 5 deaths (2.7%) had occurred. -
Chapter 6: Clinical Presentation of Venous Thrombosis “Clots”
CHAPTER 6 CLINICAL PRESENTATION OF VENOUS THROMBOSIS “CLOTS”: DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLUS Original authors: Daniel Kim, Kellie Krallman, Joan Lohr, and Mark H. Meissner Abstracted by Kellie R. Brown Introduction The body has normal processes that balance between clot formation and clot breakdown. This allows clot to form when necessary to stop bleeding, but allows the clot formation to be limited to the injured area. Unbalancing these systems can lead to abnormal clot formation. When this happens clot can form in the deep veins usually, but not always, in the legs, forming a deep vein thrombosis (DVT). In some cases, this clot can dislodge from the vein in which it was formed and travel through the bloodstream into the lungs, where it gets stuck as the size of the vessels get too small to allow the clot to go any further. This is called a pulmonary embolus (PE). This limits the amount of blood that can get oxygen from the lungs, which then limits the amount of oxygen that can be delivered to the rest of the body. How severe the PE is for the patient has to do with the size of the clot that gets to the lungs. Small clots can cause no symptoms at all. Very large clots can cause death very quickly. This chapter will describe the symptoms that are caused by DVT and PE, and discuss the means by which these conditions are diagnosed. What are the most common signs and symptoms of a DVT? The symptoms that are caused by DVT depend on the location and extent of the clot. -
Brachial Artery Embolus Mimicking Acute Stroke Christine Holmstedt and Marc Chimowitz Neurology 2011;76;E86-E87 DOI 10.1212/WNL.0B013e3182190cc0
RESIDENT & FELLOW SECTION E-Pearl: Section Editor Brachial artery embolus mimicking acute Mitchell S.V. Elkind, MD, MS stroke Christine Holmstedt, DO PEARL paroxysmal atrial fibrillation, hypertension, dyslipi- Marc Chimowitz, • Limb arterial embolism should be considered in demia, congestive heart failure, and coronary artery MBChB the differential diagnosis of acute monoparesis disease. The patient was not anticoagulated because because the diagnosis may be missed if the of a recent gastrointestinal bleeding episode. other typical manifestations of this presentation The emergency department physician diagnosed Address correspondence and (pain, pallor, pulselessness, sensory loss, and acute stroke and requested a telemedicine consulta- reprint requests to Dr. Christine tion. The patient’s blood pressure was 160/70 mm Holmstedt, Harborview Office coolness of the arm) are overlooked. Although Tower, 19 Hagwood Ave., MSC the rapid identification of acute ischemic stroke Hg, and a rhythm strip demonstrated normal sinus 805, Medical University of South rhythm at 80 beats per minute. On neurologic exam- Carolina, Charleston, SC 29464 is essential to the timely delivery of thrombolyt- [email protected] ics, care must be taken to obtain the relevant ination, the right upper extremity strength revealed history and to ensure that important signs are no effort against gravity with some preserved not missed whether the evaluation of the pa- strength in wrist and finger extension. The patient tient is done at the bedside or by telemedicine. could not localize touch on the right arm. Findings • Rapid and accurate diagnosis of ischemic stroke from the remainder of the neurologic examination, is essential for timely and appropriate treatment including speech and language, cranial nerves, coor- with thrombolytic therapy. -
Atraumatic Ischaemic Myelopathy
Paraplegia 19 (1981) 352-362 0031-1 758/8 1/006003 5 2 $02.00 © 1981 International Medical Society of Paraplegia ATRAUMATIC ISCHAEMIC MYELOPATHY By L. S. KEWALRAMANI, M.D., M.S. Orth. and R. S. R. KATTA, M.D. Louisiana Rehabilitation Institute, LSU School of Medicine New Orleans, Louisiana and Baylor College of Medicine, Houston, Texas Abstract. Significant and permanent neurological deficit due to ischaemic myelopathy continues to occur in 5-10 per cent of patients following surgery on the thoracic aorta for aneurysms, coarctation and lacerations, and following corrective surgery for scoliosis. Clinical features, patterns of neurological deficit, management and outcome in 29 patients with atraumatic ischaemic myelopathy following surgery on the aorta, aortocoronary bypass and cardiogenic shock, will be presented. Pertinent literature on the subject will also be reviewed. Key words: Secondary (non-traumatic neurological) ischaemic myelopathy; Aortic injury; Aortic aneurysms; Aortocoronary bypass surgery. Introduction INFARCTION of the spinal cord has been considered to be rare when compared with cerebral infarction (Garland et at., 1966) which may be due to the fact that the frequency of arteriosclerotic changes in major spinal arteries occur in 2·2-10 per cent of cases compared with cerebrovascular arteriosclerotic changes in 39 per cent of the population (Jellinger, 1967). Although Bastian in 1910 was firstto suggest that spinal cord softening might be a consequence of vascular occlusion but for several years the number of well documented cases of ischaemic myelopathy remained small and often anecdotal with syphilitic vasculitis. There continued to be limited interest in the spinovascular syndromes until neurological deficitfollowing surgery on the thoracic aorta brought into sharp focus the role of vascular occlusions and ischaemic injury to the spinal cord. -
A Mechanistic Model for Atherosclerosis and Its Application to the Cohort of Mayak Workers
RESEARCH ARTICLE A mechanistic model for atherosclerosis and its application to the cohort of Mayak workers Cristoforo Simonetto1*, Tamara V. Azizova2, Zarko Barjaktarovic1, Johann Bauersachs3, Peter Jacob1¤, Jan Christian Kaiser1, Reinhard Meckbach1, Helmut SchoÈ llnberger1, Markus EidemuÈ ller1 1 Helmholtz Zentrum MuÈnchen, Department of Radiation Sciences, Neuherberg, Germany, 2 Southern Urals Biophysics Institute, Ozyorsk, Chelyabinsk Region, Russia, 3 Hannover Medical School, Department of Cardiology and Angiology, Hannover, Germany a1111111111 a1111111111 ¤ Current address: RADRISK, Schliersee, Germany * [email protected] a1111111111 a1111111111 a1111111111 Abstract We propose a stochastic model for use in epidemiological analysis, describing the age- dependent development of atherosclerosis with adequate simplification. The model features OPEN ACCESS the uptake of monocytes into the arterial wall, their proliferation and transition into foam Citation: Simonetto C, Azizova TV, Barjaktarovic Z, cells. The number of foam cells is assumed to determine the health risk for clinically relevant Bauersachs J, Jacob P, Kaiser JC, et al. (2017) A events such as stroke. In a simulation study, the model was checked against the age-depen- mechanistic model for atherosclerosis and its dent prevalence of atherosclerotic lesions. Next, the model was applied to incidence of ath- application to the cohort of Mayak workers. PLoS ONE 12(4): e0175386. https://doi.org/10.1371/ erosclerotic stroke in the cohort of male workers from the Mayak nuclear facility in the journal.pone.0175386 Southern Urals. It describes the data as well as standard epidemiological models. Based on Editor: Xianwu Cheng, Nagoya University, JAPAN goodness-of-fit criteria the risk factors smoking, hypertension and radiation exposure were tested for their effect on disease development. -
University of Illinois, December 2003
Case #1 Case Presented by Virginia C. Fiedler, MD, Michelle Bain, MD and Alexander L. Berlin, MD History of Present Illness: This 9-year-old African American girl presented with hair shedding and patchy hair loss since infancy. Additionally, her hair has been brittle. Her scalp is comfortable, without pruritus. The patient’s mother has also noticed deviations of multiple finger joints since the age of 3 along with more recent similar changes in toe joints. These changes are not associated with pain or joint swelling. The patient denies decreased body sweating, but she does note increased sweating in the areas of scalp hair loss. Past Medical History: Febrile seizures as a child Multiple finger and toe joint deviations starting at 3 years of age History of ankle deformities treated with braces for 2 years Medications: None Allergies: No known drug allergies Family History: No history of autoimmune or other skin disorders; no joint abnormalities Social History: Patient is a 4th grade student and is doing well in school Review of Systems: Denies visual problems or arthralgias Diet is adequate for protein Physical Examination: The patient had patchy alopecia that was most pronounced in the ophiasis distribution and also involved the vertex. The affected areas had miniaturized hair follicles. Hair pull test was positive for 5-6 hairs in catagen and telogen phases. Ears were not low-set. There was an increased distance between the nose and the upper lip, and the philtrum was difficult to appreciate. The patient had retained deciduous teeth, as well as hypodontia and partial anodontia. -
Guidelines for the Use of Echocardiography in the Evaluation of a Cardiac Source of Embolism
ASE GUIDELINES AND STANDARDS Guidelines for the Use of Echocardiography in the Evaluation of a Cardiac Source of Embolism Muhamed Saric, MD, PhD, FASE, Chair, Alicia C. Armour, MA, BS, RDCS, FASE, M. Samir Arnaout, MD, Farooq A. Chaudhry, MD, FASE, Richard A. Grimm, DO, FASE, Itzhak Kronzon, MD, FASE, Bruce F. Landeck, II, MD, FASE, Kameswari Maganti, MD, FASE, Hector I. Michelena, MD, FASE, and Kirsten Tolstrup, MD, FASE, New York, New York; Durham, North Carolina; Beirut, Lebanon; Cleveland, Ohio; Aurora, Colorado; Chicago, Illinois; Rochester, Minnesota; and Albuquerque, New Mexico Embolism from the heart or the thoracic aorta often leads to clinically significant morbidity and mortality due to transient ischemic attack, stroke or occlusion of peripheral arteries. Transthoracic and transesophageal echo- cardiography are the key diagnostic modalities for evaluation, diagnosis, and management of stroke, systemic and pulmonary embolism. This document provides comprehensive American Society of Echocardiography guidelines on the use of echocardiography for evaluation of cardiac sources of embolism. It describes general mechanisms of stroke and systemic embolism; the specific role of cardiac and aortic sour- ces in stroke, and systemic and pulmonary embolism; the role of echocardiography in evaluation, diagnosis, and management of cardiac and aortic sources of emboli including the incremental value of contrast and 3D echocardiography; and a brief description of alternative imaging techniques and their role in the evaluation of cardiac sources of emboli. Specific guidelines are provided for each category of embolic sources including the left atrium and left atrial appendage, left ventricle, heart valves, cardiac tumors, and thoracic aorta. In addition, there are recommen- dation regarding pulmonary embolism, and embolism related to cardiovascular surgery and percutaneous procedures. -
Mechanisms of Thrombosis
Mechanisms of Thrombosis Maureane Hoffman, MD, PhD Professor of Pathology Thrombosis • Formation of a blood clot in an artery or vein of a living person • Arterial thrombosis denies oxygen and nutrition to an area of the body – Thrombosis of an artery leading to the heart causes a myocardial infarction – Thrombosis of an artery leading to the brain causes a stroke • Acute arterial thrombosis often results from the deposition of atherosclerotic material in the wall of an artery, which gradually narrows the channel, precipitating clot formation Thrombosis • Extends into vessel without blocking it completely - mural thrombus • Blocks it completely - occlusive thrombus • Extends along the blood vessel - propagative thrombus Thrombosis • Venous thrombosis blocks return of deoxygenated blood to the heart • Venous thrombosis is quite common in the lower extremities, but can also occur in the upper extremeties • Symptoms include swelling, bluish discoloration and pain. • The most feared complication of venous thrombosis is pulmonary embolism Pulmonary Emboli Lines of Zahn in a pulmonary embolus Is it thrombus or post-mortem clot? • Thrombus adheres to the vessel wall • May be red, white, or mixed • Is crumbly and layered Small pulmonary emboli Thrombosis in the Aorta What Causes Thrombosis? Virchow’s Triad: Stasis Vascular Injury Hypercoagulability Vascular Injury endothelial cell TF TF VIIa Hypercoagulability The coagulant/anticoagulant proteins and the cells each play a role Evolution of the Paradigm Old: Hypercoagulable State = Systemic