Skin and Soft Tissue Infections in the ED Cellulitis Cellulitis
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Complete Healing of Venous Leg Ulcer Using a Collagen Based Dressing a Case Report
Case Report Journal of Surgical Techniques and Procedures Published: 30 Jul, 2018 Complete Healing of Venous Leg Ulcer Using a Collagen Based Dressing a Case Report Dumont Isabelle1#, Caillava Celine2#, Dupoiron Stephanie2, Guillemin Yannis2## and Gouze Jean Noel2*## 1Department of Foot and Ankle Surgery, Center of the Foot Ransart, Belgium 2Department of Research and Development, Genbiotech, France #Dumont Isabelle and Caillava Celine Contributed Equally to this Work ##Guillemin Yannis and Gouze Jean Noel are Co-senor Authors Abstract Venous Leg Ulceration (VLU) is a common pathology which affects patients at any age. Ulcers are characterized by long-term healing, pain and frequent recurrence despite adherence to standard of care resulting in time consuming and costly treatments. Here, the authors describe the case of a diabetic, 63 years old male suffering from venous insufficiency and presenting a distal leg ulcer. The ulcer was treated using GBT013 device, a new biocompatible and biodegradable tri-dimensional collagen based matrix. GBT013 seems to be well integrated to the healing tissues and well tolerated. No complication or pain was reported during treatment. Complete healing was obtained within 36 days with no recurrence to date despite a context of stasis dermatitis. Keywords: Venous leg ulcer; Collagen dressing; Tri-dimensional matrix; Wound healing Abbreviations DFU: Diabetic Foot Ulcer; VLU: Venous Leg Ulcer Introduction Venous Leg Ulcers (VLUs) are open lesions of the lower extremities caused by venous disease. OPEN ACCESS Risk factors include all factors susceptible to increase pressure within vessels (e.g., obesity, immobility, thrombosis, varicose veins, and trauma) [1-3]. They are more common in women *Correspondence: and older people and represent 60% to 80% of leg ulcers [4-7]. -
Pilonidal Disease
Pilonidal Disease What is pilonidal disease and what causes it? Pilonidal disease is a chronic infection of the skin in the region of the buttock crease (Figure 1). The condition results from a reaction to hairs embedded in the skin, commonly occurring in the cleft between the buttocks. The disease is more common in men than women and frequently occurs between puberty and age 40. It is also common in obese people and those with thick, stiff body hair. Figure 1: Pilonidal disease is a chronic skin infection in the buttock crease area. Two small openings are shown (A). What are the symptoms? Symptoms vary from a small dimple to a large painful mass. Often the area will drain fluid that may be clear, cloudy or bloody. With infection, the area becomes red, tender, and the drainage (pus) will have a foul odor. The infection may also cause fever, malaise, or nausea. There are several common patterns of this disease. Nearly all patients have an episode of an acute abscess (the area is swollen, tender, and may drain pus). After the abscess resolves, either by itself or with medical assistance, many patients develop a pilonidal sinus. The sinus is a cavity below the skin surface that connects to the surface with one or more small openings or tracts. Although a few of these sinus tracts may resolve without therapy, most patients need a small operation to eliminate them. A small number of patients develop recurrent infections and inflammation of these sinus tracts. The chronic disease causes episodes of swelling, pain, and drainage. -
Clinical Manifestations and Management of Livedoid Vasculopathy
Clinical Manifestations and Management of Livedoid Vasculopathy Elyse Julian, BS,* Tania Espinal, MBS,* Jacqueline Thomas, DO, FAOCD,** Nason Rouhizad, MS,* David Thomas, MD, JD, EdD*** *Medical Student, 4th year, Nova Southeastern University College of Osteopathic Medicine, Ft. Lauderdale, FL **Assistant Professor, Nova Southeastern University, Department of Dermatology, Ft. Lauderdale, FL ***Professor and Chairman of Surgery, Nova Southeastern University, Ft. Lauderdale, FL Abstract Livedoid vasculopathy (LV) is an extremely rare and distinct hyalinizing vascular disease affecting only one in 100,000 individuals per year.1,2 Formerly described by Feldaker in 1955 as livedo reticularis with summer ulcerations, LV is a unique non-inflammatory condition that manifests with thrombi formation and painful ulceration of the lower extremities.3 Clinically, the disease often displays a triad of livedo racemosa, slow-healing ulcerations, and atrophie blanche scarring.4 Although still not fully understood, the primary pathogenic mechanism is related to intraluminal thrombosis of the dermal microvessels causing occlusion and tissue hypoxia.4 We review a case in which the patient had LV undiagnosed and therefore inappropriately treated for more than 20 years. To reduce the current average five-year period from presentation to diagnosis, and to improve management options, we review the typical presentation, pathogenesis, histology, and treatment of LV.4 Upon physical exam, the patient was found to have the patient finally consented to biopsy. The ACase 62-year-old Report Caucasian male presented in an a wound on the right medial malleolus measuring pathology report identified ulceration with fibrin assisted living facility setting with chronic, right- 6.4 cm x 4.0 cm x 0.7 cm with moderate serous in vessel walls associated with stasis dermatitis lower-extremity ulcers present for more than 20 exudate, approximately 30% yellow necrosis characterized by thick-walled capillaries and years. -
Cellulitis (You Say, Sell-You-Ly-Tis)
Cellulitis (you say, sell-you-ly-tis) Any area of skin can become infected with cellulitis if the skin is broken, for example from a sore, insect bite, boil, rash, cut, burn or graze. Cellulitis can also infect the flesh under the skin if it is damaged or bruised or if there is poor circulation. Signs your child has cellulitis: The skin will look red, and feel warm and painful to touch. There may be pus or fluid leaking from the skin. The skin may start swelling. The red area keeps growing. Gently mark the edge of the infected red area How is with a pen to see if the red area grows bigger. cellulitis spread? Red lines may appear in the skin spreading out from the centre of the infection. Bad bacteria (germs) gets into broken skin such as a cut or insect bite. What to do Wash your hands before and Cellulitis is a serious infection that needs to after touching the infected area. be treated with antibiotics. Keep your child’s nails short and Go to the doctor if the infected area is clean. painful or bigger than a 10 cent piece. Don’t let your child share Go to the doctor immediately if cellulitis is bath water, towels, sheets and near an eye as this can be very serious. clothes. Make sure your child takes the antibiotics Make sure your child rests every day until they are finished, even if and eats plenty of fruit and the infection seems to have cleared up. The vegetables and drinks plenty of antibiotics need to keep killing the infection water. -
Outcome of Venous Stasis Ulceration When Complicated by Arterial Occlusive Disease
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Eur J Vasc Endovasc Surg 24, 249±254 (2002) doi:10.1053/ejvs.2002.1650, available online at http://www.idealibrary.com on Outcome of Venous Stasis Ulceration when Complicated by Arterial Occlusive Disease W. T. Bohannon, R. B. McLaffertyÃ, S. T. Chaney, M. A. Mattos, L. A. Gruneiro, D. E. Ramsey and K. J. Hodgson Division Vascular Surgery, Department of Surgery, Southern Illinois University, School of Medicine, Springfield, Illinois, U.S.A. Objective: to report the outcome of patients with venous stasis ulceration (VSU) and severe arterial occlusive disease (AOD). Design: retrospective study. Methods: using the International Classification of Diseases (ICD-9), codes for VSU and AOD were cross-matched to identify patients from 1989 to 1999 at two tertiary hospitals. Entry into the study required the presence of a VSU and an ipsilateral procedure to improve AOD or major amputation during the same hospitalisation. Results: fourteen patients (15 extremities) with a mean age of 80 years (range: 47±93) were identified as having VSU and AOD. Mean duration of VSU up to the time of revascularisation or amputation was 6.4 years (range: 4 months±21 years). The mean number of VSUs per extremity was 2.1 and mean wound area was 71 cm2. Mean ankle±brachial index was 0.46 (range: 0.10±0.78). Nine extremities (60%) had a bypass procedure, 3 (20%) had an interventional procedure, 1 (0.6%) had a lumbar sympathectomy, and 2 (13%) had an amputation. -
Cutaneous Manifestations of Abdominal Arteriovenous Fistulas
Cutaneous Manifestations of Abdominal Arteriovenous Fistulas Jessica Scruggs, MD; Daniel D. Bennett, MD Abdominal arteriovenous (A-V) fistulas may be edema.1-3 We report a case of abdominal aortocaval spontaneous or secondary to trauma. The clini- fistula presenting with lower extremity edema, ery- cal manifestations of abdominal A-V fistulas are thema, and cyanosis that had been previously diag- variable, but cutaneous findings are common and nosed as venous stasis dermatitis. may be suggestive of the diagnosis. Cutaneous physical examination findings consistent with Case Report abdominal A-V fistula include lower extremity A 51-year-old woman presented to the emergency edema with cyanosis, pulsatile varicose veins, department with worsening lower extremity swelling, and scrotal edema. redness, and pain. Her medical history included a We present a patient admitted to the hospital diagnosis of congestive heart failure, chronic obstruc- with lower extremity swelling, discoloration, and tive pulmonary disease, hepatitis C virus, tobacco pain, as well as renal insufficiency. During a prior abuse, and polysubstance dependence. Swelling, red- hospitalization she was diagnosed with venous ness, and pain of her legs developed several years stasis dermatitis; however, CUTISher physical examina- prior, and during a prior hospitalization she had been tion findings were not consistent with that diagno- diagnosed with chronic venous stasis dermatitis as sis. Imaging studies identified and characterized well as neurodermatitis. an abdominal aortocaval fistula. We propose that On admission, the patient had cool lower extremi- dermatologists add abdominal A-V fistula to the ties associated with discoloration and many crusted differential diagnosis of patients presenting with ulcerations. Aside from obesity, her abdominal exam- lower extremity edema with cyanosis, and we ination was unremarkable and no bruits were noted. -
Doxium Has Been Proven to Be the Only Oral Agent Available for Delaying the Progression of Diabetic Retinopathy. It Has Also
Doxium has been proven to be the only oral agent available for delaying the progression of diabetic retinopathy. It has also shown benefits in chronic venous insufficiency and haemorrhoids. Product Indications Pack Size DOXIUM 500 Cases of microangiopathy including diabetic retinopathy, 30’s/box capsules. chronic venous insufficiency. As an adjuvant in the treatment of blister-pack Each cap. contains superficial thrombophlebitis, post-thrombotic syndrome, 500mg calcium oedema, stasis dermatitis, circulatory disturbances of dobesilate. arteriovenous origin or due to impaired microcirculation & haemorrhoidal syndrome. ACTIVE PRINCIPLE Calcium 2, 5 dihydroxybenzenesulfonate (Ca dobesilate, INN) PROPERTIES Doxium corrects capillary hyperpermeability and increases capillary resistance. It antagonises the effect of vasoactive substances (histamine, serotonin, bradykinin, prostaglandins and PAF), acts against collagen breakdown, reduces blood hyperviscosity, increases red cell flexibility, diminishes platelet hyperaggregation and improves lymphatic drainage. CONTRA-INDICATIONS No contra-indications known up to now. TOLERABILITY Doxium is particularly well tolerated, even when administered for long-term therapy. It is not toxic; it is practically not metabolized in the body and does not impair hepatic or renal function in any way. It has no effect on arterial blood pressure, blood coagulation or glucose and lipid metabolisms. Doxium has no teratogenic effects and does not cross the placental barrier. Like most drugs, it should not be administered during the first 3 months of pregnancy. Numerous published clinical trials, totaling over 5000 cases, show that the incidence of undesirable side effects is extremely low (3.4%). These usually involve slight digestive disorders. PRESENTATIONS DOXIUM 500, capsules containing 500mg calcium dobesilate. . -
Skin Disease and Disorders
Sports Dermatology Robert Kiningham, MD, FACSM Department of Family Medicine University of Michigan Health System Disclosures/Conflicts of Interest ◼ None Goals and Objectives ◼ Review skin infections common in athletes ◼ Establish a logical treatment approach to skin infections ◼ Discuss ways to decrease the risk of athlete’s acquiring and spreading skin infections ◼ Discuss disqualification and return-to-play criteria for athletes with skin infections ◼ Recognize and treat non-infectious skin conditions in athletes Skin Infections in Athletes ◼ Bacterial ◼ Herpetic ◼ Fungal Skin Infections in Athletes ◼ Very common – most common cause of practice-loss time in wrestlers ◼ Athletes are susceptible because: – Prone to skin breakdown (abrasions, cuts) – Warm, moist environment – Close contacts Cases 1 -3 ◼ 21 year old male football player with 4 day h/o left axillary pain and tenderness. Two days ago he noticed a tender “bump” that is getting bigger and more tender. ◼ 16 year old football player with 3 day h/o mildly tender lesions on chin. Started as a single lesion, but now has “spread”. Over the past day the lesions have developed a dark yellowish crust. ◼ 19 year old wrestler with a 3 day h/o lesions on right side of face. Noticed “tingling” 4 days ago, small fluid filled lesions then appeared that have now started to crust over. Skin Infections Bacterial Skin Infections ◼ Cellulitis ◼ Erysipelas ◼ Impetigo ◼ Furunculosis ◼ Folliculitis ◼ Paronychea Cellulitis Cellulitis ◼ Diffuse infection of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin – Triad of erythema, edema, and warmth in the absence of underlying foci ◼ S. aureus or S. pyogenes Erysipelas Erysipelas ◼ Superficial infection of the dermis ◼ Distinguished from cellulitis by the intracutaneous edema that produces palpable margins of the skin. -
Treatment Strategies for Patients with Lower Extremity Chronic Venous Disease (LECVD)
Evidence-based Practice Center Systematic Review Protocol Project Title: Treatment Strategies for Patients with Lower Extremity Chronic Venous Disease (LECVD) Project ID: DVTT0515 Initial publication date if applicable: March 7, 2016 Amendment Date(s) if applicable: May 6th, 2016 (Amendments Details–see Section VII) I. Background for the Systematic Review Lower extremity chronic venous disease (LECVD) is a heterogeneous term that encompasses a variety of conditions that are typically classified based on the CEAP classification, which defines LECVD based on Clinical, Etiologic, Anatomic, and Pathophysiologic parameters. This review will focus on treatment strategies for patients with LECVD, which will be defined as patients who have had signs or symptoms of LE venous disease for at least 3 months. Patients with LECVD can be asymptomatic or symptomatic, and they can exhibit a myriad of signs including varicose veins, telangiectasias, LE edema, skin changes, and/or ulceration. The etiology of chronic venous disease includes venous dilation, venous reflux, (venous) valvular incompetence, mechanical compression (e.g., May-Thurner syndrome), and post-thrombotic syndrome. Because severity of disease and treatment are influenced by anatomic segment, LECVD is also categorized by anatomy (iliofemoral vs. infrainguinal veins) and type of veins (superficial veins, perforating veins, and deep veins). Finally, the pathophysiology of LECVD is designated typically as due to the presence of venous reflux, thrombosis, and/or obstruction. LECVD is common -
Final Report of the Lyme Disease Review Panel of the Infectious Diseases Society of America (IDSA)
Final Report of the Lyme Disease Review Panel of the Infectious Diseases Society of America (IDSA) INTRODUCTION AND PURPOSE In November 2006, the Connecticut Attorney General (CAG), Richard Blumenthal, initiated an antitrust investigation to determine whether the Infectious Diseases Society of America (IDSA) violated antitrust laws in the promulgation of the IDSA’s 2006 Lyme disease guidelines, entitled “The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America” (the 2006 Lyme Guidelines). IDSA maintained that it had developed the 2006 Lyme disease guidelines based on a proper review of the medical/scientifi c studies and evidence by a panel of experts in the prevention, diagnosis, and treatment of Lyme disease. In April 2008, the CAG and the IDSA reached an agreement to end the investigation. Under the Agreement and its attached Action Plan, the 2006 Lyme Guidelines remain in effect, and the Society agreed to convene a Review Panel whose task would be to determine whether or not the 2006 Lyme Guidelines were based on sound medical/scientifi c evidence and whether or not these guidelines required change or revision. The Review Panel was not charged with updating or rewriting the 2006 Lyme Guidelines. Any recommendation for update or revision to the 2006 Lyme Guidelines would be conducted by a separate IDSA group. This document is the Final Report of the Review Panel. REVIEW PANEL MEMBERS Carol J. Baker, MD, Review Panel Chair Baylor College of Medicine Houston, TX William A. Charini, MD Lawrence General Hospital, Lawrence, MA Paul H. -
Sepsis and Septic Shock: Endothelial Molecular Pathogenesis Associated with Vascular Microthrombotic Disease Jae C
Chang Thrombosis Journal (2019) 17:10 https://doi.org/10.1186/s12959-019-0198-4 REVIEW Open Access Sepsis and septic shock: endothelial molecular pathogenesis associated with vascular microthrombotic disease Jae C. Chang Abstract In addition to protective “immune response”, sepsis is characterized by destructive “endothelial response” of the host, leading to endotheliopathy and its molecular dysfunction. Complement activation generates membrane attack complex (MAC). MAC causes channel formation to the cell membrane of pathogen, leading to death of microorganisms. In the host, MAC also may induce channel formation to innocent bystander endothelial cells (ECs) and ECs cannot be protected. This provokes endotheliopathy, which activates two independent molecular pathways: inflammatory and microthrombotic. Activated inflammatory pathway promotes the release of inflammatory cytokines and triggers inflammation. Activated microthrombotic pathway mediates platelet activation and exocytosis of unusually large von Willebrand factor multimers (ULVWF) from ECs and initiates microthrombogenesis. Excessively released ULVWF become anchored to ECs as long elongated strings and recruit activated platelets to assemble platelet-ULVWF complexes and form “microthrombi”. These microthrombi strings trigger disseminated intravascular microthrombosis (DIT), which is the underlying pathology of endotheliopathy- associated vascular microthrombotic disease (EA-VMTD). Sepsis-induced endotheliopathy promotes inflammation and DIT. Inflammation produces inflammatory response -
Organ System % of Exam Content Diseases/Disorders
Organ System % of Exam Diseases/Disorders Content Cardiovascular 16 Cardiomyopathy Congestive Heart Failure Vascular Disease Dilated Hypertension Acute rheumatic fever Hypertrophic Essential Aortic Restrictive Secondary aneurysm/dissection Conduction Disorders Malignant Arterial Atrial fibrillation/flutter Hypotension embolism/thrombosis Atrioventricular block Cardiogenic shock Chronic/acute arterial Bundle branch block Orthostasis/postural occlusion Paroxysmal supraventricular tachycardia Ischemic Heart Disease Giant cell arteritis Premature beats Acute myocardial infarction Peripheral vascular Ventricular tachycardia Angina pectoris disease Ventricular fibrillation/flutter • Stable Phlebitis/thrombophlebitis Congenital Heart Disease • Unstable Venous thrombosis Atrial septal defect • Prinzmetal's/variant Varicose veins Coarctation of aorta Valvular Disease Patent ductus arteriosus Aortic Tetralogy of Fallot stenosis/insufficiency Ventricular septal defect Mitral stenosis/insufficiency Mitral valve prolapse Tricuspid stenosis/insufficiency Pulmonary stenosis/insufficiency Other Forms of Heart Disease Acute and subacute bacterial endocarditis Acute pericarditis Cardiac tamponade Pericardial effusion Pulmonary 12 Infectious Disorders Neoplastic Disease Pulmonary Acute bronchitis Bronchogenic carcinoma Circulation Acute bronchiolitis Carcinoid tumors Pulmonary embolism Acute epiglottitis Metastatic tumors Pulmonary Pulmonary nodules hypertension Croup Obstructive Pulmonary Cor pulmonale Influenza Disease Restrictive Pertussis Asthma Pulmonary