DOCSLIB.ORG

Chapter 32 Diagnosis and Management of Hypotension and Shock in the Intensive Care Unit

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chapter 32 Diagnosis and Management of Hypotension and Shock in the Intensive Care Unit Diagnosis and Management of Hypotension and Shock in the Intensive Care Unit Chapter 32 DIAGNOSIS AND MANAGEMENT OF HYPOTENSION AND SHOCK IN THE INTENSIVE CARE UNIT JESSICA BUNIN, MD* INTRODUCTION PATHOPHYSIOLOGY AND CLINICAL PRESENTATION CATEGORIES OF SHOCK GENERAL DIAGNOSTIC APPROACH FOR HYPOTENSION GENERAL PRINCIPLES OF MANAGEMENT OF THE HYPOTENSIVE INTENSIVE CARE UNIT PATIENT MANAGEMENT OF SPECIFIC TYPES OF SHOCK Hypovolemic Shock Cardiogenic Shock Distributive Shock Obstructive Shock SUMMARY *Lieutenant Colonel, Medical Corps, US Army; Chief of the Critical Care Medicine Service, Department of Medicine, Walter Reed National Military Medical Center, 8901 Wisconsin Avenue, Bethesda, Maryland 20889 327 Combat Anesthesia: The First 24 Hours INTRODUCTION Shock is a state of impaired tissue oxygenation and than 30% of blood volume has been lost. Although perfusion that can be caused by decreased oxygen hypotension and shock are not synonymous, the goals delivery, poor tissue perfusion, or impaired oxygen of treatment are the same: to restore the body’s oxygen utilization. Hypotension is a sign of shock and an indi- balance and correct hypoperfusion. This chapter will cator of advanced derangement, requiring immediate address the categories of shock, initial evaluation of a evaluation and management. For example, in hemor- hypotensive patient, general principles of shock man- rhagic shock, hypotension is not present until greater agement, and management for specific causes of shock. PATHOPHYSIOLOGY AND CLINICAL PRESENTATION Shock represents a state of hypoperfusion that vital of organs—the heart and the brain—because of can be the final pathway for a number of conditions. the opening of arteriovenous connections to bypass Hypoperfusion from any cause results in an inflamma- capillary flow.2 tory response. A normal physiologic compensation to As these compensatory mechanisms begin to fail, improve perfusion of vital organs is sympathetic vaso- the clinical signs and symptoms of shock become evi- constriction resulting in an elevated diastolic pressure, dent. The most commonly discussed signs of shock narrow pulse pressure, and peripheral hypothermia. are hypotension, altered mental status, and oligura, There is also a sympathetically mediated tachycardia but dysfunction of any end organ can result. Labora- that helps maintain cardiac output. Hypoperfusion tory abnormalities include lactic acidosis, elevated also causes an acidosis induced by lactate production base deficit, hypoxia, elevated blood urea nitrogen and resulting in compensatory tachypnea as the body and creatinine, elevated liver-associated enzymes attempts to offset the resulting acidosis. The other and bilirubin, and coagulation abnormalities. Lactic major effect of the acidosis is a rightward shift of the acidosis and base deficit are more sensitive indicators oxyhemoglobin curve,1 allowing more of the oxygen of severity and prognosis than are blood pressure and that is bound to hemoglobin to be released. Addition- urine output (these will be covered in greater detail ally, there is increased shunting of blood to the most later in this chapter).3,4 CATEGORIES OF SHOCK It is helpful to place shock in one of the following pressure are elevated in cardiogenic shock. In this state, four distinct categories: (1) hypovolemic, (2) cardiogen- the volume is available, but pump failure causes inad- ic, (3) distributive, and (4) obstructive. Hypovolemic equate blood circulation. Physical exam is significant shock can result from hemorrhage or other forms of for distended neck veins, pulmonary edema, and a intravascular fluid loss such as capillary leak, gastroin- possible S3 gallop. testinal losses, or renal losses. Its hemodynamic profile Distributive shock is often referred to as high out- is significant for increased heart rate (HR), decreased put or hyperdynamic shock because, unlike the other cardiac output (CO), increased systemic vascular forms of shock, the cardiac output is normal to elevat- resistance (SVR), decreased cardiac filling pressures, ed. The loss of vascular tone that defines distributive decreased pulse pressures (PPs), and decreased central shock results in decreased SVR and an increased pulse venous oxygen saturation (ScvO2). Simply stated, the pressure caused by decreased diastolic pressure. Many circulatory system cannot maintain adequate blood causes of distributive shock exist, including early septic flow and the body is compensating by increasing HR shock, neurogenic shock, and anaphylactic shock. in an effort to increase CO and SVR to maintain perfu- Obstructive shock shares the hemodynamic profile sion. On physical exam, one would expect to see pallor of cardiogenic shock, and the two are often lumped and flat neck veins. together. The most significant difference between Cardiogenic shock is most often caused by a myo- the two is the cause. Obstructive shock is caused by cardial infarction, but it can have other causes such impaired cardiac filling as in cardiac tamponade, or ex- as myocardial contusion. Like hypovolemic shock, its cessive afterload as in a massive pulmonary embolus. hemodynamic profile shows increased HR, decreased Management lies in relieving the obstruction, which CO, increased SVR, and decreased ScvO2. It differs, is often readily treatable if identified, but can be fatal however, in that cardiac-filling pressures, central ve- if not detected. nous pressure (CVP), and pulmonary artery occlusion One must be cognizant that the categorization of 328 Diagnosis and Management of Hypotension and Shock in the Intensive Care Unit SHOCK Hypodynamic-Low CO Hyperdynamic-Low SVR Pulmonary Edema? No Yes JVD? No Yes Sepsis RV Failure Cardiogenic Shock Hypovolemia Neurogenic PE LV Failure Hemorrhage Adrenal Insuff Tamponade MI Dehydration Anaphylaxis Tension PTX Valve Disease Medication Treatment Treatment Treatment Treatment Hemostasis Fluids Fluid Optimization Fluid Fluids Inotropes Intropes Pressors Blood Specific TX IABP Early Goal Revascularization Directed Figure 32-1. Diagnosing and treating various forms of hypotension. CO: cardiac output; IABP: intra-aortic balloon pump; JVD: jugular vein distension; LV: left ventricular; MI: myocardial infarction; PE: pulmonary embolism; PTX: pneumothorax; RV: right ventricular; SVR: systemic vascular resistance; TX: therapeutics shock is not always clear cut and overlap often oc- have cardiac tamponade or a pneumothorax, resulting curs. For example, while septic shock is considered in obstructive shock. Additionally, shock is a dynamic distributive shock, there is often a large component state so the dominant component may change over of hypovolemia present from third spacing of fluid. time or with treatment. An overview of the causes and Alternatively, a thoracic trauma patient may suffer treatments of the various forms of shock can be seen hemorrhage, causing hypovolemic shock, but may also in Figure 32-1. GENERAL DIAGNOSTIC APPROACH FOR HYPOTENSION As with any medical illness, diagnosing the source neck veins, auscultation of cardiac and breath sounds, of hypotension should begin with a history and physi- sources of external bleeding, assessment of possible cal examination. The importance of a thorough but internal sources of bleeding, and neurologic status. focused physical exam must not be underestimated. Noninvasive vital signs are not adequate to de- Vital signs should be obtained. Airway, breathing, and termine the severity of illness or injury. Tachycardia, circulation should be immediately assessed and the tachypnea, and hypotension are highly concerning patient must be fully disrobed and inspected, front and findings, but they likely represent an advanced stage of back. Specific findings that may guide the investigation disease. Consequently, invasive monitoring and labo- are vital signs, level of consciousness, appearance of ratory evaluation should be obtained.4 CVP and ScvO2 329 Combat Anesthesia: The First 24 Hours can assist with determining the type of shock. Arterial including medication effect, altered mental status, and catheterization may be helpful in maintaining a more distracting injuries. Therefore, to improve diagnostic accurate blood pressure as well as in determining re- accuracy, many trauma centers routinely include Fo- spiratory variation of pressures. There is no apparent cused Assessment Sonography for Trauma (FAST) as benefit to using a pulmonary artery catheter.5 Lactate part of the physical exam.11 and base deficit are important values to obtain.3,4 They The FAST exam consists of four sonographic views will not assist in determining the cause of hypotension, to evaluate for pericardial and peritoneal free fluid: but they will aid in assessing severity and adequacy of (1) pericardial, (2) perisplenic, (3) perihepatic, and (4) resuscitation. Base deficit has been shown to correlate pelvic.11 This exam is most helpful when free fluid is with greater fluid requirements, ongoing blood loss,6 identified. A negative exam is less helpful because of and mortality.7 Lactate has been shown to correlate a lower sensitivity. Therefore, the Eastern Association with the development of multiorgan failure.8 for the Surgery of Trauma guidelines recommend re- Although obtaining a thorough history is not a peat exams and at least 6 hours of monitoring before requirement when assessing a hypotensive critically accepting a negative exam.10 Similarly, Advanced ill patient, at a minimum one must be aware of aller- Trauma Life Support recommends a repeat exam in gies and medications.
Load more

Recommended publications
  • Differentiating Between Anxiety, Syncope & Anaphylaxis
    Differentiating between anxiety, syncope & anaphylaxis Dr. Réka Gustafson Medical Health Officer Vancouver Coastal Health Introduction Anaphylaxis is a rare but much feared side-effect of vaccination. Most vaccine providers will never see a case of true anaphylaxis due to vaccination, but need to be prepared to diagnose and respond to this medical emergency. Since anaphylaxis is so rare, most of us rely on guidelines to assist us in assessment and response. Due to the highly variable presentation, and absence of clinical trials, guidelines are by necessity often vague and very conservative. Guidelines are no substitute for good clinical judgment. Anaphylaxis Guidelines • “Anaphylaxis is a potentially life-threatening IgE mediated allergic reaction” – How many people die or have died from anaphylaxis after immunization? Can we predict who is likely to die from anaphylaxis? • “Anaphylaxis is one of the rarer events reported in the post-marketing surveillance” – How rare? Will I or my colleagues ever see a case? • “Changes develop over several minutes” – What is “several”? 1, 2, 10, 20 minutes? • “Even when there are mild symptoms initially, there is a potential for progression to a severe and even irreversible outcome” – Do I park my clinical judgment at the door? What do I look for in my clinical assessment? • “Fatalities during anaphylaxis usually result from delayed administration of epinephrine and from severe cardiac and respiratory complications. “ – What is delayed? How much time do I have? What is anaphylaxis? •an acute, potentially
    [Show full text]
  • Hypovolemic Shock and Resuscitation Piper Lynn Wall Iowa State University
    Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1997 Hypovolemic shock and resuscitation Piper Lynn Wall Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Sciences Commons, Physiology Commons, Surgery Commons, and the Veterinary Physiology Commons Recommended Citation Wall, Piper Lynn, "Hypovolemic shock and resuscitation " (1997). Retrospective Theses and Dissertations. 11754. https://lib.dr.iastate.edu/rtd/11754 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directly fi-om the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter &ce, while others may be from any type of computer printer. The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overiaps.
    [Show full text]
  • Fluid Resuscitation Therapy for Hemorrhagic Shock
    CLINICAL CARE Fluid Resuscitation Therapy for Hemorrhagic Shock Joseph R. Spaniol vides a review of the 4 types of shock, the 4 classes of Amanda R. Knight, BA hemorrhagic shock, and the latest research on resuscita- tive fluid. The 4 types of shock are categorized into dis- Jessica L. Zebley, MS, RN tributive, obstructive, cardiogenic, and hemorrhagic Dawn Anderson, MS, RN shock. Hemorrhagic shock has been categorized into 4 Janet D. Pierce, DSN, ARNP, CCRN classes, and based on these classes, appropriate treatment can be planned. Crystalloids, colloids, dopamine, and blood products are all considered resuscitative fluid treat- ment options. Each individual case requires various resus- ■ ABSTRACT citative actions with different fluids. Healthcare Hemorrhagic shock is a severe life-threatening emergency professionals who are knowledgeable of the information affecting all organ systems of the body by depriving tissue in this review would be better prepared for patients who of sufficient oxygen and nutrients by decreasing cardiac are admitted with hemorrhagic shock, thus providing output. This article is a short review of the different types optimal care. of shock, followed by information specifically referring to hemorrhagic shock. The American College of Surgeons ■ DISTRIBUTIVE SHOCK categorized shock into 4 classes: (1) distributive; (2) Distributive shock is composed of 3 separate categories obstructive; (3) cardiogenic; and (4) hemorrhagic. based on their clinical outcome. Distributive shock can be Similarly, the classes of hemorrhagic shock are grouped categorized into (1) septic; (2) anaphylactic; and (3) neu- by signs and symptoms, amount of blood loss, and the rogenic shock. type of fluid replacement. This updated review is helpful to trauma nurses in understanding the various clinical Septic shock aspects of shock and the current recommendations for In accordance with the American College of Chest fluid resuscitation therapy following hemorrhagic shock.
    [Show full text]
  • Sepsis: a Guide for Patients & Relatives
    SEPSIS: A GUIDE FOR PATIENTS & RELATIVES CONTENTS ABOUT SEPSIS ABOUT SEPSIS: INTRODUCTION P3 What is sepsis? In the UK, at least 150,000* people each year suffer from serious P4 Why does sepsis happen? sepsis. Worldwide it is thought that 3 in a 1000 people get sepsis P4 Different types of sepsis P4 Who is at risk of getting sepsis? each year, which means that 18 million people are affected. P5 What sepsis does to your body Sepsis can move from a mild illness to a serious one very quickly, TREATMENT OF SEPSIS which is very frightening for patients and their relatives. P7 Why did I need to go to the Critical Care Unit? This booklet is for patients and relatives and it explains sepsis P8 What treatment might I have had? and its causes, the treatment needed and what might help after P9 What other help might I have received in the Critical Care Unit? having sepsis. It has been written by the UK Sepsis Trust, a charity P10 How might I have felt in the Critical Care Unit? which supports people who have had sepsis and campaigns to P11 How long might I stay in the Critical Care Unit and hospital? raise awareness of the illness, in collaboration with ICU steps. P11 Moving to a general ward and The Outreach Team/Patient at Risk Team If a patient cannot read this booklet for him or herself, it may be helpful for AFTER SEPSIS relatives to read it. This will help them to understand what the patient is going through and they will be more able to support them as they recover.
    [Show full text]
  • When the Heart Kills the Liver: Acute Liver Failure in Congestive Heart Failure
    December 14, 2009 Eu Ro PE an JouR nal oF MED I cal RE sEaRcH 541 Eur J Med Res (2009) 14: 541-546 © I. Holzapfel Publishers 2009 WHEn tHE HEaRt KIlls tHE lIvER: acutE lIvER FaIluRE In congEstIvE HEaRt FaIluRE F. H. saner1, M. Heuer1, M. Meyer1, a. canbay2, g. c. sotiropoulos1, a. Radtke1, J. treckmann1, s. Beckebaum1, c. Dohna-schwake2, s. W. oldedamink3, 4, a. Paul1 1Department of general-, visceral- and transplant surgery, university Hospital Essen, germany, 2Department of Pediatric Medicine, university Hospital Essen, germany, 3Department of surgery, university of Maastricht, netherlands, 4Department of surgery, university college london Hospital, ucl, uK Abstract gestive heart failure may be absent [5, 18]. Both, congestive heart failure as a cause of acute liver fail- chronic and acute congestive heart failure can lead to ure is rarely documented with only a few cases. hepatic dysfunction [10, 17]. although there is no although the pathophysiology is poorly under- classic pattern of abnormalities, a cholestatic bio- stood, there is rising evidence, that low cardiac output chemical profile is common, with a mild elevation in with consecutive reduction in hepatic blood flow is a total bilirubin (usually 3 g/dl), a mild elevation in al- main causing factor, rather than hypotension. In the kaline phosphatase and only occasional elevations in setting of acute liver failure due to congestive heart transaminases. another common observation is an in- failure, clinical signs of the latter can be absent, which crease in InR. the presumed causes of hepatic dys- requires an appropriate diagnostic approach. function in congestive heart failure are hepatic con- as a reference center for acute liver failure and liver gestion from venous outflow obstruction and result- transplantation we recorded from May 2003 to De- ing hypertension and decreased oxygen delivery from cember 2007 202 admissions with the primary diag- an impaired cardiac output [10].
    [Show full text]
  • Shock and Hemodynamic Monitoring
    Shock and Hemodynamic Monitoring Matthew Bank, MD, FACS Assistant Professor Hofstra North Shore‐LIJ School of Medicine Director, Surgical Intensive Care Unit North Shore University Hospital I do not have any financial conflicts of interest to disclose for this presentation Shock • Multiple different strategies for classifying shock, but all forms of shock result in impaired oxygen delivery secondary to either one or both: – reduced cardiac output (cardiogenic, septic) OR – loss of effective intravascular volume (hypovolemic, neurogenic, anaphylactic, septic). Septic Shock –Gram Negative • Gram negative septic shock: —Very studied well studied in animal models —Lipopolysaccharide (LPS) in bacterial cell wall binds to LPS binding protein. —LPS‐LBP complex then binds to cell surface CD14 receptors on monocytes and macrophages. —The LPS‐LBP‐CD14 complex then activates cells via Toll‐like receptor‐4 (TLR4). —TLR4 then “activates” cells which produce a cytokine “cascade” of proinflamatory mediators. Septic Shock –Gram Negative • Tumor Necrosis Factor (TNF) – First cytokine produced in response to gram negative sepsis – Principal mediator for acute response to gram negative bacteria – Major source of TNF is from activated macrophages – High levels of TNF predict mortality and can cause apoptosis. Septic Shock –Gram Negative • Interleukin‐1 (IL‐1) – Levels of IL‐1 increase soon after TNF production in gram negative sepsis (second cytokine to be elevated) – IL‐1 produced by macrophages, neutrophils and endothelial cells – IL‐1 increases levels of next proinflammatory cytokines in cascade, IL‐2 and IL‐12. – IL‐1 does NOT cause apoptosis Septic Shock –Gram Negative • Interleukin‐10 – Anti‐inflammatory cytokine – Inhibits production of IL‐12 – Inhibits T‐cell activation Septic Shock –Gram Positive • Gram positive sepsis – Gram positive cell wall components are also known to be involved in septic response – Peptidoglycans – Teichoic Acid – Likely act in a similar manner as LPS, but less potent on a weight bases.
    [Show full text]
  • 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.
    [Show full text]
  • Acute Kidney Injury in Cardiogenic Shock: an Updated Narrative Review
    Journal of Cardiovascular Development and Disease Review Acute Kidney Injury in Cardiogenic Shock: An Updated Narrative Review Sohrab Singh 1 , Ardaas Kanwar 2, Pranathi R. Sundaragiri 3, Wisit Cheungpasitporn 4 , Alexander G. Truesdell 5, Syed Tanveer Rab 6, Mandeep Singh 7 and Saraschandra Vallabhajosyula 8,* 1 Department of Medicine, The Brooklyn Hospital, Brooklyn, NY 11201, USA; [email protected] 2 Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA; [email protected] 3 Section of Primary Care Internal Medicine, Wake Forest Baptist Health, High Point, NC 27262, USA; [email protected] 4 Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 5 Virginia Heart/Inova Heart and Vascular Institute, Falls Church, VA 22042, USA; [email protected] 6 Section of Interventional Cardiology, Division of Cardiovascular Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; [email protected] 7 Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 8 Section of Cardiovascular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27262, USA * Correspondence: [email protected] Abstract: Acute myocardial infarction with cardiogenic shock (AMI-CS) is associated with high mortality and morbidity despite advancements in cardiovascular care. AMI-CS is associated with multiorgan failure of non-cardiac organ systems. Acute kidney injury (AKI) is frequently seen in patients with AMI-CS and is associated with worse mortality and outcomes compared to those without. The pathogenesis of AMI-CS associated with AKI may involve more factors than previously Citation: Singh, S.; Kanwar, A.; understood.
    [Show full text]
  • Characteristics and Risk Factors for Intensive Care Unit Cardiac Arrest in Critically Ill Patients with COVID-19—A Retrospective Study
    Journal of Clinical Medicine Article Characteristics and Risk Factors for Intensive Care Unit Cardiac Arrest in Critically Ill Patients with COVID-19—A Retrospective Study Kevin Roedl 1,* , Gerold Söffker 1, Dominic Wichmann 1 , Olaf Boenisch 1, Geraldine de Heer 1 , Christoph Burdelski 1, Daniel Frings 1, Barbara Sensen 1, Axel Nierhaus 1 , Dirk Westermann 2, Stefan Kluge 1 and Dominik Jarczak 1 1 Department of Intensive Care Medicine, University Medical Centre Hamburg-Eppendorf, 20246 Hamburg, Germany; [email protected] (G.S.); [email protected] (D.W.); [email protected] (O.B.); [email protected] (G.d.H.); [email protected] (C.B.); [email protected] (D.F.); [email protected] (B.S.); [email protected] (A.N.); [email protected] (S.K.); [email protected] (D.J.) 2 Department of Interventional and General Cardiology, University Heart Centre Hamburg, 20246 Hamburg, Germany; [email protected] * Correspondence: [email protected]; Tel.: +49-40-7410-57020 Abstract: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causing the coron- avirus disease 2019 (COVID-19) led to an ongoing pandemic with a surge of critically ill patients. Very little is known about the occurrence and characteristic of cardiac arrest in critically ill patients Citation: Roedl, K.; Söffker, G.; with COVID-19 treated at the intensive care unit (ICU). The aim was to investigate the incidence Wichmann, D.; Boenisch, O.; de Heer, and outcome of intensive care unit cardiac arrest (ICU-CA) in critically ill patients with COVID-19. G.; Burdelski, C.; Frings, D.; Sensen, This was a retrospective analysis of prospectively recorded data of all consecutive adult patients B.; Nierhaus, A.; Westermann, D.; with COVID-19 admitted (27 February 2020–14 January 2021) at the University Medical Centre et al.
    [Show full text]
  • Essentials of Sepsis Management
    Essentials of Sepsis Management John M. Green, MD KEYWORDS Sepsis Sepsis syndrome Surgical infection Septic shock Goal-directed therapy KEY POINTS Successful treatment of perioperative sepsis relies on the early recognition, diagnosis, and aggressive treatment of the underlying infection; delay in resuscitation, source control, or antimicrobial therapy can lead to increased morbidity and mortality. When sepsis is suspected, appropriate cultures should be obtained immediately so that antimicrobial therapy is not delayed; initiation of diagnostic tests, resuscitative measures, and therapeutic interventions should otherwise occur concomitantly to ensure the best outcome. Early, aggressive, invasive monitoring is appropriate to ensure adequate resuscitation and to observe the response to therapy. Any patient suspected of having sepsis should be in a location where adequate resources can be provided. INTRODUCTION Sepsis is among the most common conditions encountered in critical care, and septic shock is one of the leading causes of morbidity and mortality in the intensive care unit (ICU). Indeed, sepsis is among the 10 most common causes of death in the United States.1 Martin and colleagues2 showed that surgical patients account for nearly one-third of sepsis cases in the United States. Despite advanced knowledge in the field, sepsis remains a common threat to life in the perioperative period. Survival relies on early recognition and timely targeted correction of the syndrome’s root cause as well as ongoing organ support. The objective of this article is to review strategies for detection and timely management of sepsis in the perioperative surgical patient. A comprehensive review of the molecular and cellular mechanisms of organ dysfunc- tion and sepsis management is beyond the scope of this article.
    [Show full text]
  • Health Care Facilities Hospitals Report on Training Visit
    SLOVAK UNIVERSITY OF TECHNOLOGY IN BRATISLAVA FACULTY OF ARCHITECTURE INSTITUTE OF HOUSING AND CIVIC STRUCTURES HEALTH CARE FACILITIES HOSPITALS REPORT ON TRAINING VISIT In the frame work of the project No. SAMRS 2010/12/10 “Development of human resource capacity of Kabul polytechnic university” Funded by UÜtà|áÄtät ECDC cÜÉA Wtâw f{t{ YtÜâÖ December, 14, 2010 Prof. Daud Shah Faruq Health Care Facilities, Hospitals 2010/12/14 Acknowledgement: I Daud Shah Faruq professor of Kabul Poly Technic University The author of this article would like to express my appreciation for the Scientific Training Program to the Faculty of Architecture of the Slovak University of Technology and Slovak Aid program for financial support of this project. I would like to say my hearth thanks to Professor Arch. Mrs. Veronika Katradyova PhD, and professor Arch. Mr. stanislav majcher for their guidance and assistance during the all time of my training visit. My thank belongs also to Ing. Juma Haydary, PhD. the coordinator of the project SMARS/2010/10/01 in the frame work of which my visit was realized. Besides of this I would like to appreciate all professors and personnel of the faculty of Architecture for their good behaves and hospitality. Best regards cÜÉyA Wtâw ft{t{ YtÜâÖ December, 14, 2010 2 Prof. Daud Shah Faruq Health Care Facilities, Hospitals 2010/12/14 VISITING REPORT FROM FACULTY OF ARCHITECTURE OF SLOVAK UNIVERSITY OF TECHNOLOGY IN BRATISLAVA This visit was organized for exchanging knowledge views and advices between us (professor of Kabul Poly Technic University and professors of this faculty). My visit was especially organized to the departments of Public Buildings and Interior design.
    [Show full text]
  • Approach to Shock.” These Podcasts Are Designed to Give Medical Students an Overview of Key Topics in Pediatrics
    PedsCases Podcast Scripts This is a text version of a podcast from Pedscases.com on “Approach to Shock.” These podcasts are designed to give medical students an overview of key topics in pediatrics. The audio versions are accessible on iTunes or at www.pedcases.com/podcasts. Approach to Shock Developed by Dr. Dustin Jacobson and Dr Suzanne Beno for PedsCases.com. December 20, 2016 My name is Dustin Jacobson, a 3rd year pediatrics resident from the University of Toronto. This podcast was supervised by Dr. Suzanne Beno, a staff physician in the division of Pediatric Emergency Medicine at the University of Toronto. Today, we’ll discuss an approach to shock in children. First, we’ll define shock and understand it’s pathophysiology. Next, we’ll examine the subclassifications of shock. Last, we’ll review some basic and more advanced treatment for shock But first, let’s start with a case. Jonny is a 6-year-old male who presents with lethargy that is preceded by 2 days of a diarrheal illness. He has not urinated over the previous 24 hours. On assessment, he is tachycardic and hypotensive. He is febrile at 40 degrees Celsius, and is moaning on assessment, but spontaneously breathing. We’ll revisit this case including evaluation and management near the end of this podcast. The term “shock” is essentially a ‘catch-all’ phrase that refers to a state of inadequate oxygen or nutrient delivery for tissue metabolic demand. This broad definition incorporates many causes that eventually lead to this end-stage state. Basic oxygen delivery is determined by cardiac output and content of oxygen in the blood.
    [Show full text]