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Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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Adult-Gerontology Acute Care Practice Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Catherine Harris, Ph D, MBA, AGACNP, is an associate professor of graduate programs and a faculty in the Acute Care Nurse Practitioner Program at Thomas Jefferson University in Philadelphia. She earned her Ph D in nursing at the University of Pennsylvania and an MBA from Drexel University before becoming credentialed as an acute care nurse practitioner at Thomas Jefferson University in Philadelphia. Dr. Harris specializes in neurocritical care, having presented extensively on ischemic and hemorrhagic stroke. She has been a mentee for the Fellows of the American Association of Nurse Practitioner Mentorship Program and has won numerous research grants in neurocritical care and global health. | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Adult-Gerontology Acute Care Practice Guidelines Catherine Harris, Ph D, MBA, AGACNP Editor | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Copyright © 2020 Springer Publishing Company, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Springer Publishing Company, LLC, or authorization through payment of the appropriate fees to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400, fax 978-646-8600, info@copyright. com or on the Web at www. copyright. com. Springer Publishing Company, LLC 11 West 42nd Street New York, NY 10036 www. springerpub. com Acquisitions Editor : Suzanne Toppy Compositor : diacri Tech, Chennai ISBN: 978-0-8261-7004-0 e-book ISBN : 978-0-8261-7005-7 18 19 20 21 22 / 5 4 3 2 1 The author and the publisher of this Work have made every effort to use sources believed to be reliable to provide information that is accurate and compatible with the standards generally accepted at the time of publication. Because medical science is continually advancing, our knowledge base continues to expand. Therefore, as new information becomes available, changes in procedures become necessary. We recommend that the reader always consult current research and specific institutional policies before performing any clinical procedure. The author and publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers' use of, or reliance on, the information contained in this book. The publisher has no responsibility for the persistence or accuracy of URLs for external or third-party Internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Library of Congress Cataloging-in-Publication Data Names: Harris, Catherine AGACNP, editor. Title: Adult-gerontology acute care practice guidelines / [edited by] Catherine Harris, Ph D, MBA, AGACNP. Description: New York, NY : Springer Publishing Company, LLC, [2019] | Includes bibliographical references and index. Identifiers: LCCN 2019015624 |ISBN 9780826170040 |ISBN 9780826170057 (ebook) Subjects: LCSH: Geriatric nursing. |Intensive care nursing |Older people-Medical care. |Nurse practitioners. Classification: LCC RC954. A38 2019 |DDC 618. 97/0231-dc23 LC record available at https://lccn. loc. gov/2019015624 Contact us to receive discount rates on bulk purchases. We can also customize our books to meet your needs. For more information please contact: sales@springerpub. com Publisher's Note :New and used products purchased from third-party sellers are not guaranteed for quality, authenticity, or access to any included digital components. Printed in the United States of America. | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
To Matthew, My beautiful little boy, you are always in my heart, and I am so proud of you! Mom and Dad, Thank you for your encouragement and always being there for me. | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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vii Contents Contributors xi Reviewers xv Foreword Harrison Reed, MMS, PA-C xvii Preface xix Organization xxi What Is Different About This Book xxiii Acknowledgments xxv Introduction xxvii I. ACUTE CARE GUIDELINES BY SYSTEM 1. ENT Guidelines Conjunctivitis 3 Pharyngitis 5 Rhinosinusitis 8 2. Pulmonary Guidelines Acute Respiratory Distress Syndrome 11 Asthma 14 Chronic Obstructive Pulmonary Disease 17 Pleural Effusions 22 Pneumonia 24 Pulmonary Embolism 27 Restrictive Lung Disease 30 3. Cardiac Guidelines Acute Coronary Syndromes 35 Angina 40 Arrhythmias 43 Dyslipidemia 48 Heart Failure 50 Hypertension 55 Pericardial Effusions 57 Valvular Heart Disease 60 4. Gastrointestinal Guidelines Acute Abdomen 67 Cirrhosis 72 Drug-Induced Liver Injury 75 Gastroesophageal Reflux Disease 76 Gastrointestinal Bleeding 78 Hepatitis-Alcoholic 81 Hepatitis-Autoimmune 82 Hepatitis A 83Hepatitis B 84 Hepatitis C 85 Inflammatory Bowel Disease 86 Nonalcoholic Fatty Liver Disease 89 Pancreatitis 90 Peptic Ulcer Disease 93 5. Nephrology Guidelines Acute Kidney Injury 95 Benign Prostatic Hypertrophy 99 Chronic Kidney Disease 101 Hematuria 104 Hypercalcemia 107 Hyperkalemia 109 Hypermagnesemia 111 Hypernatremia 112 Hyperphosphatemia 115 Hypocalcemia 116 Hypokalemia 117 Hypomagnesemia 119 Hyponatremia 120 Hypophosphatemia 124 Metabolic Acidosis 125 Nephrolithiasis 127 Nephrotic Syndrome 129 Prostatitis 131 Pyelonephritis 133 Urinary Incontinence 135 Urinary Tract Infection 138 6. Neurology Guidelines Anoxic Brain Injury 141 Brain Death 142 Headaches 144 Intracerebral Hemorrhage 147 Ischemic Stroke/Cerebrovascular Accident 150 Contents Share: Adult Gerontology Acute Care Practice Guidelines- | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
viii Status Epilepticus 152 Transient Ischemia Attack 155 7. Targeted Temperature Management Guidelines Fever Management 157 Hypothermia or Targeted Temperature Management After Cardiac Arrest 160 8. Endocrine Guidelines Adrenal Insufficiency 165 Diabetes Mellitus—Type 1 167 Diabetes Mellitus—Type 2 170 Diabetic Ketoacidosis 175 Hyperglycemic Hyperosmolar State 177 Metabolic Syndrome 179 Pheochromocytoma 180 Prediabetes 181 Thyroid Disorder—Euthyroid Sick Syndrome 183 Thyroid Disorder—Hyperthyroidism 184 Thyroid Disorder—Hypothyroidism 186 Thyroid Disorder—Myxedema Coma 187 Thyroid Disorder—Thyroid Storm 188 9. Psychiatric Guidelines Bipolar Disorder 191 Major Depressive Disorder 194 Posttraumatic Stress Disorder 196 Schizophrenia 198 Substance Use Disorders 200 Psychiatric Patient Medical Clearance 201 10. Infection Guidelines Colitis: Infective 203 Encephalitis 206 Endocarditis: Infective 208 Influenza 212 Meningitis 214 Necrotizing Fasciitis 217 Osteomyelitis 218 Peritonitis 220 Systemic Inflammatory Response Syndrome (SIRS)/Bactermia/Sepsis 223 Septic Arthritis 227 Tuberculosis 230 11. Peripheral Vascular Guidelines Acute Limb Ischemia 235 Aortic Vessel Disease: Aneurysms of the Aorta 237 Carotid Artery Disease 239 Peripheral Artery Disease: Lower Extremity 242 Peripheral Artery Disease: Upper Extremity 243 Peripheral Vascular Disease 245 Thoracic Outlet Sydnrome 249 12. Hematology Guidelines Anemia 251 Bleeding Diatheses 254Coagulopathies 257 Deep Vein Thrombosis 258 Sickle Cell Crisis 261 13. Oncology Guidelines Brain/Central Nervous System Malignancies 265 Breast Cancer 266 Gastrointestinal Cancers: Colorectal Cancer 269 Gastrointestinal Cancers: Gastric Cancer 271 Gastrointestinal Cancers: Hepatic Cancer 273 Gastrointestinal Cancers: Pancreatic Cancer 275 Gynecologic Cancers: Cervical Cancer 276 Gynecologic Cancers: Endometrial Cancer 277 Gynecologic Cancers: Ovarian Cancer 279 Head and Neck Cancers 280 Leukemias: Acute Leukemias 281 Leukemias: Chronic Leukemias 284 Leukemias: Myelodysplastic Syndromes 287 Leukemias: Myeloproliferative Neoplasms 289 Lung Cancer 291 Lymphomas: Hodgkin Lymphoma 293 Lymphomas: Non-Hodgkin Lymphoma 294 Multiple Myeloma 296 Sarcoma 298 Skin Cancer 299 14. Immune System, Connective Tissue, and Joints Guidelines Back Pain 303 Compartment Syndrome of the Lower Leg 305 Joint Pain 308 Osteoarthritis 311 Rheumatoid Arthritis 312 Spondyloarthropathies 314 Systemic Lupus Erythematosus 315 Vasculitis-Variable Vessel 319 Vasculitis-Small Vessel 320 Vasculitis-Medium Vessel 323 Vasculitis-Large Vessel 324 15. Dermatology Guidelines Atopic Dermatitis 327 Cellulitis 329 Seborrheic Dermatitis 331 Stasis Dermatitis 333 16. Geriatric Guidelines Delirium 335 Dementia 338 Falls 340 Urinary Incontinence 343 17. Trauma Guidelines Chest Trauma 347 Penetrating Chest Injuries 349 Penetrating Intracranial Injuries 350 Shock 352 Spinal Cord Injuries 354 Traumatic Brain Injury 357Contents | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
ix II. PERIOPERATIVE CONSIDERATIONS 18. Preoperative Evaluation and Management Scope of Chapter 361 Considerations 361 Care Principles 362 Medication Management 364 19. Perioperative and Intraoperative Management Scope of Chapter 367Considerations 367 Care Principles 370 Medication Management 372 20. Postoperative Evaluation and Management Scope of Chapter 373 Outcomes 373 Wound Management 375 Medication Management 377 III. PROCEDURES Ankle-Brachial Index Measurement 381 Arterial Lines 383 Bone Marrow Aspiration and Biopsy 387 Bronchoscopy 391 Central Venous Access 394 Chest Tube Insertion 404 Chest Tube Removal 407 Digital Nerve Blocks 409 Extracorporeal Membrane Oxygenation 411 Endotracheal Intubation 415 Endotracheal Extubation 419 External Ventricular Drain 421 Intraosseous Vascular Access 423Long Leg Casting 425 Lumbar Puncture 429 Peripherally Inserted Central Catheter Placement 432 Reduction of the Ankles 435 Reduction of the Fingers 437 Reduction of the Hip 440 Reduction of the Patella 442 Reduction of the Shoulder 444 Splinting 446 Synovial Fluid Aspiration 451 Thoracentesis 454 Transpyloric Feeding Tube Placement 457 IV. SPECIAL TOPICS End-of-Life Considerations 461 Health Prevention and Screening 467 Hemodynamic Monitoring Devices 482Telemedicine in Acute Care 489 Transitional Care 493 APPENDIX Normal Laboratory Values 501 Index 515 Contents | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xi Contributors Dana A. Albinson, MSN, BSN, AGACNP Adult-Gerontology Acute Care Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Frank O. Amanze, MSN, AGACNP-BC, CFRN, CCRN, PHRN, NRP Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania M. Kamran Athar, MD Assistant Professor of Medicine and Neurological Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Ponrathi Athilingam, Ph D, RN, ACNP, FAANP, FHFSA Associate Professor, College of Nursing University of South Florida Tampa, Florida Asha Avirachen, MSN, BSN, AG, ACNP Adult-Gerontology Acute Care Nurse Practitioner Department of Neurosurgery, Hospital of University of Pennsylvania Philadelphia, Pennsylvania Suzanne Barron, MSN, RN, CRNP, FNP Adult and Gerontology Acute Care Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Karen A. Beaty, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas David Bergamo, MSPAS, PA-C, AAHIVS Physician Assistant Infectious Disease Associates and Christiana Care Health System Christiana, Delaware Amy Blake, MSN, FNP-BC Family Nurse Practitioner Team Health Hospitalist & Post Acute Care Wilmington, Delaware Ann E. Burke, MSN, CRNP, FNP-BC Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Dana Cafaro, MS, PA-C Associate Program Director & Assistant Professor Thomas Jefferson University Physician Assistant Program Atlantic City, New Jersey E. Mone ́e Carter-Griffin, DNP, RN, ACNP-BC Associate Chair for Advanced Practice Nursing University of Texas at Arlington Arlington, Texas Alexis Chettiar, Ph D, MSN, RN Director of Quality Improvement Center for Elders' Independence Oakland, California Christine M. Chmielewski, MS, CRNP, ANP-BC, CNN-NP Nephrology Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Kelly Cimino, MSN, RN, CRNP, AG ACNP-BC Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Jennifer Coates, DNP, MBA, ACNP-BC, ACNPC Critical Care Nurse Practitioner Drexel University Philadelphia, Pennsylvania Lisa Coco, MSN, CRNP, CDE Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Courtney Connolley, MSN Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Heather Warren Cook, MSN, RN, AGACNP-BC Acute Care Nurse Practitioner Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Contributors | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xii Jane S. Davis, DNP, MSN, BSN, CRNP University of Alabama at Birmingham Birmingham, Alabama Erin Michelle Dean, MS, PA-C, RD Physician Assistant Department of Surgical Oncology, MD Anderson Cancer Center Houston, Texas Michele De Castro, MSN, CRNP Nurse Practitioner Division of Hospital Medicine, Thomas Jefferson University Philadelphia, Pennsylvania Jingyi Deng, MSN, RN-BC, AGACNP-BC Cardiac Surgery Nurse Practitioner Lankenau Medical Center Philadelphia, Pennsylvania Jessica S. Everitt, Pharm D Assistant Professor University of Mississippi Medical Center Jackson, Mississippi Susan F. Galiczynski, MSN, RN, CRNP, CEN Nurse Practitioner Crozer-Chester Medical Center Philadelphia, Pennsylvania Alexis C. Geppner, MLS (ASCP), PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Bridget Gibson, CRNP, Adult Acute Care, MSN, BSN Neurocritical Care Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Debra Hain, Ph D, APRN, AGPCNP-BC, FAANP, FNKF Professor/Nurse Practitioner Florida Atlantic University, Chrisitne E. Lynn College of Nursing and Cleveland Clinic Florida, Department of Nephrology Boca Raton, Florida Catherine Harris, Ph D, MBA, AGACNP Associate Professor Thomas Jefferson University College of Nursing Philadelphia, Pennsylvania Carey Heck, Ph D, CRNP, AGACNP-BC, CCRN, CNRN Assistant Professor, Director, AGACNP Program Thomas Jefferson University, College of Nursing Philadelphia, Pennsylvania Shannon B. Holloway, MHS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas John Hurt, MPAS, PA-C Director of Clinical Education Samford University Physician Assistant Program Birmingham, Alabama Alicia John, MSN, RN, CNS Advanced Practice Provider Kingwood Medical Center Houston, Texas Cynae Johnson, DNP, MSN, WHNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Swetha Rani Kanduri, MD Assistant Professor of Medicine University of Mississippi Medical Center Jackson, Mississippi Kiffon M. Keigher, MSN, APN, ACNP-BC Program Manager, Acute Care Nurse Practitioner Advocate Aurora Health Park Ridge, Illinois Alison M. Kelley, MSN, AGACNP-BC Critical Care Nurse Practitioner Emory University Hospital Atlanta, Georgia Karthik Kovvuru, MD Assistant Professor of Medicine University of Mississippi Medical Center Jackson, Mississippi Kathryn Evans Kreider, DNP, APRN, FNP-BC, BC-ADM Assistant Professor of Nursing Duke University Durham, North Carolina Megan Krug, MHS, PA-C Physician Assistant Dana Farber Cancer Institute Boston, Massachusetts Monique Lambert, DNP, APN, ACNP-BC, FAANP Anesthesia Critical Care Northshoure University Health Care System Skokie, Illinois Sarah L. Livesay, DNP, RN, ACNP-BC, ACNS-BC, FNCS, FAHA Associate Professor Rush University, Department of Adult Health and Gerontological Nursing Chicago, Illinois Kristopher R. Maday, MS, PA-C Program Director, Associate Professor University of Tennessee Health Science Center Physician Assistant Program Memphis, Tennessee Shawn Mangan, MSN, RNFA, ANP-C, AGACNP-BC Acute Care Surgery/Trauma Intensive Care Unit Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Contributors | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xiii Amelita B. Marzan, MS, APRN, FNP-C, OCN Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Sijimol Mathew, MSN, ACNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Juan A. Medaura, MD Assistant Professor of Medicine University of Maryland Medical Center Baltimore, Maryland Heather H. Meissen, MSN, ACNP, CCRN, FCCM, FAANP Program Director NPPA Critical Care Residency Emory Healthcare Atlanta, Georgia Rose Milano, DNP, MS, BSN, RN, ACNP-BC Assistant Professor Rush University College of Nursing Chicago, Illinois Robin Miller, DNP, MPH, ACNP-BC Assistant Professor of Clinical Nursing Oregon Health & Science University Portland, Oregon Robin Miller, MSN, FNP-BC, AGACNP-BC Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Divya Monga, MD Division of Nephrology University of Mississippi Medical Center Jackson, Mississippi Madeleine Nguyen-Cao, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Karen Sheffield O'Brien, Ph D, RN, ACNP-BC Assistant Professor University of St. Thomas and Memorial Hermann Sugar Land Nurse Practitioner Houston, Texas Dominick Osipowicz, MSN, CRNP, AGACNP-BC Nurse Practitioner Christiana Care Health System Newark, Delaware Jennifer W. Parker, Ph D, MSN, BSN Acute Care Nurse Practitioner University of Pennsylvania Health System West Chester, Pennsylvania Joanne Elaine Pechar, MSN, ANP-BC, AGACNP-BC Acute Care Nurse Practitioner Department of Penn Orthopedics, Pennsylvania Hospital Philadelphia, Pennsylvania Cheryl Pfennig, MSN, RN, NP-C, AOCNP Advanced Practice Registered Nurse, Surgical Oncology MD Anderson Cancer Center Houston, Texas Allyson Price, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Rae Brana Reynolds, Ph D, RN, ACNP-BC Manager, Advanced Practice Providers MD Anderson Cancer Center Houston, Texas Monica Richey, MSN, ANP-BC Nurse Practitioner Northwell Health New York, New York Courtney Robb, MS, RN, CRNFA, FNP-C Nurse Practitioner MD Anderson Cancer Center Houston, Texas Allison Rusgo, MHS, MPH, PA-C Assistant Clinical Professor Drexel University Philadelphia, Pennsylvania Annamma Sam, Ph D, WHNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Leigh A. Samp, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Laura A. Santanna Lonergan, MHS, PA-C Physician Assistant Pennsylvania Hospital Philadelphia, Pennsylvania Syed Omar Shah, MD, MBA Assistant Professor of Neurology and Neurological Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Christina Shin, PA-C Physician Assistant Rush University Chicago, Illinois Ruth Anne Skinner, DNP, ACNP-BC, C-NP, CNRN ACNP Lead Faculty College of Nursing & Health Care Professions, Grand Canyon University Phoenix, Arizona Mary Rogers Sorey, MSN, RN, ACNP Assistant Professor Division of Nephrology, Vanderbilt University Medical Center Nashville, Tennessee Contributors | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xiv Cara M. Staley, MSN, RN-BC, AGACNP-BC Vascular Surgery Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Jerrad M. Stoddard, MS, MA, PA-C Physician Assistant Texas Oncology Round Rock, Texas Frances M. Stokes, DNP, RN, ACNP-BC, CMNL Nurse Practitioner Intensivist Austin, Texas Julie Stone, MSN, RN, ACNP-BC, BC-ADM Endocrinology Nurse Practitioner Ascension St. Vincent Heart Center Indianapolis, Indiana Siji Thomas, ACNP, OCN Acute Care Nurse Practitioner MD Anderson Cancer Center Houston, Texas Nicole Thomer, MSN, AG-ACNP Nurse Practitioner, Neuro Critcal Care Thomas Jefferson University Hospital Philadelphia, Pennsylvania Melissa Timmons, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Amber Tran, MSN, CRNP, FNP-BC Family Nurse Practitioner Department of Dermatology and Cutaneous Biology, TJU Philadelphia, Pennsylvania Fiona Unac, MN, NP, GDip AL&T Nurse Practitioner Radiology Department, Soldiers' Memorial Hospital Hastings, New Zealand Dawn Vanderhoef, Ph D, DNP, PMHNP, FAANP Assistant Professor and Academic Director Vanderbilt University School of Nursing Nashville, Tennessee Susan Varghese, MSN, RN, ANP-C Adult Nurse Practitioner MD Anderson Cancer Center Houston, Texas Valerie F. Villanueva, MSN, RN, FNP-BC Supervisor, Advanced Practice Providers MD Anderson Cancer Center GYNONC and Reproductive Medicine Houston, Texas Catherine Wells, DNP, ACNP, CNN-NP, FNKF Assistant Professor Division of Nephrology, University of Mississippi Medical Center Jackson, Mississippi Mary L. Wilby, Ph D, MSN, MPH, RN, CRNP, ANP-BC Assistant Professor, Nurse Practitioner Track Coordinator La Salle University Philadelphia, Pennsylvania Joseph Willmitch, MSPAS, PA-C, DFAAPA Director of Clinical Education University of Tennessee Health Science Center Physician Assistant Program Memphis, Tennessee Danielle Zielinski, MSN, BSN, RN, ACNP-BC Acute Care Nurse Practitioner Northwestern Medicine, Neurosurgery Chicago, Illinois Kim Zuber, MS, PAC Executive Director American Academy of Nephrology Pas Oceanside, California Contributors | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xv Reviewers M. Kamran Athar, MD Assistant Professor of Medicine and Neurological Surgery Thomas Jefferson University Philadelphia, Pennsylvania Ashley L. Barba, DNP, ANP Acute Care Nurse Practitioner Duke University Medical Center Durham, North Carolina Mark E. Baus, MSN, CRNP, RNFA Lead Orthopaedic Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Brennan Bowker, MHS, PA-C, CPAAPA Physician Assistant; Part-Time Clinical Assistant Professor of Physician Assistant Studies Yale New Haven Hospital Department of Surgery; Quinnipiac University Department of Physician Assistant Studies New Haven, Connecticut Theresa M. Campo, DNP, FNP-C, ENP-C, FAANP, FAAN Director of the Emergency Nurse Practitioner and Co-Director of the Family Nurse Practitioner Tracks, Associate Clinical Professor for the College of Nursing and Health Professions Drexel University College of Nursing and Health Professions Philadelphia, Pennsylvania Shawnna Cannaday, MSN, AGACNP, FNP-BC Acute Care Nurse Practitioner Department of Surgery, Surgical Oncology Jefferson University Physicians Department of Surgery, Hepato-Biliary-Pancreatic Surgery Philadelphia, Pennsylvania Dawn Carpenter, DNP, ACNP-BC, CCRN Coordinator, Adult-Gerontology Acute Care Nurse Practitioner Program University of Massachusetts Medical School Worcester, Massachusetts Nicole Cavaliere, MSN, AGACNP-BC Acute Care Nurse Practitioner Department of Surgery, Cardiothoracic Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Kathleen O. Chennell, MS, CNS, ACNP-BC, CCRN Adult-Gerontology Acute Care Nurse Practitioner Division of Nephrology, University of Cincinnati Cincinnati, Ohio Carolina Dimsdale Tennyson, DNP, ACNP-BC, AACC Nurse Practitioner, Clinical Associate Faculty Duke University School of Nursing Durham, North Carolina Patricia Galanis, MSN, CRNP Oncology Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Carey Heck, Ph D, CRNP, AGACNP-BC, CCRN, CNRN Assistant Professor, Director, AGACNP Program Thomas Jefferson University, College of Nursing Philadelphia, Pennsylvania Heather Hobbs, MSN, CRNP, AGACNP-BC Adult-Gerontology Acute Care Nurse Practitoner Department of Otolaryngology/Head & Neck Surgery, Thomas Jefferson University Hospital Philadelphia, Pennsylvania Robert Kirk, MSN, PMHNP-BC Psychiatric Nurse Practitioner University of Pennsylvania School of Nursing Philadelphia, Pennsylvania Stefanie La Manna, Ph D, MPH, APRN, FNP-C, AGACNP-BC Program Director for the Ph D/DNP/AGACNP Programs Nova Southeastern University Palm Beach Gardens, Florida Johannah Lebow, MSN, CRNP Oncology Nurse Practitioner University of Pennsylvania Health System Philadelphia, Pennsylvania Gail Ann Lis, DNP, ACNP-BC Professor, Graduate Chair Madonna University Livonia, Michigan Karen Bradley Lodge, MSN, CRNP Nurse Practitioner Reviewers | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xvi Northwest Internal Medicine Wydnmoor, Pennsylvania Mary Anne Mc Coy, Ph D, RN, ACNS, ACNP-BC Assistant Professor; Graduate Coordinator, AGACNP Specialty Wayne State University College of Nursing Detroit, Michigan Anne Bradley Mitchell, Ph D, MN, ANP-BC Assistant Professor of Nursing Jefferson University College of Nursing Philadelphia, Pennsylvania Dominick Osipowicz, MSN, CRNP, AGACNP-BC Nurse Practitioner Christiana Care Health System Newark, Delaware Jennifer W. Parker, Ph D, MSN, BSN Acute Care Nurse Practitioner University of Pennsylvania Health System West Chester, Pennsylvania Belbina Pereira, MSN Nephrology Nurse Practitioner Brooklyn Hospital Brooklyn, New York Marilyn Riley, Ph D, MSN, RN, APRN-BC, FNP NP Intensivist, Chief Nursing Officer Indiana University Health Indianapolis, Indiana Fred Rincon, MD, FACP Associate Professor of Medicine Thomas Jefferson University Philadelphia, Pennsylvania Tracy Setji, MD Associate Professor of Medicine Duke University Durham, North Carolina Jennifer Sheehan, MSN, CRNP, RNFA Nurse Practitioner Philadelphia VA Medical Center Philadelphia, Pennsylvania Benjamin Smallheer, Ph D, RN, ACNP-BC, FNP-BC, CCRN, CNE Assistant Professor of Nursing; Lead Faculty, Adult-Gerontology Acute Care NP Program Duke University School of Nursing Durham, North Carolina R. Shane Smith, MS, PA-C, EMT-P(NREMT), SFC (RET), US Army Trauma Surgery, Critical Care Ballad Health Systems, Milligan College Adjunct Faculty Johnson City, Tennessee Frances Stokes, DNP, RN, ACNP-BC, CMNL NP Intensivist St. Davids Medical Center Austin, Texas Kevin Tipton, MSN, CRNP Nurse Practitioner Lehigh Valley Hospital East Stroudsburg, Pennsylvania Mark Ubbens, MSN, CRNP, AG-ACNP-BC, PHRN Advanced Practice Chief, Trauma Surgery; Aquarium Medical Advisor, Ski Patroller Geisinger Medical Center, National Aquarium, Big Boulder Ski Patrol Danville, Pennsylvania; Baltimore, Maryland; Lake Harmony, Pennsylvania Karen L. Visich, MSN, RN, ANP-BC, AOCNP Nurse Practitioner, Genitourinary Oncology; Acting Associate Director of Nursing and Patient Education Rutgers Cancer Institute of New Jersey New Brunswick, New Jersey Michael Zychowicz, DNP, ANP, ONP, FAAN, FAANP MSN Program Director Duke University School of Nursing Durham, North Carolina Reviewers | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xvii Foreword There is no blueprint for acute care. The term itself is as broad and nebulous as the field it describes. Our patients reserve the right to present with any configuration of symptoms, to respond to our treat-ments when—and if—their bodies deem appropriate, and to decompensate without warning. Unlike the neat black and white lines of our textbooks, the reality of acute medicine is a messy gray. Of course, the geriatric population adds yet another wrin-kle to that hazy clinical landscape. The aging body owes no guarantees. Every tent pole of our didactic education—the classic triads and notorious eponyms—fades with the march of time. As a young clinician thrust into the halls of famous hospitals, surrounded by brilliant clinicians and the sickest patients, these lessons often landed with a painful thud. But over time I began to appreciate the subconscious calculations that registered as subtle sensations. The flutter in my chest that told me to double-check a detail, the tickle deep in my skull that said to investigate further, the lead weight in my gut that meant something was wrong. Of course, you cannot buy those instincts in any store. They are earned over the course of a career. In the meantime, you can insulate yourself with as much raw knowledge as pos-sible. And the book you are holding is a great start. The following pages provide a skeleton on which to build that knowledge. They are not a replacement for clinical acumen but a guide to help you find a deeper understanding of acute care. They are the concepts that should flash through your mind when your patients are at their most vulnerable, when time is precious, and when mistakes are costly. This book is authored by a coalition of talented physician assistants and nurse practitioners who have collaborated as we so often do in the clinical setting. They bring decades of col-lective experience and use it to distill the cloudy concoction of acute care into clear, manageable parts. They have fortified the material with threads of relevant wisdom for the geriatric patient. This is not the dense tome that will collect dust on your bookshelf. It is designed for utility, sleek and practical. It is the book I wish I would have had as a new clinician. So, while there is no blueprint for acute care, do not worry. You may have found the next best thing. Harrison Reed, MMS, PA-C Assistant Professor School of Medicine and Health Sciences George Washington University Washington, DC Foreword | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xix Preface The need for an acute care textbook has been growing. Although outpatient practices have long seen the value of uti-lizing advanced practice providers (APPs), the surge in acute care providers has been relatively recent. I remember when I was a registered nurse back in the 1990s, I had no idea there was such a role as a nurse practitioner or a physician assistant in the hospital, despite the fact they have been around since the 1960s! I was immediately fascinated and intrigued by the role of APPs. It was not long before I found myself enrolled in a nurse practitioner program. When I graduated, I was one of the first nurse practitioners on the neurosurgery service in the facility where I practiced. The service appreciated the help, but they did not really know what to do with me. It took many months for me to garner the trust of the surgeons, and to show them the true capacity of what APPs could do and how we could really become essential parts of the team. APPs have come a long way over the years. I have seen the role of nurse practitioners and physician assistants expand tremendously since I first began practicing in this role. I have seen the negative terms to describe us, such as midlevels, physician extenders, and helpers, evolve into advance prac-tice providers. I have also seen collaborative growth and mutual respect grow between nurse practitioners and physician assistants, arelationship that was previously more isolated. I respect my physician assistant colleagues, and, as a nurse practitioner, I have learned quite a bit from their struggles with role and identity. I find that I personally relate to these struggles in how I practice and how I see my own role on the healthcare team. I have also learned the value of combining resources and focusing on how we are similar, rather than different. It was important to write this textbook with physician assistants and nurse practitioners together. Both groups have immense value to provide each other in terms of knowledge, resources, and experience. Finally, it was essential to write this textbook because it fills a void in the marketplace. Countless times my students have asked if there were an acute care textbook that they could use. I have tried many different textbooks, but either I found them to be too cumbersome or the information provided was just too scant. This final iteration of the textbook came about as a result of those experiences and discussions with students about what they needed and they wanted. We all suffer from information overload and overwhelm, so the focus of this textbook was to provide the minimum of what new graduate students need to know in order to be competent when they start practice. Catherine Harris Preface | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xxi Organization This book is organized into four major sections. Part I: Acute Care Guidelines by System—In Part I, the advanced practice provider (APP) is exposed to the most common medical conditions organized by system. Although it is by no means comprehensive or inclusive of every medical condition, the section is meant to provide APP students with an overview of very common medical conditions that they should focus on during their studies. In my teachings, I have found students tend to gravitate toward understanding the “zebras” in medicine, or those conditions that are unusual, instead of diagnosing common problems or unusual variants of common problems. This phenomenon might have to do with the common practice of testing on zebras or the student perception that we (as academic institutions) are out to trick them on a test. By not introducing zebras into the context of this book, the students can maintain focus on the most common disease states. Part II: Perioperative Considerations—Part II contains an operative overview. Again, this section is not a compre-hensive review of the operating room, but it does provide APP students an overview of what they should know regard-less of where they work. In the acute care setting, operativeprocedures are very common. It does not matter if acute care practitioners work directly or indirectly with patients in the perioperative period. A review of the common issues is mandatory. Part III: Procedures—Not all APPs will perform proce-dures, but students frequently feel a sense of accomplish-ment in being able to do something tangible. It is difficult to measure the progress of one's own critical thinking, but if a student can perform a procedure, his or her confidence level goes up quickly. In this section, some of the more common procedures are listed. Part IV: Special Topics—There are many issues that we will deal with as APPs; however, these issues do not all fall neatly into predefined categories. This section was created for select topics that could not be defined by systems but were equally important to address. These topics include end-of-life issues, health promotion, hemodynamic monitoring devices, telemedicine, and transitions of care. All APPs will deal with these issues during the course of their careers. These top-ics will also continue to evolve as we conduct more research and clinical studies and as technology improves. Organization | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xxiii What Is Different About This Book This book was created for advanced practice provider (APP) students in the acute care setting. In talking to students about their wants and needs in a textbook, I found students were not able to absorb and assimilate information in heavy, dense textbooks that we had been using. I also found myself telling my students not to bother with a large portion of the text-book because it was not immediately relevant to their basic knowledge. Students struggled to understand what to focuson and what they needed to know versus what was nice to know. No one can memorize everything they need to know about medicine. As students specialize in various fields, they will learn in-depth information about their specialties that is beyond the scope of this book. However, there is a body of knowledge that every APP should know, and I have done my best to include those topics in this book. What Is Different About This Book | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xxv Acknowledgments I have so many people to acknowledge in the creation of this textbook, particularly Dr. Ksenia Zukowsky, Dr. Carey Heck, and Dr. Jack Jallo. Dr. Zukowsky saw so much poten-tial in my plans. She pushed me to do things I was scared to do, and she made them seem possible. Her incredible stories have inspired me over the years, and she remains a powerful influence in my life. Dr. Heck has been an incredible colleague. As the direc-tor of the Acute Care Nurse Practitioner Program at Thomas Jefferson University, she has entertained my “big” ideas and helped me implement them. She has been a rock of support and has contributed massively to the publication of this book as well as the profession. Dr. Jallo has been my main physician support over the years in neurocritical care and neurosurgery. He never told me something could not be done, and he has made me believe that more was always possible. I want to acknowledge all the people who contributed to my growth as a nurse and an academic, especially Dr. Bob Hess. Dr. Hess knew me as a little girl. He was my neighboracross the street. Then, he was my teacher when I went to undergraduate nursing school at the University of Pennsyl-vania. Then he became my employer when I picked up extra time doing some editing work at the nursing magazine that he edited. Finally, he became my colleague and friend who encouraged me to keep rising through the ranks. Of course, I would not be the clinician, academic, and nurse I am today without my students, fellow faculty, friends, and family. I want to express my gratitude to so many peo-ple, but it is not possible to list them all here. From my first nursing job to where I am today, I am thankful for everyone in my life who has taught me so much. It has been an absolute pleasure to work with Springer Publishing Company. I worked most closely with Suzanne Toppy. Her talent, expertise, and encouragement were the guiding light for me through this entire process. I need to acknowledge all the work done by the edit-ing team. What you produced is absolutely amazing. I really appreciate everything you have done in the editorial process. Acknowledgments | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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xxvii Introduction Information Overload No book can serve all the needs of students, nor should that be the goal. This book was specifically designed to provide a foundation of basic information about acute care that stu-dents or any advanced practice provider (APP) should know about a body system. Acute care is defined as treatment that is received in the short term for an injury, emergency, or episode of illness. Acute care can be delivered in the hos-pital setting, EDs, or even outpatient clinics and includes a vast array of conditions and issues. However, patients come to the acute care setting with chronic problems as well that APPs need to address, and the table of contents was developed with this in mind. The table of contents is divided into four parts to accommodate the large scope of acute care. In Part I, the contents are arranged by body system and include the most commonly encountered diseases and conditions that are seen in acute care. In Part II, perioperative considerations are included because surgery is often the main reason for hos-pitalization in the acute care setting. In Part III, procedures that are commonly performed by APPs are included, as well as videos for certain procedures when a visual demonstration can be particularly helpful. Part IV is designed to address special issues that are unique to the acute care setting. The topics addressed are transi-tional care, end-of-life issues, health promotion, hemody-namic monitoring devices, and telemedicine. When a patient comes into the acute care setting, it is an opportunity for all healthcare providers to address health promotion. Not every-one sees healthcare providers on a regular basis or gets eval-uated for routine screening. Therefore, it is essential for all acute care providers to be well versed on the types of health promotion that are necessary based on a patient's age and other demographic factors. Telemedicine is also addressed because it is becoming increasingly prevalent. The ICUs in rural areas can now be monitored by intensivists and APPs in central regions. There is a burgeoning role for APPs in this area. Transitional care is the point where a patient either comes into the acute care setting or returns to the outpatient community. This period of transition is the most vulnerable time for patients. Care-ful attention must be devoted to updating and informing the accepting provider on patient status and the management plan. Finally, end-of-life issues often are addressed in the hos-pital system after an acute episode. Knowledge of these issues is essential to practice. The appendix provides normal lab values as a refer-ence tool for APPs. There may be slight variations frominstitution to institution that may be attributed to different vendors. Please use these values as guides for quick reference, but defer to your institutional normal reference range. Medicine is clearly and overwhelmingly a vast body of knowledge. Students who try to take it all on at once make learning seem like an unsurmountable task. The brain can only absorb so much information at once. When students pick up a dense textbook and see there are hundreds of con-ditions that could exist with just one body system, it makes it difficult for them to focus on the relatively few conditions that we treat commonly. The goal of this book is to decon-struct large topics into focused, core conditions. Students will not learn everything they need to know about a topic by using this book, but they will get what they need to know as a new graduate. Practicing APPs can refer to this resource as a quick review of what they need to know. Continuing to strive for more learning is a lifelong duty as an APP. Furthering the learning process far beyond graduate school and continuing to search out information that is unfamiliar is essential. In this day and age, the Internet is a quick and easy resource to utilize. Patients will be using it as well. While no one expects any one person to know everything at all times, there is an expectation that the providers are resourceful and will know how to find the information. Imposter Syndrome At the end of the day, students will never feel like they know enough to get started, and much of this anxiety can be attributed to what we know about imposter syndrome. Going from the role of an expert in one area to a novice is extremely challenging and creates feelings of uneasiness. This is a com-pletely natural transition mode. In fact, I would be more concerned about a student who thinks he or she knows everything than a student who feels like his or her peers just have not “figured out” that they do not belong. This unease and uncertainty of feeling like an imposter will help students be cautious and humble when they enter the healthcare system as an acute care provider. Developing clin-ical judgment is an art that is guided by science and occurs over time and through experiential learning. Being unsure will motivate new graduates to consult evidence-based mate-rials to search for answers. Frequently textbooks, articles, and case studies provide classic presentations that are useful for learning a concept. However, in practice, the APP quickly discovers that didac-tic content in a lecture or a book does not account for the number of variables that are present in real clinical situations. Introduction | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
xxviii Hence, textbook learning has limitations that can only be remedied with practice. A student in the novice stage of a new role would be best advised to spend as much time as possible with patients, practicing active, focused listening and asking questions. This practice will help the new graduate APP gain confidence quickly. Role of APPs The role of APPs continues to evolve and expand in the healthcare system. New opportunities open up as the health-care system begins to depend heavily on the utilization of APPs, particularly in the acute care system. It was not too long ago that most nurse practitioners (NPs) and physician assis-tants (PAs) worked primarily in primary care settings. Now, NPs and PAs work in primary care, all aspects of the acute care system, and beyond. More and more collaborative efforts are being established between NPs and PAs as we move away from contrasting how we are different and focus on achieving the same goals. Both NPs and PAs struggle with practice issues, prescrib-ing issues, and levels of autonomy. However, many legislative advancements have been achieved over the past 10 years that have created a growing demand for APPs. As the roles and responsibilities of APPs continue to expand, the stronger the collaboration between them needs to be. This book is one step forward in developing and creating these collaborative efforts for NPs and PAs. Future Opportunities There are many opportunities for APPs. One of the major next steps I see for APPs is acute care billing. Billing pro-vides visibility of the extent of work that is truly being done by APPs. Billing can also be leveraged for improved working conditions and better pay. In the current system where APP billing is absorbed by physician groups, APPs are left withbasically nothing to show for their efforts. How can a hospi-tal administration effectively determine if more or fewer APPs are needed in a particular department? How can a practice group determine if an APP is exceeding expectations in his or her work or even underperforming? How can an APP justify a raise for himself or herself when there is nothing quantifiable to show the value of what has been done? Billing is more than just sending off charges to insurance companies to get paid. Billing provides visibility, which in turn comes with responsibilities and challenges. At the time of the writing of this book, there were no models (or too few to use) of acute care billing for APPs to devote an entire section to the issue; however, it is definitely coming. Insur-ance companies and compliance programs are taking steps to implement a structure that recognizes the contribution of the APP to the patient's care. Acute care billing is going to be a controversial issue in the years to come, and APPs would be well advised to keep on top of how it is implemented and to participate in any committees that are designated to discuss such planning. Final Note Being an APP is an exciting and excellent career choice that has countless opportunities. Learning about disease states and management of patients is one aspect of the role of the APP. There is so much to learn, and it can be incredibly over-whelming. My advice to students, new graduates, and even seasoned APPs would be this: Acknowledge that there is a massive amount of information to be learned... over time. Accept that you have roles and responsibilities to the health-care system and your community that extend beyond treat-ing disease states. And accelerate your learning curve by being present with your patients, collaborating with your team, and staying involved in your profession. Best of luck in this amazing profession as an APP. Introduction | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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I Acute Care Guidelines by System 1. ENT Guidelines 2. Pulmonary Guidelines 3. Cardiac Guidelines 4. Gastrointestinal Guidelines 5. Nephrology Guidelines 6. Neurology Guidelines 7. Targeted Temperature Management Guidelines 8. Endocrine Guidelines 9. Psychiatric Guidelines10. Infection Guidelines 11. Peripheral Vascular Guidelines 12. Hematology Guidelines 13. Oncology Guidelines 14. Immune System, Connective Tissue, and Joints Guidelines 15. Dermatology Guidelines 16. Geriatric Guidelines 17. Trauma Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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3 1 ENT Guidelines Carey Heck Conjunctivitis Carey Heck Definition A. Inflammation of the conjunctiva, a thin transparent membrane that lines the inside of the eyelids and covers the sclera. B. Commonly called “pink eye. ” Incidence A. Allergic conjunctivitis. 1. Most common cause of conjunctivitis (15%-40% of population). 2. Most frequently occurs in spring and summer. B. Viral conjunctivitis. 1. Most common cause of infectious conjunctivitis. 2. Most common type in adults. 3. More frequently occurs in the summer months. C. Bacterial conjunctivitis. 1. Most common cause of infectious conjunctivitis in children. 2. Most frequently occurs in the winter and early spring months. Pathogenesis A. Allergic. 1. Not contagious. 2. Common in individuals with other signs of allergic disease. 3. Reaction to allergic triggers. B. Infectious. 1. Bacterial. a. Highly contagious. b. Most common causative agents. i. Staphylococcus aureus. ii. Haemophilus influenzae. iii. Streptococcus pneumoniae. iv. Moraxella catarrhalis. 2. Viral. a. Highly contagious. b. Most common causative agent. i. Adenoviruses. ii. Rubella virus. iii. Rubeola virus. iv. Herpes viruses. C. Noninfectious. D. Other causes. 1. Environmental irritants. 2. Medications. 3. Toxins. 4. Chemicals. Predisposing Factors A. Exposure to allergens. B. Exposure to environmental irritants. C. Contact lens wearers. D. Use of ophthalmic drops. E. Old makeup products. F. Occupational exposure to chemicals. Subjective Data A. Common complaints/symptoms. 1. Redness. 2. Discharge. a. From the eye. b. Crusts over the eyelid, especially after sleep. 3. Itching, burning. 4. Increased tearing. 5. Blurred vision. 6. Painless. 7. Feeling of foreign body in the eye. B. Common/typical scenario. 1. Specific presentation varies dependent on type of con-junctivitis. 2. Symptoms of eye redness and discharge are common regardless of specific cause. 3. Contributing history and appearance of discharge often determines diagnosis. C. Family and social history. 1. Review of symptoms. a. Elicit the onset and duration of symptoms. b. Determine if the patient or close contacts have any systemic illnesses. c. Assess the patient for any risk factors. d. Associated symptoms. i. Rhinorrhea. ii. Earache. iii. Sore throat. iv. Rash. e. Single or both eyes. 2. Past medical history. a. Recent illnesses. b. Sick contacts. c. Allergies. d. Possible occupational exposure history. e. Sexual history. f. Contact lens use. Conjunctivitis | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
4 D. Review of systems. 1. Recent illnesses. Determine the onset and duration of symptoms. a. Abrupt or gradual onset. b. Determine if the patient or close contacts have any systemic illnesses. 2. Allergies. 3. Possible occupational exposure history. 4. Sexual history. 5. Pertinent systems review. a. Head, ear, eyes, nose, and throat (HEENT). i. Headache. ii. Vision loss. iii. Eye pain. iv. Eye discharge. v. Ear pain. vi. Rhinorrhea. vii. Nasal congestion. viii. Cough. b. Integumentary. i. Rash. ii. Lesions. Physical Examination A. Perform an eye examination, assessing for vision loss and eye discharge. 1. Appearance of eyes. a. Allergic: Typically both eyes are infected. b. Bacterial: Typically one eye is infected but may spread to other eye. c. Viral: Typically both eyes are infected. 2. Discharge. a. Allergic: Stringy. b. Bacterial: Mucopurulent. i. Copious yellow-green discharge is consistent with gonorrheal infection. c. Viral: Watery. 3. Visual acuity. 4. Corneal opacity. 5. Pupil size and shape. 6. Eyelid swelling. 7. Presence of proptosis. B. Red flags. 1. Reduction of visual acuity. 2. Ciliary flush. 3. Photophobia. 4. Severe foreign body sensation. 5. Corneal opacity. 6. Fixed pupil. 7. Severe headache with nausea. 8. Dendriform lesion indicative of herpes simplex virus (HSV). Diagnostic Tests A. Diagnosis is made with history and physical examination. B. Imaging studies are not indicated unless underlying con-dition is suspected. C. Culture should be considered. 1. In severe cases. 2. In patients who wear contact lenses. 3. In patient unresponsive to initial treatment. 4. If sexually transmitted disease (STD) is suspected. Differential Diagnosis A. Conjunctivitis. 1. Allergic: Likely with accompanying allergic symptoms and contributing history. 2. Bacterial: Likely with thick, yellow-green discharge. 3. Viral: Likely with accompanying cold or respiratory symptoms and watery discharge from the eye. B. Corneal abrasion. 1. Different from conjunctivitis in that there is a subjec-tive complaint of severe pain that worsens over time. C. Foreign body in the eye. D. Keratitis. E. Varicella zoster ophthalmicus. F. Glaucoma. Evaluation and Management Plan A. General plan. 1. Symptomatic relief is adequate for all forms of con-junctivitis. a. Most symptoms: Resolve without treatment. b. Supportive care. i. Over-the-counter (OTC) products. 1)Topical OTC medications are of limited efficacy for allergic conjunctivitis. 2)Systemic antihistamines may be useful for allergic conjunctivitis. ii. Moist cold compresses to eyes. iii. Avoidance of allergic triggers. 2. Antibiotics are not indicated in most cases of bacterial conjunctivitis. a. Return to work or school requirements. These may necessitate initiation of antibiotic for confirmed cases of bacterial conjunctivitis. i. Antibiotics initiated within the first 2 to 5 days can hasten the resolution of symptoms. ii. Initiation of antibiotics after 5 days of the start of symptoms has a minimal effect, and use is not recommended. b. Indications for antibiotic therapy. i. Cases caused by gonorrhea infection. ii. Cases caused by chlamydia infection. iii. Contact lens wearers. 1)Consider pseudomonas infection. B. Patient/family teaching points. 1. Use handwashing to prevent spread. 2. Avoid touching eyes. 3. Instruct patients to dispose of current contact lenses and to avoid wearing contact lenses until irritation/infec-tion is cleared. 4. Instruct patients to dispose of all eye makeup. C. Pharmacotherapy. 1. Allergic. a. Artificial tears. b. Antihistamine/decongestant drops (OTC). c. Mast cell stabilizer/antihistamine drops (OTC). 2. Viral. a. Antibiotics not indicated. b. Antihistamine/decongestant drops (OTC). c. Artificial tears (OTC). d. Viral therapy for HSV infection. 3. Bacterial conjunctivitis. a. Topical (eye drops or ointment) antibiotic therapy. i. Erythromycin 5 mg/g ophthalmic ointment: One-half inch (1. 25 cm) four times daily for 5 to 7 days. ii. Ciprofloxacin 0. 3% ophthalmic drops (pre-ferred agent in contact lens wearer): 1 to 2 drops four times daily for 5 to 7 days. b. Systemic antibiotics indicated for gonorrhea and chlamydia infections. i. 1 gm ceftriaxone IM plus azithromycin 1 gm PO for one dose. 1. ENT Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
5 D. Discharge instructions. 1. Symptoms should resolve in 5 to 7 days. 2. If symptoms continue or different symptoms appear, then follow-up is recommended. Follow-Up A. Instruct patients with acute bacterial conjunctivitis to follow-up in 1 to 2 days if symptoms worsen or do not improve. B. Instruct patients with other forms of conjunctivitis to follow-up within 2 weeks if symptoms worsen or do not improve. Consultation/Referral A. Consider referral to allergy specialist for allergen testing in severe cases of allergic conjunctivitis. B. Referral to ophthalmologist for cases that are resistant to initial treatment. C. Urgent referral to ophthalmologist due to increased risk of vision loss. 1. Hyperacute bacterial conjunctivitis. 2. Keratitis. 3. Varicella zoster ophthalmicus. Special/Geriatric Considerations A. Infants (highly susceptible to conjunctivitis). 1. At risk for more serious complications. 2. Prophylactically treated with optic antibiotics at birth. B. Contact lens wearers. 1. Higher risk for keratitis: Careful evaluation to rule out keratitis is essential before diagnosis of conjunctivitis is made. 2. Discontinue use until eye has healed. Use can begin again when eye is white and patient has no discharge for 24 hours after completion of antibiotics. C. Returning to school or work. This is appropriate 24 hours after antibiotics have been initiated or there is no discharge. D. Awareness of local board of health reporting laws for STDs. This is essential when the diagnosis of conjunctivitis is made in the setting of gonorrhea and chlamydia. Bibliography Alfonso, S. A., Fawley, J. D., & Lu, X. A. (2015). Conjunc-tivitis. Primary Care: Clinics in Office Practice, 42 (3), 325-345. doi:10. 1016/j. pop. 2015. 05. 001 Azari, A., & Barney, N. (2013). Conjunctivitis: A systematic review of diagnosis and treatment. Journal of the American Medical Association, 310(16), 1721-1729. doi:10. 1001/jama. 2013. 280318 Bielory, B. P., O'Brien, T. P., & Bielory, L. (2012). Management of seasonal allergic conjunctivitis: Guide to therapy. Acta Ophthalmologica, 90 (5), 399-407. doi:10. 1111/j. 1755-3768. 2011. 02272. x Gore, J. (2013). Conjunctivitis. Journal of the American Academy of Physician Assistants, 26 (3), 60. Mc Anena, L., Knowles, S. J., Curry, A. S., & Cassidy, L. (2015). Prevalence of gonococcal conjunctivitis in adults and neonates. Eye, 29 (7), 875-880. doi:10. 1038/eye. 2015. 57 Segal, K., Lai, L., & Starr, E. (2014). Management of acute conjunctivitis. Current Ophthalmology Reports, 2 (3), 116-123. doi:10. 1007/s40135-014-0046-4 Pharyngitis Carey Heck Definition A. Inflammation of the pharynx. B. Commonly referred to as a “sore throat. ”Incidence A. Acute pharyngitis accounts for more than 12 million office and emergency/urgent care visits in the United States annually. B. Viral pharyngitis occurs most frequently; increased inci-dence in adult population. C. Bacterial pharyngitis occurs more frequently in children and adolescents. 1. Particularly the Group A beta-hemolytic streptococci (GAS). a. Peak incidence occurs in 5 to 15 year age group. b. Only 5% to 15% of adults present with GAS. 2. Bacterial pharyngitis occurs most frequently in winter and early spring months. Pathogenesis A. Infectious. 1. Viral. a. Adenoviruses and rhinoviruses responsible for most cases of viral pharyngitis. b. Other causes include. i. Herpes simplex virus (HSV) 1 and 2. ii. Coxsackievirus. iii. Human herpes virus 4 (Epstein-Barr virus [EBV]). iv. Human herpes virus 5 (cytomegalovirus). v. HIV. 2. Bacterial. a. The most important causative agent is the GAS. i. Severe complications of GAS warrant prompt identification and treatment. b. Other causes include. i. Group C streptococci. ii. Neisseria gonorrhoeae. iii. Corynebacterium diphtheriae. iv. Treponema pallidum. v. Mixed anaerobes. B. Noninfectious. 1. Allergy. 2. Irritants. 3. Gastrointestinal reflux. Predisposing Factors A. Exposure to infectious agents. 1. Bacteria. 2. Viruses. B. Exposure to allergens. C. Exposure to environmental irritants. D. History of gastrointestinal reflux. E. History of immunosuppression. Subjective Data A. Common complaints/symptoms. 1. “Sore throat. ” 2. Difficulty swallowing. 3. Nasal congestion. 4. Sinus tenderness. 5. Cough. 6. Malaise. 7. Headache. 8. Distinguishing features of pharyngitis associated with GAS. a. Absent cough. b. Fever. Pharyngitis | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
6 c. Tonsillar exudates. d. Anterior cervical lymphadenopathy. B. Common/typical scenario. 1. Patients typically complain of sore or scratchy throat, fever, and general malaise. C. Review of systems. 1. Past medical history. a. Recent illnesses. Determine the onset and duration of symptoms. i. Abrupt or gradual onset. ii. Duration longer than 3 weeks unlikely to be pharyngitis. b. Sick contacts. Determine if the patient or close contacts have any systemic illnesses. c. Assess the patient for any risk factors. 2. Allergies. 3. Possible occupational exposure history. 4. Travel history. 5. Sexual history. 6. Pertinent systems review. a. Constitutional. i. Fever. ii. Malaise. b. Head, ear, eyes, nose, and throat (HEENT). i. Sore throat. ii. Cough. iii. Rhinorrhea. iv. Nasal congestion. v. Headache. vi. Sinus tenderness/pain. c. Integumentary. i. Rash. ii. Lesions. Physical Examination A. Appearance of pharynx. 1. Pale to red. 2. Mild erythema to profound edema. 3. Vesicular lesions. a. HSV. b. Coxsackievirus. B. Appearance of tonsils. 1. Redness. 2. Edema. 3. Exudates. a. White (oropharyngeal candidiasis, GAS). b. Grayish membrane (diphtheria). C. Lymph nodes. 1. Cervical lymphadenopathy. 2. Tonsillar lymphadenopathy. D. Integumentary. 1. Scarlatiniform rash may be present in GAS infections. 2. Palatine petechiae may be present in GAS infection. E. Red flags. 1. “Hot potato” voice. a. Garbled speech due to pharyngeal edema. b. Suggestive of peritonsillar abscess. 2. Unilateral neck swelling. 3. Difficulties with secretion management. a. Drooling. b. Compromised airway. i. Tonsillar pillars touching. ii. “Kissing tonsils. ” 4. Uvula deviation. a. Indicative of peritonsillar abscess. TABLE 1. 1 Modified Centor Criteria Clinical Finding Score Fever +1 Absence of cough +1 Anterior cervical lymphadenopathy +1 Tonsillarexudates +1 Age (years) 2-14 +1 15-44 0 45+-1 Source:Fine,A. M.,Nizet,V.,&Mandl,K. D. (2012,June11). Large-scale validation of the Centor and Mc Isaac scoresto predictgroup A streptococcalpharyngitis. Archives of Internal Medicine, 172 (11), 847-852. Diagnostic Tests A. Clinical examination: Modified Centor criteria. 1. Scoring system developed to quickly diagnose the like-lihood of GAS. 2. One point assigned for each of the following clin-ical findings: History of fever, tonsillar exudates, ante-rior cervical lymphadenopathy, and absence of cough (see Table 1. 1). 3. Empiric treatment based on symptoms and higher Centor score is no longer recommended by the Infectious Disease Society of America. B. Rapid antigen detection testing (RADT). 1. Indicated because clinical examination alone cannot differentiate between viral and bacterial pharyngitis. Modified Centor Score Guidelines for Treatment 0-1 No further evaluation necessary Providesupportive care Antibiotics not recommended 2-3 Assess for GAS pharyngitis Consider throatculturesand RADT Treatif culturespositive >4 Assess for GAS pharyngitis Throatculturesand RADT indicated Empiric treatmentcontroversial IDSA does not recommendempiric treatment Treatif culturespositive GAS, group A beta-hemolytic streptococci; IDSA, Infectious Disease Society of America; RADT,rapid antigen detection testing. 2. May not be necessary if overt viral symptoms are present (i. e., cough, rhinorrhea). a. Throat culture. 3. Pediatric: Indicated in children with negative RADT and clinical symptoms supportive of bacterial pharyngitis. 4. Adults. a. Not necessary in adults with negative RADT due to low incidence of GAS in adults. 1. ENT Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
7 b. Possibly indicated. i. In adults with negative RADT if high suspi-cion of GAS. ii. In adults at high risk for infection (immuno-compromised or other comorbidities). iii. Those who are in close contact with high risk populations. Differential Diagnosis A. Viral pharyngitis. B. Bacterial pharyngitis. C. Oropharyngeal candidiasis (thrush). 1. Immunocompromised patients. 2. Patients receiving broad spectrum antibiotics or cor-ticosteroids. D. Gonococci. Possible in patients engaging in orogenital sex. E. Diphtheria. F. Mononucleosis. Evaluation and Management Plan A. General plan. 1. Pain relief. a. Over-the-counter (OTC) oral analgesics. i. Nonsteroidal anti-inflammatory drugs. ii. Acetaminophen. iii. Aspirin. b. Topical therapies. i. Lozenges. ii. Sprays. iii. Fluids (i. e., tea, honey). c. Environmental measures. i. Humidified air. ii. Avoidance of irritants. d. Glucocorticoid. i. Not recommended for routine use. ii. Limited role in the patient with extreme sore throat and inability to swallow. 2. Antibiotics for confirmed bacterial infection. B. Patient/family teaching points. 1. Handwashing to prevent spread. C. Pharmacotherapy. 1. Avoidance of empiric antibiotics. a. Overprescribing contributes to antibiotic resis-tance. b. Antimicrobial therapy generally does not benefit bacterial pharyngitis caused by infection other than streptococcal bacteria. c. Infections due to other organisms are possible but tend to be the exception. i. N. gonorrhoeae. ii. C. diphtheriae. 2. Bacterial pharyngitis. a. Penicillin is antibiotic of choice for GAS pharyn-gitis. i. 10-day course recommended. b. First generation cephalosporin for penicillin aller-gies. c. Alternatively 5-day course of azithromycin is acceptable. i. Local and regional resistance has been reported. 3. Viral pharyngitis. a. Supportive care. D. Discharge instructions. 1. Follow-up is recommended if symptoms do not improve in 3 to 4 days. Follow-Up A. Instruct patients to follow-up if pharyngitis does not improve in 5 to 7 days. B. Further evaluation indicated if no improvement or wors-ening of symptoms. 1. Possible suppurative complication. 2. Alternative diagnosis. Consultation/Referral A. Urgent referral to otolaryngologist for suppurative com-plications. 1. Peritonsillar abscess. 2. Retropharyngeal abscess. 3. Epiglottitis. Special/Geriatric Considerations A. Suppurative complications. 1. Rare but potentially life threatening complications of GAS pharyngitis. 2. Early recognition and appropriate treatment essential to avoid associated morbidity and mortality. 3. Complications include: a. Peritonsillar abscess. b. Retropharyngeal abscess. c. Streptococcal bacteremia. d. Epiglottitis. B. Nonsuppurative complications. 1. Rheumatic fever. a. Rare in developed countries. 2. Poststreptococcal glomerulonephritis. C. Other considerations. 1. Morbilliform rash may develop in patients with pharyngitis caused by EBV who have been treated with penicillin or amoxicillin. Bibliography Fine, A. M., Nizet, V., & Mandl, K. D. (2012, june 11). Large-scale valida-tion of the Centor and Mc Isaac scores to predict group a streptococcal pharyngitis. Archives of Internal Medicine, 172 (11), 847-852. Gore, J. (2013). Acute pharyngitis. Official Journal of the American Academy of Physician Assistants, 26 (2), 57-58. doi:10. 1097/01720610-201302000-00012 Mc Isaac, W. J., White, D., Tannenbaum, D., & Low, D. E. (1998). A clinical score to reduce unnecessary antibiotic use in patients with sore throat. Canadian Medical Association Journal, 158 (1), 75-83. Nicoteri, J. (2013). Adolescent pharyngitis: A common complaint with potentially lethal complications. Journal for Nurse Practitioners, 9 (5), 295-300. doi:10. 1016/j. nurpra. 2013. 02. 023 Shapiro, D., Lindgren, C., Neuman, M., & Fine, A. (2017). Viral features and testing for streptococcal pharyngitis. Pediatrics, 139 (5), e20163403. doi:10. 1542/peds. 2016-3403 Shulman, S., Bisno, A., Clegg, H., Gerber, M., Kaplan, E., Lee, G., & Van Beneden, C. (2012). Executive summary: Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngi-tis: 2012 update by the Infectious Diseases Society of America. Clinical Infectious Diseases, 55 (10), 1279-1282. doi:10. 1093/cid/cis847 Weber, R. (2014). Pharyngitis. Primary Care: Clinics in Office Practice, 41, 91-98. doi:10. 1016/j. pop. 2013. 10. 010 Pharyngitis | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
8Rhinosinusitis Carey Heck Definition A. Inflammation of the nasal cavity and paranasal sinuses. B. Preferred terminology: “Rhinosinusitis” rather than “sinusitis” since inflammation of the sinuses rarely occurs without inflammation of the nasal mucosa as well. C. Classification. 1. Acute rhinosinusitis (ARS): Symptoms lasting less than 4 weeks. 2. Acute bacterial rhinosinusitis (ABRS): ARS with bac-terial etiology. 3. Chronic rhinosinusitis (CRS): Symptoms lasting greater than 12 weeks. Incidence A. Viral infection due to rhinopharyngitis (common cold) is the most common cause of ARS. B. Annually, 1 in 7-8 persons in the United States will expe-rience an episode of ARS. C. More frequent in women. D. Higher in 45-to 64-year-ld age group. E. ABRS accounts for less than 2% of the cases of ARS. Pathogenesis A. Viral. 1. Rhinovirus. 2. Influenza virus. 3. Parainfluenza virus. B. Bacterial. a. Streptococcus pneumoniae. b. Haemophilus influenzae. c. Moraxella catarrhalis. Predisposing Factors A. Older age. B. Smoking. C. Air travel. D. Exposure to changes in atmospheric pressure. E. Asthma and allergies. F. Swimming. G. Dental disease. H. Immunodeficiency. Subjective Data A. Common complaints/symptoms. 1. Nasal congestion. 2. Nasal discharge. 3. Facial pressure or feeling of fullness. 4. Reduced sense of smell. B. Other complaints. 1. Fatigue. 2. Headache. 3. Difficulty sleeping. 4. Toothache. 5. Ear pain or fullness. C. Family and social history. 1. Family and social history is noncontributory. D. Common/typical scenario. 1. Common complaints are: a. Fever. b. Sore throat. c. Nasal discharge. d. Facial pain. e. Frontal pain or pressure that worsens when patient bends forward. 2. Patients frequently complain of headaches. E. Review of systems. 1. Past medical history. a. Recent illnesses. Elicit onset and duration of symp-toms. b. Sick contacts. Determine if patient or close con-tacts have any systemic illnesses. c. Asthma. 2. Allergies. 3. Possible occupational exposure history. 4. Travel history. 5. Pertinent systems review. a. Constitutional. i. Fever. ii. Malaise. b. Head, ear, eyes, nose, and throat (HEENT). i. Sinus pain/tenderness. ii. Headache. iii. Nasal congestion. iv. Cough. v. Rhinorrhea. vi. Purulent discharge with bacterial infection. Physical Examination A. Appearance. 1. Erythema and/or edema of involved cheek. 2. Erythema and/or edema of periorbital area. B. Drainage. 1. Mucopurulent more likely ABRS. 2. Clear more likely viral ARS. C. Percussion. 1. Increased pain or tenderness of sinuses. 2. Not specific or sensitive test for diagnosis of rhinosi-nusitis. D. Transillumination of frontal and maxillary sinuses. 1. Limited diagnostic value. 2. Not specific or sensitive test for diagnosis of rhinosi-nusitis. E. Nasal examination. 1. Diffuse mucosal edema. 2. Narrowing of middle meatus. 3. Inferior turbinate hypertrophy. 4. Presence or absence of polyps. a. Presence may indicate anatomic risk for develop-ment of ABRS. Diagnostic Tests A. Generally not indicated for uncomplicated cases of rhi-nosinusitis. B. Nasal cultures are not useful in the diagnosis of ABRS. C. Gold standard for culture identification: Sinus aspiration. 1. Reserved for complicated cases. 2. Referral to otolaryngologist. D. CT. 1. Persistent symptoms. 2. Recurrent symptoms. 3. Complicated ABRS. 4. Planning for sinus surgery. Differential Diagnosis A. Rhinosinusitis. B. Allergic rhinitis. 1. ENT Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
9 C. Rhinopharyngitis. D. Headache. Evaluation and Management Plan A. General plan. 1. Use pain relief: Over-the-counter (OTC) analgesics and antipyretics. 2. Reduce mucosal inflammation: Topical nasal corticos-teroids. 3. Enhance sinus drainage: Saline irrigation. 4. Modulate environmental triggers. a. Treat concurrent allergic rhinitis symptoms if present with OTC antihistamines and allergy therapy as needed. 5. Eradicate infection indicated for ABRS. B. Patient/family teaching points. 1. Use handwashing to prevent spread. C. Pharmacotherapy. 1. Acute sinusitis. a. Most cases of acute sinusitis are viral and pharma-cotherapy is targeted to symptomatic relief. i. OTC analgesics and antipyretics. ii. Saline nasal irrigation. iii. Possibly topical corticosteroids. 1)Literature suggests that high-volume cor-ticosteroid irrigations are more effective than low-volume corticosteroid sprays. iv. Topical decongestants. 1)Use not to exceed 3 to 5 days to avoid rebound congestion. v. Antihistamines. 1)No clinical studies support use in viral sinusitis. vi. Expectorants and cough suppressants. 1)Clinical studies do not support efficacy in use for viral sinusitis. b. Suspected bacterial sinusitis. i. Classic progression is mild symptoms that begin to resolve and then suddenly become worse. ii. Watchful waiting: Plan to follow-up if symp-toms worsen or do not improve in 7 days. iii. Nonmacrolide therapy. 1)Amoxicillin/clavulanate 875/125 mg orally twice daily ×5 to 7 days. 2)Doxycycline 200 mg orally daily ×5 to 7 days for PCN allergies. iv. OTC analgesics and antipyretics. v. Saline irrigation. 1)Use as adjuvant to corticosteroids in chronic sinusitis. vi. Topical corticosteroids. 1)Literature suggests that high-volume cor-ticosteroid irrigations are more effective than low-volume corticosteroid sprays. 2. Chronic sinusitis. a. Initial management is high-volume saline irriga-tion with topical corticosteroid therapy. b. Consider short course of nonmacrolide therapy if active mucopurulence is present on examination. c. For patients with persistent symptoms. i. Consider systemic corticosteroids. ii. Use long-term macrolide therapy for patients without nasal polyps. d. Topical antibiotics and antifungals are not recom-mended in the treatment of chronic sinusitis. D. Discharge instructions. 1. Follow-up is recommended in 3 to 4 days if no improvement in symptoms. Follow-Up A. Patients should be instructed to follow-up if symptoms do not improve in 7 days. B. Further evaluation is indicated if no improvement or worsening of symptoms. Consultation/Referral A. Persistent cases should be referred to otolaryngology. 1. Endoscopic nasal evaluation. 2. Endoscopic nasal surgery. Special/Geriatric Considerations A. Long-term use of nasogastric tubes can put patients at risk for developing sinusitis. Bibliography Bird, J., Biggs, T., Thomas, M., & Salib, R. (2013). Adult acute rhinosinusi-tis. British Medical Journal, 346, f2687. doi:10. 1136/bmj. f2687 Cevc, G. (2017). Differential diagnosis and proper treatment of acute rhi-nosinusitis: Guidance based on historical data analysis. Allergy & Rhinol-ogy, 8(2), e45-e52. Advance online publication. doi:10. 2500/ar. 2017. 8. 0206 Cho, S. H., Kim, D. W., & Gevaert, P. (2016). Chronic rhinosinusitis with-out nasal polyps. Journal of Allergy and Clinical Immunology: In Practice, 4(4), 575-582. doi:10. 1016/j. jaip. 2016. 04. 015 Rosenfeld, R., Piccirillo, J., Chandrasekhar, S., Brook, I., Kumar, K., Kram-per, M.,... Corrigan, M. (2015). Clinical practice guideline (Update): Adult sinusitis. Otolaryngology-Head and Neck Surgery, 152 (2 Suppl. ), S1-S39. doi:10. 1177/0194599815572097 Rudmik, L., & Soler, Z. (2015). Medical therapies for adult chronic sinusitis: A systematic review. Journal of the American Medical Association, 314 (9), 926-939. doi:10. 1001/jama. 2015. 7544 Rhinosinusitis | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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11 2 Pulmonary Guidelines Acute Respiratory Distress Syndrome E. Mone ́e Carter-Griffin Definition A. Acute respiratory distress syndrome (ARDS) is defined by three variables. 1. Bilateral opacities on imaging. 2. Onset within 7 days of a clinical event or worsening respiratory symptoms. 3. Origin of pulmonary edema not fully explained by cardiac failure or volume overload. B. ARDS is identified as mild, moderate, or severe based on the PF ratio (Pa O2/Fi O2). C. Acute lung injury does not exist in the new definition of ARDS. D. Exclusion of heart failure is not required in the new defi-nition of ARDS. Incidence A. It is difficult to obtain an accurate incidence due to vari-ations in the definition used to identify or describe ARDS. B. An estimated 200,000 cases of ARDS occur each year in the United States. C. The incidence increases with advancing age. D. ARDS has not been shown to occur more in one sex than the other. E. Mortality and morbidity are associated with worsening of the PF ratio. Pathogenesis A. An indirect or direct insult causes an inflammatory response and accumulation of pro-inflammatory mediators in the lung microcirculation. Injury occurs to the microvascu-lar endothelium and alveolar epithelium. Endothelium injury leads to capillary permeability and migration of protein-rich fluid into the alveolar space. Due to injury of the alveolar epithelium, pulmonary edema forms and damage occurs to the cells lining the alveoli. B. Damage to type I and II cells leads to decreased clear-ance of fluid in the pleural space, increased fluid entry into the alveoli, and decreased surfactant production resulting in decreased alveolar compliance and alveoli collapse. C. An influx of fibroblasts leads to collagen deposition and possibly fibrosis. Predisposing Factors A. Aspiration, including gastric content and drowning. B. Sepsis. C. Pneumonia. D. Massive transfusions. E. Pancreatitis. F. Burns. G. T rauma, including cases with and without pulmonary injury. H. Underlying interstitial lung disease. Subjective Data A. Common complaints/symptoms. 1. Severe dyspnea. 2. Chest discomfort. 3. Tachypnea. B. Common/typical scenario. 1. Onset is typically 12 to 48 hours after the insult. 2. History shows progressive worsening symptoms. 3. Extrapulmonary complaints may have led to the development of ARDS. Physical Examination A. Dyspnea (see Figure 2. 1). B. Tachypnea. C. Abdominal retractions; obvious respiratory distress. D. Hypoxia and possibly cyanosis. E. Tachycardia. F. Altered mental status, agitation, or confusion. G. Rales during auscultation. H. Additional findings that may relate to the underlying eti-ology of ARDS (e. g., febrile, hypotension, an acute abdomen, or nausea and vomiting seen in pancreatitis). Diagnostic Tests A. Chest x-ray (CXR). 1. Patchy infiltrates rapidly evolve and progress to dif-fuse, bilateral infiltrates. 2. Daily CXRs may be required, especially for patients on mechanical ventilation. B. Arterial blood gas (ABG). 1. Regular ABGs are required to evaluate management. 2. Development of respiratory acidosis (decreased p H and rising CO2). 3. Hypoxemia is defined by the PF ratio. a. Less than 300: As mild ARDS. b. Less than 200: Moderate ARDS. c. Less than 100: Severe ARDS. C. Complete blood count (CBC). 1. Evaluate the white blood cell count and platelets. D. Comprehensive metabolic panel. 1. Evaluate renal and liver function. Acute Respiratory Distress Syndrome E. Mone ́e Carter-Griffin | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
12 Respirat ory ABG: Assess for hypercapnia or hypoxemia D-dimer, ag e-adj usted : Can aid in ru ling out a pulm onary embolus. Chest CT/A ngiogr aphy: Assess for pne umonia, emph ysematous c hange s, /f_luid, honeycombing sugge stive of /f_ibrosis, pulmo nary embo lus. Pulmona ry function t esti ng: Assess for obstr uctiveorrestric tive dise ase. Addit ional Testin g Thyroid studies: Assess for hyperthyroidism (high card iac output sta te). Hemogl obin/Hematocrit: Assess for anemia. Cardiopulmonary exercis e test: Can help di stinguish between the two by indicating ischemic changeson ECG (cardiac),bronchospasmduringexercise(respiratory), and so forth. Obtain the History Quality/sensation, timing, precipitating factors, allev iating factors, a ny associated factors. Gradual or sudden onset? Continuous or episod ic? Occur with exertion or at rest? Positional? Physical Ex amin ation General: Positioning? Accessor y muscle use? Paradoxical abdominal movement? O vert distress ? Able to speak in full sentences? Audible stridor? Vital Signs: Tachycardia? Tachypnea? Pulsus para doxus? Oxygen desat urations? Cardiac: Elevated JVD? Murmur? S3 or S4 gallop? Edema? Resp iratory: Adventitious b reath sounds such as cra ckles/rales, wheezes, or diminished? Chest shape? Dullness or h yperre sonance on percussio n? R espiratory pattern? Symmetrical chest movement? Extremities: Cyanosis? Edema? Clubbing? *The physical exam shoul d always focus on airway, breathing, circulation /f_irst. Proceed with a full exam in the stab le patient* Initial Diagn ostics Chest x-ray: Evidence of pulmonary edema? Pneumonia? Pleural effusion ? Hyperin/f_lation of the lungs suggestive of obstru ctive disease? Heart size? L ung volumes? Elevation of hemidiaphragm? ECG: Toassess for myocardial injury or ischemia. Cardiovasc ular Echoc ardio gram :Assess heart siz e, func tion, valves, pulmonary pressures, pericardial effusion, and so forth. NT-pro BN P: Can a id in the diagnosis of heart failure in the appro priate clinical context. FIGURE 2. 1 Algorithm for the evaluation of dyspnea. JVD, jugular venous distention; NT-pro BNP, N-Terminal pro brain natriuretic peptide. 2. Magnesium and phosphorus. Strict electrolyte reple-tion is necessary for cardiac stability and prevention of arrhythmias, especially in the setting of profound tissue hypoxia and/or septic shock, which is often concomitant. E. Coagulation studies. 1. Prothrombin time and international normalized ratio. 2. Fibrinogen level. 3. Fibrin degradation products. F. N-Terminal pro brain natriuretic peptide level. 1. This is used to assess for heart failure causing or con-tributing to the bilateral infiltrates and hypoxemia. 2. It is important for the clinician to note that this value may be elevated secondary to etiologies other than heart failure, such as sepsis and renal failure. G. Blood cultures. 1. Evaluate infective etiology as a source for ARDS devel-opment. H. Systemic infection markers. 1. Lactic acid. Measure level of end-organ tissue hypoxia and consider trend. 2. Procalcitonin. Consider trend every 24 hours and monitor for effectiveness of treatment of the primarily offending process. I. Urinalysis and urine culture. 1. Evaluate infective etiology as source for ARDS devel-opment. J. Sputum culture. 1. Evaluate infective etiology as source for ARDS devel-opment. Differential Diagnosis A. Asthma. B. Chronic obstructive pulmonary disease (COPD). C. Congestive heart failure (CHF). D. Acute lung injury. E. Pleural effusions. F. Pneumonia. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
13 Evaluation and Management Plan A. T reatment is dependent on the severity of ARDS. 1. Oxygen therapy (e. g., high flow nasal cannula, non-invasive positive pressure ventilation, invasive mechanical ventilation). a. In acute hypoxemic respiratory failure, high flow nasal cannula may be necessary. It resulted in improved mortality at 90 days compared to nonin-vasive and invasive mechanical ventilation. b. Invasive mechanical ventilation: Recommended tidal volume of 6 to 8 m L/kg and maintaining plateau pressures less than 30 cm H2O. i. It may be necessary to reduce the tidal volume to 4 to 5 m L/kg if one is unable to obtain a plateau pressure less than 30 cm H2O. ii. Plateau pressures less than 30 cm H2O may not be attainable in obese patients. iii. Low tidal volumes usually result in hypoven-tilation. Permissive hypercapnia is typically accepted to a p H of 7. 20. c. The use of lung recruitment measures and titrated positive end-expiratory pressure (PEEP) is contro-versial in patients with moderate to severe forms of ARDS due to recent studies indicating negative con-sequences. Recent recommendations are conditional for use of higher levels of PEEP. d. Weaning from mechanical ventilation is typically initiated once the patient requires 50% or less Fi O2, physiologic levels of PEEP, hemodynamically stable, assessed neurological status, and so forth. 2. Positioning. a. Studies have shown that prone positioning results in decreased mortality. i. Recommended to start in early and severe ARDS. b. Prone positioning requires the patient to be hemo-dynamically stable while proning, adequate seda-tion and paralytics, well-trained staff to care for the patient, and adequate space for the equipment. 3. Conservative fluid management. a. Increased ventilator-free days but no difference in mortality. b. Initial fluid resuscitation depends on the under-lying etiology for the development of ARDS. Con-ditions such as hemorrhagic shock and pancreatitis initially require more aggressive fluid management. c. Guidelines for fluid resuscitation should be fol-lowed for certain diagnoses such as sepsis, pancreatitis, and so forth. B. Pharmacotherapy. 1. Paralytics and sedatives. a. Paralytics should be administered in combination with sedatives. i. Minimal sedation to achieve compliance with ventilation and early mobilization show improved outcomes in the ICU setting when clinically appropriate in mild-moderate ARDS. ii. Daily sedation vacation and ventilator libera-tion procedures should be initiated when oxygen requirements are compatible with extubation. b. Paralytics should be considered with ventilatory dyssynchrony and difficulty with ventilation such as poor airway compliance. c. Early administration in severe ARDS has not been associated with increased muscle weakness. d. A commonly used paralytic is cisatracurium. 2. Corticosteroids: Evidence is lacking to recommend for or against steroid use in ARDS. 3. Antibiotics are indicated in patients with an infective etiology. 4. Nitric oxide has not shown to improve outcomes. 5. Deep vein thrombosis (DVT) and stress ulcer prophy-laxis is required. a. DVT prophylaxis is held in patients with signif-icant coagulopathies using subcutaneous heparin or lovenox. b. Proton pump inhibitors and fluoroquinolones are used with caution due to increasing incidence of renal complications and Clostridium difficile colitis with concurrent use. C. Other treatment methods. 1. High frequency ventilation: Has not shown to improve outcomes and some evidence suggests it may increase mortality. 2. Extracorporeal membrane oxygenation. a. Limited evidence to support regular use and no guidelines for widespread use. b. Limited to certain institutions. Follow-Up A. This is dependent on the patient's clinical course, out-comes, and length of hospital stay. Consultation/Referral A. Consultation with a pulmonologist and/or intensivist would be required for management of mechanical ventilation and critical care needs. B. Additional consultation may be required depending on the underlying etiology for ARDS (e. g., trauma, infectious disease). Special/Geriatric Considerations A. Open communication with the family is required. B. Nutritional support is recommended. The preferred route is enteral. C. Patients with prolonged mechanical ventilation— typically greater than 14 days—should undergo tra-cheostomy placement. Bibliography Adhikari, N. K., Dellinger, R. P., Lundin, S., Payen, D., Vallet, B., Gerlack, H.,... Friedrich, J. O. (2014). Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: Systematic review and meta-analysis. Critical Care Medicine, 42, 404-412. doi:10. 1097/CCM. 0b013e3182a27909 Cavalcanti, A. B., Suzumura, R. A., Laranjeira, L. N., de Mores Paisani, D., Damiani, L. P., Guimaraes, H. P.,... Ribeiro de Carvalho, C. R. (2017). Effect of lung recruitment and titrated positive end-expiratory-pressure (peep) vs low peep on mortality in patients with acute respiratory dis-tress syndrome: A randomized clinical trial. Journal of American Medical Association, 318, 1335-1345. doi:10. 1001/jama. 2017. 14171 Fan, E., Del Sorbo, L., Goligher, E. C., Hodgson, C. L., Munshi, L., Walkey, A. J.,... Brochard, L. J. (2017). An official American Tho-racic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline: Mechanical ventila-tion in adult patients with acute respiratory distress syndrome. Ameri-can Journal of Respiratory and Critical Care Medicine, 195, 1253-1263. doi:10. 1164/rccm. 201703-0548ST Ferguson, N. D., Fan, E., Camporota, L., Antonelli, M., Anzueto, A., Beale, R., & Ranieri, V. M. (2012). The Berlin definition of ARDS: An expanded rationale, justification, and supplementary material. Intensive Care Medicine, 38, 1573-1582. doi:10. 1007/s00134-012-2682-1 Frat, J. P., Thille, A. W., Mercat, A., Girault, C., Ragot, S., Perbet, S., & Robert, R. (2015). High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. New England Journal of Medicine, 372, 2185-2196. doi:10. 1056/NEJMoa1503326 Acute Respiratory Distress Syndrome | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
14 Guerin, C., Reignier, J., Richard, J. C., Beuret, P., Gacouin, A., Boulain, T.,... Ayzac, L. (2013). Prone positioning in severe acute respiratory distress syndrome. New England Journal of Medicine, 368, 2159-2168. doi:10. 1056/NEJMoa1214103 Papazian, L., Forel, J.-M., Gacouin, A., Penot-Ragon, C., Perrin, G., Loun-dou, A.,... Roch, A. (2010). Neuromuscular blockers in early acute respiratory distress syndrome. New England Journal of Medicine, 363, 1107-1116. doi:10. 1056/NEJMoa1005372 Rhodes, A., Evans, L. E., Alhazzani, W., Levy, M. M., Antonelli, M., Ferrer, R.,... Dellinger, R. (2017). Surviving sepsis campaign: International guidelines for management of sepsis and septic shock: 2016. Critical Care Medicine, 45, 486-552. doi:10. 1097/CCM. 0000000000002255 Tenner, S., Baillie, J., De Witt, J., & Vege, S. S. (2013). American College of Gastroenterology Guideline: Management of acute pancreatitis. Ameri-can Journal of Gastroenterology, 108, 1400-1415. doi:10. 1038/ajg. 2013. 218 Asthma E. Mone ́e Carter-Griffin Definition A. A chronic airway inflammatory disease defined by a vari-ation of expiratory airflow limitation and history of respi-ratory symptoms that vary in intensity over time. There are various asthma phenotypes, such as allergic asthma and late-onset asthma. Incidence A. Approximately 39. 5 million people in the United States have been diagnosed with asthma in their lifetime. B. It is estimated that 18. 9 million adults still have asthma. C. Asthma accounts for greater than 400,000 hospitaliza-tions, 1. 8 million ED visits, and 14. 2 million office visits. D. The prevalence in adults is highest in women and African Americans. Pathogenesis A. Interplay among host factors and environmental expo-sures, resulting in airway inflammation, airflow obstruction, and bronchial hyperresponsiveness. 1. Immune response to antigen, causing activation of T-lymphocytes. 2. Release of cytokines and interleukins, leading to a release of mast cells, eosinophils, and basophils. 3. Subsequent release of inflammatory mediators (e. g., histamine, prostaglandins) that cause airway inflamma-tion and mucus secretion. B. Resulting development of airway hyperplasia, airway obstruction, and bronchial hyperresponsiveness. Predisposing Factors A. Direct and indirect exposure to tobacco smoke. B. Allergens (e. g., animals such as cats and dogs, dust mites, pollen). C. Occupational exposures or irritants (e. g., paint, sprays). D. Pollution. E. Respiratory infections. F. Exercise. G. Stress. H. Gastroesophageal reflux disease. I. Obesity. J. Sex (more likely in female adults). K. Viral infections. Subjective Data A. Common complaints/symptoms. 1. Respiratory symptoms (e. g., wheezing, dyspnea, chest tightness, and cough). 2. Possible extrapulmonary manifestations (e. g., allergic skin conditions or conjunctival irritation). B. History of the present illness. 1. Onset of asthma and/or symptoms. 2. Precipitating factors. 3. Asthma severity such as frequency of rescue inhaler use. 4. Comorbid conditions that may predispose the patient to developing asthma. 5. Number of exacerbations in the past year. 6. History of ED visits, hospitalizations, and intubations related to asthma. C. Family and social history. 1. Family history of asthma. 2. Social history such as smoking and inhaled illicit drug use. 3. Employment/environmental factors (e. g., working outside, mining operations, military service). Physical Examination A. The physical examination may vary depending on the severity of the asthma and if the patient is having an exac-erbation. B. Expiratory wheezing on auscultation may be audible (see Figure 2. 2). C. Dyspnea may be evident (see Figure 2. 1). D. Changes in mentation (e. g., confusion, lethargy) may be apparent. E. Patients with moderate to severe asthma exacerbations may be in a tripod position and have tachypnea, absent breath sounds (silent chest) on auscultation, accessory muscle use (e. g., intercostal), and tachycardia. F. As previously stated, some patients may have extrapul-monary symptoms such as dermatitis, conjunctival irritation, and a swollen nasal mucosa. Diagnostic Tests A. Lung function. Initial diagnosis is based on a history of variable symptoms and confirmed variation in expiratory air-flow limitation. Lung function is typically normal between symptoms. 1. Evidence of obstruction with reduction in the forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) and at least one low FEV1. 2. One or more tests documented with excessive variabil-ity in lung function. a. Positive bronchodilator reversibility test with a greater than 12% and 200 m L increase from baseline in the FEV1. b. Excessive variability of greater than 10% in twice-daily peak expiratory flow (PEF) over 2 weeks. c. Positive exercise challenge test with decrease in FEV1of greater than 10% and 200 m L from base-line. d. Positive bronchial challenge test. e. Increase in the FEV1by greater than 12% and 200 m L OR a greater than 20% increase in the PEF from baseline after 4 weeks of treatment. f. Variation of lung function between office visits. B. PEF. 1. Can be routinely monitored in the outpatient setting. 2. Repeat values compared with personal best or pre-dicted value by patients. 3. Typically, severe symptoms: At or less than 50% predicted. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
15 Physical Ex amin ation General: Accessory muscle use? Diaphoresis? Flushing? Vital Signs: Febrile? Tachypnea? Tachycardia? Oxygen desaturations? HEENT: Facial or lip/oropharynx swelling? Central cyanosis? Rhinorrhea? Redness and/or watery eyes? Assessment of voice quality? Neck: Surgical scars? Old tracheostomy sites? Swelling? Goiter? Tracheal deviation? High pitched noises or stridor on auscultation? Cardiac: Elevated JVD? Murmur? S3 or S4 gallop? Edema? Respiratory: Inspiratory or expiratory wheezing? Other adventitious breath sounds such as crackles? Diminished breath sounds? Chest shape? Respiratory pattern? Retractions? Dullness or hyperresonance on percussion? Extremities: Cyanosis? Edema? Clubbing? Skin: Rash? Hives? Noted insect stings or bites? Diagnostics Pulse oximetry: Assess oxygen saturations ABG: Assess oxygenation and ventilation Chest x-ray: Assess for lung mass, consolidation/infiltrate, pulmonary edema, or hyperinfiation Pulmonary function testing: Assess for obstructive or restrictive disease Chest CT/Angiography: Assess for pneumonia, changes associated with obstructive disease, fluid, fibrosis, pulmonary embolus, mass, tracheal narrowing/stenosis, and so forth Allergy testing Respiratory viral testing: Such as RSV Bronchoscopy: Assess for tracheomalacia, tracheal narrowing/stenosis, foreign objects, masses/tumors Echocardiogram: To evaluate for heart failure Esophagram/barium swallow: Assess for reflux disease or aspiration Obtain the hist ory. Onset, quality, precipitating factors, alleviating factors, any associated f actors. Acute or gradual onset ? Associated with other sym ptoms such as dyspnea, cou gh, hoarsen ess, ushing, pruritus, chest discomfort/tightness, and so forth? Triggers such as exerc ise, fumes/smoke, allergens, and so forth? Medicati on or food allergies? Initiation of new medications? Com orbid conditions such as asthm a, COPD, heart failure, myocard ial infarction, GERD, and so forth? Recent respiratory infections? Curre nt or history of smoking? Prior intubations? History of throat or neck cancer, surgeries, and so forth? Aspiration? **Completed in the stab le patient with wheezing** FIGURE 2. 2 Algorithm for the evaluation of wheezing. ABG, arterial blood gas; COPD, chronic obstructive pulmonary disease. GERD, gastroesophageal reflux disease; JVD, jugular venous distention; RSV, respiratory syncytial virus C. Allergy skin testing. 1. Positive allergen test: Allergen not necessarily causing asthma symptoms. 2. Essential to account for the timing of symptoms in relation to allergen exposure and the patient's history. D. Chest x-ray. 1. Usually normal in patients with asthma but may reveal hyperinflation. 2. If a patient has a fever in conjunction with respiratory symptoms: May be diagnostic for pneumonia. E. Pulse oximetry and arterial blood gas (ABG). 1. Used to evaluate for hypoxemia. 2. ABG: Can also be used to evaluate for hypercapnia and respiratory acidosis, especially in those patients pre-senting with an acute exacerbation. Differential Diagnosis A. Chronic obstructive pulmonary disease (COPD). B. Pulmonary embolism. C. Congestive heart failure (CHF). D. Chronic rhinosinusitis. E. Alpha-1 antitrypsin deficiency. Evaluation and Management Plan A. General plan. 1. The goal is to control symptoms and minimize the risk of asthma exacerbations. 2. T reatment includes assessment, adjustment of medi-cations, and response review. 3. Emergency treatment: Patients with progressively worsening symptoms may present to the ED. a. Evaluation of ABCs, physical assessment, and PEF is necessary. b. Medication management consists of a short-acting beta2agonist (SABA) via continuous nebulizer or a metered-dose inhaler, corticosteroids, oxygen therapy, and ipratropium bromide. c. Patients with a more severe exacerbation as demonstrated by a PEF less than 50% will receive Asthma | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
16 intravenous instead of oral corticosteroids (OCS) and possibly intravenous magnesium sulfate. d. Posttreatment, the PEF should be reassessed. e. Patients with an alteration in mental status (e. g., somnolence, confusion), absent breath sounds, worsening hypoxemia or hypercapnia, and hemo-dynamic instability should be placed on invasive mechanical ventilation and admitted to the ICU. B. Patient/family teaching points. 1. Nonpharmacological interventions should be addressed such as smoking cessation, engagement in regular physical activity, and avoidance of known occu-pational exposures and allergen triggers. 2. Patients should be provided with self-management education to reduce morbidity. Essential components included in self-management are: a. Self-monitoring of symptoms and/or PEF. b. A written action plan that includes recognition and response to worsening asthma symptoms. c. Regular review of asthma control and treatment by a healthcare provider. C. Pharmacotherapy. 1. A daily controller treatment is recommended once an asthma diagnosis has been confirmed. 2. Early treatment with an inhaled corticosteroid (ICS) has been shown to improve lung function. a. A controller treatment is not indicated in patients with rare asthma symptoms, no night awakenings, no exacerbations in the past year, and a normal FEV1. b. An ICS (controller treatment) is recommended in patients with two or more asthma symptoms monthly, waking from asthma more than one night per month, and asthma symptoms plus risk factors for exacerbations. 3. A stepwise approach is used for treatment adjustment. See Table 2. 1 for commonly used medications in asthma management. a. Step 1: SABA as needed with consideration of a controller treatment with an ICS. b. Step 2: Low dose ICS plus a SABA as needed. i. The provider can consider a leukotriene recep-tor antagonist (LTRA) but research has shown it to be less effective. ii. An ICS and long-acting beta2agonist (LABA) combination leads to improvement in symptoms but is more expensive and has similar exacerbation rates compared to an ICS alone. c. Step 3: Low dose ICS/LABA plus a SABA as needed ORICS/formoterol and reliever therapy. d. Step 4: Low dose ICS/formoterol plus a reliever therapy ORmedium dose ICS/LABA plus a SABA as needed. The provider can add on tiotropium in patients with a history of exacerbations. e. Step 5: Patients should be referred to an expert. Additional medication management includes chang-ing the patient to a high dose ICS/LABA plus oral corticosteroids OCS. 4. With the stepwise approach, the treatment regimen can be adjusted up or down by the provider based on fre-quency and severity of asthma symptoms. 5. Asthma exacerbations are characterized by an increase or worsening in respiratory symptoms and lung function compared to the patient's baseline. 6. Patients with acute exacerbations and an asthma action plan in place can increase their SABA or usual reliever, as well as maintenance controller. OCS can be TABLE 2. 1 Asthma Medications Beta2agonists SABA Levalbuterol Salbutamol (albuterol) Terbutaline Anticholinergics/Antimuscarinics SAMA Ipratropium bromide (reduces risk of admissions in acute asthma; less effective in the long term) LAMA Tiotropium (add-on option in patients with history of exacerbations on controller medications) ICSs Beclometasone Budesonide Fluticasone furoate Fluticasone propionate Mometasone Triamcinolone acetonide Combination ICS plus LABA ICS/LABA Beclometasone/formoterol Budesonide/formoterol Fluticasone furoate/vilanterol Fluticasone propionate/formoterol Fluticasone propionate/salmeterol Mometasone/formoterol Systemic corticosteroids Prednisone (oral) Methylprednisolone (intravenous) LTRA Montelukast Pranlukast Zafirlukast Zileuton ICS, inhaled corticosteroid; LABA, long-acting beta2agonist; LAMA, long-acting muscarinic antagonist; LTRA, leukotriene receptor antagonist; SABA, short-acting beta2agonist; SAMA, short-acting muscarinic antagonist. added for patients who fail to respond to treatment or severe exacerbations with a PEF or FEV1less than 60% predicted or their personal best (see Exhibit 2. 1). D. Discharge instructions. 1. Discharge criteria. Patients should a. Show improvement in symptoms such as resolu-tion of accessory muscle use and dyspnea, improved respiratory rate, and O2saturation greater than 94% on room air. b. Improved PEF of greater than 60% predicted or personal best. c. Have adequate home resources. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
17 2. Diet. a. Restrictions: Specific diet based on whether the patient has underlying comorbid conditions such as diabetes or renal disease. b. No restrictions: Patient can resume a regular diet. 3. Medications. a. OCS: Usually prescribed for 5 to 7 days. b. Reliever medications such as SABA: Can be resumed on an as-needed basis. c. ICS prior to discharge. i. ICS/LABA ORICS/formoterol. ii. If the patient is already on an ICS: Increase the dose for 2 to 4 weeks. d. Medication reconciliation and continuation of appropriate medications for comorbid conditions. 4. T reatment plan. a. Identification of risk factors that contribute to exacerbations. b. Individualized written asthma action plan. c. Evaluation of maintenance therapy understand-ing. d. Assessment of inhaler technique. e. Assessment of PEF meter technique if applicable outside of an acute exacerbation. f. Smoking cessation counseling. g. Immunizations such as influenza. Influenza can trigger acute and severe asthma exacerbations that could potentially result in necessitating ventilatory support. h. Management of comorbid conditions. 5. Discuss with patient. a. Importance of medication compliance and proper inhaler technique to reduce symptoms and exacerba-tions. b. As previously stated, avoidance of known risk fac-tors that worsen asthma symptoms or lead to exacer-bations such as smoking or other known allergens. c. Signs and symptoms of an impending exacerbation such as increasing reliever inhaler use, frequent awak-ening at night with coughing or dyspnea, and PEF less than 60% of predicted or personal best. Follow-Up A. Regular follow-up is dependent on symptom control and exacerbation risk but should last for 1 to 3 months after treat-ment initiation and every 3 to 12 months once stabilized. B. Patients should see their primary care provider or pulmo-nologist 1 to 2 weeks after self-management of an exacerba-tion. C. Patients should see their primary care provider or asthma specialist/pulmonologist within 2 to 7 days of discharge from the ED or hospital. Consultation/Referral A. Patients with progressively worsening asthma despite increasing treatment may require a referral to a pulmonolo-gist or allergist. B. A pulmonologist and/or intensivist consultation is indi-cated for patients with a moderate to severe exacerbation necessitating ICU admission and/or noninvasive and inva-sive mechanical ventilation. Special/Geriatric Considerations A. Poor inhaler technique needs to be considered in patients with persistent symptoms. B. Comorbid conditions may contribute and complicate asthma management. C. Routine chest x-rays and antibiotic therapy are not indi-cated in asthma management. D. In the elderly population, asthma can be underdiagnosed or overdiagnosed due to varying assumptions and perceptions over dyspnea. Bibliography Centers for Disease Control and Prevention. (2013). Asthma facts: CDC's National Asthma Control Program Grantees. Atlanta, GA: U. S. Depart-ment of Health and Human Services. Retrieved from https://www. cdc. gov/asthma/pdfs/asthma_facts_program_grantees. pdf Global Initiative for Asthma. (2017). Global strategy for asthma man-agement and prevention. Retrieved from https://ginasthma. org/wp-content/uploads/2016/01/wms-GINA-2017-main-report-tracked-changes-for-archive. pdf Chronic Obstructive Pulmonary Disease E. Mone ́e Carter-Griffin Definition A. A chronic and progressive respiratory disease character-ized by expiratory airflow limitation. Incidence A. Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States and fourth leading cause of death worldwide. B. The incidence is much higher in smokers and ex-smokers compared to nonsmokers. C. It is more prevalent in individuals greater than 40 years with the greatest prevalence in those greater than 65 years. D. T raditionally, prevalence has been higher in men but recent literature suggests the occurrence may be rising in women, and women may be more susceptible to poorer out-comes. Pathogenesis A. The lungs are exposed to a stimulus (e. g., smoking, fumes) that causes inflammation of the airways. Neutrophils and var-ious other immune cells are recruited to the airways lead-ing to breakdown of elastin fibers and increasing oxidative stress. B. Ultimately, there is destruction of alveolar walls, decreased repair of the alveoli, fibrosis, and bronchiolar wall thickening leading to narrowed airways, impaired gas exchange, and enlarged air spaces. Predisposing Factors A. Tobacco smoke: Leading environmental risk factor. B. Individuals greater than 40 years. C. Occupational exposures to lung irritants (e. g., dust, chemical agents, fumes). D. Alpha-1 antitrypsin is a genetic condition leading to COPD that should be tested in a new diagnosis of COPD. E. Airway hyperresponsiveness (e. g., asthma). F. Allergies. G. Recurrent respiratory infections. Subjective Data A. Common complaints/symptoms. 1. Dyspnea (see Figure 2. 1): Chronic and progressive. This is a cardinal symptom. Chronic Obstructive Pulmonary Disease | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
18 2. Pulmonary Guidelines FIGURE 2. 3 Algorithm for the evaluation of cough. ACE, angiotensin-converting enzyme; COPD, chronic obstructive pulmonary disease; GERD, gastroesophageal reflux disease; HEENT, head, ear, eyes, nose, and throat. 2. Cough (see Figure 2. 3) with or without sputum pro-duction. a. Not uncommon for individuals to produce small amounts of sputum. b. Increasing sputum production, especially with change in color: May indicate bacterial infection. 3. Wheezing (see Figure 2. 2) and/or chest tightness. 4. Severe COPD: Possible fatigue, weight loss, and anorexia. B. Family and social history. 1. Inquire about environmental risk factors and family history. 2. Inquire about smoking because it can accelerate or exacerbate COPD symptoms. C. Review of symptoms. 1. Evaluate for symptom onset, duration, severity, asso-ciated symptoms (e. g., increased wheezing or sputum), and aggravating and alleviating factors. 2. Inquire about early onset of COPD. 3. Assess for risk factors such as a history of allergies, asthma, or recurrent respiratory infections. Physical Examination A. The physical examination for COPD is rarely diagnostic. Physical signs of COPD may or may not be present, depend-ing on the severity of disease. However, it is still important to assess for the respiratory and systemic symptoms that may be associated with COPD. B. General examination. 1. Assess the respiratory rate. It may be normal or increased. 2. Assess the patient's posture. Leaning forward with out-stretched palms is associated with an attempt to relieve dyspnea. 3. Check breathing. In advanced disease or severe dysp-nea, pursed-lip breathing is possible. Obtain the hist ory. Onset, timing, description of cough, alleviating factors, any assoc iated f actors. Acute (<3 wee ks), subacute (3-8 weeks), or chronic (>8 wee ks)? Associated with other sym ptoms such as dyspnea, wheezing, chest tightne ss, or hemoptysis? Recent respiratory infection? Occupational or environmental exposures? Medicati ons such as ACE inhibitors? Known comorbid conditions such as asthma, COPD, GERD, and so forth Curre nt or history of smoking? Occurrence of cough? Upon awaken ing? Lying down? During exercise? Initial Diagnostic Chest x-ray: All individuals with a chronic cough. All individuals with an acu te cough AND dyspnea, chest pa in, fever, hemoptysis, or weight loss Physic al Ex amination The initial physical exam focuses on clues suggestive of cardiopulmonary disease. A thorough full exam should follow because a cough may be a manifestation of a more systemic disease process. General: Weight loss? Fatigue? Vital Signs: Usually normal unless associated with another disease process. May have tachypnea, tachycardia, oxygen desaturations, and/or fever. HEENT: Red and/or watery eyes? Fluid behind eardrum? Boggy, swollen, and/or pale mucus membranes? Nasal polyps? Thin, watery, or purulent secretions? Congestion? Throat redness? Hoarseness? Respiratory: Adventitious breath sounds such as crackles or wheezing? Chest shape? Respiratory pattern? Dullness or hyperresonance on percussion? Extremities: Clubbing? Edema? Acute/Subacute Usually does not req uire further testing. Additional testing focuses on a susp ected etiology. Allergy testing Chest CT/Angiography: Assess f or pneumonia, changes a ssociated w ith obstructive disea se, fluid, fibrosis, pulmonary embolus Pulmon ary function testing: Assess for obstructive or restrictive disea se Tuberculosis skin tes ting Pertus sis testing Chron ic Pulmona ry funct ion testi ng: Assess for obstructive or restrictive disease Additional work-up may follow after empirical treat ment for disorders suc h as GERD. Bronchoscopy: To evaluate for chronic infla mmation Sinus Imaging High-resolution Chest CT: Used in cough with atypical presentations a nd concern for chronic pulmonary disea se Eso phagram or swallow evaluation: Assess for reflu x disease or aspiration Echocardigram: To evaluate for heart failure or elevated p ulmonary pressures ? | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
19 4. Inspect for clubbing. 5. In more severe disease, cyanosis, elevated jugular venous pressure, and peripheral edema may be present. C. Respiratory examination. 1. Inspect the chest. a. Check for an increased anteroposterior chest diameter due to hyperinflation of the lungs, giving a barrel chest shape. b. Assess for use of accessory muscles (e. g., sternoclei-domastoids, scalenes, intercostals). 2. Percuss the chest wall. a. Observe for hyperresonance due to overinflation of the lungs. 3. Auscultate bilaterally. a. Diminished breath sounds throughout. b. Occasional expiratory wheezing. c. Prolonged expiratory phase. d. Coarse rhonchi throughout the respiratory phase, especially during times of increased sputum pro-duction. Diagnostic Tests A. Pulmonary function test: Spirometry. 1. Objective measurement of airflow limitation. 2. Ratio between the volume of air forcibly exhaled after maximal inspiration (forced vital capacity [FVC]) and the volume of air forcibly exhaled during the first second (forced expiratory volume [FEV1]). A ratio less than 0. 7 after bronchodilator testing indicates obstruction. 3. Reduced FEV1(reduction in expiratory flow rates). 4. Possibly reduced FVC, usually to a lesser extent than the FEV1. B. Chest x-ray (see Figure 2. 3). 1. Hyperinflation, as evidenced by a flattened diaphragm and increased retrosternal air space. 2. Hyperlucency of the lungs. 3. Rapid tapering of the vascular markings. C. Arterial blood gas (ABG). 1. May reveal hypercapnia and/or hypoxemia. a. Early or mild COPD: Typically normal. b. Worsening as COPD progresses. Individuals with moderate to severe disease may have a chronic respi-ratory acidosis often with metabolic compensation as evidenced by increased serum bicarbonate. 2. Can provide clues to the acuteness and severity of COPD in those individuals with an exacerbation. D. Pulse oximetry. 1. Used to assess arterial oxygen saturation. If the pulse oximetry is less than 92%, then an ABG is warranted. E. Exercise testing (e. g., 6-minute walking distance). 1. Objectively measures functional capacity by evaluat-ing whether the individual has a reduction in walking dis-tance. 2. Useful for disability assessment, risk of mortality, and indicator of impairment of health status. F. Laboratory evaluation. 1. Alpha-1 antitrypsin screening: This should be assessed in those individuals with a family history of COPD at an early age and less than 45 years. Differential Diagnosis A. Bronchitis. B. Chronic cough. C. Congestive heart failure (CHF). D. Emphysema. E. Asthma. Evaluation and Management Plan A. General plan. 1. The interventions listed in the following are part of the general plan for a COPD patient. We should incorpo-rate these interventions in all COPD patients who meet criteria. 2. Specific interventions. a. Smoking cessation. i. Literature has indicated that counseling from healthcare professionals increases cessation rates compared to self-initiated strategies. ii. A five-step program initiated by healthcare providers offers a helpful framework for cessation. iii. Nicotine replacement (e. g., gum, lozenge, transdermal patch) can increase long-term cessa-tion rates. iv. Pharmacologic agents, such as varenicline and bupropion, can increase long-term cessation rates but should be used as an adjunct to an interven-tion program. b. Individuals should receive the influenza and pneu-mococcal. c. Reduction of risk factors such as avoidance of occupational irritants can help. d. Pulmonary rehabilitation lasting from 6 to 8 weeks has been shown to improve dyspnea, health status, exercise intolerance, and hospitalizations in patients with a recent exacerbation. This requires collaboration among multiple healthcare professionals. e. T reatment recommendations should consider the symptomatic assessment (ABCD group) and the indi-vidual's spirometric classification (GOLD 1-4). In addition, they should consider comorbid conditions and other medications. f. The GOLD categories one through four (spiro-metric grade) are used to classify the degree or severity of airflow limitation, which is identified using: i. GOLD 1: Mild, FEV180% or greater than the predicted. ii. GOLD 2: Moderate, FEV1greater than or equal to 50% predicted but less than 80% predicted. iii. GOLD 3: Severe, FEV1greater than or equal to 30% predicted but less than 50% predicted. iv. GOLD 4: Very severe, FEV1is less than 30% predicted. g. Symptom assessment can be evaluated using the COPD Assessment Test (CAT) or the COPD Control Questionnaire (CCQ). The CAT is commonly used in the clinical setting and a score greater than t10 is associated with symptoms. h. The ABCD Assessment Tool (Groups A-D) is a measure of the individual's symptoms and history of exacerbations. i. Groups A and B indicate the individual has no more than one exacerbation with no hospitaliza-tions and a CAT score less than 10 or greater than 10, respectively. ii. Groups C and D indicate the individual has more than two exacerbations or more than one exacerbation leading to hospitalization and a CAT score less than 10 or greater than 10, respectively. 3. Management of stable COPD. a. T reatment should be individualized based on symptoms and risk for exacerbations. 4. Goals of treatment. a. Symptom relief. Chronic Obstructive Pulmonary Disease | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
20 b. Increased exercise tolerance. c. Improved health status. d. Reduction of mortality. e. Prevention of disease progression and exacerba-tions. f. Management should include pharmacological and nonpharmacological interventions. g. Smoking cessation and avoidance of occupational irritants are important. h. The GOLD guidelines suggest treatment escala-tion or de-escalation in those with persistent symp-toms or resolution of symptoms, respectively. T rials are needed to investigate treatment escalation and de-escalation. 5. Management of exacerbations. a. Acute worsening in symptoms from baseline occurs. i. Increased sputum, including purulence, increased dyspnea, and increased cough and/or wheezing. b. Can be classified as: i. Mild: T reatment with short-acting bron-chodilators. ii. Moderate: T reatment with short-acting bron-chodilators plus antibiotics and/or oral steroids. iii. Severe: Requires hospitalization or ED visits. c. Symptoms can last 7 to 10 days and contribute to disease progression. d. Severity of exacerbation is based on the individ-ual's symptoms and whether respiratory failure is present. i. No respiratory failure to respiratory rate 20 to 30/minute; no accessory muscle use, mental status change, or elevation in Pa CO2; hypoxemia improved with less than 35% of inspired oxygen. ii. Respiratory failure, nonlife threatening to res-piratory rate greater than 30/minute; use of acces-sory muscles, no change in mental status, Pa CO2 above baseline or 50 to 60 mm Hg; hypoxemia improved with less than 30% of inspired oxygen. iii. Respiratory failure, life threatening to res-piratory rate greater than 30/minute; accessory muscle use, mental status changes, Pa CO2above baseline or greater than 60 mm Hg or presence of a respiratory acidosis with a p H less than 7. 25; hypoxemia requiring greater than 40% of inspired oxygen or not improving with supplemental oxygen. B. Pharmacotherapy. 1. See Table 2. 2. 2. Adequate pharmacotherapy can reduce symptoms and severity of exacerbations, and improve overall health status. 3. Most medications are inhaled. It is essential that indi-viduals receive education on proper technique. 4. Bronchodilators. a. Often prescribed in COPD to prevent or reduce symptoms. b. Central to symptom management. c. Inhaled beta2agonists. i. Functional antagonism to bronchoconstric-tion by relaxing airway smooth muscle. ii. Short-acting (SABA) and long-acting (LABA) beta2agonists. iii. SABAs: Typically last 4 to 6 hours; shown with regular use to improve symptoms and FEV1in COPD. TABLE 2. 2 COPD Medications Beta2agonists (inhaled) SABA Fenoterol Levalbuterol Salbutamol (albuterol) Terbutaline LABA Arformoterol Formoterol Salmeterol Anticholinergics/Antimuscarinics (inhaled) SAMA Ipratropium bromide Oxitropium bromide LAMA Aclidinium bromide Glycopyrronium bromide Tiotropium Combination SABA plus short-acting anticholinergic (inhaled) SABA/SAMA Fenoterol/ipratropium Salbutamol/ipratropium Combination LABA plus long-acting anticholinergic (inhaled) LABA/LAMA Formoterol/aclidinium Formoterol/glycopyrronium Combination LABA plus ICS (inhaled) LABA/ICS Formoterol/budesonide Formoterol/mometasone Salmeterol/fluticasone Vilanterol/fluticasone furoate Methylxanthines (oral and intravenous) Theophylline (SR) Systemic Corticosteroids Prednisone (oral) Methylprednisolone (intravenous) Phosphodiesterase-4 inhibitors (oral) Roflumilast Antibiotics (oral) Azithromycin Erythromycin COPD, chronic obstructive pulmonary disease; ICS, inhaled corticosteroid; LABA, long-acting beta2agonist; LAMA, long-acting antimuscarinics; SABA, short-acting beta2agonist; SAMA, short-acting antimuscarinics. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
21 iv. LABAs: Duration of 12 hours or more; shown to improve lung function, dyspnea, and reduce exacerbations. d. Anticholinergics/antimuscarinics. i. Blockage of acetylcholine on muscarinic receptors leading to relaxation of airway smooth muscle. ii. Short-acting (SAMA) and long-acting (LAMA) antimuscarinics. iii. SAMAs: Shown to improve symptoms and FEV1with regular or as needed use. iv. LAMAs: Shown to improve lung function, dyspnea, and health status. Literature has shown that LAMAs compared to LABAs reduce exacer-bations and decrease hospitalizations. e. Methylxanthines. i. Need to monitor therapeutic drug levels and for signs and symptoms of toxicity. f. Inhaled corticosteroids (ICS). i. No mortality benefit or modification in the long-term decline of the FEV1with ICS monotherapy. ii. Severe COPD and regular use of ICS: Increased risk for pneumonia. g. Combination inhaled therapy. i. Combination of a SABA and SAMA: Superior in improving symptoms compared to either med-ication used alone. ii. Combination of an LABA and LAMA: Improves FEV1and reduces symptoms and exac-erbations compared to either medication used alone or compared to those individuals treated with a combination of ICS and LABA. iii. Combination therapy with an ICS and LABA compared to monotherapy with either medica-tion: Improves lung function and health status as well as reduces exacerbations. h. Oral glucocorticoids. i. Long-term risks: Preclude use in stable COPD. ii. In acute exacerbations in hospitalized patients: Decreased treatment failure and relapse as well as improved lung function. i. Phosphodiesterase4inhibitors. i. Only one approved drug, roflumilast: Used for patients with a history of exacerbations and severe to very severe COPD. ii. Has been shown to improve lung function and decrease moderate to severe exacerbations. iii. Requires caution in those with depression and those who are underweight. j. Antibiotics. i. Reduced exacerbations: Azithromycin 250 mg daily or 500 mg three times a week OR ery-thromycin 500 mg twice daily for 1 year. 1)Use of azithromycin: Association with increased antibiotic resistance. ii. No data indicating efficacy of chronic antibi-otic therapy beyond 1 year. k. Mucolytics. i. Reduced risk of exacerbation in select popula-tions. 5. Pharmacologic treatment using the ABCD Assess-ment Tool. a. Utilization of an algorithm based on the ABCD Assessment Tool Groups A-D. b. Group A. i. Should be placed on a bronchodilator. ii. The provider should evaluate drug effective-ness and decide to continue, stop, or try an alter-native bronchodilator class. c. Group B. i. Should be initiated on a long-acting bron-chodilator. Choice of long-acting bronchodilator should be based on symptom relief. ii. T wo bronchodilators: Recommended for indi-viduals with persistent dyspnea. d. Group C. i. Should be initiated on a bronchodilator; pre-ferred choice is a LAMA secondary to superior exacerbation prevention. ii. Individuals with persistent dyspnea: T wo long-acting bronchodilators (LABA/LAMA) OR combination of long-acting bronchodila-tor and ICS (LABA/ICS). The primary choice is LABA/LAMA secondary to the increased risk of pneumonia in certain individuals on ICS. e. Group D. i. LABA/LAMA combination for certain patients. In individuals with findings suggestive of asthma-COPD overlap, initiation of LABA/ICS may be the first choice. ii. Individuals with persistent exacerbations despite being on LABA/LAMA triple inhaled therapy with a LABA/LAMA/ICS OR switch to a LABA/ICS. However, there is no clinical evidence that switching to a LABA/ICS from LABA/LAMA will improve symptoms. iii. For continued exacerbations despite triple inhaled therapy, possible: 1)Addition of roflumilast. 2)Addition of a macrolide, specifically azithromycin. 3)Stopping the ICS. 6. Hospital medication management and medical ther-apy of COPD exacerbations. a. Combination of SABA and anticholinergics. b. Possible systemic steroids. i. Have been shown to shorten recovery time, improve oxygenation, and improve the risk of early relapse and treatment failure. ii. Oral prednisone recommended at 40 mg daily for 5 days. c. Consideration of oral antibiotics when signs of bacterial infection are present. d. Possible O2therapy and noninvasive ventilation. i. Noninvasive ventilation: Shown to reduce intubation rates, mortality, and hospital length of stay. 7. Invasive mechanical ventilation: Warranted in patients who are unable to undergo or fail noninva-sive ventilation, are hemodynamically unstable, have status postarrest, have profound hypoxemia in patients not able to tolerate noninvasive ventilation, massive aspi-ration, and encounter significant changes in levels of consciousness. C. Discharge instructions. 1. Be aware that these vary based on the severity of the underlying COPD and exacerbation. 2. Review all clinical (e. g., improved dyspnea, sputum production, cognition) and laboratory data. Chronic Obstructive Pulmonary Disease | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
22 3. Assess continual need for oxygen therapy. Patients on chronic home O2should resume their baseline O2 requirements. 4. Check functional status. 5. Ensure adequate home resources. 6. Activity. a. Pulmonary rehabilitation. i. Shown to reduce hospitalizations, as well as improve dyspnea and health status. ii. Indicated in all patients with symptoms and/or high risk for exacerbation. iii. Early rehabilitation has been associated with improved mortality. b. Regular physical activity. i. Combination interval training with strength training. ii. Strong predictor of mortality. 7. Diet. a. May vary depending on underlying comorbid conditions such as diabetes, heart failure, or renal disease. b. Nutritional supplementation: Recommended; should be considered in malnourished COPD patients. 8. Medications (see section “Pharmacotherapy”). a. Bronchodilators. i. Most patients are likely to receive two long-acting bronchodilators (LABA/LAMA) or a long-acting bronchodilator and ICS (LABA/ICS). b. Additional agent: The provider may choose to ini-tiate a long-term macrolide or roflumilast in patients who meet criteria and continue to have exacerba-tions despite multimedication inhaled therapy. c. Other drugs: Medication reconciliation and con-tinuation of medications for comorbid conditions are necessary. 9. T reatment plan. a. Evaluation of psychosocial needs and home resources such as availability of home O2. b. Inclusion of family in the treatment and educa-tion plan. c. Evaluation maintenance therapy understanding. d. Ensuring of understanding of withdrawal medi-cations prescribed for an acute exacerbation such as steroids. e. Assessment of inhaler technique. f. Pulmonary hygiene (e. g., deep breathing). g. Smoking cessation counseling. h. Encouragement of pneumococcal and influenza vaccinations. i. Setting up of pulmonary rehabilitation. j. Management of comorbid conditions such as gastroesophageal reflux disease (GERD) and heart failure. 10. Discuss with patient. a. Discuss signs and symptoms associated with infection and/or exacerbations such as fever, chills, increased dyspnea, and increasing sputum produc-tion or change in sputum color. b. Instruct patients on the importance of medica-tion compliance and physical activity to reduce the occurrence of exacerbations, reduce symptoms, and improve quality of life. Follow-Up A. Follow-up with a primary care physician or pulmonolo-gist, ideally within 1 to 4 weeks of discharge. 1. Especially during initiation, escalation, and de-escalation in therapy. 2. With new or worsening symptoms. 3. Posthospitalization. B. Association of early follow-up with fewer readmissions. Consultation/Referral A. Consultation with a pulmonologist: In patients with pro-gressively worsening symptoms, severe or very severe COPD, frequent exacerbations, and respiratory failure. Special/Geriatric Considerations A. Chronic use of oxygen is indicated for patients with severe hypoxemia at rest and chronic respiratory failure. B. Patients should be evaluated and treated for comorbid conditions such as heart failure, obstructive sleep apnea, obe-sity, hypoventilation syndrome, and so forth. C. Education alone has not been shown to change behaviors; however, education and self-management with a case man-ager may prevent exacerbation complications. D. Physical activity is highly encouraged given its strong mortality prediction. E. Nutritional supplements may be indicated in malnour-ished patients. F. Patients should be considered for lung volume reduction surgery if they have upper-lobe predominance emphysema. G. Patients with very severe COPD and advanced systemic symptoms may be considered for lung transplantation. H. Discussions with patients and families regarding palliative and end-of-life care should take place in the event the patient becomes critically ill. Bibliography American Lung Association. (2013). T aking her breath away: The rise of COPD in women. Chicago, IL: Author. Retrieved from https://www. lung. org/assets/documents/research/rise-of-copd-in-women-full. pdf Decramer, M. L., Chapman, K. R., Dahl, R., Frith, P., Devouassoux, G., Fritscher, C., & Mc Bryan, D. (2013). Once-daily indacaterol versus tiotropium for patients with severe chronic obstructive pulmonary dis-ease (INVIGORATE): A randomized, blinded, parallel-group study. The Lancet Respiratory Medicine, 1, 524-533. doi:10. 1016/S2213-2600(13) 70158-9 Global Initiative for Chronic Obstructive Lung Disease. (2017). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from https://www. goldcopd. org Karner, C., Chong, J., & Poole, P. (2012). Tiotropium versus placebo for chronic obstructive pulmonary disease. Cochrane Database of System-atic Reviews, 2014 (7), CD009285. doi:10. 1002/14651858. CD009285. pub3 Vogelmeier, C., Hederer, B., Glaab, T., Schmidt, H., Rutten-van Molken, M., Beeh, K.,... Fabbri, L. M. (2011). Tiotropium versus salmeterol for the prevention of exacerbations of COPD. New England Journal of Medicine, 364, 1093-1103. doi:10. 1056/NEJMoa1008378 Pleural Effusions E. Mone ́e Carter-Griffin Definition A. Result of excess fluid production or decreased absorption of fluid in the pleural space. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
23 Incidence A. There are an estimated 1 to 1. 5 million cases annually. B. In general, the incidence is similar in both males and females. However, certain causes are more likely in males or females. Pathogenesis A. Pleural effusions are a manifestation of an underlying dis-ease process. B. Effusions can be transudative or exudative. 1. T ransudative effusions are typically due to imbalance that occurs between the hydrostatic pressure and oncotic pressure. 2. Exudative effusions are the result of an alteration of the pleural surface such as pleural or lung inflammation, impairment of lymphatic drainage, and so forth. Predisposing Factors A. Any disease that may lead to accumulation of pleural fluid. The most common causes of pleural effusions are heart failure, malignancy, and pneumonia. B. Diseases that can predispose a patient to a transudative effusion. 1. Heart failure. 2. Cirrhosis. 3. Nephrotic syndrome. C. Diseases that can predispose a patient to an exudative effusion. 1. Pneumonia (parapneumonic effusion or empyema). 2. Malignancy. 3. Pancreatitis/pancreatic disease. 4. T rauma. Subjective Data A. Common complaints/symptoms. 1. Patients may have complaints of cough, pleuritic chest pain, and dyspnea. 2. Patients may have additional symptoms or clinical manifestations secondary to the underlying etiology for the pleural effusion. B. Review of systems. 1. Depending on the suspected etiology of the effusion, the provider may want to inquire about heart failure, known liver disease or chronic alcoholism, recent trauma, history of cancer, occupational exposures, recent signs and symptoms of respiratory infection, and so on. Physical Examination A. Typically, no physical findings when the pleural effusion is less than 300 m L. B. Other findings. 1. Diminished breath sounds. 2. Dullness on percussion. 3. Pleural friction rub. 4. Decreased tactile fremitus. C. Possible other findings such as fever and edema, depend-ing on the etiology. Diagnostic Tests A. Chest x-ray (see Figure 2. 4). 1. Blunting of costophrenic angle in upright posteroan-terior x-ray when 175 m L or more is present. B. Smaller pleural effusions observed in lateral decubitus x-rays. C. Failure of a pleural effusion to layer on a lateral decubitus x-ray. This may indicate a loculated pleural effusion. D. Chest CT: Possible for evaluation of a loculated pleural effusion. E. Ultrasonography: Can be used to evaluate the size of the pleural effusion and location. F. Diagnostic thoracentesis. 1. Should be performed in patients whose etiology is unclear and who fail to respond to therapy. 2. Pleural fluid for diagnosis. Send for glucose, lactate dehydrogenase (LDH), p H, cell count, protein, and cul-ture to aid with a possible diagnosis. Serum blood levels of LDH, total protein, and glucose are needed for com-parison. 3. Light's criteria: Used to differentiate between tran-sudative and exudative pleural effusions. a. Exudative if one of the following is present. i. Ratio of pleural fluid to serum protein is greater than 0. 5. ii. Ratio of pleural fluid to serum LDH is greater than 0. 6. iii. Pleural fluid LDH is greater than two-thirds the normal serum LDH. 4. Additional testing may be indicated when trying to identify the etiology. Differential Diagnosis A. First, it is important to determine if the pleural effusion is transudate or exudate using Light's criteria in order to estab-lish a differential diagnosis. B. T ransudate pleural effusion. C. Congestive heart failure (CHF). D. Cirrhosis. E. Exudate pleural effusion. F. Pneumonia. G. Cancer. H. T uberculosis. I. Pulmonary embolism. Evaluation and Management Plan A. General plan. 1. For transudative effusions, manage the underlying dis-ease process such as diuretics for patients with effusions due to heart failure. 2. Specific interventions. a. Monitoring of chest x-rays: As needed pending the size, symptoms associated with the effusion, and fol-lowing treatment to evaluate for reaccumulating fluid. b. Therapeutic thoracentesis: Used for patients with refractory, large pleural effusions and/or severe respi-ratory compromise to relieve symptoms. Diagnostic evaluation may be required if concerned for malig-nancy, infectious process, and so forth. i. Patients with malignant pleural effusions may require more than one thoracentesis due to reac-cumulating fluid. ii. Patients who need frequent thoracentesis may require a pleurodesis or indwelling tunneled pleu-ral catheter for home drainage. The patient and family will require teaching about home use of the tunneled pleural catheter. c. Chest tube. i. Required for a parapneumonic effusion or an empyema, but ultimately the patient will need to be treated with antibiotics and possible surgical intervention. Pleural Effusions | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
24 FIGURE 2. 4 Chest x-ray of left pleural effusion. Source: By Tomatheart/Shutterstock. ii. Required for patients with a hemothorax (bloody pleural effusion). B. Patient/family teaching points. 1. Teach patients that it may help to cough or take a deep breath by holding a pillow against your chest to prevent pain. 2. Practice smoking cessation and avoid secondhand smoke. 3. Keep hydrated. 4. Use an incentive spirometer for frequent deep breath-ing and coughing exercises. C. Pharmacotherapy—depends on the etiology of pleural effusion. 1. Antibiotics. a. For use in parapneumonic effusions, empyemas, and abscesses. b. Use empiric coverage and consider the patient's age, comorbidities, and clinical picture before tailor-ing the final selection of antibiotics. c. In general, the antimicrobial coverage should cover anaerobic organisms. 2. Vasodilators and diuretics: For use in pleural effusions related to CHF and pulmonary edema. 3. Anticoagulants: For use in pleural effusions due to pulmonary emboli. D. Discharge instructions. 1. Instruct patients to report any increased work in breathing, fevers, and pain that does not go away or gets worse. Take medications as prescribed. Follow-Up A. Patients in the hospital: Monitor with serial chest x-rays and/or based on their symptoms. B. Etiology of the effusion: Determines the course and fre-quency of outpatient follow-up. Consultation/Referral A. Thoracentesis: This can be completed by a hospitalist, pulmonologist, or interventional radiologist. If a more inva-sive procedure such as a surgical intervention is indicated, then a cardiothoracic surgeon will need to be consulted. B. Further referrals may be indicated depending on the eti-ology of the effusion. If the effusion is malignant, then oncol-ogy will need to be consulted. Bibliography Bhatnagar, R., & Maskell, N. (2015). The modern diagnosis and manage-ment of pleural effusions. British Medical Journal, 351, 26-30. doi:10. 1136/bmj. h4520 Kummerfeldt, C. E., Pastis, N. J., & Huggins, J. T. (2017). Pleural diseases. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1923-1932). New York, NY: Mc Graw-Hill. Saguil, A., Wyrick, K., & Hallgren, J. (2014). Diagnostic approach to pleu-ral effusion. American Family Physician, 90, 99-104. Retrieved from https://www. aafp. org/afp/2014/0715/p99. html Pneumonia E. Mone ́e Carter-Griffin Definition A. An infection of the lungs that can have varying degrees of severity. B. Caused by bacteria, viruses, or fungi. C. Can be further divided into four types: Community, hospital, ventilator acquired, and aspiration. Incidence A. Pneumonia (combined with influenza) is the eighth lead-ing cause of mortality in the United States, accounting for approximately 50,000 deaths annually. B. Thirty-day mortality is higher in elderly patients treated for hospital-acquired pneumonia (HAP) compared to community-acquired pneumonia (CAP). C. Pneumonia is the third leading cause of ED visits that led to a hospitalization, with the highest prevalence in patients 65 to 84 years. D. It is the most common cause of readmissions for the elderly population. E. It accounts for the top 10 most costly hospitalizations in the United States, with approximately $10. 6 billion spent for 1. 1 million hospital stays. F. Most common cause of sepsis and septic shock. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
25 Pathogenesis A. A pathogenic microorganism invades the lung parenchyma. Neutrophils aggregate to the site of invasion and begin to phagocytize the microorganisms and release an extracellular trap. B. The immune response is activated. Inflammatory media-tors are released, causing the capillaries to become permeable and an exudative fluid to be formed. The protein rich fluid containing neutrophils, bacteria, fibrin, and so forth, fills the alveoli, leading to a lung consolidation. Predisposing Factors A. An impaired immune response and/or dysfunction of the body's defense mechanism, HIV. B. Advanced age. C. Smoking. D. Chronic lung disease (e. g., chronic obstructive pul-monary disease [COPD] and asthma). E. Other chronic comorbid conditions (e. g., heart failure, diabetes). F. Recent respiratory viral infection. G. Excessive alcohol consumption. Subjective Data A. Common complaints/symptoms. 1. Cough with sputum production (see Figure 2. 3). 2. Fever. 3. Chills. 4. Altered mental status or confusion, especially in the elderly. 5. Pleuritic chest pain. B. Common/typical scenario. 1. Patients typically present with sudden onset of symp-toms such as shortness of breath, productive cough, and fever. They may also complain of chills and malaise. C. Family and social history. May be more prevalent in smokers, among the elderly, and in the chronically ill. D. Review of symptoms. 1. Symptoms may vary depending on the age, activity level, and underlying comorbid conditions. Elderly peo-ple typically present differently than younger adults. 2. The provider should inquire about onset, severity, and associated symptoms. 3. Assessment of recent respiratory viral illnesses is important, especially given the correlation of pneumonia following influenza. 4. It may help to enquire about recent sick contacts. Physical Examination A. General: Vital signs. 1. Fever, which may occur. Note that approximately 30% of patients are afebrile on presentation. 2. Tachycardia, which may or may not be present. 3. Possibly high respiratory rate; this may be normal or increased. B. Neurological. 1. More likely to see changes in the elderly. Patients can be described as having confusion, decreased interactions, and/or “acting differently. ” C. Respiratory. 1. Rales/crackles on auscultation in the affected area. Patients may also have rhonchi. 2. Dullness on percussion in the affected area. 3. Increased tactile fremitus in the affected area. 4. Possible pleural friction rub. 5. Decreased breath sounds. D. Possible other findings. 1. Cyanosis, respiratory failure, and septic shock in patients with a more virulent type of pneumonia, mul-tilobar pneumonia, age, and/or comorbid conditions. Diagnostic Tests A. Chest x-ray. 1. Evidence of an infiltrate, which can be patchy or a dense consolidation of a lobe(s) or segment. B. Sputum culture and gram stain. 1. Used to identify the microorganism responsible for the pneumonia. 2. Most sensitive if the patient can provide an adequate specimen and has not recently been treated or is not cur-rently receiving treatment with antibiotics. 3. Intubated patient: Obtain an endotracheal aspirate. C. Blood cultures. 1. Usually indicated for patients with more severe forms of pneumonia, specifically CAP. 2. Most common pathogen isolated in patients with CAP: Streptococcus pneumoniae. However, in more severe infections, other microorganisms may be present. D. Urinary antigen testing. 1. Used to assess for pneumococcal pneumonia, mycoplasma pneumonia, and Legionnaire's disease. 2. Rapid and simple; however, do not provide informa-tion for narrowing of antibiotics. E. Serum procalcitonin. 1. Can assist the provider with antibiotic duration in conjunction with the patient's clinical presentation. 2. No recommended use of procalcitonin in patients with hospital or ventilator-acquired pneumonia accord-ing to Infectious Diseases Society of America and the American Thoracic Society guidelines. F. Comprehensive metabolic panel. 1. Can assist with risk stratification and sequela of pneu-monia. G. Complete blood count. 1. Assessment of a leukocytosis or leukopenia. H. Arterial blood gas (ABG). 1. May be indicated in more severe presentations such as cyanosis or respiratory failure to evaluate for hypoxemia and/or hypercapnia. I. Chest CT scan. 1. Not typically indicated, especially if one is able to obtain a good-quality chest x-ray. Differential Diagnosis A. COPD. B. Asthma. C. Pulmonary edema. D. Bronchiectasis. E. Lung cancer. F. Pulmonary embolism. G. Bronchitis. H. Viral or bacterial pneumonia. I. Pneumocystis pneumonia (PCP). Evaluation and Management Plan A. General plan. 1. Management of pneumonia: Dependent on the sever-ity of the disease, classification or type of pneumonia (e. g., community vs. hospital acquired), and pathogens involved. 2. Supportive care, such as oxygen therapy or other methods of respiratory support (e. g., noninvasive Pneumonia | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
26 ventilation, invasive mechanical ventilation); this should be considered in those patients with hypoxemia and/or respiratory failure. 3. Patients presenting with sepsis due to pneumonia. These patients should receive care in accordance with the sepsis guidelines. 4. Guidelines suggest that antimicrobial therapy be de-escalated rather than fixed therapy. 5. T ransitioning to oral therapy. Oral therapy is appro-priate once patients' clinical status has improved, and they are hemodynamically stable. 6. Patients with coexisting Influenza A. Early treatment with oseltamivir or zanamivir is appropriate. 7. Systematic corticosteroids: May be appropriate in cer-tain patient populations who present with severe CAP. B. CAP. 1. Evaluation of patients for hospital admission. Use the CURB-65 criteria, which evaluates/looks at confu-sion, uremia, respiratory rate, low blood pressure, and age 65 years or greater, or pneumonia severity index (PSI) to identify patients who can be treated as outpatient versus inpatient. 2. Duration of treatment. Patients should receive a min-imum of 5 days of treatment and literature suggests that more than 7 days is typically not needed. 3. Antibiotic therapy, which focuses on the likely pathogen and severity. a. The most common outpatient pathogens are S. pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella, and respiratory viruses. i. Previously healthy patients with no exposure to antibiotics within the past 3 months should be started on a macrolide. If they are unable to toler-ate a macrolide, then doxycycline may be used. ii. Patients with chronic comorbid conditions (e. g., heart failure, liver or renal disease, diabetes) or antibiotic therapy within the past 3 months should be started on a respiratory fluoroquinolone (e. g., moxifloxacin, levofloxacin, or gemifloxacin) ORbeta-lactam plus a macrolide. Remember, a beta-lactam alone will not work for atypical pneu-monia because of the lack of a beta-lactam ring. b. The most common inpatient, non-ICU pathogens are S. pneumoniae, M. pneumoniae, C. pneumoniae, H. influenzae, Legionella species, aspiration, and respira-tory viruses. i. Patients should be treated with a respira-tory fluoroquinolone OR a beta-lactam plus a macrolide. c. The most common inpatient, ICU pathogens are S. pneumoniae, Staphylococcus aureus, Legionella species, gram-negative bacilli, and H. influenzae. i. Patients should be started on a beta-lactam (e. g., cefotaxime, ceftriaxone, or ampicillin-sulbactam) plus either azithromycin or a respira-tory fluoroquinolone. ii. If the patient has a penicillin allergy, then a res-piratory fluoroquinolone and aztreonam are rec-ommended. iii. Gram-negative organisms are selectively responsive to aztreonam treatment. d. If a pseudomonal infection is suspected, then providers should prescribe one of the following. i. Antipneumococcal, antipseudomonal beta-lactam plus levofloxacin OR,ii. Beta-lactam plus an aminoglycoside and azithromycin OR, iii. Beta-lactam plus an aminoglycoside and antipneumococcal fluoroquinolone. e. If methicillin-resistant Staphylococcus aureus ( MRSA) is suspected, then intravenous vancomycin or linezolid is indicated. C. HAP. 1. Develops 2 or more days after admission to the hospital. 2. Use of a local antibiogram tailored to HAP pathogens and susceptibilities for empiric coverage as recommended by guidelines. 3. Antibiotic treatment: Recommended 7-day course. a. Empiric coverage depends on the patient's mortal-ity risk and suspicion for multidrug resistant (MDR) pathogens. b. Patients not at high risk for mortality or likelihood of MDR pathogens can be placed on piperacillin-tazobactam (Zosyn) ORcefepime ORlevofloxacin. c. Patients not at high risk for mortality but who have factors that may increase their likelihood of MRSA should be placed on cefepime ORlevofloxacin OR meropenem ORaztreonam plus vancomycin or line-zolid (second line due to toxic effects if vancomycin cannot be used). d. Patients with a high mortality risk, coverage for pseudomonas, or who have received intravenous antibiotics in 3 months should be started on: i. Piperacillin-tazobactam (Zosyn) OR cefepime ORlevofloxacin ORmeropenem OR amikacin/gentamicin/tobramycin ORaztreonam plus vancomycin or linezolid. ii. Providers should cover for MRSA and pick two additional medications while avoiding pre-scribing two beta-lactams. D. Ventilator-acquired pneumonia (VAP). 1. A pneumonia that develops more than 2 days after intubation and mechanical ventilation. 2. Use of a local antibiogram tailored to the ICU popu-lation, VAP pathogens, and susceptibilities for adequate coverage as recommended per guidelines. 3. Antibiotic treatment: Recommended 7-day course. a. S. aureus, Pseudomonas, and other gram-negative bacilli coverage should be included in all empiric reg-imens. b. Patients with risk factors for MRSA should receive empiric coverage with vancomycin or linezolid. c. Patients with no known risk factors for MRSA and suspected of methicillin-susceptible Staphylococcus aureus (MSSA), then the suggested regimen includes piperacillin-tazobactam, cefepime, levofloxacin, or meropenem. If the patient has proven MSSA, then the preferred agents are cefazolin or nafcillin. d. Patients with risk factors for gram-negative infection, including pseudomonas and resistant microorganisms, should receive treatment with two antipseudomonal drugs. i. Piperacillin-tazobactam OR, ii. Cefepime OR, iii. Meropenem OR, iv. Aztreonam OR, v. Ciprofloxacin. e. Guidelines recommend against the routine use of aminoglycosides and colistin if adequate coverage is available with alternative antibiotics. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
27 E. Discharge instructions. 1. Discharge criteria. These primarily focus on improve-ment in the clinical status/condition. a. Resolution of fever (e. g., <38∘C). b. Improving symptoms (e. g., dyspnea, cough, spu-tum production). c. Heart rate less than 100 bpm. d. Respiratory rate less than 24/minute. e. Oxygen saturations greater than 90%. f. Diminishing leukocytosis. g. Maintaining oral intake. h. Systolic blood pressure greater than 90 mm Hg. i. Return to baseline mentation. 2. Activity. a. Regular or baseline activity as tolerated. 3. Diet. a. Comorbid conditions such as diabetes, heart fail-ure, or renal disease: May vary. b. No underlying comorbid conditions: Resumption of regular diet. 4. Medications. a. Antibiotics: Duration of 7 days. This includes the days the patient received antibiotics while hospital-ized. b. Other drugs. Medication reconciliation and con-tinuation of medications for comorbid conditions. 5. T reatment plan. a. Important for patient to complete the full course of antibiotics even if feeling better. b. Coughing with sputum production: Normal. This should improve over time. c. Vaccinations such as influenza annually and pneu-mococcal disease necessary for those at risk. d. Pulmonary hygiene (e. g., deep breathing). e. Smoking cessation counseling. f. Remaining hydrated. g. Managing comorbid conditions. 6. Discuss with patient. a. Stress that patients should contact their provider if they develop fever or worsening symptoms such as increased cough and dyspnea despite antibiotic therapy, decreased appetite, nausea, and mentation changes. b. Reemphasize the importance of completing antibiotic therapy to reduce reoccurrence and avoid resistance emergence. Follow-Up A. Follow-up is highly dependent on the type and severity of pneumonia as well as functional status and comorbid con-ditions. B. Patients in the outpatient setting typically see improve-ment in symptoms within 3 to 7 days, so failure to see improvement or clinical deterioration should be dealt with immediately. C. Patients discharged from the hospital should be seen 1 to 2 weeks after discharge. Consultation/Referral A. Outpatient management typically does not require a referral unless the patient's clinical status worsens, in which case the patient should be sent to the hospital. B. Inpatient management may include a pulmonologist and infectious disease pending the severity of the pneumonia and the patient's condition. Special/Geriatric Considerations A. The elderly should be instructed to receive pneumococcal and influenza vaccinations. B. All patients should be counseled regarding smoking cessation. Bibliography American Thoracic Society. (2018). Top 20 pneumonia facts. Retrieved from https://www. thoracic. org/patients/patient-resources/resources/ top-pneumonia-facts. pdf Hines, A. L., Barrett, M. L., Jiang, J., & Steiner, C. A. (2014). Con-ditions with the largest number of adult hospital readmissions by payer, 2011. Retrieved from https://www. hcup-us. ahrq. gov/reports/statbriefs/ sb172-Conditions-Readmissions-Payer. pdf Kalil, A. C., Metersky, M. L., Klompas, M., Muscedere, J., Sweeney, D. A., Palmer, L. B., & Brozek, J. L. (2016). Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases, 63, e61-e111. doi:10. 1093/cid/ciw353 Klompas, M. (2017). Health care and hospital-acquired pneumonia. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1514-1518). New York, NY: Mc Graw-Hill. Kochanek, K. D., Murphy, S. L., Xu, J., & Tejada-Vera, B. (2016). Deaths: Final data for 2014. National Vital Statistics Reports, 65, 1-122. Retrieved from https://www. cdc. gov/nchs/data/nvsr/nvsr65/ nvsr65_04. pdf Mandell, L. A., Wunderlink, R. G., Anzueto, A., Bartlett, J. G., Campbell, G. D., Dean, N. C., & Whitney, C. G. (2007). Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical Infectious Diseases, 44, S27-S72. doi:10. 1086/511159 Musher, D. M. (2017). Community-acquired pneumonia. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1503-1513). New York, NY: Mc Graw-Hill. Musher, D. M., & Thorner, A. R. (2014). Community-acquired pneumo-nia. New England Journal of Medicine, 371, 1619-1628. doi:10. 1056/ NEJMra1312885 Wunderlink, R. G., & Waterer, G. W. (2014). Community-acquired pneu-monia. New England Journal of Medicine, 370, 543-541. doi:10. 1056/ NEJMcp1214869 Pulmonary Embolism E. Mone ́e Carter-Griffin Definition A. A blockage of a pulmonary artery or one of the smaller branches. Most commonly, pulmonary embolism (PE) is the result of an embolic thrombus formation elsewhere in the body (e. g., lower extremity). Incidence A. PE is more common in patients with deep vein thrombo-sis (DVT). B. It affects more than 600,000 people annually. C. An estimated 60,000 to 100,000 people die annually. D. Approximately one-third of patients will have a recur-rence within 10 years. Pathogenesis A. A thrombus forms secondary to a hypercoagulable state, injury to the vascular endothelium, and venostasis, which concentrates blood clotting factors at the site of vessel injury. Clot formation occurs as a result of blood pooling. B. The clot can dislodge from the extremity, travel through the venous system, move through the right side of the heart, and obstruct a pulmonary artery or the smaller branches. Pulmonary Embolism | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
28 Large enough obstructions can prevent blood flow to the affected area, creating a ventilation/perfusion mismatch lead-ing to respiratory failure and/or increase the pulmonary artery pressure, resulting in right-sided heart failure. Predisposing Factors A. Factor V mutation. B. Protein C or S deficiency. C. Malignancy. D. Immobility. E. T rauma. F. Surgery. G. Smoking. H. Obesity. I. Prior PE. J. Chronic diseases such as heart failure and chronic obstructive pulmonary disease (COPD). K. Prolonged travel. Subjective Data A. Common complaints/symptoms. 1. These can vary depending on the degree of clot burden. 2. Patients may be asymptomatic, especially in the setting of a small segmental branch PE. The condition is usually found incidentally in these cases. 3. Symptoms may include: a. Pleuritic chest pain. b. Dyspnea/Tachypnea. c. Hypoxia. d. Cough with possible blood-tinged sputum pro-duction. e. Tachycardia. f. Dizziness or syncope. g. Hypotension/shock with a massive PE. h. Recent symptoms associated with a DVT (e. g., extremity pain, warmth, erythema, edema). B. Family and social history. C. The provider should assess symptom onset and any asso-ciated risk factors for PE development such as history or cur-rent malignancy, decreased mobility, travel, recent surgeries, and so forth. D. It is important for the provider to assess for family history of clot formation or known factor deficiencies. Physical Examination A. Findings depend on the degree of clot burden. B. Perform a general examination, which may reveal diaphoresis, fever, and tachycardia. On presentation, most patients are hemodynamically stable. C. Assess neurological status. Patients may present with syn-cope, altered mentation, or agitation. D. Assess the respiratory rate. In more significant PEs, the rate will be increased. Auscultation of breath sounds may reveal rales or crackles. E. Perform a cardiac examination. Patients may have a murmur, accentuated second heart sound, or S3/S4 gallop. F. Extremities may reveal signs of a deep vein thrombosis such as pain, edema, or erythema. Diagnostic Tests A. D-dimer (age adjusted). 1. High sensitivity: With negative results and a low prob-ability of a PE. 2. Most reliable in young patients with no comorbid conditions and short symptom onset. 3. Can have nonspecific elevations in the elderly and those with other acute illnesses requiring hospitalization. B. Chest CT Angiography (CTA). 1. Allows for direct visualization of the emboli. 2. Considered the standard of care for diagnosing patients with high probability of a PE or low/interme-diate probability but positive D-dimer. 3. Right ventricular (RV) dilation: Associated with short-term adverse outcomes. C. Ventilation/Perfusion (V/Q) Lung Scan. 1. An alternative to the chest CTA, especially in the set-ting of contraindications such as renal failure. 2. Evaluates for perfusion defects, which are nonspecific and only present in one-third of patients with PE. 3. Increased likelihood of nonconclusive results in patients older than 75 years. D. Echocardiography. 1. Often indirectly helps diagnose PE in conjunction with the patient's clinical presentation. 2. Can also be utilized as a prognostic factor in PE. 3. Possible findings consistent with a PE: Acute RV enlargement and in some cases dysfunction, evidence of pulmonary hypertension with elevated RV systolic pres-sures, and possible flattening of the septum. 4. May be able to visualize an intracardiac thrombi. 5. RV dilation: Associated with an increased risk for adverse outcomes. E. Ultrasonography. 1. Can assist in the diagnosis of PE. F. Additional diagnostics for acute risk stratification. 1. Pulmonary embolism severity index (PESI). a. Used to predict the 30-day outcomes/mortality in patients with acute PE. b. Score greater than 106 on the original PESI: High risk for morbidity and mortality. c. Score greater than 1 on the simplified PESI: High risk for morbidity and mortality. 2. T roponin. a. Elevated troponin levels in patients presenting or receiving treatment for PE: Associated with adverse outcomes. 3. N-Terminal pro brain natriuretic peptide (NT-pro BNP). 4. Elevated levels: Associated with adverse outcomes (in literature). Differential Diagnosis A. Pericarditis. B. Pleuritis. C. Musculoskeletal pain. Evaluation and Management Plan A. General plan. 1. Diagnosis of a PE requires the provider to account for the patient's clinical presentation as well as evaluat-ing diagnostic tests. 2. T reatment recommendations are highly dependent on the patient's clinical status including respiratory and hemodynamic stability at the time of presentation. 3. In the clinical setting and literature, PEs have been described as low risk, submassive, and massive. a. Low risk PEs: Patients with hemodynamic stabil-ity, no elevation in biomarkers, and no evidence of RV dysfunction on imaging. 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
29 b. Submassive PEs: Patients with hemodynamic sta-bility but evidence of RV dysfunction on imaging and/or biomarker elevation. c. Massive PEs: Patient with hemodynamic instabil-ity, elevation in biomarkers, and evidence of RV dys-function. 4. Ideally, patients should have pretest clinical assess-ment, diagnostics with consideration of risk stratification, and initiation of treatment. 5. Low to intermediate probability of PE. a. Pretest clinical assessment. i. Wells Clinical Prediction Rule for PE. Patients are evaluated using seven variables in which they can receive 1 to 3 points. A score of 2 to 6 points indicates a moderate risk and a score greater than 6 indicates high risk. ii. Revised Geneva Score. Patients are evaluated using eight variables in which they can receive 1 to 5 points. A score of 4 to 10 points indi-cates an intermediate risk and a score greater than 11 indicates high risk. iii. Appropriate for patients who are hemody-namically stable. Patients with a high probability of PE should proceed immediately to diagnostic testing. b. Age-adjusted D-dimer. i. If negative: No further imaging needed. ii. If positive: Further imaging needed. iii. It is important that the provider use an age-adjusted scale due to decreased specificity in the elderly population. Using the appropriate scale can reduce the number of false-positive results. c. Chest CTA versus V/Q Lung Scan. i. If no contraindications to CTA: Chest CTA is preferred. d. T reatment: Anticoagulation therapy. 6. High probability of PE. a. Patients likely to be hemodynamically unstable; pretest clinical assessment not appropriate. b. Immediate chest CTA. If unable to obtain a chest CTA due to hemodynamic instability/uncontrolled hypotension, then findings consistent with a PE on echocardiography may be a suitable alternative. B. Pharmacotherapy. 1. Decision about medication management should consider whether the PE was provoked (caused by an identifiable risk factor such as cancer) and duration of therapy. 2. Patients should be routinely reevaluated for antico-agulation needs if receiving extended therapy. 3. T reatment with dabigatran, rivaroxaban, apixaban, or edoxaban is recommended over a vitamin K antagonist in patients with a PE. 4. A vitamin K antagonist is recommended for patients with an unprovoked PE if not receiving treatment with dabigatran, rivaroxaban, apixaban, or edoxaban. 5. It is suggested that a provider treating a patient with a PE and cancer use a low molecular weight heparin (LMWH). It is also recommended that patients receive extended therapy (e. g., no stop date) depending on their bleeding risk. 6. Anticoagulation is recommended for 3 months in patients with a PE provoked by surgery or transient risk factors. 7. For patients with an unprovoked PE at a low or mod-erate bleeding risk, initiation of extended anticoagulationtherapy (e. g., no stop date) is suggested. For patients with a high bleeding risk, it is recommended to initiate anti-coagulation for 3 months. 8. Surveillance is suggested in patients with a distal (subsegmental) PE who have no proximal DVTs and a low risk for recurrent venous thromboembolism (VTE). 9. Systemic thrombolytic therapy is suggested for hemodynamically unstable patients. 10. Additional management: Catheter-directed throm-bolysis. C. Patient/family teaching. 1. Prevent more blood clots from forming by taking the medication as prescribed. 2. Be sure to follow-up with lab tests as directed. 3. Encourage patients to get up and be active. 4. Smoking cessation. 5. On long trips, make frequent stops to get out and move about. 6. On airplane rides, perform exercises that keep your legs, feet, and toes moving. D. Discharge. 1. Call your healthcare provider if there is any increase in symptoms. Follow-Up A. Patient follow-up is variable in the literature primarily due to the type of medication, cause of PE, and severity of illness due to the PE. B. A vitamin K antagonist requires that the patient follow-up 2 to 3 days postdischarge for international normalized ratio (INR) evaluation. Consultation/Referral A. Pulmonologist may be consulted due to the pulmonary symptoms associated with a PE. B. Hematologist may be warranted especially if concerned for a procoagulant defect. C. An interventional radiologist or interventional cardiolo-gist may be consulted for catheter-directed thrombolysis. D. Critical care may be needed if the patient is admitted to the ICU or becomes hemodynamically unstable. Special/Geriatric Considerations A. Inferior vena cava (IVC) filters are not recommended for patients treated with anticoagulation. B. IV anticoagulation therapy should be started prior to administering dabigatran and edoxaban. Bibliography Beckman, M. G., Hooper, W. C., Critchley, S. E., & Ortel, T. L. (2010). Venous thromboembolism: A public health concern. American Journal of Preventive Medicine, 38, S495-S501. doi:10. 1016/j. amepre. 2009. 12 017 Jaff, M. R., Mc Murtry, S., Archer, S. L., Cushman, M., Goldenberg, N., Goldhaber, S. Z., & Zierler, B. K. (2011). Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombo-sis, and chronic thromboembolic pulmonary hypertension. Circulation, 123, 1788-1830. doi:10. 1161/CIR. 0b013e318214914f Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez, D., Bounameaux, H., Huisman, M., & Moores, C. L. (2016). Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest, 149, 315-352. doi:10. 1016/j. chest. 2015. 11. 026 Konstantinides, S. V., Barco, S., Lankeit, M., & Meyer, G. (2016). Man-agement of pulmonary embolism: An update. Journal of the American College of Cardiology, 67, 976-990. doi:10. 1016/j. jacc. 2015. 11. 061 Meyer, N. J., & Schmidt, G. A. (2015). Pulmonary embolic disorders: Thrombus, air, and fat. In J. B. Hall, G. A. Schmidt, & J. P. Kress Pulmonary Embolism | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
30 (Eds. ), Hall, Schmidt, and Wood's principles of critical care (4th ed., pp. 318-336). New York, NY: Mc Graw-Hill. Raja, A. S., Greenberg, J. O., Qaseem, A., Denberg, T. D., Fitterman, N., & Schuur, J. D. (2015). Evaluation of patients with suspected acute pulmonary embolism: Best practice advice from the clinical guidelines committee of the American College of Physicians. Annals of Internal Medicine, 163, 701-711. doi:10. 7326/M14-1772 Restrictive Lung Disease E. Mone ́e Carter-Griffin Definition A. A reduction in the total lung capacity secondary to a decrease in lung elasticity or disease of the chest wall, pleura, or neuromuscular etiology. Disorders can be classified as intrinsic or extrinsic. Incidence A. The incidence is highly variable and dependent on the etiology of restriction. B. The incidence of some disorders is not well known. C. Interstitial lung diseases (ILDs), although rare, are a cause of restrictive lung disease affecting approximately 500,000 individuals each year and resulting in 40,000 deaths. D. Nonidiopathic and idiopathic pulmonary fibrosis (type of ILD) are a common cause of restrictive lung disease. E. Approximately 30 cases per 100,000 of restrictive lung disease are due to idiopathic pulmonary fibrosis. F. The prevalence of disease increases with age. G. Frequency of occurrence is typically higher in men. Pathogenesis A. An exogenous or endogenous stimulus causes repetitive injury to the lung parenchyma, leading to epithelial and endothelial damage. Activation of local and systemic factors (e. g., fibroblasts, growth factors, clotting, factors, cytokines) occurs. B. A provisional matrix is formed. There is a dysregulation of the intricate network and lack of matrix degradation, leading to aberrant wound healing and progressive lung remodeling, ultimately causing pulmonary fibrosis. Predisposing Factors A. Predisposing factors depend on the etiology of the restric-tive lung disease. B. Risk factors include: 1. Obesity. 2. Kyphoscoliosis. 3. Myasthenia gravis. 4. Chronic pleural disease (e. g., trapped lung). 5. Autoimmune disease (e. g., scleroderma, systemic lupus erythematosus). 6. Occupational exposures. 7. Medications such as amiodarone, bleomycin, and methotrexate. 8. Idiopathic lung disease such as pulmonary fibrosis, more common in the elderly and men. 9. Sarcoidosis. Subjective Data A. Common complaints/symptoms. 1. Symptoms and complaints may vary depending on the underlying cause of the restrictive lung disease. 2. Dyspnea (see Figure 2. 1): Most common complaint. It can be present with exercise or at rest as the disease progresses. 3. Possible chronic cough (see Figure 2. 3), wheezing (see Figure 2. 2), or chest discomfort. 4. Possible hemoptysis. 5. Fatigue. B. Common/typical scenario. 1. Duration of illness (e. g., acute onset, chronic). C. Family and social history. 1. Smoking history. 2. Occupational history or exposures. 3. Family history of fibrotic lung disease. D. Review of symptoms. 1. Neurologic—any confusion, fatigue, muscle weak-ness. 2. Respiratory—shortness of breath at rest, upon exer-tion, or that is progressive; dry cough; bloody spu-tum; pain on inspiration; recent or frequent colds. 3. Use of medications such as nitrofurantoin, amio-darone, or others that have the potential to cause lung disease. Physical Examination A. Dyspnea, which may be more evident with activity. B. Tachypnea. C. Cyanosis or oxygen desaturation with activity. D. Possible bibasilar inspiratory crackles, scattered inspira-tory rhonchi, or wheezing. E. Digital clubbing. F. Obese. G. Other disease-specific signs and symptoms (e. g., rash, Raynaud's, muscle weakness), depending on the underlying etiology. Diagnostic Tests A. Laboratory studies. 1. Usually nonspecific. 2. Serologic testing. This may be appropriate in patients suspected of having an underlying disorder causing restrictive disease such as rheumatoid arthritis. B. Chest x-ray. 1. Typically nonspecific findings, which may vary with the type of restrictive disease. 2. Possible evidence of increased interstitial markings, bibasilar reticular pattern, or a nodular pattern. 3. Honeycombing, which is typically noted as a late or advanced finding. 4. If an extrinsic factor is suspected, then imaging may reveal a trapped lung, pleural effusion, etc. C. Chest CT 1. More sensitive and better assessment of the extent of disease compared to a chest x-ray. 2. May reveal findings characteristic of specific restric-tive diseases. Some restrictive diseases such as idiopathic pulmonary fibrosis can be diagnosed solely with a chest CT. 3. If an extrinsic factor is suspected, then imaging may reveal a trapped lung, pleural effusion, etc. D. Pulmonary Function Testing 1. Valuable for assessing the response to therapy and monitoring disease progression. 2. Does not diagnosis a specific disease. 3. Characteristic findings include a reduced total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV). 2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
31 4. The forced expiratory volume in one second (FEV1) and forced vital capacity ratio is usually normal or increased. 5. The diffusing capacity of carbon monoxide is reduced in patients with an intrinsic etiology of restrictive disease. If the diffusing capacity is normal, then the etiology of restrictive disease is an extrinsic factor such as neuromus-cular disease. E. Arterial blood gas 1. May be normal or indicate hypoxemia and a respira-tory alkalosis. 2. May reveal an increased alveolar-arterial gradient. F. Bronchoscopy and/or lung biopsy 1. Beneficial for identifying diseases associated with intrinsic factors or the lung parenchyma. 2. A bronchoalveolar lavage (BAL) may be useful in nar-rowing the differential diagnoses. a. The clinical usefulness of the BAL has not been well established. 3. A lung biopsy can confirm the diagnosis, evaluate dis-ease activity, and exclude other diagnoses. a. Open thoracotomy b. Video-assisted thoracoscopic lung biopsy c. T ransbronchial lung biopsy via bronchoscopy G. Additional imaging or testing may be warranted to assess for complications resulting from restrictive diseases such as an echocardiogram to evaluate for pulmonary hypertension or right-sided heart failure. Evaluation and Management Plan A. T reatment may vary depending on the underlying etiol-ogy for restrictive disease. B. Intrinsic etiologies are defined as diseases of the lung parenchyma. Extrinsic etiologies are extra-pulmonary causes including neuromuscular disorders, the chest wall, etc. C. Patients should receive smoking cessation counseling. D. Avoidance of environmental and/or occupational expo-sures. E. Medications suspected of causing restrictive disease should be stopped immediately. F. Supplemental oxygen therapy should be administered for all patients with oxygen saturations less than 88% on room air at rest or upon exertion. G. Pulmonary rehabilitation or regular activity/exercise should be encouraged because it has been shown to improve endurance and quality of life. H. Patients should receive vaccinations for influenza and pneumococcal. I. T reatment regimens for intrinsic causes usually includes: 1. Corticosteroid therapy a. Use of corticosteroids is generally accepted; however, timing, dosing, and continuation versus discontinuation of treatment is highly variable and dependent on the intrinsic cause for restrictive disease as well as patient responsiveness. b. The long-term effects of corticosteroid therapy must be considered. c. Pulse high dose corticosteroids are typically used for acute exacerbations. 2. Immunosuppressive agents (e. g. cyclosporine, aza-thioprine) may be used in certain diagnoses. These medi-cations should not be routinely or empirically used with-out a definitive diagnosis. 3. If worsening respiratory symptoms, patients may require invasive mechanical ventilation. 4. Patients with refractory disease to treatment and pro-gressive worsening, may be a candidate for lung trans-plantation and should be referred to lung transplant spe-cialist and center. J. T reatment for extrinsic causes include: 1. Weight loss counseling and plan for obese patients 2. Non-invasive positive pressure ventilation for patients who have impaired gas exchange 3. Identification of the extrinsic disorder and treatment accordingly. 4. For patients with a trapped lung, chronic effusion, or empyema, a decortication may be required. Follow Up A. Follow-up is variable and dependent on the patient's symptoms and medical management. It should be individ-ualized. B. Post-hospital discharge, patients will follow-up with their provider in one week. Consultation/Referral A. Patients with restrictive lung disease should be referred to a pulmonologist for diagnosis and management. B. Patients with an extrinsic etiology for restrictive disease such as myasthenia gravis should be referred to a neurologist or the appropriate consultant for the disorder. Individual/Special/Geriatric Considerations A. To adequately assess responsiveness to immunosuppres-sive medications, the provider should note it may not be evi-dent until eight to twelve weeks after therapy initiation. B. Patients with parenchymal restrictive disease (e. g. idio-pathic or non-idiopathic pulmonary fibrosis) receiving treat-ment with high dose steroids should receive prophylactic treatment for pneumocystis jiroveci pneumonia (PJP). C. Patients with progressive disease are typically discharged on home oxygen therapy. Increased oxygen requirements may be necessary to maintain a goal saturation greater than 88%. The patient and family is instructed that oxygen ther-apy may be tailored to maintain oxygen saturations at rest and with exertion. If the patient is requiring increased oxygen therapy from baseline, then an immediate follow-up appoint-ment with their pulmonologist or hospital admission may be warranted. Restrictive Lung Disease | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
32 EXHIBIT 2. 1 Stepwise Approach for Managing Asthma Long Term The stepwise approach tailors the selection of medication to the level of asthma severity or asthma control. The stepwise approach is meant to help, not replace, the clinical decision making needed to meet individual patient needs. ASSESS CONTROL:STEP UP IF NEEDED (first, check me dication adherence, inhaler technique, environmenta l control, and comorbiditie s) STEP DO WN IF POSSIBLE (and a sthma is well controlled for at le ast 3 month s) STEP 1 STEP 6 STEP 5 STEP 4 STEP 3 Ateach step: Patient education, envir onmental contr ol,and management ofcomorbidities0-4 years of age 5-11 years of age Intermittent Asthma Persistent Asthma: Daily Medication. Consult with asthma spec ialist ifstep3car eorhigher isrequir ed. Consider consul-tation atstep 2. Preferred Treatmentb SABAaas needed Low-dose ICSa Medium-dose ICSa Medium-dose ICSa+ either LABAaor montelukast High-dose ICSa+either LABAaor montelukast High-dose ICS a+either LABA or montelukast+ oralcorticoster oids Alternative Treatmentb,c Cromolyn or montelukast If clear bene/f_it is not observed in 4-6 weeks, and medication technique and adherence are satisfactory,consider adjusting therapy or alternate diagnoses. Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms; intensity oftreatment depends onseverity ofsymptoms. /uni25A0With viral respiratory symptoms: SABA every 4-6hours upto24hours (longer with physician consult). Consider short course oforalsystemic corticoster oids ifasthma exacerbation issever e orpatient hashistory ofsever eexacerbations. /uni25A0Caution: Frequent useof SABA may indicate theneedtostep uptreatment. Intermittent Asthma Persistent Asthma: Daily Medication. Consult with asthma spec ialist ifstep4car eorhigher isrequir ed. Consider consul-tation atstep 3. Preferred Treatmentb SABAaas needed Low-dose ICS a Low-dose ICSa +either LABA, LABA ,a theophyllinebor Medium-dose ICS a + LABAa High-dose ICS a+LABAa High-dose ICSa +LABAa+ OCS Alternative Treatmentb,c Cromolyn, LTRAa,or theophyllined Medium-dose ICSa+ either LTRAa or theophyllined High-dose ICSa+either LTRAaor theophyllined High-dose ICSa +either LTRAa ortheophyllined +OCS Consider subcutaneous allergenimmunotherapy for patients who have persistent, allergicasthma. e Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms. Theintensity oftreatment depends onseverity ofsymptoms: Uptothreetreatments every 20minutes asneeded. Short course oforalsystemic corticoster oids may beneeded. /uni25A0Caution: Increasing useof SABA oruse >2days/week forsymptom relief (nottoprevent EIB) generally indicates inadequate contr olandtheneed tostep uptreatment. (continued )STEP 2 medium-dose ICSa2. Pulmonary Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
33 Restrictive Lung Disease EXHIBIT 2. 1 Step wise Approach for Managing Asthma Long Term (continued ) Ateach step: Patient education, envir onmental contr ol,and management ofcomorbid Ities Preferred Treatmentb SABAaas needed Low-dose ICSa Low-dose ICSa +LABAa OR medium-dose ICSa Medium-dose ICSa+ LABAa High-dose ICSa+LABAa AND consider omalizumab forpatients who have allergiesf High-dose ICSa +LABAa+ OCSh AND consider omalizumab for patients who have allergiesf Alternative Treatmentb,c Cromolyn, LTRAa,or theophyllined Low-dose ICSa +either theophylline , or zileutong Medium-dose ICSa+either theophylline , orzileutong Consider subcutaneous allergenimmunotherapy forpatients who have persistent, allergicasthma. e Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms. Theintensity oftreatment depends onseverity ofsymptoms: Up tothreetreatments every 20minutes asneeded. Short course oforalsystemic corticoster oids may beneeded. /uni25A0Caution: Use of SABA >2days/week forsymptom relief (nottoprevent EIBa)generally indicates inadequate contr olandtheneed tostep uptreatment. ASSESS CONTROL:STEP UP IF NEEDED (first, check medication adherence, inhaler technique, environment al control, and comorbiditi es) STEP DO WN IF POSSIBLE (and asthma is well controlled for at least 3 mont hs) STEP 1 STEP 6 STEP 5 STEP 4 STEP 3 STEP 2 a EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting beta 2agonist; LTRA, leukotriene receptor antagonist; OCS, oral corticosteroids ;SABA, short-a cting beta 2agonist. b Treatment option sarelisted inalphabetical order,ifmorethan one. c Ifalternative treatment isused andresponse isinadequate, discontinue andusepreferredtreatment befor estepping up. d Theophylline isalessdesirable alternative because oftheneed tomonitor serum concentration levels. e Based onevidence fordust mites, animal dander,andpollen; evidence isweak orlacking formolds andcockr oaches. Evidence isstrongest for immunotherap ywith single allergens. Theroleofallergyinasthma isgreater inchildr enthan inadults. f Clinicians who administer immunotherapy oromalizumab should bepreparedtotreatanaphylaxis thatmay occur. h Befor eoralcorticoster oids areintroduced, atrialofhigh-dose ICS + LABA + either LTRA, theophylline, orzileuton, may beconsider ed,although this approach hasnotbeen studied inclinical trials. SABA,short-act ingbeta Source: U. S. Department of Health and Human Services. (2012). Asthma carequick reference: Diagnosing and man aging asthma. Retrieved from https://www. nhlbi. nih. gov//f_iles/docs/guidelines/asthma_qrg. pdf /uni2265 12 years of age Intermittent asthma Persistent asthma: Daily medication. Consult with asthma spec ialist ifstep4careorhigher isrequir ed. Consider consul-tation atstep 3. LTRAa, LTRAa d,d g Zileuton islessdesirable because oflimited studies asadjunctive therapy andtheneed tomonitor liver function. | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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35 3 Cardiac Guidelines Allison Rusgo Acute Coronary Syndromes Allison Rusgo Definition A. Umbrella term encompassing unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). B. UA: No cardiac damage, no elevation in cardiac labora-tory biomarkers, and no ST-segment elevation on ECG, but may show ST-segment depression. 1. Indicates narrowing of coronary arteries secondary to thrombosis, hemorrhage, or plaque rupture. In variant angina (Prinzmetal) cause is vasospasms. 2. Myocardial oxygen demand: Unchanged but available blood supply is decreased because of overall reduced coro-nary blood flow. C. NSTEMI: Evidence of cardiac damage, evidence of ele-vation in cardiac laboratory biomarkers, and no ST-segment elevation on ECG (but may show ST-segment depression and other ECG abnormalities; T wave inversion, or peaked T waves). 1. Indicates partial blockage of coronary artery sec-ondary to atherosclerotic narrowing. 2. Cardiac damage at the area of the heart supplied by the partially blocked artery. D. STEMI: Evidence of cardiac damage, evidence of eleva-tion in cardiac biomarkers, and positive ST-segment elevation on ECG. Infarction may produce Q waves (pathologic). 1. Indicates complete blockage of an artery, damaging the area of the heart supplied by the completely occluded vessel. E. Important note: Patients with stable coronary artery dis-ease (CAD) can have acute coronary syndrome (ACS) with-out atherosclerotic plaque rupture where physiologic stress (i. e., trauma, anemia, infection, acute blood loss) increases the myocardial oxygen demand of the heart. Incidence A. Ischemic heart disease is the leading cause of death among U. S. adults, estimated to be 405,000/annually. B. Approximately 1. 4 million individuals are hospitalized for ACS; of these, 810,000 experience an myocardial infarction (MI). C. STEMI is more common in middle-aged patients, and NSTEMI is more common in elderly patients. Pathogenesis A. Mismatch between myocardial oxygen supply and demand, where supply is affected by coronary blood flow and oxygen-carrying capacity of the blood. B. Overall oxygen-carrying capacity determined by hemoglobin level and oxygen saturation. C. Coronary artery blood flow: Interplay between periph-eral vascular resistance and ability of the heart to relax during diastole. D. Primary cardiac ischemia caused by atherosclerotic nar-rowing of the coronary vasculature. E. Secondary cardiac ischemia (less common) secondary to causes unrelated to atherosclerotic narrowing of the coronary vasculature. 1. Increased myocardial oxygen demand (i. e., infection, tachyarrhythmias, thyrotoxicosis). 2. Decreased blood flow (i. e., hypotension). 3. Decreased oxygen availability (i. e., anemia). F. Atherosclerotic-related ACS: Coronary arteries undergo a cascade of reactions leading to increased plaque accu-mulation, resulting in plaque rupture, and finally artery blockage. 1. Vascular injury: T riggered by factors such as tobacco by-products, elevated blood pressure (BP), elevated glu-cose, and oxidized low-density lipoproteins. 2. Results in increased vascular permeability and inflammation. 3. Inflammatory mediators (macrophages and smooth muscle cells) activated: Create “fatty streaks” in vasculature. 4. “Fatty streaks”: T ransformed into foam cells (i. e., plaque), which form fibrous caps. 5. When the top layer of the fibrous cap ruptures, platelets are activated. 6. Platelet response: Consists of adhesion, aggrega-tion, and activation; potentiates further damage to affected artery via platelet-laden thrombi, hemorrhage, and inflammation (overall blood flow decreased). 7. Immediate onset of the artery blockage created by ischemia secondary to rapid decrease in blood flow. 8. Amount and duration of the myocardial oxygen sup-ply and demand mismatch related to whether person experiences reversible ischemia (UA) or irreversible dam-age with cell death (STEMI or NSTEMI). Predisposing Factors A. Hypertension (HTN). B. Hyperlipidemia. C. Diabetes mellitus (DM). D. Metabolic syndrome. E. Obesity and sedentary lifestyle. F. Tobacco use. G. Family history of cardiovascular disease. H. Medications/toxins (cocaine, ergonovine, serotonin). Acute Coronary Syndromes | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
36 Subjective Data A. Common complaints/symptoms. 1. Chest discomfort (vise-like or crushing, aching, pres-sure, tightness, or burning); less likely sharp/stabbing or knife-like. a. Reproducible chest tenderness in some cases. b. Classic: Left-sided or substernal chest discomfort that radiates to the jaw or left arm. c. Can also radiate to the upper abdomen, back, or shoulders. 2. Nausea/vomiting. 3. Diaphoresis. 4. Palpitations. 5. Dyspnea. 6. Lightheadedness or syncope. 7. Feelings of anxiety. 8. Women, elderly persons, and those with DM: More likely to experience atypical ACS presentations. a. Fatigue. b. Weakness. c. Generalized malaise. d. Nonspecific chest or back discomfort. e. Decreased exercise tolerance. f. Altered mental status (elders). g. Gastrointestinal symptoms radiating the back (women). h. No pain (elders and DM persons). B. History of the present illness. 1. Information regarding onset, provoking and alleviat-ing factors, duration, quality, severity, and timing of chest discomfort. a. Compared to stable angina or UA, MIs cause more severe chest discomfort that is prolonged ( >20 min-utes) and unrelieved by nitroglycerin. b. Can be potentiated by exposure to cold, physical activity, or emotional stress. c. Possible previous history of angina and any recent changes in anginal symptoms over the past several months. d. Possible recent decrease in activity level due to decreased tolerance. 2. More likely to experience associated symptoms with MIs as opposed to angina (i. e., nausea, dyspnea, fatigue, diaphoresis). C. Family and social history. 1. Family history of premature CAD or MI in first-degree relative (males <45 years and females <55 years). 2. Tobacco or illegal substance use, especially cocaine. 3. Lifestyle factors, including level of exercise and dietary habits. D. Review of systems. 1. General: Fatigue and diaphoresis. 2. Cardiovascular: Chest pain/discomfort (with radia-tion) and palpitations. 3. Pulmonary: Dyspnea on exertion and shortness of breath. 4. Abdominal: Epigastric discomfort, indigestion, nau-sea, and vomiting. 5. Neurological: Dizziness, lightheadedness, near-syncope/syncope, and mental status changes. Physical Examination A. General appearance (one of the following). 1. Unremarkable and appearing well without any signs of distress, resting calmly. 2. Insignificant clinical/respiratory distress and insta-bility. 3. Cyanotic, in respiratory distress. B. Vital signs: Assess pulse, BP, respirations, oxygen satura-tion, and temperature. 1. Pulse: Can be regular, irregular, tachycardic, or brady-cardic (bradycardia can occur with anterior or inferior wall MIs). 2. BP: Can be elevated (due to anxiety, pain, underly-ing HTN, catecholamine surge) or decreased (indicates ventricular dysfunction). C. Skin: Diaphoresis, cool/clammy skin (concern for cardio-genic shock), and peripheral edema. D. Neck: Possible jugular venous distention (JVD). E. Cardiac. 1. Inspect for lifts, heaves, and pulsations. 2. Palpate for possible chest wall tenderness. 3. Auscultate. a. Extra heart sounds. S3 is present in approximately 15% of cases and indicates acute MI with heart failure. b. A new systolic murmur. This is concerning for papillary muscle dysfunction, ventricular septal defect, or new mitral regurgitation from a flail seg-ment of the valve. F. Pulmonary: Auscultate lung sounds for evidence of rales/crackles; concern for pulmonary edema or congestive heart failure. G. Abdominal: Inspect, auscultate for bruits, and palpate for tenderness and evidence of pulsatile abdominal mass (con-cern for abdominal aortic aneurysm). Diagnostic Tests A. ECG: Should be performed within 10 minutes of presen-tation to healthcare provider. Note that a normal ECG or one unchanged from the patient's baseline does not rule out the possibility of ischemic cardiac damage. 1. Fixed ST-segment elevations (STEMI). 2. Fixed ST-segment depressions (shows ischemia). 3. T-wave changes (can indicate ischemia). 4. T ransient ST-segment elevations (consider pericardi-tis, Prinzmetal angina, left ventricular aneurysm). B. Cardiac biomarkers. 1. Serial troponins (c Tn I or c Tn T): Sensitive and spe-cific for ACS diagnosis (biomarker of choice); recom-mended as set of three drawn approximately 4 to 6 hours apart. 2. Complete blood count: Useful for baseline informa-tion and ruling out anemia as cause of ACS. C. Basic metabolic panel. 1. To assess electrolytes, especially magnesium and potassium (causes of cardiac arrhythmias). 2. To assess renal function: Important if going to use angiotensin-converting enzyme (ACE) inhibitors for future therapy and/or contrast dye during catheterization (want to avoid contrast-induced nephropathy). D. Chest radiography: To assess for pulmonary edema and cardiomegaly, and rule out other causes of chest pain such as pneumonia or thoracic aneurysm. E. Cardiac echocardiography: Can be especially helpful if diagnosis is questionable. It is used to : 1. Assess left ventricular function. 2. Evaluate for regional wall motion abnormalities. 3. Check for pericardial effusions or valvular abnormal-ities (i. e., acute mitral regurgitation). 3. Cardiac Guidelines | Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf |
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