2012 washington manual of critical care medicine 2nd edition

Louis, Missouri Professor of Medicine and Pediatrics Division of Pulmonary and Critical Care Associate Professor of Medicine Division of Pulmonary and Critical Care Director of Intervent

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r i

OF CRITICAL CARE

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P1: Trim: 5in × 8in Top: 0.394in Gutter: 0.581in

ii

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Director, Respiratory Care ServicesDirector, Critical Care ResearchDivision of Pulmonary and Critical Care MedicineWashington University School of Medicine

Barnes-Jewish Hospital

St Louis, Missouri

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Library of Congress Cataloging-in-Publication Data

The Washington manual of critical care / [edited by] Marin H Kollef, Warren Isakow.

p ; cm.

Manual of critical care

Includes bibliographical references and index.

ISBN 978-1-4511-1022-7

I Kollef, Marin H II Isakow, Warren III Title: Manual of critical care.

[DNLM: 1 Critical Care–methods–Handbooks 2 Critical Illness–therapy–

Handbooks WX 39]

LC classification not assigned

Care has been taken to confirm the accuracy of the information presented and to describe generally accepted

practices However, the authors, editors, and publisher are not responsible for errors or omissions or for any

consequences from application of the information in this book and make no warranty, expressed or implied,

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information in a particular situation remains the professional responsibility of the practitioner.

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set forth in this text are in accordance with current recommendations and practice at the time of publication.

However, in view of ongoing research, changes in government regulations, and the constant flow of

information relating to drug therapy and drug reactions, the reader is urged to check the package insert for

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particularly important when the recommended agent is a new or infrequently employed drug.

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We dedicate this manual to all health care providers involved in

the care of critically ill patients and their families We acknowledge their efforts and sacrifices and hope that this manual

can assist them in some meaningful manner.

To our families for their support and to the critical care and academic communities of Washington University and

Barnes-Jewish Hospital for their commitment to the education and

well-being of medical students and house staff physicians.

v

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vi

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Director, Cardiac Intensive Care Unit

Washington University School of Medicine

Director, Marfan Syndrome ClinicWashington University School ofMedicine

St Louis, Missouri

FellowDivision of Cardiothoracic SurgeryWashington University School ofMedicine

Washington University School ofMedicine

St Louis, Missouri

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v i i i C O N T R I B U T O R S

Assistant Professor of Medicine

Division of Pulmonary and Critical Care

Division of Infectious Diseases

Associate Hospital Epidemiologist

Washington University School of

Department of Obstetrics and Gynecology

St Louis, Missouri

Professor of Medicine and Pediatrics

Associate Professor of Medicine

Director of Interventional Pulmonology

St Louis, Missouri

Marilyn Bornefeld Chair inGastrointestinal Research and TreatmentDivision of Gastroenterology

Medical Director, Liver TransplantationWashington University School ofMedicine

St Louis, Missouri

Associate ProfessorDivision of OncologyDirector, Inpatient OncologyWashington University School ofMedicine

St Louis, Missouri

FellowCardiovascular DivisionWashington University School ofMedicine

St Louis, Missouri

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Associate Hospital Epidemiologist

Division of Pulmonary and Critical CareMedicine

St Louis, Missouri

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St Louis, Missouri

Fellow

Director, Medical Intensive Care Unit

Cardiovascular DivisionWashington University School ofMedicine

St Louis, Missouri

FellowDivision of Pulmonary and Critical CareMedicine

St Louis, Missouri

Professor of MedicineVirginia E and Sam J Golman Chair inRespiratory and Intensive Care MedicineDirector, Respiratory Care ServicesDirector, Critical Care ResearchDivision of Pulmonary and Critical CareMedicine

St Louis, Missouri

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St Louis, Missouri

Professor of MedicineDivision of Pulmonary and Critical CareMedicine

St Louis Veterans Affairs Medical Center

St Louis, Missouri

Professor of SurgeryDivision of General SurgeryWashington University School of MedicineBarnes-Jewish Hospital

St Louis, Missouri

Assistant Professor of SurgeryDepartment of Acute and CriticalCare Surgery

Emory UniversityAtlanta, Georgia

Clinical PharmacistDepartment of PharmacyWashington University School of MedicineBarnes-Jewish Hospital

St Louis, Missouri

Assistant Professor of MedicineDepartment of AnesthesiologyDepartment of Emergency MedicineWashington University School of MedicineBarnes-Jewish Hospital

St Louis, Missouri

Attending PhysicianDepartment of HematologySoutheast HospitalCape Girardeau, Missouri

Assistant Professor of MedicineDivision of GastroenterologyWashington University School of MedicineBarnes-Jewish Hospital

St Louis, Missouri

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St Louis, Missouri

Assistant Professor of Surgery

Division of General Thoracic Surgery

Division of Endocrinology, Metabolism,

and Lipid Research

St Louis, Missouri

Fellow

Divisions of Hematology and Oncology

St Louis, Missouri

Associate Professor of SurgeryDirector of Trauma

Director of Surgical CriticalCare FellowshipDivision of General SurgeryWashington University School ofMedicine

St Louis, Missouri

FellowCardiovascular DivisionWashington University School ofMedicine

St Louis, Missouri

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Assistant Professor of Surgery

Division of General Surgery

Department of Food and Nutrition

St Louis, Missouri

Clinical FellowRenal DivisionWashington University School ofMedicine

St Louis, Missouri

Instructor in MedicineDepartment of MedicineWashington University School ofMedicine

St Louis, Missouri

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x i v C O N T R I B U T O R S

Professor of Medicine

Director, Clinical Advisory Group

and Healthcare Informatics

Washington University School of MedicineBarnes-Jewish Hospital

St Louis, Missouri

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This is the second edition of The Washington Manual TM of Critical Care, building

upon the first edition and adding to the long tradition of medical education promoted

by The Washington Manual TM of Medical Therapeutics and the associated medical and

surgical subspecialty manuals published from Washington University Our continuedgoal in publishing this manuscript is to provide experienced clinicians and trainees aresource containing comprehensive and current treatment algorithms for the bedsidediagnosis and management of the most frequently encountered illnesses and problems

in the intensive care unit (ICU) In this edition, we continue to focus on the delivery

of concise algorithms in order to expedite bedside decision-making The chaptersinclude annotated bibliographies of select references to guide more in-depth readingwhen time permits We again include sections on common ICU procedures, equations,nutrition, and pharmacology All chapters were written by Washington Universityfaculty physicians and experts in their respective fields, often with the assistance ofsubspecialty fellows and residents

We recognize that the field of critical care is constantly changing with the ability of new study results Therefore, this manual is meant to be a starting place forthe initial care and stabilization of critically ill patients The tables and figures thataccompany each chapter are meant as guides and may not be applicable for all patients

avail-We strongly encourage further reading of the literature and consultation with moreexpert clinicians to optimize the outcomes of critically ill patients

We again especially give our sincerest thanks to Becky Light for her devotedefforts in preparing chapters and for acting as the liaison between the chapters’ authorsand Lippincott Williams & Wilkins We also thank the entire production staff atLippincott Williams & Wilkins and Wolters Kluwer for their efforts in the production

of this manual

M.H.K would like to thank his loving family for all their support and agement W.I would like to thank his wife for her support and understanding

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The editors thank Becky Light who expertly coordinated all of the chapter cations, preparation, and revisions

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xviii

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Marin H Kollef and Scott T Micek

Sundeep Viswanathan and Richard G Bach

Timothy J Bedient and Marin H Kollef

Howard J Huang

Warren Isakow

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Saad Ghafoor and Mario Castro

Chad A Witt and Marin H Kollef

Tonya D Russell

Right Ventricular Failure in the Intensive

Murali M Chakinala

Hannah C Otepka and Roger D Yusen

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C O N T E N T S x x i

Jeremiah P Depta and Andrew M Kates

Sundeep Viswanathan and Marin Kollef

Jay Shah and Alan C Braverman

Shane J LaRue and Gregory A Ewald

Derrick R Fansler and Daniel H Cooper

Ahsan Usman and Seth Goldberg

Peter Juran and Steven Cheng

Andrew Labelle

William E Clutter

Timothy J Bedient and Marin H Kollef

David A Rometo, Marin H Kollef, and Garry S Tobin

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x x i i C O N T E N T S

David A Rometo, Marin H Kollef, and Garry S Tobin

Ryan Roop and Alex Denes

Derek E Byers

Nicholas M Mohr, Devin P Sherman, and Steven L Brody

Hitoshi Honda and Keith F Woeltje

Kevin W McConnell, John P Kirby, and John E Mazuski

David K Warren

Toshibumi Taniguchi and Keith F Woeltje

Stephen Y Liang and Steven J Lawrence

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Linda D Bobo and Erik R Dubberke

Tingting Li and Anitha Vijayan

Anupam Aditi and Jeffrey S Crippin

Mrudula V Kumar and Kevin M Korenblat

Chandra Prakash Gyawali

Mrudula Kumar and Daniel K Mullady

Rajat Dhar

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Warren Isakow

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James C Mosley, III

Jeanine F Carbone and Molly V Houser

Molly J Stout and Laura A Parks

Kevin W McConnell and Douglas J.E Schuerer

Jennifer L Gnerlich, Robb R Whinney, and John P Kirby

Stephen R Broderick and Varun Puri

Beth E Taylor and Robert Southard

Jeremy Kilburn

Chad A Witt

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Jennifer Shaffer and Warren Isakow

Jonathan M Green

Warren Isakow

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C O N T E N T S x x v i i

Jamie M Rosini and Scott T Micek

Lee P Skrupky and Scott T Micek

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xxviii

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MANAGEMENT OF SHOCK SECTION I

Marin H Kollef

Shock is a common problem in the intensive care unit, requiring immediate diagnosisand treatment It is usually defined by a combination of hemodynamic parameters(mean blood pressure<60 mm Hg, systolic blood pressure <90 mm Hg), clinical

findings (altered mentation, decreased urine output), and abnormal laboratory values(elevated serum lactate, metabolic acidosis) The first step is to identify the cause ofshock, as each condition will require different interventions The overall goal of therapy

is to reverse tissue hypoperfusion as quickly as possible in order to preserve organfunction Table 1.1 and Algorithms 1.1 and 1.2 offer an approach for determining themain cause of shock Specific management of the various shock states is presented inthe following chapters Early evaluation with echocardiography, intraesophageal aorticwaveform assessment, or right heart catheterization will allow determination of thecause of shock and will assist in management

TABLE 1.1 Hemodynamic Patterns Associated with Specific Shock Statesa

aEqualization of RAP, PAOP, diastolic PAP, and diastolic RVP indicates cardiac tamponade.

CI, cardiac index; SVR, systemic vascular resistance; PVR, pulmonary vascular resistance;

SvO 2 , mixed venous oxygen saturation; RAP, right arterial pressure; RVP, right ventricular

pressure; PAP, pulmonary artery pressure; PAOP, pulmonary artery occlusion pressure;

↑, increased; ↓, decreased; N, normal.

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2 M A N A G E M E N T O F S H O C K

ALGORITHM 1.1 Main Causes of Shock

SBP: systolic blood pressure

MAP: mean arterial pressure

CI: cardiac index

Clinical Picture of Shock SBP <90 mm Hg MAP <60 mm Hg Lactate ≥4 mmol/L

Reduced Cardiac Output

CI <2.2 L/min/m 2 measured by thermodilution method or aortic waveform assessment with esophageal Doppler

Cardiogenic Shock

Hypovolemic Shock

Septic Shock

No Yes

↓

↓ Cool Slow

↑

+++

Large heart, pulmonary edema –

↓

↓ Cool Slow

↓

–

– Diminished cardiac size

–

↑

↓↓ ↓ Warm Rapid

↓

–

– Normal, unless pneumonia present +++

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Management of Shock rIntroduction to Shock 3

ALGORITHM 1.2 Miscellaneous Causes of Shock

CI: cardiac index Assess cardiac output by

thermodilution or aortic waveform assessment with esophageal Doppler

High cardiac output

Consider

• Spinal shock

• Anaphylaxis

• Adrenal insufficiency

Low to normal cardiac output

CI = 2.2−3.5 L/min/m 2

Low to normal right atrial pressure and fluid unresponsive

High right atrial pressure and fluid responsive

Consider

• Pulmonary embolism

• Cardiac tamponade

• Right ventricular infarction

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Marin H Kollef

Hypovolemic shock occurs as a result of decreased circulating blood volume, most

commonly from acute hemorrhage It may also result from heat-related intravascular

volume depletion or fluid sequestration within the abdomen Table 2.1 provides a

classification of hypovolemic shock based on the amount of whole blood volume

lost In general, the greater the loss of whole blood, the greater the resultant risk of

mortality However, it is important to note that other factors can influence the outcome

of hypovolemic shock including age, underlying comorbidities (e.g., cardiovascular

disease), and the rapidity and adequacy of the fluid resuscitation

Lactic acidosis occurs during hypovolemic shock because of inadequate tissue

perfusion The magnitude of the serum lactate elevation is correlated with mortality in

hypovolemic shock and may be an early indicator of tissue hypoperfusion, despite

near-normal–appearing vital signs The treatment of lactic acidosis depends on reversing

organ hypoperfusion This is reflected in the equation for tissue oxygen delivery shown

here Optimizing oxygen delivery to tissues requires a sufficient hemoglobin

concen-tration to carry oxygen to tissues In addition, ventricular preload is an important

determinant of cardiac output Providing adequate intravascular volume will ensure

that stroke volume and cardiac output are optimized to meet tissue demands for oxygen

and other nutrients If, despite adequate preload, cardiac output is not sufficient for

the demands of tissues, then dobutamine can be employed to further increase cardiac

output and oxygen delivery

TABLE 2.1 Classification of Hypovolemic Shock

Whole Blood

preserve blood flow to criticalorgans (brain and heart)

such as the kidneys, intestine,and pancreas

and heart

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injury to internal bleeding vessel or tissue, esophageal banding or tamponade of rapid variceal bleeding

Continue intravenous fluidresuscitation and exclude concomitant causes of

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6 M A N A G E M E N T O F S H O C K

TABLE 2.2 Adjunctive Therapies for Hypovolemic Shock

lungs and to prevent aspirationCardiac/hemodynamic

The prothrombin time and partial tin time should be corrected and the platelet

ongoing bleeding

or nonoperative ongoing hemorrhage whenclotting abnormalities have been correctedCalcium chloride,

magnesium chloride

To reverse ionized hypocalcemia andhypomagnesemia resulting from theadministration of citrate with transfused blood,which binds ionized calcium and magnesiumRewarming techniques (e.g.,

warm fluids, blankets,

radiant lamps, head covers,

warmed humidified air,

heated body cavity lavage)

Hypothermia is a common consequence ofmassive blood transfusion that can contribute

to cardiac dysfunction and coagulationabnormalities

Monitor and treat for

present to prevent and treat bacterial infections

and patients unable to mount an appropriatestress response

˙

CaO2 = (Hb × 1.34 × SaO2)+ 0.0031 PaO2

where ˙DO2= oxygen delivery, CaO2= arterial oxygen content, CO = cardiac output,

Hb= hemoglobin concentration, SaO2 = arterial hemoglobin oxygen saturation,

PaO2= arterial oxygen tension, SV = stroke volume, and HR = heart rate

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Management of Shock rHypovolemic Shock 7

The treatment goals in hypovolemic shock are to control the source of hemorrhageand to administer adequate intravascular volume replacement Control of the source ofhemorrhage may be as simple as placing a pressure dressing on an open bleeding wound,

or it may require urgent operative exploration to identify and control the bleedingsource from an intra-abdominal or intrathoracic injury Angiographic embolization

of a bleeding vessel may also be helpful for bleeding injuries that are not amenable

to surgical intervention (e.g., multiple pelvic fractures with ongoing hemorrhage).Therefore, most episodes of hypovolemic shock are managed by trauma specialists,usually in the emergency department setting However, all clinicians caring for criticallyill patients should be able to recognize the early clinical manifestations of hypovolemicshock and to initiate appropriate fluid management

An algorithm for the fluid management of hypovolemic shock is provided inAlgorithm 2.1 At least two large-bore (14 to 16 gauge or larger) peripheral veincatheters and/or an 8.5 French central vein catheter should be placed to allow rapidblood product and crystalloid administration A mechanical rapid transfusion deviceshould also be used to decrease the time required for each unit of blood or liter ofcrystalloid to be infused In a patient with ongoing hemorrhage, initial administration

of 2 to 4 L of crystalloid (0.9 NaCl or lactated Ringer solution) and group O bloodshould be given Most hospitals will employ four units of Rh-positive O blood for menand women who are not in childbearing age and Rh-negative O blood for women whoare in childbearing age Type-specific blood is usually administered after the first fourunits of nontyped blood are given The goal of blood transfusion therapy duringongoing hemorrhage is to maintain the hemoglobin value above 8 g/dL

In addition to the initial administration of crystalloid and red blood cells, othertherapies will be required in patients with hypovolemic shock These are summarized

in Table 2.2 and are especially important for patients requiring massive transfusions

or those with ongoing blood loss

pene-Kelley DM Hypovolemic shock: an overview Crit Care Nurs Q 2005;28:2–19.

A concise review of hypovolemic shock including initial evaluation and management.

Nunez TC, Cotton BA Transfusion therapy in hemorrhagic shock Curr Opin Crit Care.

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Septic Shock

Marin H Kollef and Scott T Micek

Severe sepsis is an infection-induced syndrome resulting in a systemic inflammatory

response that is complicated by dysfunction of at least one organ system In the United

States, approximately 750,000 cases of sepsis occur each year The mortality associated

with severe sepsis ranges from 30% to 50%, with mortality increasing with advancing

age Although complex, the pathophysiology of sepsis involves a series of interacting

pathways involving immune stimulation, immune suppression, hypercoagulation, and

hypofibrinolysis Cardiovascular management plays an important role in the treatment

of septic shock Hypotension occurs because of failure of vasoconstriction by

vascu-lar smooth muscle resulting in peripheral vasodilation Goal-directed cardiovascuvascu-lar

resuscitation has been demonstrated to be an important determinant of survival in

patients with septic shock In addition to cardiovascular management, appropriate

initial antimicrobial treatment of patients with severe sepsis also appears to be an

important determinant of patient outcome

The unscrambling of the complex pathophysiology associated with severe sepsis

and septic shock has made much progress, and current understanding of this process

is no longer rudimentary Novel drug entities and new therapeutic strategies targeting

these pathways have demonstrated efficacy in reducing patient mortality (Table 3.1)

The challenge for clinicians is the integration of these pharmacotherapies to confer the

recognized survival benefit into critical care practice The Surviving Sepsis Campaign

has teamed with the Institute for Healthcare Improvement to create the Severe Sepsis

Bundles, which are designed in an effort to optimize the timing, sequence, and goals

of the individual elements of care as delineated in the Surviving Sepsis Guidelines

The benefits associated with the use of comprehensive treatment protocols integrating

goal-directed hemodynamic stabilization, early appropriate antimicrobial therapy, and

associated adjunctive severe sepsis therapies initiated in the emergency department

and continued in the intensive care unit have been reported in several prospective

trials (Algorithms 3.1–3.3) However, several ongoing trials evaluating the individual

elements of goal-directed therapy and drotrecogin alfa (activated) in shock will likely

lead to modification of these recommendations

The significance of early, aggressive, volume resuscitation and hemodynamic

sta-bilization was demonstrated in a randomized, controlled, single-center trial in patients

who presented to the emergency department with signs of the systemic inflammatory

response syndrome and hypotension, as published by Rivers et al Administration of

crystalloids, red blood cell transfusions, vasopressors, and inotropes based on

aggres-sive monitoring of intravascular volume and a tissue oxygen marker within 6 hours of

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Management of Shock rSevere Sepsis and Septic Shock 9

TABLE 3.1 Medications Commonly Used in Septic Shock

CO, cardiac output; MAP, mean arterial blood pressure; SVR, systemic vascular resistance.

presentation to the emergency department resulted in a 16% decrease in absolute day mortality The major differences in treatment between the intervention and controlgroups were in the volume of intravenous fluids received, the number of patients trans-fused packed red blood, the use of dobutamine, and the presence of a dedicated studyteam for the first 6 hours of care

28-The implementation of treatment pathways mimicking the interventions of thewell-scripted, carefully performed procedures employed by Rivers et al has been putinto practice in the clinical setting Micek et al employed standardized order sets thatfocused on intravenous fluid administration and the appropriateness of initial antimi-crobial therapy for severe sepsis and septic shock Patients managed in this mannerwere more likely to receive intravenous fluids>20 mL/kg of body weight prior to

vasopressor administration, and consequently were less likely to require vasopressoradministration at the time of transfer to the intensive care unit Patients managed withthis approach were also more likely to be treated with an appropriate initial antimi-crobial regimen As a result of the aggressive management initiated in the emergencydepartment and continued in the intensive care unit, patients managed via the severesepsis order sets had statistically shorter hospital lengths of stay and a lower risk for28-day mortality Similar results have recently been reported from a multicenter studycoordinated by the Surviving Sepsis Campaign Group

In summary, the initial management of patients with septic shock appears to becritical in terms of determining outcome Institution of standardized physician ordersets, or some other systematic approach, for the management of patients with severeinfections appears to consistently improve the delivery of recommended therapies and,

as a result, may improve patient outcomes Given that evidence-based treatment ways typically have no additional risks and are associated with little to no acquisition

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• Moribund state (or) • Not expected to survive 28 days (or) • DNR

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2012 washington manual of critical care medicine 2nd edition

Diagnosis and Management of Altered

Initial Approach to a Patient with