ACS/ASE Medical Student Core Curriculum Postoperative Care
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Caring for Yourself After Surgery: Preventing Surgical Site Infections
CARE AT HOME SERIES CARE AT HOME SERIES Caring for Yourself After Surgery Caring for Yourself After Surgery Preventing Surgical Site Infections Preventing Surgical Site Infections Wounds Canada has developed this simple guide that can be used by patients and their care partners when they are looking after a surgical wound. It provides guidance on things to do before and after surgery to help prevent infections and recognize the signs of infections if they do occur. In the past, people stayed in hospital for days or weeks following surgery. In those days, many of the complications that can occur soon after surgery (like infections, heart problems or bleeding) were treated when patients were still recovering in hospital. Today, patients having surgery get home Uninfected, healed surgical incision site. (See page 4 for faster than ever, often even the same day. Surgical uninfected and infected surgical incision sites.) site infections (SSIs) that were once treated in hospital are now being managed by patients at home. The good news is that there are actions you can take before and after your surgery to reduce the chances of developing a serious SSI. What is a surgical site infection? A surgical site infection is a problem where there are too many bacteria or really dangerous, active bacteria in your surgical incision. SSIs cause pain and delay wound healing. In more severe cases, SSIs can spread into the bloodstream (a condition called sepsis), which can lead to tissue loss, organ failure and death. A surgical site infection can be on the surface or deep. How much damage it does depends on how healthy you are as well as how strongly the bacteria affect your tissues. -
Complication Prevention for Patients with Diabetes a Noncommunicable Disease Education Manual for Primary Health Care Professionals and Patients
Complication prevention for patients with diabetes A noncommunicable disease education manual for primary health care professionals and patients Complication prevention for patients with diabetes A noncommunicable disease education manual for primary health care professionals and patients The Noncommunicable Disease Education Manual for Primary Health Care Professionals and Patients results from the contributions and hard work of many people. Its development was led by Dr Hai-Rim Shin, Coordinator, and Dr Warrick Junsuk Kim, Medical Officer, of the Noncommunicable Diseases and Health Promotion unit at the WHO Regional Office for the Western Pacific (WHO/WPRO/NCD) in Manila, Philippines. WHO graciously acknowledges the intellectual contributions of Dr Jung-jin Cho, Co-director, Community-based Primary Care Project Committee and Professor, Department of Family Medicine, Hallym University Sacred Heart Dongtan Hospital, Republic of Korea; Dr Hyejin Lee, Volunteer, WHO/WPRO/NCD (currently PhD candidate, Department of Family Medicine, Seoul National University, Republic of Korea); Ms Saki Narita, Volunteer, WHO/WPRO/NCD (currently PhD candidate, Department of Global Health Policy, Graduate School of Medicine, University of Tokyo, Japan); and Mr Byung Ki Kwon, Technical Officer, WHO/WPRO/NCD (currently Director, Division of Health Promotion, Ministry of Health and Welfare, Republic of Korea). Many thanks to Dr Albert Domingo, Dr Sonia McCarthy, Ms Marie Clem Carlos, Dr Katrin Engelhardt, Mr Kelvin Khow Chuan Heng and Dr Roberto Andres Ruiz from the WHO Regional Office for the Western Pacific and Dr Ma. Charina Benedicto, Physician-in-Charge, Bagong Barangay Health Center & Lying-in Clinic, Pandacan, Manila, Philippines for reviewing the draft publication. Financial support for this publication was received from the Korea Centers for Disease Control and Prevention, Republic of Korea. -
Risk Factors and Complications in Type 2 Diabetes Outpatients
RISKORIGINAL FACTORS AND COMPLICATIONS ARTICLE IN TYPE 2 DIABETES OUTPATIENTS Risk factors and complications in type 2 diabetes outpatients ELLEN FERNANDES FLávIO SILVA1, CRISTIANE MARIA MENDES FERREIRA2*, LUCINEIA DE PINHO3 1Medical Student, Faculdades Unidas do Norte de Minas (Funorte), Montes Claros, MG, Brazil 2Endocrinologist, Universidade Estadual de Montes Claros (Unimontes), Montes Claros, MG, Brazil 3PhD in Health Sciences, Unimontes and Funorte, Montes Claros, MG, Brazil SUMMARY Objective: Our study investigated type 2 diabetes mellitus (T2DM) outpatients attending a university hospital in Montes Claros, MG, to estimate the prevalence of risk factors and their association with diabetes complications. Method: This was a quantitative, documental, retrospective and analytical study. Medical records of 95 outpatients with T2DM treated in this hospital from 2011 to 2015 were analyzed. Data were collected according to a structured questionnaire surveying sociodemographic, anthropometric and biochemical data and clinical and lifestyle aspects. Regression analysis was used to evaluate the association between risk factor variables and complications. Results: With a mean age of 54 years, the study population showed irregular blood glucose control, despite the use of hypoglycemic medication, and did not Study conducted at Universidade have a healthy lifestyle. The main complication reported was high blood pressure Estadual de Montes Claros (Unimontes), Montes Claros, MG, Brazil (HBP), occurring in 70.9% of patients. The prevalence of complications was positively associated with patients receiving insulin treatment (p=0.042) and Article received: 11/13/2016 Accepted for publication: 12/19/2016 multidisciplinary monitoring (p=0.050). Conclusion: The associations identified reflect the condition of patients that *Correspondence: Address: Av. Dr. -
Drug Class Review Antianginal Agents
Drug Class Review Antianginal Agents 24:12.08 Nitrates and Nitrites 24:04.92 Cardiac Drugs, Miscellaneous Amyl Nitrite Isosorbide Dinitrate (IsoDitrate ER®, others) Isosorbide Mononitrate (Imdur®) Nitroglycerin (Minitran®, Nitrostat®, others) Ranolazine (Ranexa®) Final Report May 2015 Review prepared by: Melissa Archer, PharmD, Clinical Pharmacist Carin Steinvoort, PharmD, Clinical Pharmacist Gary Oderda, PharmD, MPH, Professor University of Utah College of Pharmacy Copyright © 2015 by University of Utah College of Pharmacy Salt Lake City, Utah. All rights reserved. Table of Contents Executive Summary ......................................................................................................................... 3 Introduction .................................................................................................................................... 4 Table 1. Antianginal Therapies .............................................................................................. 4 Table 2. Summary of Agents .................................................................................................. 5 Disease Overview ........................................................................................................................ 8 Table 3. Summary of Current Clinical Practice Guidelines .................................................... 9 Pharmacology ............................................................................................................................... 10 Table 4. Pharmacokinetic Properties -
Causes of Surgical Wound Dehiscence: a Multicenter Study
J Wound Manag Res 2018 September;14(2):74-79 pISSN 2586-0402 https://doi.org/10.22467/jwmr.2018.00374 eISSN 2586-0410 Journal of Wound Management and Research Causes of Surgical Wound Dehiscence: A Multicenter Study Jeong Jin Chun1, Seok Min Yoon1, Woo Jin Song1, Hyun Gyo Jeong1, Chang Yong Choi2, Syeo Young Wee1 1Department of Plastic and Reconstructive Surgery, College of Medicine, Soonchunhyang University, Gumi; 2Department of Plastic and Reconstructive Surgery, College of Medicine, Soonchunhyang University, Bucheon, Korea Abstract Surgical wound dehiscence is a postoperative complication involving breakdown of surgical incision site. Despite the in- creased knowledge of wound healing mechanism before and after surgery, wound dehiscence may increase the length of hospital stay, increase patient inconvenience and rates of re-operation. The purpose of this study was to analyze the causes of wound dehiscence in patients undergoing reoperation at 4 hospitals of Soonchunhyang Medical Center. The number of patients in each hospital and those operated previously were compared. In addition, other characteristics of patients were compared in patients who underwent reoperation. In 22 out of 1,026 patients consulted at the Seoul hos- pital, 32 cases out of 1,295 at Bucheon hospital, 14 cases out of 1,687 at Cheonan hospital and 15 cases out of 374 at Gumi hospital, wound revision was performed for wound dehiscence. Patients at the Department of Obstetrics and Gy- necology were the most common and included 33 patients (39.8%). The most common intervention before wound revi- sion was Cesarean section in 14 patients (19.3%). In this study, we retrospectively reviewed patients who underwent wound revision due to wound dehiscence and analyzed the underlying causes of the postoperative complication. -
The Practice of Gastrointestinal Motility Laboratory During COVID-19 Pandemic
J Neurogastroenterol Motil, Vol. 26 No. 3 July, 2020 pISSN: 2093-0879 eISSN: 2093-0887 https://doi.org/10.5056/jnm20107 JNM Journal of Neurogastroenterology and Motility Review The Practice of Gastrointestinal Motility Laboratory During COVID-19 Pandemic: Position Statements of the Asian Neurogastroenterology and Motility Association (ANMA-GML-COVID-19 Position Statements) Kewin T H Siah,1,2* M Masudur Rahman,3 Andrew M L Ong,4,5 Alex Y S Soh,1,2 Yeong Yeh Lee,6,7 Yinglian Xiao,8 Sanjeev Sachdeva,9 Kee Wook Jung,10 Yen-Po Wang,11 Tadayuki Oshima,12 Tanisa Patcharatrakul,13,14 Ping-Huei Tseng,15 Omesh Goyal,16 Junxiong Pang,17 Christopher K C Lai,18 Jung Ho Park,19 Sanjiv Mahadeva,20 Yu Kyung Cho,21 Justin C Y Wu,22 Uday C Ghoshal,23 and Hiroto Miwa12 1Department of Medicine, Yong Loo Lin School of Medicine, The National University of Singapore, Singapore; 2Division of Gastroenterology and Hepatology, Department of Medicine, National University Hospital, Singapore; 3Department of Gastroenterology, Sheikh Russel National Gastroliver Institute and Hospital, Dhaka, Bangladesh; 4Department of Gastroenterology and Hepatology, Singapore General Hospital, Singapore; 5Duke-NUS Medical School, Singapore; 6School of Medical Sciences, Universiti Sains Malaysia, Malaysia; 7St George and Sutherland Clinical School, University of New South Wales, Kogarah, NSW, Australia; 8Department of Gastroenterology and Hepatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; 9Department of Gastroenterology, GB Pant Hospital, New Delhi, India; -
Guidelines for Management of Acute Renal Failure (Acute Kidney Injury)
Guidelines for management of Acute Renal Failure (Acute Kidney Injury) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the author(s) reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Feb 2009 Guidelines on management of Acute Renal Failure (Acute Kidney Injury) Definition of ARF (now referred to as AKI) • Acute renal failure is a sudden decline in glomerular filtration rate (usually marked by rise in serum creatinine & urea) which is potentially reversible with or without oliguria. • Oliguria defined as urine output <300ml/m²/day or < 0.5 ml/kg/h (<1 ml/kg/h in neonates). • Acute on chronic renal failure suggested by poor growth, history of polyuria and polydipsia, and evidence of renal osteodystrophy However, immediately after a kidney injury, serum creatinine & urea levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (e.g., cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the serum urea level can occur without renal injury, such as in GI or mucosal bleeding, steroid use, or protein loading. -
Current Current
CP_0406_Cases.final 3/17/06 2:57 PM Page 67 Current p SYCHIATRY CASES THAT TEST YOUR SKILLS Chronic enuresis has destroyed 12-year-old Jimmy’s emotional and social functioning. The challenge: restore his self-esteem by finding out why can’t he stop wetting his bed. The boy who longed for a ‘dry spell’ Tanvir Singh, MD Kristi Williams, MD Fellow, child® Dowdenpsychiatry ResidencyHealth training Media director, psychiatry Medical University of Ohio, Toledo CopyrightFor personal use only HISTORY ‘I CAN’T FACE MYSELF’ during regular checkups and refer to a psychia- immy, age 12, is referred to us by his pediatri- trist only if the child has an emotional problem J cian, who is concerned about his “frequent secondary to enuresis or a comorbid psychiatric nighttime accidents.” His parents report that he wets disorder. his bed 5 to 6 times weekly and has never stayed con- Once identified, enuresis requires a thorough sistently dry for more than a few days. assessment—including its emotional conse- The accidents occur only at night, his parents quences, which for Jimmy are significant. In its say. Numerous interventions have failed, including practice parameter for treating enuresis, the restricting fluids after dinner and awakening the boy American Academy of Child and Adolescent overnight to make him go to the bathroom. Psychiatry (AACAP)1 suggests that you: Jimmy, a sixth-grader, wonders if he will ever Take an extensive developmental and family stop wetting his bed. He refuses to go to summer history. Find out if the child was toilet trained and camp or stay overnight at a friend’s house, fearful started walking, talking, or running at an appro- that other kids will make fun of him after an acci- priate age. -
Antianginal Drugs
Antianginal Drugs Angina medications are used for angina pectoris or chest pain. The types of chest pain are chronic stable angina (which is associated with atherosclerosis), unstable angina (early stage of progressive coronary artery disease), and vasospastic angina (which results from spasms in the layer of smooth muscle that surrounds atherosclerotic coronary arteries). The three main classes of drugs used to treat angina pectoris are nitrates and nitrites, beta-blockers, and calcium channel blockers. The goal of the treatment is: 1. Minimize the frequency of attacks and decrease the duration and intensity of angina pain 2. Improve the patient’s functional capacity with as few adverse effects as possible 3. Increase blood flow to ischemic heart muscle and decrease myocardial oxygen demand 4. Prevent or delay the worst possible outcome, which is a myocardial infarction Nitrates and Nitrites Nitrates are available on many forms including sublingual, chewable tablets, oral capsules/tablets, IV solutions, transdermal patches, ointments and translingual sprays. They are broken down into rapid-acting forms and long-acting forms. The rapid-acting forms include sublingual and IV solutions. These are used to treat acute angina attacks. The long-acting forms are used to prevent angina episodes. Mechanism of Action Nitrates dilate all blood vessels; however, they predominately affect venous vascular beds and have a dose-dependent arterial vasodilator effect. This vasodilation happens because of relaxation of smooth muscle cells. 1. Vasodilation results in reduced myocardial oxygen demand and therefore more oxygen to ischemic myocardial tissue and reduction of angina symptoms. 2. By causing venous dilation, the nitrates reduce venous return and in turn reduce the leftventricular end-diastolic volume (preload) and results in a lower left ventricular pressure. -
Your Guide to Living Well with Heart Disease
YOUR GUIDE TO Living Well Wi t h H e a rt Disease U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Heart, Lung, and Blood Institute NIH Publication No. 06–5270 November 2005 Written by: Marian Sandmaier U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Heart, Lung, and Blood Institute C o n t e n t s Introduction . 1 Heart Disease: A Wakeup Call . 2 What Is Heart Disease? . 4 Getting Tested for Heart Disease . 7 Controlling Your Risk Factors . 10 You and Your Doctor: A Healthy Partnership . 12 Major Risk Factors . 13 Smoking . 13 High Blood Pressure . 14 High Blood Cholesterol . 18 Overweight and Obesity . 23 Physical Inactivity. 26 Diabetes . 27 What Else Affects Heart Disease? . 31 Stress . 31 Alcohol . 31 Sleep Apnea. 32 Menopausal Hormone Therapy . 33 C-Reactive Protein . 33 Treatments for Heart Disease . 34 Medications . 34 Managing Angina . 38 Procedures. 41 Coronary Angioplasty, or “Balloon” Angioplasty. 42 Plaque Removal . 42 Stent Placement . 42 Coronary Bypass Surgery . 44 Getting Help for a Heart Attack. 46 Know the Warning Signs. 46 Get Help Quickly . 46 Plan Ahead. 49 Recovering Well: Life After a Heart Attack or Heart Procedure. 51 Your First Weeks at Home. 52 Cardiac Rehabilitation . 55 Getting Started . 55 How To Choose a Cardiac Rehab Program . 56 What You’ll Do in a Cardiac Rehab Program. 56 Getting the Most Out of Cardiac Rehab . 57 Getting Your Life Back . 59 Coping With Your Feelings . 60 Caring for Your Heart . 63 To Learn More . 64 1 I n t r o d u c t i o n Chances are, you’re reading this book because you or someone close to you has heart disease. -
Bradycardia; Pulse Present
Bradycardia; Pulse Present History Signs and Symptoms Differential • Past medical history • HR < 60/min with hypotension, acute • Acute myocardial infarction • Medications altered mental status, chest pain, • Hypoxia / Hypothermia • Beta-Blockers acute CHF, seizures, syncope, or • Pacemaker failure • Calcium channel blockers shock secondary to bradycardia • Sinus bradycardia • Clonidine • Chest pain • Head injury (elevated ICP) or Stroke • Digoxin • Respiratory distress • Spinal cord lesion • Pacemaker • Hypotension or Shock • Sick sinus syndrome • Altered mental status • AV blocks (1°, 2°, or 3°) • Syncope • Overdose Heart Rate < 60 / min and Symptomatic: Exit to Hypotension, Acute AMS, Ischemic Chest Pain, Appropriate NO Acute CHF, Seizures, Syncope, or Shock Protocol(s) secondary to bradycardia Typically HR < 50 / min YES Airway Protocol(s) AR 1, 2, 3 if indicated Respiratory Distress Reversible Causes Protocol AR 4 if indicated Hypovolemia Hypoxia Chest Pain: Cardiac and STEMI Section Cardiac Protocol Adult Protocol AC 4 Hydrogen ion (acidosis) if indicated Hypothermia Hypo / Hyperkalemia Search for Reversible Causes B Tension pneumothorax 12 Lead ECG Procedure Tamponade; cardiac Toxins Suspected Beta- IV / IO Protocol UP 6 Thrombosis; pulmonary Blocker or Calcium P Cardiac Monitor (PE) Channel Blocker Thrombosis; coronary (MI) A Follow Overdose/ Toxic Ingestion Protocol TE 7 P If No Improvement Transcutaneous Pacing Procedure P (Consider earlier in 2nd or 3rd AVB) Notify Destination or Contact Medical Control Revised AC 2 01/01/2021 Any local EMS System changes to this document must follow the NC OEMS Protocol Change Policy and be approved by OEMS 1 Bradycardia; Pulse Present Adult Cardiac Adult Section Protocol Pearls • Recommended Exam: Mental Status, HEENT, Skin, Heart, Lungs, Abdomen, Back, Extremities, Neuro • Identifying signs and symptoms of poor perfusion caused by bradycardia are paramount. -
Hypovolemic Shock
Ask the Expert Emergency Medicine / Critical Care Peer Reviewed Hypovolemic Shock Garret E. Pachtinger, VMD, DACVECC Veterinary Specialty & Emergency Center Levittown, Pennsylvania You have asked… What is hypovolemic shock, and how should I manage it? Retroperitoneal effusion in a dog The expert says… hock, a syndrome in which clinical deterioration can occur quickly, requires careful analy- All forms of shock share sis and rapid treatment. Broad definitions for shock include inadequate cellular energy pro- a common concern: Sduction or the inability of the body to supply cells and tissues with oxygen and nutrients and remove waste products. Shock may result from a variety of underlying conditions and can be inadequate perfusion. classified into the broad categories of septic, hemorrhagic, obstructive, and hypovolemic shock.1-3 Regardless of the underlying cause, all forms of shock share a common concern: inadequate per- fusion.1,2 Perfusion (ie, flow to or through a given structure or tissue bed) is imperative for nutri- ent and oxygen delivery, as well as removal of cellular waste and byproducts of metabolism. Lack of adequate perfusion can result in cell death, morbidity, and, ultimately, mortality. Hypovolemic shock is one of the most common categories of shock seen in clinical veterinary medicine.4 In hypovolemic shock, perfusion is impaired as a result of an ineffective circulating blood volume. During initial circulating volume loss, there are a number of mechanisms to com- pensate for decreases in perfusion, including increased levels of 2,3-Bisphosphoglycerate, result- ing in a rightward shift in the oxyhemoglobin dissociation curve and a decreased blood viscosity.