Ebook Critical care update 2017: Part 1

CRITICAL CARE UPDATE 2017


Editors
Subhash Todi MD MRCP
Director

Department ofCritical Care

Advanced Medicare Research Institute

Kolkata, West Bengal, India


Atul PKulkarni MD FISCCM PGDHHM FICCM
Professor and Head
Department of Anesthesiology, Critical Care Medicine and Pain
Tata Memorial Hospital .
Mumbai, Maharashtra, India

Kapil Zirpe MD FCCM F1CCM
Director

Neuro Trauma Unit

Ruby Hall Clinic

Pune, Maharashtra, India

The Health Sciences Publisher
New Delhi I London I Panama


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Critical Care Update 2017 /Subhash Todi, Atul PKulkarni, Kapil Zirpe
First Edition: 2017

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ISBN: 978-93-86261-15-1
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Contributors

EDITORS

Subhash Todi MD MRCP
Director
Department of Critical Care
Advanced Medicare Research
Institute
Kolkata, West Bengal, India

Atul PKulkarniMD FISCCM PGDHHM
Professor and Head
Department of Anesthesiology, Critical
Care Medicine and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Kapil Zirpe MD FCCM FICCM
Director
Neuro Trauma Unit
Ruby Hall Clinic
Pune, Maharashtra, India

Rahul A Pandit MD FJFICM FCICM EDIC
FCCP DA
Director, Department of Intensive Care
Fortis Hospital and Healthcare
Mumbai, Maharashtra, India

Pradeep Rangappa DNB FJFICM EDIC
FClCM, P9DipECHO MBA FICCM PGDMLE

Senior Specialist
Department of Intensive Care
Columbiaasia Referral Hospital
Bangalore, Karnataka, India

SECTION EDITORS
Arvind KBaronia MD
Professor and Head
Department of Critical Care Medicine
Sanjay Gandhi Postgraduate Institute of
Medical Sciences
Lucknow, Uttar Pradesh, India
Rajesh Chawla MD FCCM FCCP
Senior Consultant .
Department of Respiratory, Critical Care
and Sleep Medicine
Indraprastha Apollo Hospitals,
New Delhi, India
Shivakumar Slyer MD DNB EDIC
Professor and Head
Department of Critical Care Medicine
Bharati Vidyapeeth Deemed University
Medical College
Pune, Maharashtra, India
Dilip RKarnad MD FACP FRCP
Consultant
Department of Critical Care
Jupiter Hospital
Thane, Maharashtra, India

Vijaya P Patil MD
Professor, Department of
Anesthesiology, Critical Care and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India
BananiPoddarMDDNB
Professor
Department of Critical Care Medicine
Sanjay Gandhi Postgraduate Institute of
Medical Sciences
Lucknow, Uttar Pradesh, India
Ramakrishnan NAB (Int Med)
AB (Crit Care) AB (Sleep Med) MMM FACP FCCP
FCCMFICCM
Senior Consultant
Department of Critical Care and
Sleep Medicine, Apollo Hospitals
Chennai, Tamil Nadu,lndi:

Jayant RShelgaonkar DA MD FRCA FICCM
Associate Director
Department of Critical Care
Aditya Birla Memorial Hospital.
Pune, Mahrashtra, India
Shrikanth Srinivasan MD DNB
FNB EDIC
Senior Consultant
Department of Critical Care Medicine
Medanta-The Medicity
Gurgaon, Haryana, India

KVinodanMD DA
Head
Department of Anesthesia and
Critical Care
Medical Trust Hospital
Cochin, Kerala, India


Critical Care Update 2017
.~

CONTRIBUTING AUTHORS
Chu-Chu A MBBS

Nikhill\l Balankhe MD

Devawrat RBuche MD FNB

Department of Anesthesia
Kingston Hospital
Kingston, United Kingdom

Director

Department of Critical Care

Orange City Hospital and Research

Institute

Nagpur, Maharashtra, India


Clinical Associate
Department of Centre for Critical Care
BLK Superspeciality Hospital
New Delhi, India

Ankur Agrawal MDDM
DMFeilow
Department of Pulmonary and Critical
Care Medicine
Post Graduate Institute of
Medicine Sciences
Rohtak, Haryana, India

~

""

""'"

Vignesh C MD FNB EDIC
Susruta Bandyopadhyay MD
Director

Department of Critical Care

AMRI Hospitals

Kolkata, West Bengal, India


Consultant
Department of Critical Care
Apollo Hospitals
Chennai, Tamil Nadu, India

Chandrashish Chakravarty MD
Vandana Agarwal MD FRCA

Rajan Barokar MD EDIC

MNAMSEDIC

Professor
Department of Anesthesia, Critical Care
and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Director and Consultant

Aditya Hospital Critical Care and

Emergency Centre

Nagpur, Maharashtra, India

Consultant
Department of ICU
Apollo Gleneagles Hospitals
Kolkata, West Bengal, India

Rinaldo Bellomo MD FRACP FClCM


Matthew JChan BMedSci

PGDipEcho FAHMS


Research Fellow
Department of Intensive Care
Austin Health
Heidelberg, Victoria, Australia

Nayana SAmin MD

Protessor

Department of Anesthesiology, Critical
Care and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Andrew CArgent MBBCh Mmed MD
FCPeds DCH FRCPCH

Professor and Medical Director PICU
Department of Pediatric Intensive Care
Red Cross War Memorial Children's
Hospital and University of Cape Town
Cape Town, South Africa

• Professor
. Department of Intensive Care Medicine
University of Melbourne
Parkville, Victoria, Australia

Dhruva Chaudhry MD DNB OM

Vikas Bhagat MD DOMS

FICCM FICP


Senior Registrar

Department of Anesthesiology,

Critical Care and Pain

Tata Memorial Hospital

Mumbai, Mahrashtra, India


Senior Professor and Head

Department of Pulmonary and
Critical Care Medicine
Post Graduate Institute of
Medicine Sciences
Rohtak, Haryana, India

lata Bhattacharya MD
Consultant

Department of Critical Care Medicine

Fortis Memorial Research Institute

Gurgaon, Haryana, India


Gagan Brar MD FNB IDCC EDIC

Pradip KBhattacharya MD FICCM

Aakanksha Chawla MD FCCM FCCP

Consultant
Department of Critical Care and
Emergency Services
Narayana Health
Bangalore, Karnataka, India

FCCCM

Senior Resident

Department of Respiratory,

Critical Care andSleep Medicine

Indraprastha Apollo Hospitals

New Delhi, India


Mildhur Arora MD IDCCM
Attending Consultant
Department ofCritical Care Medicine
Fortis Memorial Research Institute
Gurgaon, Haryana, India

Director
Emergency and Critical Care Services
Chirayu Medical College and
Hospital
Bhopal, Madhya Pradesh, India

Vipal Chawla MD IDCCM

Khusrav BBajan MD EDIC

..

..

Consultant
Depatement of Critical Care
PD Hinduja National Hospital and
Medical Research Centre
Mumbai, Maharashtra, India

vi

Munish Chauhan MD FNB EDIC

Senior Consultant
Department of Anesthesiology and
Critical Care
JLN Cancer Hospital
Bhopal, Madhya Pradesh, India

Neeta Bose. MD

.

Associate Professor

Department of Anesthesia

GMERS Medical College

Vadodara, Gujarat, India

Associate Consultant

Medanta Institute of Critical Care and

Anesthesia

Medanta-The Medicity

Gurgaon, Haryana, India


,"


Contributors

Maurizio Cecconi MD FRCA FFICM MD

Supradip Ghosh Dip. Intensive Care

Sushma KGurav DNB IDCCM

Consultant and Reader
Department of Anesthesia and
Intensive Care Medicine
StGeorge's University Hospitals NHS
Foundation Trust
StGeorge's University of London
London, United Kingdom

Additional Director and Head
Department ofCritical Care medicine
Fortis Escorts Hospital
Faridabad, Haryana, India

Intensivist
Neuro-trauma Unit
Grant Medical Foundation
Ruby Hall Clinic
Pune, Maharashtra, India

Ravi Varma Durai Pandian MD FNB
EDIC

Associate Consultant
Department of Intensive Care Medicine
Apollo Hospital
Chennai, Tamil Nadu, India

Raymond D MD DM EDIC
Consultant
Department of Critical Care
Apollo Hospitals
Chennai, Tamil Nadu, India

Kanishka Davda DNB
Fellow of National Board
Department of Infectious Diseases
PD Hinduja National Hospital and
Medical Research Centre

Mumbai, Maharashtra, India

Palepu BGopal MD FRCA CCST FICCM FCCM
Consultant and HOD
Department of Critical Care Medicine
Continental Hospitals
Hyderabad, Telangana, India

Prabhas PGiri MD MRCPCH
Assistant Professor and In-Charge PICU
Department of Pediatrics
Institute of Child Health
Kolkata, West Bengal, India

Anish Gupta MD
Fellow FNB
Institute of Critical Care Medicine
Max Super Speciality Hospital
New Delhi, India

Rahul BAmte MD IDCCM EDIC
Consultant
Department of Critical Care Medicine
Yashoda Hospitals
Hyderabad, Telangana, India

Nimita Deora MSc
Clinical Research Assistant
Department of Anesthesiology and
Critical Care

Chirayu Medical College and
Hospital
Bhopal, Madhya Pradesh, India

Deepak Govil MD FCCM EDIC FICCM

Sandeep Dewan DA DNB IDCCM

James Hanison FRCA
Consultant
Department of Anesthesia and
Intensive Care Medicine
Manchester Royal Infirmary
United Kingdom

Ashit V Hegde MD MRCP
Consultant
Department of Medicine and
Critical Care
PD Hindula National Hospital
Mumbai, Maharashtra, India

Javed Ismail MD DM •
• Consultant
. Department of Pediatrics
Post Graduate Institute of Medical
Education and Research
Chandigarh, India

Jose Chacko MD DA DNB EDIC

Director
Department of Critical Care Medicine
Medanta-The Medicity
Gurgaon,_ Haryana, India

Consultant and Head
Department of Critical Care and
Emergency Services
Narayana Health
Bangalore, Karnataka, India

Navya Guwalani PG

Gaurav Jain MD PDCC

Director and Head
Department ofCritical Care Medicine
Fortis Memorial Research Institute
Gurgaon, Haryana, India

Clinical Reseacrh Officer
Department of Anesthesiology and
Critical Care
Chirayu Medical College and Hospital
Bhopal, Madhya Pradesh, India

Assistant Professor
Department of Anesthesiology
Institute of Medical Sciences

Banaras Hindu University
Varanasi, Uttar Pradesh, India

Jigeeshu VDivatia MD FCCM FISCCM

Abhinav Gupta MD DNB FNB EDIC

Professor and Head
Department of Anesthesiology,
Critical Care andPain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Additional Medical Superintendent and
Head
School of Medical Sciences and
Research, Sharda Hospital
Sharda University
Greater Noida, Uttar Pradesh, India

Subhal BDixit MD IDCCM FICCM FCCM
,Director
Department of Intensive Care
Sanjeevan Hospital and
MJM Hospital
Pune, Maharashtra, India

Sachin Gupta MD IDCCM IFCCM EDIC
Senior Consultant
Department of Critical Care Medicine

Medanta-The Medicity
Gurgaon, Haryana, India

Yash Javeri DAIDCCM
Director
Department ofCritical Care Medicine
Apex Healthcare Consortium
New Delhi, India

Sameer AJog MD IDCCM EDIC
Consultant Intensivist
Department of Emergency Medicine
and Critical Care
Deenanath Mangeshkar Hospital
Pune, Maharashtra, India

vii


Critical Care Update 2017

Deven Juneja DNB FNB EDIC FCCM

Krishna PMulavisala MD FRCA

Saumen Meur DCH MRCPCH FRCPCH CCT

Principal Consultant
Department of Critical Care Medicine
Max Super Speciality Hospital

New Delhi, India

Consultant
Department of Anesthesiology
Global Hospitals
Hyderabad, Telangana, India

Consultant Pediatric Intensivist
Department of Pediatric Cardiology
BM Birla Heart Research Centre
Kolkata, West Bengal, India

Sunil Karanth MD FNB EDIC FCICM

Rajesh Pande MD PDCC FICCM FCCM

Sheila NMyatra MD FCCM FICCM

Chairman, Consultant, and Head
Department of Critical care services
Manipal Health Enterprise (P) Ltd
Bangalore, Karnataka, India

Director
BLK Center forCritical Care
BLK Superspeciality Hospital
New Delhi, India

Professor
Department of Anesthesiology, Critical

Care and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, Idia

Mohit Kharbanda MD IDCCM FNB

Samidh BPatel MD

Director

Department of Critical Care

Desun Hospital

Kolkata, West Bengal, India


In-Charge
Department of Critical Care
Manik Hospital and Research Center
Aurangabad, Maharashtra, India

Ruchira WKhasne DA DNB IDCCM

Kinjal Patel MD

EDAICEDIC

Consultant

Department of Critical Care

Apollo Hospital

Nashik, Maharashtra, India


Clinical Assistant
Department of Lab Medicine
Hinduja Hospital and Medical Research
Centre
Mumbai, Maharashtra, India

Khalid I Khatib MD

Sweta Patel MD IDCCM

Professor
Department of Medicine
Shrimati Kashibai Navale Medical
College
Pune, Maharashtra, India

Consultant, Medanta Institute of Critical
Care and Anesthesia
Medanta-The Medicity
Gurgaon, Haryana, India

.

Harish M Maheshwarappa MD DNB
Jagadeesh KN MBBS

IDCCM DM EDIC

Consultant, Medanta Institute of Critical
Care and Anesthesia
Medanta-The Medicity
Gurgaon, Haryana, India

Consultant and Head
Department of Critical Care Medicine
Yashoda Hospitals
Secunderabad, Telangana, India

Niranjan Kissoon FRCPC FAAP FACPE

Arghya Majumdar MD DNB MR~P

MCCMCPE

Director and Head

Department of Nephrology

AMRI Hospitals

Kolkata, West Bengal, India

Professor
Department of Pediatrics
University of British Columbia and
BC Children's Hospital
British Columbia, Vancouver, Canada

Rohit V Kodagali MD
Medical Advisor
Medical Department
Boehringer Ingelheim
Mumbai, Maharashtra, India

•

viii

Amit M Narkhede MD DNB
Senior Resident
Department of Anesthesiology, Critical
Care and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Prashant Nasa MD FNB EDIC ClC FCCP
FICCM

Specialist and Head
Department of Critical Care Medicine
NMC Speciality Hospital
Dubai, United Arab Emirates

Anand M Nikalje MD
Medical Director and In-Charge
Department of Medicine and
Critical Care
MIT Hospital and Research Institute
Aurangabad, Maharashtra, India

Odiraa ( Nwankwor MD MPH FAAP
Consultant
Department of Pediatrics
Children's Regional Hospital atCooper
University Hospital
Camden, New Jersey, USA
Consultant
Department of Pediatrics
Alfred I. DuPont Hospital for Children
Wilmington, Delaware, USA

Mohan AMathew MD
Director

Department of Anesthesia and

Critical Care

Lakeshore Hospital

Kochi, Kerala, India

Divya Pal MD IDCCM
Fellow (FNB) Critical Care

Institute of Critical Care and

Anesthesiology

Medanta-The Medicity

Gurgaon, Haryana, India


Yatin Mehta MD MNAMS FRCA FAMS


Sadanand SKulkarni MD

FIACTA FICCM FTEE

Vice-President
Department of Medical Affairs and
Clinical Research
Fresenius Kabi India Pvt. Ltd
Pune, Maharashtra, India

Chairman

Institute of Critical Care and

Anesthesiology

Medanta-The Medicity

Gurgaon, Haryana, India


•


JV Peter MD DNB MAMS FRACP FJFICM

FClCM FICCM


Professor and Head

Medical Intensive Care Unit

Christian Medical College

Vellore, Tamil Nadu, India



Contributors

Natesh RPrabu MD DNB DM EDIC

Sriram Sampath MD

Manoj KSingh MD DNB FNB

Specialist Registrar
Department of Anesthesiology, Critical
Care and Pain
Tata Memorial Hospital
Mumbai, Maharashtra, India

Professor and Director
Department of Critical Care Medicine
StJohn's Medical College and
Hospital
Bangalore, Karnataka, India

Consultant
Department of Critical Care
Apollo Hospital International Ltd
Ahmedabad, Gujarat, India

Ramesh Venkataraman AB (1M) AB (CCM)

Gauri Saroj MD IDCCM EDIC

Senior Consultant
Department of Critical Care Medicine
Apollo Hospitals
Chennai, Tamil Nadu, India

Consultant

Department of Critical Care
Jupiter Hospital
Thane, Maharashtra, India

Suresh Ramasubban FACP FCCP AB

Sanjith Saseedharan IDCCM EDIC

Senior Consultant
Department of Pulmonary and Critical
Care Medicine
Apollo Gleneagles Hospital
Kolkata, West Bengal, India

Head
Department of Critical Care
SL Raheja Hospital-AFortis Associate
Mumbai, Maharashtra, India

Banambar Ray MD FICCM

Pratik Savaj DNB

Omender Singh MD FCCM
Director
Institute of Critical Care Medicine
Max-Super Speciality Hospital
New Delhi, India

Saswati Sinha MD IDCCM EDIC

.

FNNCC DA FIMSA

Chief Consultant
Department of Critical Care and
Anaesthesia'
Apollo Hospitals
Bhubaneswar, Odisha, India

Fellow of National Board
Department of Infectious Diseases
PD Hinduja National Hospital and
Medical Research Centre
Mum,bai, Maharashtra, India

Sumit Ray MD FICCM

Mozammil Shafi MD FNB

Senior Consultant and Vice-Chairperson
Department of Critical Care and
Emergency Medicine
Sir Gangaram Hospital
New Delhi, India

Associate Consultant
Institute of Critical Care and
Anesthesiology

Medanta-The Medicity
Gurgaon, Haryana, India

Camilla Rodrigues MD

Prakash Shastri MD FRCA FICCM

Consultant
Department of Lab Medicine
Hinduja Hospital and Medical Research
Centre
Mumbai,Maharashtra, India

Senior Consultant and Vice-Chairman
Department of Critical Care and
Emergency Medicine
SirGangaram Hospital
New Delhi, India

Samir Sahu MD FICCM

Suhail SSiddiqui MD FCCM DM

Director

Department of Critical Care and

Pulmonology

AMRI Hospitals

Bhubaneswar, Odisha, India


Specialist Senior Resident

Department of Anesthesiology,

Critical Care and Pain

Tata Memorial Hospital

Mumbai, Mahrashtra, India


Arijit Samanta DA MD FNB

Dinesh KSingh MD FICCM

FNB trainee

Department of Critical Care and

Emergency Medicine

Sir Gangaram Hospital

New Delhi, India

Professor

Department of Anesthesiology

Institute of Medical Sciences ...

Banaras Hindu University

Varanasi, UttarPradesh, India


Consultant
Department of Critical Care
AMRI Hospitals
Kolkata, West Bengal, India

Mehul KSolanki MD FNB
Consultant
Department of Critical Care
BAPS Yogiji Maharaj Hospital
Ahmedabad, Gujarat, India

Rajeev Soman MD
Consultant
Department of Internal Medicine and
Infectious Diseases
PD Hinduja National Hospital and
Medical Research Centre
Mumbai, Maharashtra, India

Peter ESpronk MD PhD EDIC FCCP
Director

Department of Intensive Care

Medicine

Gelre Hospitals Apeldoorn

Apeldoorn, The Netherlands


T Shyam Sunder MD PDCC FICCM
Medical Director

Thumbay Hospital

Hyderabad, Telangana, India


Nisha Tipparaju MBBS
ICU Medical Officer

Thumbay Hospital

Hyderabad, Telangana, India


Deeksha STomar DA IDCCM IFCCM
Associate Consultant

Department of Critical Care Medicine

Medanta-The Medicity

Gurgaon, Haryana, India


ix


Critical Care Update 2017

Younsuck Koh MD PhD FCCM

Sushma Patil MD •

Sharmili Sinha MD DNB EDIC

Professor
Department of Pulmonary and Critical
Care Medicine Asan Medical Center
University of Ulsan College of Medicine
Songpa-gu, Seoul, Korea

Consultant In-Charge
Neuro Trauma Unit, Ruby Hall Clinic
Pune, Maharashtra, India

Senior Consultant

Department of Critical Care Medicine
Apollo Hospitals
Bhubaneswar, Odisha, India

Mahesh Nirmalan MD FRCA PhD FFICM
Faculty of Biology, Medicine and Health
Consultant, Intensive Care Medicine
Manchester Royal Infirmary
University of Manchester and Central
Manchester Foundation Trust
Manchester, United Kingdom

Saroj KPattnaik DNB IDeCM
Consultant, Department of Critical Care
Medicine, Apollo Hospitals
Bhubaneswar, Odisha, India

Srinivas Samavedam MD FNB EDIC FRCP
Head, Department of Critical Care
Virinchi Hospitals
Hyderabad, Telangana, India

x

EDIC

Sunit CSinghi MD FlAP FAMS FISCCM

Consultant Intensivist
Department of Emergency Medicine

and Critical Care
Deenanath Mangeshkar Hospital
Pune, Maharashtra, India

FICCMFCCM

•

Head
Department of Critical Care
Niramaya Hospital
Pune, Maharashtra, India

DNBDMLE

Swapnil RPatharekar MD IDCCM IFCCM

.

Sunitha BVarghese DNB IDeCM EDIC

Director-Principal
Maharishi Markandeshwar Institute of
Medical Sciences and Research
Ambala, Haryana, India

Ximena Watson MbCHb
Department of Anesthesia
Kingston Hospital
Kingston, United Kingdom

Preface


Dear Friends
It is indeed a proud moment for Indian Society of Critical Care Medicine (ISCCM) to launch the first Critical Care
Update 2017 book during itsannual congress in Kochi. Over theyears, attendance atISCCM congress has been increasing
exponentially and ascientific congress book highlighting the key topics discussed inthecongress was long overdue. This
book has around 80 chapters authored by national and international faculty covering all the major topics which will be
discussed during thecongress. This update will highlight therecent advances made inthefieldofcritical care with special
reference to its relevance and application in resource limited settings. A special section on "Economics of ICU" is worth
mentioning. We sincerely hope this book will be useful bothfor young intensivists to promote analytical thinking, post
graduates to keep abreast of recent advances, and also to senior clinicians. The publication of thls book was possible only
through ajoint effortfrom themembers of theeditorial board, authors, and the publisher. We hope this book willcontinue
to bepublished in thefuture congresses.
-

Subhash Todi
Atul PKulkarni
Kapil Zirpe


Acknowledgment


The Indian Society of Critical Care Medicine (ISCCM) acknowledges the enthusiastic support of allthe members of the
society and isever grateful to themfor it.This book isdedicated to allthese members. .

Contents


Section 1:Hemodynamic Monitoring and Resuscitation
Section Editor: Vijaya PPatil
1. Fluid Therapy in Resource-limited Settings

3

Sameer AJog, Maurizio Cecconi, Swapnil RPatharekar

2. How Much Fluid isToo Much Fluid?

8

Srinivas Samavedam

3. Blunt Chest Trauma

13

Mahesh Nirmalan, James Hanison

4. Guidelines for Cardiopulmonary Resuscitation: 2015 Update

20

Jigeeshu VDivatia, Suhail SSiddiqui, AmitMNarkhede

5. Prognostication in Postcardiac Arrest Status

30

Kapil Zitpe, Sushma Patil

6. Barriers and Controversies in Implementation of Induced Hypothermia

40

Palepu BGopal, Rahul BAmte, Krishna PMulavisala

7. Quick Sequential Organ Failure Assessment: New Trigger for Rapid Response Teams

49

Vijaya PPatil, Nayana SAmin

8. Ventricular Preload Optimization Therapies: Science or a Dark Art?

52

Mahesh Nirmalan, James Hanison

9. How to Assess and Improve Microcirculation?

56

JVPeter

10. How to InterpretVenoarterial Partial Pressure of Carbon Dioxide?

63

Sheila NMyatra, Vikas Bhagat

11. Heart-lung Interactions

71

Suresh Ramasubban

Section 2:Respiratory System
Settion Editor: Rajesh Chawla •
12. High Flow Oxygen Therapy: Current Status

79

Jose Chacko, Gagan Brar

13. Oxygen Reserve Index
Subhash Todi

85


Critical Care Update 2017

14. End-tidal Carbon Dioxide: What's !\lew?

89

AtulPKulkarni, Harish MMaheshwarappa

15. Noninvasive Ventilation in the Perioperative Period

93

Vandana Agarwal

16. Identifying Correctable Factors in Difficult Weaning

98

Dhruva Chaudhry; Ankur Agrawal

17. Driving Pressure in Acute Respiratory Distress Syndrome: IsIt Relevant?

105

AtulPKulkarni, Natesh RPrabu, Vikas Bhagat

18. Prone Ventilationin Acute Respiratory Distress Syndrome: Why, When, and for HowLong?

109

Rajesh Chawla, Aakanksha Chawla

115

19. Viral Pneumonia

Ruchira WKhasne

20. Corticosteroids in Severe Community-acquired Pneumonia: Current Status

124

Dilip RKarnad, Gauri Saroj

21. Extracorporeal Carbon Dioxide Removal/Respiratory Dialysis:
Future of Hypercapnic Respiratory Failure

128

Sachin Gupta, Deeksha STomar, Deepak Govil

22. Extracor'poreal Membrane 'Oxygenation In Acute Hypoxemic Respiretoryfailure:
Current Status in India

134

Sandeep Dewan, Munish Chauhan, Madhur Arora

23. Synchrony During Assisted Mechanical Ventilation

144

Atul PKulkarni, Suhail SSiddiqui, Vikas Bhagat

Section 3:Gastroenterology
Section Editor: KVinodan

24. Care of Post LiverTransplant in Intensive Care Unit

155

Yatin M~hta, Deepak Govil, Mozammil Shafi, Divya Pal

25. Challenges in Identifying Sepsis in Liver Failure

161

Sunitha BVarghese, Sushma KGurav

26. Coaqulopathyin LiverDisease

165

Sumit Ray; ArijitSamanta

27. Permissive Underfeeding in Intensive Care Unit: Current Status

171

Saswati Sinha

28. Making Parenteral Nutrition Safer

173

Subhash Todi, Sadanand SKulkarni

29. Autophagy: Relevance to Critical Care

•

Subhash Todi, Sriram Sampath

176

•

30. Nutrition Guidelines: What is New?

180

Rajesh Pande

xvi

31. Fungal Sepsis in Acute Necrotizing Pancreatitis
Ashit VHegde

187


Contents
32. Acute Colonic Pseudo-obstruction

190

Pradip KBhattacharya, Lata Bhattacharya, Navya Guwalani, Nimita Deora

33. Acid Suppression in Critically III:IsIt Really Necessary?

196

SamirSahu

Section 4: Infectious Diseases
Section Editor: Rahul A Pandit
201

34. Sepsis 3:What's New?
Manoj KSingh, Mehul KSolanki

35. Neurological Manifestations of Scrub Typhus: AGreat Mimic


204

Rahul A Pandit


207

36. Rationale for Procalcitonin in the Intensive Care Unit
Ravi Varma Durai, Ramesh Venkataraman

37. Aerosolized Antibiotic

211

Anand MNikalje, Samidh BPatel

38. Rapid Diagnostic Tests for Bacterial or Fungal Identification in Intensive Care Unit

218

Kinjal Patel, Camilla Rodrigues

39. Biomarkers in Invasive Fungal Infections

225

Rajeev Soman, Pratik Savaj, Kanishka Davda

40. Extracorporeal Therapies for Sepsis: Current Status

229

Deven Juneja, Yash Javeri, Anish Gupta, Omender Singh

41. Optimum Dose of Colistin in Intensive Care Unit

235

Abhinav Gupta, Mohit Kharbanda

42. Early and Empiric Antibiotics in Sepsis: Current Controversy

239

Rajan Barakar, Devawrat RBuche

43. Fever Control in Intensive Care Unit:Is It Helpful?

242

Prashant Nasa

Section 5:Nephrology
Section Editor: JayantRShelgaonkar
44. Perioperative Dysnatremia


251

Ximena Watson, Chu-Chu A, Maurizio Cecconi


45. Hypophosphatemia in Intensive Care Unit

254

Jayant RShelgaonkar

46. Anticoagulation: The Various Options in Renal Replacement Therapy
Khu~avBB0an

258

•

47. Furosemide Stress Test

262

Arghya Majumdar

48. Continuous Renal Replacement Therapy in India: Is It Cost-effective?
Yash Javeri, Deven Juneja

267

xvii


Critical Care Update 2017

Section 6: Neurology

-

SectionEditors: Arvind K Baronia, Shivakumar Slyer
275

49. Declaration of Brain Death in India: Current Status
Dinesh KSingh, Gaurav Jain

280

50. Blood Pressure Management in Stroke
Susruta Bandyopadhyay

287

51. Use of Newer Antiepileptics in Status Epilepticus
Arvind KBaronia

289

52. Mechanical Devices and Pharmacological Thrombolysis in Stroke
Nikhil NBalankhe

294

53. Cerebral Tissue Oxygen Saturation Monitoring in Cardiac Surgical Patients
Matthew JChan, Rinaldo Bellomo

306

54. Induced Hypothermia: Current Status-Benefits andHarms
Subhal BDixit, Khalid I Khatib

314

55. Management of the Brain-dead Organ Donor
Mohan AMathew

Section 7: Hematology/Imaging/Metabolic
Section Editor: Shrikanth Srinivasan

323

56. Lung Ultrasound in Intensive Care Unit:Current Application
Shrikanth Srinivasan, Sweta Patel, Jagadeesh KN, Vipal Chawla

337

57. Metrics of Glucose Control in the Intensive Care Unit
Sunil Karanth

344

58. Reversal of Bleeding on Anticoagulants: New Options
Supradip Ghosh

351

59. Coagulopathy in Trauma
Chandrashish Chakravarty

355

60. Current Blood Transfusion Threshold in Intensive Care Units
NeetaBose

,

.'

8:

Section , Quality
,

.

Section Editor: Pradeep Rangappa
61. Post-intensive Care Unit Syndrome

369

Vignesh C, Raymond D, Ramakrishnan N

62. End-of-Iife Care of Intensive Care Units in Asia: Ethical Aspect
• Younsuck Koh

375

•

63. Principles ofTeam Science in Intensive Care Unit

380

TShyam Sunder, Nisha Tipparaju

Kviii

64. "Big Data" in Critical Care: Current Status
Subhash Todi

384


Contents

Section 9: Pediatrics
Section Editor: Banani Poddar
65. What Really Makes the Difference to Outcomes in Pediatric Sepsis?

389

Odiraa CNwankwor, Niranjan Kissoon

66. Fluid Balance: Where areWe Going with Fluids and Electrolytes in
the Pediatric Intensive Care Unit?

399

Andrew CArgent

67. Antibiotic Resistance: A Global Threat

407

Banani Poddar

68. Management of Pediatric Acute Respiratory Distress Syndrome

416

Prabhas PGiri

69. Electroencephalography Monitoringin the Intensive Care Unit:Fancy Tool or
Important Device?

423

Sunit CSinghi, Javed Ismail

70. Pediatric Neuromonitoring: Electroencephalography

426

SaumenMeur

Section 10:Economics of Intensive Care Unit Care
Section Editors: Ramakrishnan N,Dilip RKarnad
71. Methods of Costing in Intensive Care

433

AtulPKulkarni, Natesh RPrabu

72. Attributable Cost of Hospital-acquired Infection

437

Prakash Shastri

73. Cost Minimization in Intensive Care Unit

439

Pradeep Rangappa

74. Methods of Cost-effectiveness Analysis

446

Banambar Ray, Sharmili Sinha, Saroj KPattnaik

75. Intensive Care Unit Costs andResource-limited Settings

452

JVPeter

76. Severity of Illness Scores andTheir Role in Assessing Intensive Care Unit Costs

457

Dilip RKarnad, Sanjith Saseedharan

77. Stroke Units: Are They Cost Effective?

461

Kapil Zitpe, Rohit VKodagali

78. Regaining Qualityof Life in Intensive Care UnitSurvivors isPossible, but at What Cost?

465

Peter ESpronk

79. Ethical Issues in Resource Allocation for Critical Care in Resource-limited Countries

470

Shivakumar Slyer

xix


e

ec Ion
Hemodynamic Monitoring

and Resuscitation

SECTION EDITOR: VIJAYA PPATIL


--

"

CHAPTER

Fluid Therapy in

Resource-limited Settings

Sameer AJog, Maurizio Cecconi, SW9pnil RPatharekar

Intravenous fluid administration is the most common
therapy used in the intensive careunit (ICU). Judicious use
ofintravenous fluids is essential in an ICU. The challenge is
greater in limited resource settings since thereis paucity of
reliable parameters to guide fluid therapy. The "resource­
limited setting" need not always be' associated with
economical aswell as situational constraints like availability
of appropriate ambulance or emergency room services in
mass casualty situations.
Hypotension present at the hospital admission is asso­
ciated with a significant mortality and studies have shown
thatearly fluid therapy isassociated withbetteroutcomes.P
On the other hand, overzealous fluid therapy is also
associated withmany complications, e.g., pulmonary edema.
Excessive fluid administration may be proinflammatory and
potentially injurious.v' It is, thus, imperative toknow howto
give theright amount offluid.
Unfortunately, there is a paucity of good quality data
in the field of fluid therapy. Hence, the decision-making in
an individual patient is always a difficult task. Considering
this background, optimum fluid therapy in a given patient,
in a given setting, always remains a challenge for a treating

physician even in a well-equipped, resource-rlch.It.ll, In a
resource-limited setting, thisproblem iseven more complex.

I DEFINING RESOURCE-LIMITED SETTING
"'.=.:"'-........-7"-'~ ........ ~ ...~_.~'"'--- . .-....--~.-... ..... -~ ......~.~

~'"~~~I.~

...,_on

........·"...,._.......,·~_ ... _ - ,... ~ .... ' --~-."'~. - ..... '"'~. 7


When we say resource-limited setting in the context of
intensive care medicine or emergency medicine, at leastthe
following resources should be available for patient care. They
are:
• Good clinical examination, especially to detect
hypoperfusion
• At least3-lead electrocardiogram monitoring for rhythm
andrate
• Accurate noninvasive blood pressure measurement
instrument

I

• Instrumentfor measuring oxygen saturation
• Facility for urinary catheterization and measuring halfor
onehourly urineoutput
• Peripheral intravenous access bya large borecannulas

• Incaseoftotal vascular collapse-centralvenous access
• -Necessary intravenous fluids like crystalloids and
dextrose solutions
• Pressure bags to deliver thefluids at fast rate
• Oxygen therapy devices like oxygen cylinders, masks, and
venturi
• Basic resuscitation drugs.

It is a life-threatening, generalized form ofacute circulatory

failure associated withinadequate perfusion to the tissues. 1
It could be hypovolemic, cardiogenic, obstructive, or
distributive. The presentation of these shocks can overlap
with each other, like patient presenting with shock due
to hypovolemia owing to external blood loss can develop
infection andleadtoworsening ofshock.
~ FLUID
fIt
_ _ THERAPY
'_"".'''''' .. __

.

The most importa!1t physiological target of fluid adminis­
tration. is to improve tissue perfusion. Hemodynamic
optimization with fluids has shown to improve patient
outcome when applied in the early phases ofsepsis and in
the perioperative period.?" Fluid administration is, hence,
considered astherapy.
The following points should beconsidered while adminis­

trating fluid therapy in ICU in resource-limited settings.

Baseline Patient Demographics
This isoneofthemostimportant determinants offluid therapy.
Following patientgroups barely respond to fluid and, in
fact, overzealous fluid therapy in these patient groups can be
detrimentalf"


....


..,..
SECTION 1: Hemodynamic Monitoring and Resuscitation

•
•
•
•

Chronic renalfailure withanuria
Acute coronary syndrome
Acute and chronic decompensated heartfailure
Pulmonary embolism.

Indications
The indications relevant to resource-limited settings are:"
• Hypotension due to anycause
• Increased requirement ofvasopressors
• Decreased urineoutput

• Increased skinmottling.
Most common indication for fluid therapy, as suggested
bythe FluidChallenges in Intensive Care (FENICE)8 study, is
hypotension due to anyreason.

Type of Fluid 7

4

Resuscitation fluids can be divided into two broad
categories-colloids and crystalloids.
1. Colloids: The colloids are aqueous solutions that contain
both large organic macromolecules and electrolytes.
Colloids are subdivided into natural and synthetic
colloids.
a. Natural colloid: Albumin is the prototype of natural
colloid. It was also the first colloid solution used
clinically. It is harvested from humanplasmaand is
available in different concentrations like 4, 5, 20, and
25%.
Saline versus Albumin Fluid Evaluation (SAFE)9
and Albumin Italian Outcome Sepsis (ALBIOS)IO
trials have clearly shown that use of albumin does
not offer any advantage over crystalloids. In fact,
use of albumin can be detrimental in patients with
traumatic brain injury.'! Though there is some
advantage for.using albumin in early sepsis.P the
evidence is not strong enough to recommend its use
in resource-limited settings. The cost of albumin is
alsoa deterring factor to use it in thesesettings.

b. Synthetic colloids:" They are divided into three
groups-starches [hydroxy ethyl starch (HES)I,
gelatins, and dextran. These colloids were promoted
as cheaperalternative to albumin.
i. Gelatins: These are derived from bovine gelatin,
theircolloid baseisprotein.
ii. Dextran: It is a carbohydrate based colloid.
Bacteria make this polysaccharide molecule
duringethanolfermentation.
iii. Hydroxy ethyl starch: Hydroxy ethyl starch are
derived from the starch of potatoes or maize,
and their colloid base is a large carbohydrate
molecule. Solutions ofmolecular weight like130,
200, and 450 kD areavailable.
Based on current evidence, colloid use is not
recommended in the ICU. Colloid usage has shown
to increase incidence of acute kidney injury (AKI)

and need for renal replacement therapy. 13, 14 Though
there is somecontroversy due to emerging evidence
from recent trials,15,16 the overall consensus is to
avoid their usage in the ICU. Also, as colloids are
costlier than crystalloids, their usage in resource­
limited settings islimited.
2 Crystalloid solutions: These fluids are the first choice for
fluid resuscitation. They arewell-tolerated andinexpensive. .
a. Sodium chloride (saline): This isthemostcommonly
used crystalloid solution globally. There are few
concerns about the high chloride content of normal
saline, incidence of hyperchloremic metabolic

acidosis, and renal replacement therapy;17,18 then
again, evidence is not strong enough to discard its
useroutinely.
b. Balanced or physiological solutions: These are
derivatives ofHartmann's and Ringer's solutions.
Dueto their cost, regular use of thesefluids in resource­
limited settings is not recommended. In addition,
currently there is no strong evidence to support the
routineuseofbalanced crystalloids in the ICU. 19

Volume and Dose
It isverydifficult to generalize dose and volume offluid. The
requirements as well as response vary greatly during the
course of any critical illness. Also, no single physiological or
biochemical parameter is particularly useful to decide about
fluid responsiveness. However, systolic hypotension and
oliguria are usedas triggers to administer a fluid challenge. It
ranges from 200 to 1,000 mLofcrystalloid foran adultpatient.
Surviving Sepsis Campaign has recommended an initial
fluid resuscitation of30 mLlkg ofcrystalloids inseptic patients
withhypotension and/or lactate morethan4mmol/L. Afluid
challenge shouldconsist ofa volume large enough (nomore,
no less in theory) to raisethe meansystemic filling pressure'"
and increase venous return (cardiac output) in a preload
responsive patient. Also, importantly, fluid resuscitation
needs to be individualized to the patients need and clinical
indication. In the perioperative period volumes between
250 and 500 mL of fluids is routinely used." Most studies
involving nonsurgical patients have used fluid challenges of
500 mL given within30 minutes.F

Initiation and Endpoints
In resource-limited settings, where advanced laboratory
testing or hemodynamic monitoring are lacking, the task of
identifying early stages ofcirculatory dysfunction mainly relies
onproperclinical examination
andbasic laboratory testing.
.

Heart Rate
Heart rate (HR) is an easily available tool to assess fluid
responsiveness in resource-limited settings. The contribution
of HR to cardiac output and regulation of blood pressure


CHAPTER 1: Fluid Therapy in Resource-limited Settings
is crucial. Tachycardia is an important early sign of shock,"
However, tachycardia in shock could partly be due to other
factors, including pain, stress, or anemia. In addition,
bradycardia could be present in severe hypovolemia. The
specific value of HR to guide resuscitation has been poorly
studied. It is also obvious that a decrease in HR after a fluid
challenge indicate fluid responsiveness. However, the HR
responses in studies testing the fluid responsiveness in ICU
patients were variable. While somestudies found a significant
decrease in HR after fluid administration in responders."
othersreported no change in HR after fluid challenge in spite
of having a significant increase in cardiac index." Therefore,
HR alone cannotbe usedto predict fluid responsiveness.

volume can also be due to cardiac failure. In patients with
stiffarteries due to aging orcomorbidities, PPmay not below
in spite oflow stroke volume.
Inspiteofthis, changes inPPfollow thechanges incardiac
outputinducedbyfluid infusion more reliably than MAP.
More importantly, results are more or less similar
irrespective of the method ofmeasurement of arterial blood
pressure which may be arterial catheter or noninvasive
oscillometric automated brachial cuff. Also, the presence of
arrhythmias do not change the results" Hence, PP is one
of better index for fluid administration in resource-limited
settings.

Shocklnpex
Blood Pressure
Components ofbloodpressure are25 systolic arterial pressure
(SAP), diastolic arterial pressure (DAP), mean arterial
pressure (MAP), and pulsepressure (PP).

Systolic arterial pressure
A SAP value lower than normal (e.g., 90 mmHg) may be
associated either with a normal DAP (e.g., 80 mmHg) or
a low DAP (e.g., 50 mmHg). If PP is not low, then no clear
information on stroke volume can be drawn. Also, if pulse
pressure is low as in first case, stroke volume is expected to
be low, especially in cases of stiff arteries. Knowledge of the
sole value of SAP is, thus, not good guide to decide about
requirement ofintravenous fluids.

Diastolic arterial pressure

The factors which determine DAP are arterial tone and HR.
Therefore, a low DAP (e.g., 50mmHg) suggests a low arterial
tone,especially in the caseoftachycardia. AlowDAP, thus,is
indication foruse ofvasopressor, although fluids can also be
given in septic shock patients. Hence, DAP value alone also
cannotindicate fluid requirement.

Mean arterial pressure
A low MAP may be associated with cardiogenic shock
(right or left) for which fluid therapy can be detrimental.
Conversely, during hypovolemia, MAP can be maintained
due to compensatory mechanisms that increase vascular
resistance. Thus, any particular level of MAP as trigger for
fluid challenge can be misleading.
Again, MAP alone may not be sufficient to determine
adequacy of fluid resuscitation. An increase in MAP after
fluid challenge may indicate positive response but absence
ofit doesnotsuggest that patientisnotfluid responsive.

Pulse pressure
Alow PP suggest low stroke volume and in the presence of
shock, this would encourage fluid administration, unless
signs of pulmonary edema are present. However, the need
of fluid therapy is not absolutely certain since low stroke

Shock index (SI) is the ratio of HR divided by SAP (HR/
SAP). Normal value fer SI range is 0.5-0.7 in healthy adults.
Since isolated HR or SAP may not be sufficient to detect
early phases of shock or hypovolemia. An SI was originally
described in trauma patients." Shock index has a linear

inverse relationship to cardiac output and stroke volume.!?
An SI ~1.0 has been associated witha bad outcome in shock
patients." In trauma patients, it can be used to stratify
patients for increased transfusion requirements and early
mortality." Therefore, it is considered asthe mostimportant
vital signto detectacutehypovolemia and circulatory failure
in trauma patients. It has also shown relevance in septic
shock patientas well and correlate well withlactate levels. In
summary, SIis one ofeasiest, reliable, and inexpensive vital
sign whichcan be used in patients with shockto determine
volume responsiveness.

Capillary Refill Time
It isdefined asthetimetakenfor color toreturntoan external
capillary bed afterpressure is applied to cause blanching. It

can be measured by holding a hand higher than heart level
and pressing the softpadofa finger orfingernail untilitturns
white, then taking note of the time needed for the color to
returnoncepressure is released.P
Normal values for capillaryrefill time (CRT) are<2 seconds
in young individuals andvalues up to 4.5 seconds are normal
in the elderly."Capillary refill time can assist in assessment
and prognostication of trauma, major abdominal surgery,
and early septic shock patient.29-32 Patients with abnormal
peripheral perfusion presented with higher lactate levels and
have a higher incidence ofcirculatory complications.
Capillary refill time is a rapid flow-responsive parameter
that can be used in limited-resource settings as a trigger and
response during fluid resuscltation.P A recent study has

demonstrated that the useofCRT as a guide for fluid therapy
is associated withalmost 2Loflesser fluids in comparison to
the classic approach, and also toa lesser organdysfunction.F
Despite this, itwasusedasatrigger for fluid resuscitation in
lessthan8% ofcases intheFENICE trial. 8 Limitations foruseof S


SECTION 1:Hemodynamic Monitoring and Resuscitation

CRT canbe interobserver variability, skin color, andinfluence
ofambient temperature.P Inspiteofthis, easeofdoing it and
valuable information that it can give, this parameter needs
justice in resource-limited settings. Routine use of CRT is
highly recommended for trigger, guide, prognostication,
and stratification during fluid resuscitation process. Normal
CRT after fluid challenge denotes good prognosis while the
opposite is associated with increased mortality.

Mottling Index
Mottling is defined as patchy skin discoloration that usually
starts around the knees. It is due to heterogeneous, small
vessel vasoconstriction, and is thought to reflect abnormal
skin microperfusion. Mottling iseasily available signthat can
be usedfor assessment ofcirculatory dysfunction."
It has been shown to predict mortality in septic shock.
Mottling is quantified according to a mottling score. Score
varies between 0 and 5. A higher score correlates with
increased mortality. High doses of vasopressors can also
increase skinmottling and leadto purpuricchanges.

Jugular Venous Pressure
The jugular venous pressure (JVP) is the indirectly observed
pressure over the venous system via visualization of the
internal jugular vein." The patient is positioned at 30°, and
the filling level of the internal jugular vein determined. In
healthy people, the filling level of the jugular vein should
be <3 em vertical height above the sternal angle. Low JVP
usually indicated fluid responsiveness. With high NP, one
should be cautious about fluid resuscitation.P There are
many limitations of JVP, like assessment of JVP is technically
complex, difficult to interpret, and isvery subjective. The JVP
also doesnotcorrelate well withCVP. More importantly, itcan
be used as a safety limitforfluid resuscitation. Asignificant
increase in JVP before' or during fluid resuscitation should
alert clinician offluid overload.

Urine Output
During early shock, multiple neurological and hormonal
mechanisms get activated to maintain blood flow to vital
organs including kidney. Secondary functional changes in
renal blood flow, glomerular filtration, or tubular function
may result in oliguria." However, oliguria is a nonspecific
symptom and could also be present in mild dehydration
without hypoperfusion and in major surgery which mayor
may not reflect renal orsystemic hypoperfusion duringearly
shock. Impoqantly, during septic shock and J20st major
surgery, the presence ofprofound intrarenal microcirculatory
abnormalities that are triggered by proinflammatory
mediators are the main mechanisms for pathophysiology

6

of AKI than hypoperfusion and these abnormalities do not
revert withsystemic flow increasing maneuvers."
Despite these limitations, oliguria is used as a trigger
and target for fluid resuscitation in 18% patients." On the
contrary, several studies have shown that positive fluid
balance is associated with morbidity and mortality in
patients with AKI in different settings." Fluid overload in
these situations maylead to cardiac dysfunction and intra­
abdominal hypertension which may hasten the onsetofAKI
andperpetuateoliguria.

Blood Lactate Levels39 (Box 1)
The normal serum lactate level in resting humans is
approximately 1 mmollL (0.7-2.0). The value is the same
in venous or arterial blood. Use of a tourniquet can lead to
pseudoelevation oflactate level. An increase in serumlactate
levels mayindicate poortissueperfusion. Large data arenow
available to indicate serum lactate levels as an appropriate
target for fluid resuscitation, and is recommended to use
as surrogate measure of tissue microperfusion. Repeated
measurements of lactate concentrations over time are
particularly useful formonitoring the response totherapy.
Box 1:Factors that may contribute to hyperlactat~mia
• Increased production of lactate
o Tissue hypoxia
o Increased aerobic glycolysis
o Inhibition of pyruvate dehydrogenase (insepsis)
o Methanol/ethylene glycol/propofol toxicity

o Thiamine deficiency
• Decreased clearance of lactate
o Liver dysfunction orfailure
o Cardiopulmonary bypass (minor reduction in clearance)
• Exogenous sources of lactate
o Lactate buffered solutions used in continuous venovenous
hemodiafiltration
o Medications (metformin, nucleoside reverse transcriptase
inhibitors, long-term linezolid use, intravenous lorazepam, and
val prole acid)
o Hematologic malignancies

;f~~~NCLUSIO(\J
Appropriate fluid therapy in a resource-limited setting is
really a challenging issue. On the background of paucity of
evidence basedguidelines, this taskismore complex. Use of
basic parameters andsoundunderstanding ofphysiology will
definitely enhance th~ decision-making ability ofa physician.
However, at the bedsidein an emergency situation, one may
have to use his/her own discretion to answer the million
dollar question "how muchfluid?"


CHAPTER 1:fluid Therapy in Resource-limited Settings

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25, Le Manach Y, Hofer CK, Lehot JJ, et al. Can changes in arterial pressure be
. used to detect changes in cardiac output during volume expansion in the
peroperatve period? Anesthesiology, 2012;117:1165-74.
26. Lakhal K, Ehrmann S, Perrotin D, et al. Fluid challenge: tracking changes in
cardiac output with blood pressure monitoring (invasive or non-invasive),
Intensive Care Med. 2013;39:1953-62,
27. Rady MY, Rivers EP, Martin GB, et al. Continuous central venous oximetry and
shock index in the emergency department: use in the evaluation of clinical
shock, Am ,IEmerg Med, 1992;10:538-41,
28. Mutschler M, Nienaber U, Munzberg M, et al; TraumaRegister DGU. The shock
index revisited-a fast guide to transfusion requirement? A retrospective
analysis on 21,853 patients derived from the TraumaRegister DGU, .Crit Care,
2013;17:R172,
29, Liniij A, Bakker J. Clinical assessment of peripheral circulation, Curr Opin Crit
Care, 2015;21 :226-31,
30, van Genderen ME, Engels N, van der Valk RJ, et al. Early peripheral pertusion­
guided fluid therapy in patients with septic shock, Am JRespir Crit Care Med,
.2015;191:477-80,
31. van Genderen ME, Paauwe J, de Jonge J, et al. Clinical assessment of peripheral
pertusion to predict postoperative complications after major abdominal
surgery early: aprospectve observational study in adults, Crit Care. 2014;18:
R114,
32, Ait-Oufella H, Bige N, Boelle PY, et al. Capillary refill time exploration during
septic shock. Intensive Care Med, 2014;40:958-96,

33, Hernandez G, Pedreros C, Veas E, etal. Evolution of peripheral vs metabolic
pertusion parameters during septic shock resuscitation. Aclinical-physiologic
study, JCrit Care, 2012;27:283-8,
34, Coudroy R, Jamet A, Frat ,IP, et al.lncidence and impact of skin mottling over the
'Knee and its duration on outcome in critically illpatients. Intensive Care Med,
·2015;41:452-9.
35, Chua Chiaco JM, Parikh N, Fergusson D, The jugular venous pressure revisited,
Clev Clin JMed, 2013;80:638-44.
36, Prowle J, Bagshaw SM, Bellomo R. Renal blood flow, fractional excretion of
sodium and acute kidney injUry: time for anew paradigm? Curr Opin Crit Care.
2012;18:585-92, .
37. Payen D, de Pont AC, Sal(SDAP) Investigators, A positive fluid balance is associated with a worse
outcome inpatients with acute renal failure, Crit Care, 2008;12:R74,
38: Eskesen TG, Wetterslev M, Perner A, Systematic review including re-analyses
of 1148 individual data sets of central venous pressure as apredictor of fluid
responsiveness, Intensive Care Med, 2016;42:324-32.
39. Wacharasint P, Nakada TA, Boyd JH, et al. Normal-range blood lactate con­
centration in septic shock is prognostic and predictive, Shock, 2012;38(1):
4-10.

7


CHAPTER

How Much Fluid is

Too Much Fluid?

Srinivas Samavedam

l

jij INTRODUCTION
..

I;~il~-~-·- - « -~"'.< ~_"",."4'

_.__.".

'~

.•. __,,_, ~_'"

"".,~

TABLE 1 Side effects ofa positive fluid balance

, _..~.,.

Intravenous fluid therapy is one of the most common
interventions performed on hospitalized patients. Patients in
theemergencyroom, intensive careunit(ICU), andoperating
room probably receive this intervention more often than
others. Fluid therapy, when'.drlven by scientific rationale
and principles is the cornerstone of most resuscitation
algorithms. The benefits of prompt fluid resuscitation in
terms of organ perfusion, hemodynamics, and acid-base
homeostasis cannot be overemphasized. However, like any

other pharmacological intervention, fluid therapy, when
excessive canincrease themortality andaddstothemorbidity
ofcritically ill patients. It is, therefore, important to know the
limits towhich thisintervention canbe stretched. This review
will attempt to summarize the methods of identification of
fluid overload (FO) and ·the parameters which define too
much fluid.

m
i ll .IS
__ ...THIS
. A .RELEVANT
......__ .__-'..._.. QUESTION?
..._.. _...__ ..

..._"_'

.... __ .

The adverse effects of fluid therapy, which is either delayed
or denied, are well known. The effects of sedatives and
vasoactive drugs are also influenced bythe volume status of
an individual. However, over the last detade or so, evidence
hasemerged, questioning the unmeasured and unqualified
administration offluids. In fact, fluid therapy during critical
illness has been labeled ~ double-edged sword. J The advent
ofbiolmpedance, widespread availability ofultrasonography
(USG), reemergence of thermodilution techniques for the
assessment ofextravascular lungwater (EVLW), coupled with
theunderstanding ofthe natureofthe endothelial glycocalyx,

have shed more lighton the adverse effects of positive fluid
balance (PFB) on the outcomes ofcritically ill patients.

.

.

WHAT DOES POSITIVE FLUID BALANCE DO?
Almost every organ system suffers from the adverse effects
of PFB. The most well-recognized complication of PFB is

Site
, Brain
~._---

. Adverse effects

'

: Cognitive changes delirium

.

---------+------.--,------.-.--.---..---.----.----.-~"' . ---i

Myocardium i Contractility change, diastolic dysfunction,
i conduction disorders

~---,_._.-._- .. -.--.--.----+~-.,-------._--------

, Lungs
r-U~;----'-

..-.

...,--.---..------.-- .---- --.-.----- ..

-_.. -i

. Gas exchange effects, compliance change
:
I Cholestasis/~;~th~·i~d~~iun~i;~-·---_··-·_--·1

1------------- ..-..- .---.---.-:----.----

...__._-.---.------....--.,---.-----.---- -_...__..__.,­

-~,--,.-.-.-

, Kidneys

' Glomerular filtration rate reduction, salt and fluid
, retention

l Bowel

! Malabsorption, ileus, compartment syndrome

i--Pe;;~h~r~'-l Mic~;i;~I~t;r~-~h~·;,_;~~:d~I~~ed ~;~~d'he~i;ng I

: tissues

intra-abdominal hypertension. Encapsulated organs, suchas
the liver and kidney, havelimited capacity to accommodate
excessive interstitial fluid. As a result, PFB results inareduced
perfusion or venous drainage of such organs resulting in
ischemic injury. Table 1depicts the adverse effects ofPFB on
various organ systems. Enough evidence exists in literature
outlining the consequences of PFB on several outcomes
among critically ill patients. This has included patients
enrolled inmedical,2,3 surgical," andburns" ICUs. The adverse
effects include worsening of pulmonary function, delayed
renalrecovery, compromise in myocardial contractility, and
rise in intracranial pressures. Minor outcomes like wound
healing, pressure sores, and cholestasis were also adversely
influenced bydelayed PFB.6
~

WHAT DO WE USUALLY TARGET
DURING
--' FLUID
-- -- ~_ --.._..~.. _..
-- -._._RESUSCITATION?
~" --

II

..

,- .. '

..

"

-'

Traditionally, fluid challenge and resuscitation have been
triggered by clinical and pathophysiological parameters or
byidentification ofmarkers oftissue hypoperfusion. Oliguria
has always been a trigger for fluid challenge, on the valid
assumption, that oliguria is a marker of decreased cardiac


CHAPTER 2: How Much Fluid isToo Much Fluid?

-

output. A fluid bolus is presumed to increase the cardiac
preload translating into enhanced cardiac output? However,
persistent oliguria should be viewed as a marker of organ
dysfunction rather than as a marker of reduced preload.
Continuedattemptsat fluid challenges afterthe initialphase
could predisposeto significant PFB.
Lactate is another marker, which triggers a decision
of fluid therapy. Although lactate clearance is a reliable
indication of a successful resuscitation, persistent elevation
of lactate has multiple confounding causes including
hepatic clearance and systemic oxygenation. Continuing to
resuscitate a patient-based solely on lactatevaluesmightnot

achieve the desiredresults.
Static parameters, like centralvenouspressure(CVP) and
pulmonary arterial occlusion pressure (PAOP), have been
proven to be unreliable markers of either hypovolemia or
FO. They seem to be incapable of predicting the effect of a
fluid bolus on the cardiac output. It is now an accepted fact
that more than halfthe patients with a lowCVP are actually
unresponsive to fluids. Targeting a normal CVP for these
patientsis more likely to resultin an ineffective PFB.
Variations in stroke volume induced by mechanical
ventilation have been an established indicator of preload
status of both ventricles. However, it is equallywell-known
that its applicability to a spontaneously breathing patient
as well as to a patient with a nonsinus rhythm is not valid.
Moreover, the validation of this variation relates to tidal
volumes, which are much higher than what is currently
prescribed as safe. Considering the fact that fluid balance
plays a crucial role among patients with acute respiratory
distress syndrome (ARDS), where tidal volumes are
maintainedlow, the application ofstrokevolumevariation to
limitfluidtherapyappears impractical,"

i'&1 DO WE HAVE
.
. BETTER TOOLS?
00

••

._ . . . . . _

.......

•

.........

•

•


Current availability of ultrasound, bioimpedance, and less
invasive methods of thermodilution makes EVLW and
pulmonary vascular permeability index measurements
feasible. Similarly, widespread availability and increasing
understanding of the dynamics of brain natriuretic peptide
(BNP) have made this biomarker a potential candidate for
assessing FO. Intra-abdominal pressuremonitoring might be
another potentialcandidate."

Extravascular Lung Water
Extravascular lung water is the amount of water that is
contained in the lungsoutside the pulmonaryvasculature."
It is influencedbymultiple fluidinputs-alveolar, interstitial,
intracellular, and lymphatic. However, pleural effusions
do not form part of EVLW, The volume of EVLW is mainly
controlled by the lymphatic system, which returns the
volume to the systemic circulation. The normal value of
EVLW indexedto bodyweight is <7 mLlkg bodyweight.

How is Extravascular Lung Water Measured?
Thegross method to assessEVLW is by a chest X-ray (CXR).
However, there is always a scopeforinterobserver variability
in interpretation. Moreover, the exact index of EVLW when
pulmonary edema appears on CXR was never studied.
From a theoretical standpoint, the gold standard method
of assessmentof EVLW would be gravimetry, which implies
weighing the lung ex vivo before and after drying out. This
automatically excludes its applicability in clinical practice.
Several other methods have been described for measuring
EVLW, each with its own strong and weak points. Table 2
depictsthe characteristics ofthesetests.
Currently, transpulmonarythermodilution and lungUSG
seem to be practical methods of assessment of EVLW. The
roleofUSG in measuringEVLW will be discussed later in this
review.
Transpulmonary thermodilution has emerged as a
tool, which is validated experimentally against gravimetry.
The principle revolves around a central venous catheter
inserted in the superior vena cava territory coupled with
a femoral thermistor-tipped arterial catheter. Cold saline .
is injected into the venous catheter and the decrease in
temperature is measured at the arterial catheter. This will
yield a thermodilution curve. Using this curve, the EVLW is
estimated by using the Stewart-Hamilton principle. As per
this principle, the intrathoracic thermal volume (ITrV) is
assessed as'a product of cardiac output and mean transit
time. The difference between the total pulmonary volume
and the ITrV will represent global end-diastolic volume

(GEDV). Multiplying the GEDVwith a factor of 1.25 gives the
intrathoracicblood volume (ITBV). The difference between
ITTV and ITBV yields the EVLW. Extravascular lung water
has been shown to have a good correlation to mortality
amongcritically illpatients, especially, thosewithsepsisand
ARDS. 1O-13 Thisis the subset of patients, who are likely to be
adversely affected bya PFB. Although traditionally EVLWhas
been indexedto bodyweight, scientifically, indexing it to the
heightofthe individual appearsto be a morerobustsystem.

Brain Natriuretic Peptide
Serum BNP is a neurohormone, whose release is a direct
consequence of increase in ventricular walltension. One of
the advantages of BNP as a markerofwallstressis its short
half-life (<20 minutes). In effect, thisimplies that an elevated
BNP almost always indicatesa recentincreasein ventricular
wallstress.Sepsisand ARDS arebothconditionswhere early
detection of PFB is likely to improve the ultimate outcome.
A sustained rise in BNP might indicate an increased fluid
related ongoing Stress on the ventricular wall. Zhang et al."
evaluated the prognostic value of BNP and its potential
role in guiding fluid therapy among septic patients.
While admission BNP was an independent predictor of
mortality, ~BNP correlated with other outcomes such as

9


~

SECTION 1: Hemodynamic Monitoring andResuscitation
TABLE'2
Method

Methods of assessment of extravascular lung water

,
Accuracy

Gravimetry

,


Reference experimental technique

... _...

Chest X-ray

---"

..

-

-,

.., .

--_ ....- ..---_._-_.

~_

.. --.

--

-

Magnetic resonance imaging

.....- .. ---

Nil

Low

Can miss interstitial edema

Low


---­

Regional changes picked up
. _--.--_.._.-

Cost

­

, 35% increase in EVLW isneeded to show
pulmonary edema


Computed tomography

Clinical valu~

-_....

-------

.,

Cannot beused bedside, nonspecific

..,....., --,. _.._.

--

EVLW cannot besubtracted from
intravascular volume


_..

Long-image acquisition time.

High


Notbedside

Positron emission tomography

EVLW can be separated fromtotal waterby Not meant for repeated assessments
1S0 labeled carbon monoxide


Bioimpedance

Does not differentiate intrathoracic fluid

. Multiple inert-gas-exchange

High

. ... _...

. Assesses only EVLW accessible to airways

Very high

Low

Alternative to dyedilution
. Not uses

Relatively low

L~echni~u~ ..
, Double thermo-dye dilution
>._-_.. --_. -_...._ ...- ._--_. -

.__....----_ ..-._-_._-_._---.

Single thermos dilution

Uses heavy water that increases accuracy
_ .. _....__.-

..,_. _.._._-_.. _.. _-...

Acceptable

.

Invasive, cumbersome

Relatively high
-----

Repeated measurements possible

-

-- --

---_...__.. _ __ .­
..•

Relatively low

EVLW, extravascular lung water.

ICU length of stayand duration of ventilation. In addition,
the authors reported that the BNP values could change
with as little as 100 mL of PFB. A Brazilian study involving
close to 100 patientsin the outpatient demonstrated a good
correlation between the ·presence of B lines on lung USG '.
and elevation ofBNP levels. IS
While the significance of B lines and their correlation
with EVLW will be discussed in the following paragraphs, the
relevance of BNP to the sonographic patternof FO needs to
be noted.

markers. Conjunctival edema, pleural effusions, etc. are not
consistent and are morelikely to be delayed markers of Fa.
Measurement of lAP couldbe a useful tqolfor identification
of PFB. Grades of intra-abdominal hypertension are well­
validated. Ina patient, whohasundergone fluid resuscitation,
it maybe pertinentto initiate the measurement oflAP at least
for the first 72hours, when the riskof PFB is high. Progress
of lAP beyond grade I should be viewed with caution and
shouldtrigger a moremeticulous attention tofluid balancein··­
the least. This will particularly be valid among patients with
generalized increase permeability states.

Lung Ultrasonography
Assessment ofthe lungsbysonography has become standard
of care in most ICUs. The readily availability, noninvasive
nature, repllcability, and lackof radiation hazardmake USG
an idealtoolfor repeated assessment of lungabnormalities.
Definite profiles havebeen identified to represent interstitial
fluid, alveolar fluid, and extraparenchymal collections. Lung
USG has the ability to identify interstitial edema, which
precedes pulmonary edema." A definite change in profile
represents the appearance of interstitial edema, which
warrants cessation offluid therapy..
:~!

HOW MUCH IS TOO MUCH?

i??s ,

_~._'_~_.

~"""".~~~n"., ~ ...... ~ __ .~_,:,

,_.. ~. __.•

Clinical Evaluation

10

Clinical examination is a useful tool for identifying signs of
Fa in an outpatientsetting. Sacral edema and pedal edema

would be useful markers of a PFB in an ambulant patient.
However, in a critically ill, bed-bound, hypoalltuminemic
patient receiving vasopressor support will always have
some degree ofthese clinical markers. Early detection of Fa
in this subset of patients is, therefore, likely to need other

Chart Review
A meticulous review of the fluid balance for daily as well as
cumulative PFB could be the simplest method to identify
and correct a PFB of clinical significance. Literature review
shows enough evidence linking a PFB withworse outcomes
amongst a widesubsetofcritically ill patients.
The Fluids and Catheters Treatment Trial (FACTT) is
probably the most well-recognized publication, which
draws attention to the deleterious effects of PFB of as little
as 1.1 Lin 24hours, while also questioning the relevance of
CVP and PAOPY Lee et al. studied the association between
fluid balance and survival among critically ill patients,"
The authors identified a hazard ratio of 1.04 for dying with
a positive balance of I L on day 2, within 90 days of ICU
discharge. This hazard ratio was 1.07 for ICU mortality.
This effect was even more pronounced amongst those who
had a condition predisposing to fluid retention like acute
kidney injury and congestive heart failure. Cumulative
fluid balance seems to have a greater impact on mortality
than the peak PFB. The Randomized Evaluation of Normal
vs. Augmented Level (RENAL) study demonstrated the
beneficial effects ofa net negative balance on 90-day survival