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aVol. 1 - No.2; April - June, 2018 CRITICAL CARE PEDIATRICS

Vol.1 No.2April-June 2018

Critical Care PediatricsAn Official Journal of College of Pediatric Critical Care

EditorialMedical Staffi ng Patterns in Pediatric Intensive Care UnitsAnil Sachdev

Pediatric MRI SedationNameet Jerath

Do Bronchiolitis Babies Like Salty Airways?Krishan Chugh

Original ArticlesClinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs)V.S.V. Prasad, Aniket Parashar

Intermittent Dose of Propofol for Parenteral Sedation in Outpatient Pediatric MRI - A single centre experienceBhaskar Saikia, Pradeep Kumar Sharma, Rachna Sharma, Praveen Khilnani

Nebulized 3% Hypertonic Saline with Epinephrine Vs Normal Saline with Epinephrine in the Treatment of Acute Bronchiolitis in the Emergency DepartmentKaran Raheja, Ashish Prakash, Azay Punj

Review ArticlesSynergy of Antimicrobial Stewardship and Infection Prevention and ControlAparna Chakravarty, Chandrasekhar Singha

Case Reports Negative Pressure Pulmonary Edema in a Case of Adeno-tonsillectomyManish Kori, Krishan Chugh, Vikas Taneja

Exchange Transfusion as a Treatment Strategy in Severe Pertussis with Hyperleukocytosis in an Infant - A case reportAbdul Rauf, Anil Sachdev, Dhiren Gupta

Letter to EditorSpontaneous Retrograde Coiling of Central Venous Catheter into the Ipsilateral Internal Jugular Vein – Can it happen?Ankur Khandelwal, Surya K. Dube, Gyaninder P Singh

Best EvidenceJournal ScanNaresh Lal, Rachna Sharma

Critical ThinkingPICU QuizNaresh Lal, Rachna Sharma

www.criticalcarepediatrics.in

International Pediatric Critical Care

Conference of India - IPCCCI 2018

Theme : Do it NTheme : Do it Now, Do it Right...ow, Do it Right...Main Conference: 20th and 21st October, 2018

Workshops/CME: 22nd & 23rd October 2018

Venue: HICC Hyderabad

Conference Venue: HICC Hyderabad

Conference Secretariat: Dr Dinesh K Chirla. Rainbow Children’s HospitalRoad No.2, Banjara Hills, Near L.V. Prasad Eye Institute. Hyderabad - 500034.

Email: [email protected], [email protected], [email protected]

Pradeep

Typewritten Text

www.collegeofpediatriccriticalcare.org

1Vol. 1 - No.2; April - June, 2018 CRITICAL CARE PEDIATRICS

Contents

Editorial Board 3

From Editors Desk 5

From the Desk of the Vice-Chancellor 6

College of Pediatric Critical Care Executive Board 7

CCP Copyright Form 8

Author Instructions 11

Publisher Detail 18

Editorial

Medical Staffi ng Patterns in Pediatric Intensive Care Units 19Anil SachdevDirector, Department of Pediatric Intensive care, Sir Ganga Ram Hospital, New Delhi, India

Pediatric MRI Sedation 21Nameet JerathSenior Consultant, Pediatric Intensive Care, Apollo Hospital, Sarita Vihar, New Delhi, India

Do Bronchiolitis Babies Like Salty Airways? 23Krishan ChughDirector and Head, Department of Pediatrics, Fortis Memorial Research Institute, Gurugram, Haryana, India

Original Articles

Clinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs)

26

V.S.V. Prasad, Aniket ParasharPediatric Critical Care, Lotus Hospitals for Women & Children, Lakdikapul, Hyderabad, India

Intermittent Dose of Propofol for Parenteral Sedation in Outpatient Pediatric MRI - A single centre experience

32

Bhaskar Saikia, Pradeep Kumar Sharma, Rachna Sharma, Praveen KhilnaniPediatric Critical Care and Pulmonology, Max Super Speciality Hospital, Sri Balaji Action Medical Institute, B L Kapur Super Speciality Hospital, Rainbow Children Hospital, New Delhi, India

Nebulized 3% Hypertonic Saline with Epinephrine Vs Normal Saline with Epinephrine in the Treatment of Acute Bronchiolitis in the Emergency Department

35

Karan Raheja, Ashish Prakash, Azay PunjDepartment of Pediatrics Yashoda Hospital, Ghaziabad, Department of Pediatrics, Subharti Medical College, Meerut, India

Vol. 1 - No.2; April - June, 2018 2 CRITICAL CARE PEDIATRICS

Review Article

Synergy of Antimicrobial Stewardship and Infection Prevention and Control 41Aparna Chakravarty, Chandrasekhar SinghaDepartment of Pediatrics, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, Pediatric Intensive Care Unit, Madhukar Rainbow Children’s Hospital, Malviya Nagar, New Delhi, India

Case Reports

Negative Pressure Pulmonary Edema in a Case of Adeno-tonsillectomy 48Manish Kori, Krishan Chugh, Vikas TanejaPediatric Intensive Care, Department of Pediatrics, Fortis Memorial Research Institute, Gurugram, Haryana, India

Exchange Transfusion as a Treatment Strategy in Severe Pertussis with Hyperleukocytosis in an Infant - A case report

54

Abdul Rauf, Anil Sachdev, Dhiren GuptaDepartment of Pediatric Intensive Care, Sir Ganga Ram Hospital, New Delhi, Delhi, India

Letter to Editor

Spontaneous Retrograde Coiling of Central Venous Catheter into the Ipsilateral Internal Jugular Vein – Can it happen?

57

Ankur Khandelwal, Surya K. Dube, Gyaninder P SinghDepartment of Neuro-anaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi, India

Best Evidence

Journal scan 59Naresh Lal, Rachna SharmaConsultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India

Critical Thinking

PICU Quiz 67Naresh Lal, Rachna SharmaConsultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India

IPCCCI - 2018

Abstract Submission Guideline 78

Registration Form 79

Workshop Details 82

Scientifi c Programme 83


Critical Care Pediatrics (CCP)

Editorial Board

Executive MembersDr Ebor Jacob (Vellore)

Dr Partha Bhattacharya (Kolkatta)

Dr Prabhat Maheshwari (Gurgaon)

Dr Dinesh Chirla (Hyderabad)

Dr Deveraj Raichur (Hubbali)

Dr Mritunjay Pao (Assam)

Dr Deepika Gandhi (Chennai)

Dr Shipra Gulati (New Delhi)

Dr Vikas Taneja (Gurgaon)

Dr Indira Jayakumar (Chennai)

Dr Sanjay Bafna (Pune)

Dr Sagar Lad (Pune)

Dr Nikhil Vinayak (Delhi)

BiostatisticsDr M Jayshree (Chandigarh)

Dr Jhuma Sankar (New Delhi)

EthicsDr Urmila Jhamb (New Delhi)

Dr Rakesh Lodha (New Delhi)

Dr Meera Ramakrishnan (Bangalore)

Dr Vinay Joshi (Mumbai)

WebsiteDr Zahid (Gurgaon)

Dr Anjul Dayal (Hyderabad)

PublicationDr Rachna Sharma (New Delhi)

Dr Chandrashekhar (New Delhi)

International Advisory BoardDr Niranjan Kissoon (Canada)

Dr Jerry Zimmerman (USA)

Dr Joseph Carcillo (USA)

Dr Ashok Sarnaik (USA)

Dr Peter Cox (Canada)

Dr Vinay Nadkarni (USA)

Dr Shekhar Venkataraman (USA)

Dr Mohan Mysore (USA)

Dr Utpal Bhalala (USA)

Dr Suneel Poobani (UK)

Dr Ravi Samraj (USA)

Dr Dipankar Gupta (USA)

Dr Rahul Bhatia (USA)

National AdvisorsDr Y Amdekar (Mumbai)

Dr S C Arya (New Delhi)

Dr R N Srivastava (New Delhi)

Dr Digant Shastri (Mumbai)

Dr M P Jain (Gurgaon)

Dr Anupam Sachdeva (New Delhi)

Senior Editors and ReviewersDr K Chugh (Fortis Hospital, Gurgaon)

Dr S Udani (Hinduja Hospital, Mumbai)

Dr S Ranjit (Apollo Childrens Hospital, Chennai)

Dr Rajiv Uttam (Max Hospital, New Delhi)

Dr Anil Sachdev (Sir Ganga Ram Hospital, New Delhi)

Dr Madhu Otiv (KEM Hospital, Pune)

Dr Bala Ramachandran (Child Trust Hospital, Chennai)

Dr S Soans (AJIMS, Mangalore)

Associate EditorsDr Nameet Jerath (IP Apollo Hospital, Delhi)Dr Rakshay Shetty (Rainbow Hospital Bangalore)Dr Basavaraj (Banglore)Dr Gnanam (Manipal Hospital, Bangalore)Dr Sandeep Kanwal (New Delhi)Dr Dhiren Gupta (Sir Ganga Ram Hospital, New Delhi)Dr Bhaskar Saikia (New Delhi)

Executive EditorDr V S V Prasad (Lotus Hospital, Hyderabad)

Managing EditorDr Pradeep Sharma (Action Balaji Hospital, Delhi)

Editor-In-Chief:Dr Praveen Khilnani


Dear colleagues and readers

April june 2018 issue of “Critical care Pediatrics”(CCP), a journal dedicated to Pediatric critical care by the College of Pediatric critical care, India, is now published. It is an open access journal with fully functional on line process of submission and review of manuscripts (www.criticalcarepediatrics.in). For fi rst few years publication of har-d copy print issue will also be continued.

Important highlights of this issue include original articles such as “Clinical Service and Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units ”By Prasad et al from Pediatric Critical Care department, Lotus Hospitals for Women & Children, Hyderabad.

“Intermittent dose of Propofol for parenteral sedation in Outpatient Pediatric MRI- A single centre experience” is published by Saikia; et al : a study conducted at BLK superspeciality hospital PICU, New Delhi, India.

“Use of Nebulized 3% hypertonic saline with Epinephrine Vs normal saline with Epinephrine in the Treatment of Acute bronchiolitis…” in the Emergency Department is published by Raheja;et al from Department of Pediatrics Yashoda Hospital and Department of Pediatrics, Subharti Medical College, Meerut, India

Rarest of rare case reports are a prominent highlight of CCP. Refer to case reports on Negative Pressure Pulmonary Edema in a case of Adeno-tonsillectomy By Kori;et al from FMRI, Gurgaon. “Exchange transfusion as a treatment strategy in Severe Pertussis with Hyperleukocytosis in an infant “ by Rauf ;et al from SGRH New Delhi. A rare complication related to central venous catheters : “Spontaneous retrograde coiling of central venous catheter into the ipsilateral internal jugular vein – Can it happen?” has been high lighted by Khandelwal;et al from AIIMS, Delhi. H a special review article highlighting issues related to antibiotic stewardship and infection control:“Synergy of Antimicrobial Stewardship and Infection Prevention and Control”is published by Chakravarty ;et al from Department of Pediatrics, Hamdard Institute of Medical Sciences and Madhukar Rainbow Children’s Hospital, Malviya Nagar, New Delhi, India

As regular features to review whats new in the fi eld of Pediatric critical care ; Journal scan and a short PICU Quiz for readers remains as the regular feature of the journal.

Its gives me a great pleasure and pride to announce the FIRST-EVER College Conference, the International Pediatric Critical Care Conference of India (IPCCCI-2018)to be held at the beautiful HICC centre, Hyderabad between 20-23rd October 2018. A true scientifi c feast of international calibre and a grand convocation honouring faculty and graduates of fellowship courses in pediatric critical care as well as critical care nursing. For further information please visit www.collegeofpediatriccriticalcare.org

All IPCCI2018 abstracts and poster presentations will be published in subsequent issues of CCP. On behalf of team at CCP

I would like to thank all the reviewers and senior editors who have tirelessly reviewed the articles as well as contributed editorials.

Happy reading of the second issue of CCP !

Praveen Khilnani, MD FAAP MCCM(USA)Editor in Chief, Critical Care PediatricsChancellor College of Pediatric Critical Care and Organizing Chairman IPCCI 2018Clinical Director and Senior consultant Pediatric Critical Care and Pulmonology Rainbow Childrens Hospital, New Delhi

From the Editors Desk

Pradeep

Cross-Out

hard


From the Desk of the Vice-Chancellor

Dear friends and colleagues

Its gives us great pleasure and pride to announce the FIRST-EVER College Conference, the International Pediatric Critical Care Conference of India (IPCCCI-2018) to be held at the beautiful HICC centre, Hyderabad between 20-23rd October, 2018.

In keeping with the College hallmark, the IPCCCI will have the highest quality of academics, teaching and learning. The extraordinary scientifi c content promises to provide a breath-taking array of topics on Pediatric Intensive Care that will leave you spell-bound!

We have a large galaxy of international speakers well-known for their expertise and teaching skills such as Shekar Venkataraman, Peter Cox, Mohan Mysore, Utpal Bhalala from USA, Akash Deep (UK), Santhosi Nagakawa (Japan), Manu Sundaram (Qatar), Rahul Joshi (Australia) and others.

Not to be outdone is the constellation of Indian faculty, all Teachers of the College of Pediatric Critical Care who have a fantastic track record of teaching for many years as well as many years of international experience.

In view of Dusserha preceding the conference weekend, we have planned the IPCCCI such that we start with the conference on 20-21st October, and then have 2 days of great workshops and courses developed by College of Pediatric critical care.

The workshops and courses include a two day Fundamental Pediatric intensive care course (FPICC) and a two day Advanced Pediatric intensive care course (APICC), one day Pediatric ventilation, Critical care ultrasound, Non-invasive ventilation (NIV) as well Pediatric critical care Nursing (PCCN) workshops.

Highlights of the main conference include a full day Advanced CME, plenaries, Case-based practical discussions, pro-con debates, and “how I do it” sessions. Suffi cient time has been planned to permit adequate audience interaction and questions and answers.

Best wishes and look forward to meeting all of you at Hyderabad between 20-23 October 2018 at the IPCCCI! We hope that all of you will register and spread the word to your colleagues.

Suchitra Ranjit, MD FCCMVice-Chancellor, College of Pediatric Critical Carea nd Scientifi c Chair IPCCI2018


Dr Krishan ChughImmediate Past

Chancellor

Dr Soonu UdaniPast Chancellor

Dr Praveen KhilnaniChancellor

Dr Suchitra RanjitVice Chancellor

Rajiv UttamSecretary

Dr Anil SachdevTreasurer

Dr Nirmal Choraria

Dr Sajith KDr Rajeshwari N

Dr Rakshay ShettyDr Bala Ramachandran Dr M JayshreeDr Dinesh Chirla Dr Nameet Jerath

Executive Members

Executive Board College of Pediatric Critical Care

Dr Anjul Dayal

Dr Madhumati Otiv Dr Dhiren Gupta

Nominated Members

Dr Farhan Shaikh


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Author Instructions

Critical care Pediatrics (CCP) is an international online and print journal published quarterly (January, April, July and October) by College of Pediatric Critical Care. Journal’s full text is available at http://criticalcarepediatrics.in. Journal allows free access (open access) to its contents; therefore, authors are to self-archive the fi nal accepted version of the article.

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Standard Journal ArticlesFor up to six authours: Arrawal A, Singh VK, Varma A, Sharma R. Intravenous arginine vasopressin infusion in refractory vasodilatory shock: clinical study. Indian J Pediatr.2012;79(4):488-493.

b. For more than six authors: List the frst six authors followed by et al. Nobili V, Marcellini M, Giovannelli L, Girolami E, Muratori F, Giannone G, et al. Association of serum interleukin-8 levels with the degree of f brosis in infants with chronic liver disease. J Pediatr Gastroenterol Nutr. 2004;39(5):540-4.

Personal author (book): Leung AK. Common Problems in Ambulatory Pediatrics: Symptoms and Signs, 1st ed. New York: Nova Science Publishers, Inc.; 2011.

Chapter in a book: Leung AK. Oral rehydration therapy and early refeeding in the management of childhood gastroenteritis. In: Overton LT, Ewente MR, eds. Child Nutrition Physiology. New York: Nova Biomedical Books; 2008. p. 127-152.

Conference proceedings: Harnden P, Joffe JK, Jones WG, editors. Germ cell tumours V. Proceedings of the 5th Germ Cell Tumour Conference; 2001 Sep 13-15; Leeds, UK. New York: Springer; 2002.

Conference paper: Christensen S, Oppacher F.An analysis of Koza’scomputational effort statistic for genetic


CCPprogramming. In: Foster JA, Lutton E, Miller J, Ryan C, Tettamanzi AG, editors. Genetic programming. EuroGP 2002: Proceedings ofthe 5th European Conference on Genetic Programming; 2002Apr 3-5; Kinsdale, Ireland. Berlin: Springer; 2002. p. 182-91.

Unpublished Material: Children and adolescents with chronic constipation: How many seek healthcare and what determines it? Rajindrajith S, Devanarayana NM, Benninga MA. J Tropical Pediatr.2011 Dec 6. [Epub ahead of print]

Electronic Material CD-ROM: Neonatal Resuscitation Program (NRP) Training Aids [on CDROM]. National Neonatology Forum, New Delhi, 2006. Hemodynamics III: the ups and downs of hemodynamics [computer program].Version 2.2. Orlando (FL): Computerized Educational Systems; 1993.

Journal article on the Internet: Abood S. Quality improvement initiative in nursing homes: the ANA acts in an advisory role. Am J Nurs [Internet].2002 Jun [cited 2002 Aug 12];102(6):[about 1 p.]. Available from:http://www.nursingworld.org/ AJN/2002/june/Wawatch.htm

Article Homepage/Web site: Cancer-Pain.org [Internet]. New York:Association of Cancer Online Resources, Inc.; c2000-01 [updated 2002 May 16; cited 2002 Jul 9]. Available from: http://www.cancerpain. org/.

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Publisher details: Critical Care PediatricsCritical Care Pediatrics is a peer reviewed quarterly journal published by College of Pediatric Critical Care

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EditorialMedical Staffi ng Patterns in Pediatric Intensive Care Units

Anil SachdevDirector, Department of Pediatric Intensive Care, Sir Ganga Ram Hospital, New Delhi, India-110060

Received:5-June-18/Accepted: 6-June-18/Published online:18 -Jun-18

Corresponding authorDr Anil Sachdev, Director, Department of Pediatric Intensive Care and Pulmonology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi-110060Email: [email protected]

Pediatric critical care specialty has taken leaps forward ever since John Downes established the fi rst recorded PICU in the United States at Children’s Hospital of Philadelphia in 1967. In the ensuing 50 years, considerable progress has been made in this fi eld across globe, though developing countries are still lagging. The physician staffi ng pattern in ICU has been a topic of discussion ever since its inception.According to the evidence based ICU-physician staffi ng standard set by Leapfrog group and recommendations by international societies like European Society of Intensive Care Medicine, intensivists must manage or co-manage ICU patients, and should exclusively provide clinical care in the ICU during daytime hours.1,2 Studies suggest that having a full-time pediatric intensivist in the PICU improves patient care and effi ciency.3 Pediatric Section of the Society of Critical Care Medicine recommended that all PICUs must have at least one physician in house 24 hrs/day to provide bedside care to patients.4 This physician must be skilled in and have credentials to provide emergency care to critically ill. Attending Intensivist should remain on-call and be available within 30 minutes to assist with patient management. In a large metaanalysis, it was showed that High-intensity staffi ng is associated with reduced ICU and hospital mortality. However, it was surprising to note that 24-hour in-hospital intensivist coverage did not reduce hospital, or ICU, mortality within a high-intensity model.5

Literature regarding the physician staffi ng pattern in PICUs from India is scarce. For a vast and populous country like India, there is still a shortage of pediatric intensivists. Very few PICUs in the country have dedicated PICU consultants staying in-house in the

hospital during off-hours. It needs to be evaluated whether the quality of patient care gets compromised during off- hours, when the patients are managed by fellows/residents.In this issue of Critical Care Pediatrics, Prasad et al report the fi ndings of a cross sectional survey about clinical services and physician staffi ng pattern, done across 59 accredited level 3 PICUs in the country.6

All the PICUs which participated in the survey were manned with at least 2 certifi ed pediatric intensivists. One-fi fth PICU were manned by 3 intensivists and another one-fi fth with 4 intensivists. The average working hours were more than 8 hours for the majority (66.1%) intensivists. Only one-fourth of the intensivists dedicated their entire time exclusively for PICUs and the rest three-quarters practiced allied pediatric specialties like pediatrics and neonatology during regular working hours. Consultants were able to attend to patients at short notice during off-hours in the majority of the PICUs. In-house presence of intensivists in night were available in only one-third of PICUs. Most of the PICUs were managed by critical care fellows or post graduate residents during off-hours. Instances of patient deterioration during off-hours reported by majority of PICUs is a matter of concern and needs to be attended.Apart from trained physician care, critically ill children also require comprehensive care involving a multi-disciplinary team. Most of PICUs in the survey had back up of other specialties round the clock; Pediatric surgery (94.9%), Radiology (84.7%), Anesthesia (86.4%), Orthopedics and Neurosurgery (78%).Bulk of the studies about staffi ng pattern in ICUs were done in adult population. Survey reports about staffi ng pattern in PICUs are available from developed world and few developing countries like Turkey, Nepal and Pakistan.7-9 Findings in survey by Prasad et al, like number of PICUs manned with pediatric intensivists (100%), proportion of PICUs


EDITORIAL Medical Staffi ng Patterns in Pediatric Intensive Care Units

with back up of other specialties like neurosurgery and pediatric surgery (>90%) are comparable with fi gures from developed countries and far better than those from other developing countries. A head to head comparison is unfair as surveys in those countries were done few years back. Another confounding factor for comparison is that present survey included only accredited PICUs. Hence, it should be noted that the results cannot be generalized as the current state of pediatric intensive care in the country. The very fact that there are still only 59 accredited PICUs in this vast country needs attention. It means that there are still many sick children who are denied of quality critical care. Or in the other way, if we include the non-accredited centers where critically ill children are managed in the country, the quality indices found wouldn’t have been so soothing.Cross-sectional survey by Prasad et al is a good attempt and deserves applause. The survey may be repeated periodically to monitor the progress and the changes in staffi ng patterns. Majority of pediatric intensivists in the country still practice other allied specialties and they are over burdened. Only practical solution is to train more quality pediatric intensivists to serve the sick children in the country. College of Pediatric Critical Care is committed to this mission and has been conducting standardized, structured training programs in accredited centers to create pediatric critical care specialists.

References1. Milstein A, Galvin RS, Delbanco SF, Salber P, Buck CR.

Improving the safety of health care: the leapfrog initiative. Eff Clin Pract 2000;3: 313-316.

2. Valentin A, Ferdinande P; ESICM Working Group on Quality Improvement. Recommendations on basic requirements for intensive care units: structural and organizational aspects. Intensive Care Med. 2011;37(10):1575-87.

3. Pollack MM, Cuerdon TT, Patel KM, Ruttimann UE, Getson PR, Levetown M. Impact of quality-of-care factors on pediatric intensive care unit mortality. JAMA. 1994;272(12):941-6.

4. Rosenberg DI, Moss MM; American College of Critical Care Medicine of the Society of Critical Care Medicine. Guidelines and levels of care for pediatric intensive care units. Crit Care Med. 2004;32(10):2117-27.

5. Wilcox ME, Chong CA, Niven DJ, Rubenfeld GD, Rowan KM, Wunsch H, et al. Do intensivist staffi ng patterns infl uence hospital mortality following ICU admission? A systematic review and meta-analyses. Crit Care Med. 2013;41(10):2253-74.

6. Prasad VSV, Parashar A. Clinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs). Crit care Pediatr. 2018;1(2):26-31.

7. Bayrakci B, Kesici S, Kendirli T, Kalkan G, Sari A, Tokmak N, et al. Evaluation report of pediatric intensive care units in Turkey. Turk J Med Sci. 2014;44(6):1073–86.

8. Haque A, Ladak LA, Hamid MH, et al: A National Survey of Pediatric Intensive Care Units in Pakistan. J Crit Care Med. 2014:1–4.

9. A Khanal, A Sharma, S Basnet. Current state of pediatric intensive care and high dependency care in Nepal. PediatrCrit Care Med. 2016;17:1032–40.

How to cite this articleSachdev A. Medical Staffi ng Patterns in Pediatric Intensive Care Units. Crit Care Pediatr. 2018;1(2):19-20

How to cite this URLSachdev A. Medical Staffi ng Patterns in Pediatric Intensive Care Units. Crit Care Pediatr. 2018;1(2):19-20Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01021.html


EditorialP ediatric MRI Sedation

Nameet JerathSenior Consultant, Pediatric Intensive Care, Apollo Hospital, Sarita Vihar, New Delhi-110076, India

Received:5-June-18/Accepted:6-June-18/Published online:18 -Jun-18

Children often require sedation for procedures for reasons varying from pain prevention and control, anxiety, need for immobilization to parental apprehension and psychological “trauma”, to name a few. MRIs require varying periods of keeping still which often is a challenge in children and sedation is frequently sought for them. It being a painless procedure a pure sedating agent with minimal or no analgesia is often used.In this issue of the Critical Care Pediatrics Saikia et al have reported their experience of use of intermittent propofol doses for sedation children for MRIs done as an outpatient over a period of 3 years in a retrospective review.1 They found propofol to be safe and effective. The mean total cumulative dose used was 4.36±0.9mg/kg. The authors did not mention the mean duration of sedation for the procedures or the time to discharge but do report a recovery time of 6±1.9 minutes after the procedure. They report apnea in 2 children requiring bag-and-mask ventilation, one requiring aborting the procedure but none needed mechanical ventilation. Two children developed rashes and itching requiring antihistamines with good response.With adequate patient selection, appropraite monitoring during and post procedure and trained staff with competency to deal with levels of sedation deeper than intended most procedures can be safely done by non-anesthetists. Krauss B et al report the need for mechanical ventilation in just 2 of 1140 children (0.17 percent) in their series of procedural sedation and analgesia in children by trained non-anesthesiologists.2

Propofol has its benefi ts of quick onset, short duration of action and quick offset making it a desired choice for non-painful sedation procedures. It is known

to cause bradycardia and hypotension, in some instances life threatening.3 The authors have not shared their data of bradycardia and/or hypotension but have interestingly used atropine as premedication as a part of their sedation protocol. Though not a standard practice, investigators have reported varying responses to premedication with atropine. Horiguchi T et al reported no benefi ts, while Kitagawa N et al reported reduction in propofol induced bradycardia when propofol was used for induction alone and not for maintenance of anesthesia.4,5 The concerns of Propofol Infusion Syndrome with prolonged and high dose propofol in children has not been shown with short term infusions.6

Dexmedetomidine has been available for use in India of late. A potent alpha-2 agonist provides comparable sedation with lesser cardiovascular effects as compared to propofol. A meta-analysis of dexmedetomidine vs propofol use for MRI sedation in children showed propofol to have shorter onset of sedation and recovery time and lower incidence of emergence delirium compared to dexmedetomidine.7

The role of adequate patient selection, trained personnel and adequate monitoring cannot be ovewremphasized for a successful sedation. Propofol in good hands and given in right patient is a safe and effi cacious sedative option in children undergoing MRI or similar non-painful procedures.

References1. Saikia B, Sharma PK, Sharma R, Khilnani P. Intermittent

dose of Propofol for parenteral sedation in Outpatient Pediatric MRI- A single centre experience. Crit Care Pediatr. 2018;1(2):32-34

2. Krauss B, Green SM. Sedation and analgesia for procedures in children. N Engl J Med 2000;342:938-945.

3. Freysz M, Timourt Q, Betrix L, Faucon G. Propofol and bradycardia. Can J Anaesth 1991;38:137–8.

4. Horiguchi T, Nishikawa T. Heart rate response to intravenous atropine during propofol anesthesia. Anesth Analg 2002;95:389–92.

5. Kitagawa N, Katoku M, Kasahara T, Tsuruta T, Oda M,

Corresponding authorDr Nameet Jerath, Senior Consultant, Pediatric Intensive Care, Apollo Hospital, Sarita Vihar, New Delhi-110076, IndiaEmail: [email protected]


Totoki T. Does atropine reduce the risk of propofol-induced cardiovascular depression? Anesth Analg. 2006;103(6):1606-8.

6. Indra S, Haddad H, OʼRiordan MA Short-Term Propofol Infusion and Associated Effects on Serum Lactate in Pediatric Patients. Pediatr Emerg Care. 2017;33(11):e118-e121.

7. Qiang Zhou, Lingli Shen, Xinxian Zhang, Jiong Li and Yong Tang. Dexmedetomidine versus propofol on the sedation of pediatric patients during magnetic resonance imaging (MRI) scanning: a meta-analysis of current studies. Oncotarget, 2017; 8(60):102468-102473.

How to cite this articleJerath N. Pediatric MRI Sedation. Crit Care Pediatr. 2018;1(2):21-22

How to cite this URLJerath N. Pediatric MRI Sedation. Crit Care Pediatr. 2018;1(2):21-22Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01022.html

EDITORIAL P ediatric MRI Sedation


EditorialDo Bronchiolitis Babies Like Salty Airways?

Krishan ChughDirector and Head, Department of Pediatrics, Fortis Memorial Research Institute, Gurugram, Haryana-122002, India

Received:10-April-18/Accepted: 26-May-18/Published online:18-Jun-18

Bronchiolitis is one of the commonest causes of visit of infants to the Pediatric Emergency Services, especially in the winter months. While many of these children can be sent back home within a short period, a high proportion of them need admission in the pediatric wards and a few in the Pediatric Intensive Care Units (PICU). With modern intensive care, including intensive monitoring and respiratory support, mortality is low. Factors that may determine the outcome include severity of illness, presence of co-morbid conditions (like prematurity, low birth weight, congenital heart disease etc.), early vs. late arrival in the health care facility and the type and quality of care received there.Except for supportive care, there is no consensus even on the threshold for starting intravenous fl uids and oxygen therapy. Recent American Academy of Pediatrics Guidelines1 do not encourage the use of even these therapies in all cases, albeit under close monitoring. Bronchiolitis being a self-limiting disease, it has been observed that many of these infants do well without much treatment.Edema of the smaller bronchi and bronchioles resulting in the narrowing of these airways appears to the main pathophysiological change in bronchiolitis. There is also some shedding of the epithelial lining causing mechanical block of these smaller airways. Thus, therapies which are known to decrease the bronchial wall edema may have only limited positive clinical response unless muco-ciliary clearance and macrophage activity are also enhanced. Given this background it is not surprising that a number of interventions like salbutamol, epinephrine, hypertonic saline, inhaled corticosteroids, systemic corticosteroids, antibiotics, antivirals and their various combinations produce variable results. Recently there

have been a slew of research articles on the subject, including clinical trials, meta-analysis and reviews. Debate on the best available treatment (if any) in the ward/PICU or emergency department (ED) appears to have further hoted up in 2017 and 2018.Despite these guidelines being widely disseminated, there is a signifi cant gap in their implementation. In a study from Australia2, it was noted that 42% of all bronchiolitis infants received at least one medication (salbutamol most commonly) and this fi gure was much higher (81.6%), in ICU admissions.Interest in evaluation of role of hypertonic saline for treatment of bronchiolitis appears to be very high from among the various therapeutic options available. A study published in 2018 from China3 compared 7 therapeutic options while another one in 2017 from Turkey4, compared 5 regimens emphasizing the desperate search for the best one. Hypertonic saline (HS) was a component of several of the options tried in these two studies. It has been studied alone as well as in combination with epinephrine, inhaled corticosteroids and salbutamol.Several studies published in past 18 months support the use of hypertonic saline in bronchiolitis, however there are also some which do not. Indeed, one trial in France5 was stopped when only 61 of the planned 168 children had been enrolled because of no benefi cial effects and possibly severe adverse events in the 3% hypertonic saline group. In this study salbutamol / epinephrine were not being given with HS. Authors attributed 75% of the severe adverse events to high aerosol output of the type of nebulizer used.Angoulvant F et al6 administered 2 doses of (4 ml each) 3% saline, 20 minutes apart to 385 bronchiolitis infants and normal saline (NS) to 387. Nebulized HS did not signifi cantly reduce the rate of hospital admissions among infants with fi rst episode of moderate to severe acute bronchiolitis treated in the French pediatric ED. Also, mild adverse events were more frequent in the HS group.

Corresponding authorDr Krishan Chugh, Department of Pediatrics, Fortis Memorial Research Institute, Sector -44, Opposite HUDA City Centre, Gurugram, Haryana-122002Email: [email protected]


A study from Japan7 enrolled moderately ill, hospitalized patients of RSV bronchiolitis from 5 hospitals for randomized controlled trial of 3% HS vs NS and found no difference in length of stay (LOS), although HS was well tolerated.Kanjanapradap et al8 reported in Pediatric Pulmonology in Feburary 2018, that in children 6 months to 5 years admitted with acute viral wheezing, nebulized 3% HS + salbutamol signifi cantly shortened hospital LOS, time of oxygen therapy and improved asthma clinical severity score faster than NS + salbutamol.A meta-analysis9, in the same issue of Pediatric Pulmonology concluded that HS inhalation offered only limited clinical benefi ts (LOS and hospitalization rate). They found that heterogeneity (using Higgins heterogeneity test) in the studies included in their meta-analysis was substantial.Uysalol from Turkey4, in a double blind randomized controlled trial, found that nebulized epinephrine mixed with 3% HS was associated with signifi cantly higher discharge rate at 4th hour (and shorter LOS), as compared with other options. Authors interpreted this as a “better acute response”.The double blind randomized controlled trial by Raheja et al10, in this issue of the Journal also reports favorable results with Epinephrine + HS, compared to Epinephrine + NS in terms of Respiratory Distress Assessment Instrument, respiratory rate, and SpO2. However, it must be pointed out that their study enrolled bronchiolitis infants with only moderate severity (SpO2 92.09% in HS group and 91.96% in NS group). These infants had no comorbidity (like prematurity) and they all had come in their fi rst episodes. Further, 3% HS and not 7% HS was used and always with epinephrine. This study was conducted in the ED where children were monitored for 4 hours only. Any benefi t of the study drugs on LOS was not studied. This study used a very different protocol for administration of epinephrine + HS – 2.5 ml of HS + 0.5 ml of 1:1000 epinephrine, given every ½ hour for 4 hours (8 doses). More studies would be required to see if the positive response in this study can be attributed to higher dose frequency and that too for 4 hours.

In majority of studies included in the Cochrane review of 2017 December11, the benefi ts of HS with or without epinephrine were modest in terms of hospitalization rate, clinical scores and LOS. Further, the reviewers assessed the quality of evidence also to be low to moderate. A decision analysis published in 2018, the cost effectiveness of hypertonic saline inhalations for infant bronchiolitis found the benefi ts to be very modest12.Very interesting observations were made in a multicenter observational study13 of the use of nebulized HS to treat children hospitalized for bronchiolitis from 2008 to 2014. More children in ICUs received HS than in the wards. Further, use of HS increased during 2008 to 2012 winter seasons and then declined, (2% in 2008 – 09, 27% in 2011 – 12 and 17% in 2013 – 14). These fi ndings parallel trends in HS literature, with positive articles encouraging HS use in early years, followed by a growing number of neutral and negative articles after 2012!Going by the above interesting observation, one can expect the use of epinephrine + HS to increase as many of the clinical studies, meta – analysis and reviews in 2017 – 18 are favoring the use of this combination. However, the dosage schedule required (e.g. 8 doses in 4 hours, 4 – 5 times a day in the wards) defi nitely remains to be further studied.

References1. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical

Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics. 2014;134(5):e1474–e1502.

2. Oakley E, Brys T, Borland M, Neutze J, Phillips N, Krieser D, Dalziel SR, Davidson A, Donath S, Jachno K, South M. Medication use in infants admitted with bronchiolitis. Emergency Medicine Australasia. 2018;30(3):389-97.

3. Guo C, Sun X, Wang X, Guo Q, Chen D. Network Meta Analysis Comparing the Effi cacy of Therapeutic Treatments for Bronchiolitis in Children. Journal of Parenteral and Enteral Nutrition. 2018;42(1):186-95.

4. Uysalol M, Haşlak F, Özünal ZG, Vehid H, Uzel N. Rational drug use for acute bronchiolitis in emergency care. Turkish Journal of Pediatrics. 2017;59(2):155-161.

5. Carsin A, Sauvaget E, Bresson V, Retornaz K, Cabrera M, Jouve E, Truillet R, Bosdure E, Dubus JC. Early Halt of a Randomized Controlled Study with 3% Hypertonic Saline in Acute Bronchiolitis. Respiration. 2017;94(3):251-7.

EDITORIAL Do Bronchiolitis Babies Like Salty Airways?


6. Angoulvant F, Bellêttre X, Milcent K, Teglas JP, Claudet I, Le Guen CG, de Pontual L, Minodier P, Dubos F, Brouard J, Soussan-Banini V. Effect of nebulized hypertonic saline treatment in emergency departments on the hospitalization rate for acute bronchiolitis: a randomized clinical trial. JAMA pediatrics. 2017;171(8):e171333.

7. Morikawa Y, Miura M, Furuhata MY, Morino S, Omori T, Otsuka M, Chiga M, Obonai T, Hataya H, Kaneko T, Ishikura K. Nebulized hypertonic saline in infants hospitalized with moderately severe bronchiolitis due to RSV infection: A multicenter randomized controlled trial. Pediatric pulmonology. 2018;53(3):358-65.

8. Kanjanapradap T, Deerojanawong J, Sritippayawan S, Prapphal N. Does nebulized hypertonic saline shorten hospitalization in young children with acute viral wheezing?. Pediatric pulmonology. 2018;53(2):138-44.

9. Heikkilä P, Renko M, Korppi M. Hypertonic saline

inhalations in bronchiolitis—A cumulative meta analysis. Pediatric pulmonology. 2018;53(2):233-42.

10. Raheja K, Prakash A, Punj A. Nebulized 3% hypertonic saline with Epinephrine Vs normal saline with Epinephrine in the Treatment of Acute Bronchiolitis in the Emergency Department. Crit Care Pediatr. 2018;1(2):35-40.

11. Zhang L, Mendoza-Sassi RA, Wainwright C, Klassen TP. Nebulised hypertonic saline solution for acute bronchiolitis in infants. Cochrane Database of Syst Rev. 2017;12:CD006458.

12. Heikkilä P, Mecklin M, Korppi M. The cost-effectiveness of hypertonic saline inhalations for infant bronchiolitis: a decision analysis. World J Pediatr. 2018;14(1):26-34.

13. Davis J, Thompson AD, Mansbach JM, Piedra PA, Kasagawa K, Sullivan AF et al. Multicenter Observational Study of the Use of Nebulized Hypertonic Saline to Treat Children Hospitalized for Bronchiolitis From 2008 to 2014. Hosp Pediatr. 2017;7(8):483-91.

How to cite this articleChugh K. Do Bronchiolitis Babies Like Salty Airways? Crit Care Pediatr. 2018;1(2):23-25

How to cite this URLChugh K. Do Bronchiolitis Babies Like Salty Airways? Crit Care Pediatr. 2018;1(2):23-25Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01023.html

EDITORIAL Do Bronchiolitis Babies Like Salty Airways?


Original ArticleClinical Service & Medical Staffi ng Patterns in Indian Pediatric

Intensive Care Units (PICUs)V.S.V. Prasad1, Aniket Parashar2

1Chief Consultant Pediatric Intensivist, 2Senior Resident, Pediatric Critical Care, Lotus Hospitals for Women & Children, Lakdikapul, Hyderabad-500004, India

Received:10-April-18/Accepted: 10-May-18/Published online:18 -Jun-18

Corresponding authorDr V.S.V Prasad, Chief Consultant Pediatric Intensivist & CEO, Lotus Hospitals for Women & Children, Lakdikapul, Hyderabad-500004Email: [email protected]

IntroductionPICUs across India have varying levels of care (Level 2 and Level 3), as well as staffi ng patterns. Studies evaluating staffi ng patterns in Intensive care units have been conducted mainly from adult

critical care units, while those conducted for PICUs are scarce.1,2 The American Academy of Pediatrics’ (AAP) and Indian Academy of Pediatrics’ guidelines for PICUs recommend round the clock in-house cover by critical care physicians for children.3,4 However very few PICUs in India have dedicated pediatric intensivists who provide their clinical time exclusively for their PICU and do not engage themselves for provision of clinical services for other specialties, such as Pediatrics, Neonatology, etc. It is

ABSTRACTObjective: To study the clinical service and medical staffi ng patterns in Indian PICUs in the private sector, government and semi-private / or charity supported hospitals.Methods: This was an e-mail and social media based cross sectional survey conducted between Aug-Sep 2017. The participants were PICU directors of Level 3 PICUs in the country. The questionnaire contained items enquiring staffi ng patterns of the doctors in the PICU along with queries pertaining to quality of care in the PICU. Data was presented descriptively using proportions, mean and standard deviation.Results: A total of 59 Level 3 PICUs participated in the survey. All the PICU were staffed by a qualifi ed Intensivists. Majority (95%) of the Intensivists worked for more than 8 hours in a day. Only 25% of the Intensivists could dedicate their time exclusively for their PICUs while the rest were also engaged in other subspecialties. Most directors and consultant intensivists of the PICUs were involved in clinical services like bedside rounds (98%), parental counseling (93%), attending bedside emergencies (91.5%) and procedures (76.3%) during routine hours. Qualifi ed intensivists were present in premises in only 32.3% of PICUs at night whereas fellows and post graduate residents provided in house physician coverage for major part of the week (84.7%). Fellows/ residents also performed patient transport in majority of the PICUs (89.8%). Majority of the PICUs had back up of other specialties at night. A greater proportion of PICUs (64.4%) reported instances of deterioration in patient condition at night. Majority of the PICUs reported compliance with quality of care indicators like infection control practices and prevention of drug errors.Conclusions: PICUs in India function as multidisciplinary units. Majority of pediatric intensivist are overburdened as they need to cover emergency hours also (as on call). However, most of patients at night were attended within the prescribed time norms (<30min) by them. Two thirds of pediatric intensivists engage in non PICU clinical activities either of their own choice and accord or as a need in allied pediatric specialties. Most of the PICUs comply with standard patient safety measures.Keywords: Intensivist, Staffi ng, PICU, India.


also well known that very few PICUs have dedicated PICU consultants (pediatric intensivists) staying overnight in the hospital premises to provide clinical cover and have either their fellows/postgraduates manning their ICUs at night. Consultant Intensivists are mostly available for emergencies from their residence, travelling and attending to their patients as and when necessary.5,6 It is also not clear if the quality of clinical service is assured after hours when the senior and consultant faculty of the PICU are not physically available in the premises. Studies indicate that the standard of patient care during afterhours is inferior to that during working hours under the care of an Intensivist.7,8 The purpose of this study is to survey the existing patterns of clinical service and medical staffi ng of PICUs in India and identify defi ciencies and gaps in patient care, so that solutions may be found by addressing these. This study aims to evaluate Level 3 PICUs (admitting a broad spectrum of common pediatric critical care patients) and does not take into account highly specialized critical care services such as pediatric and neonatal cardiac surgery, bone marrow or solid organ transplants.Study design: Cross sectional survey.

MethodologyThis is a cross sectional survey-based study. A questionnaire was designed for the survey after reviewing the literature pertaining Physician staffi ng patterns and clinical services provided in PICUs. The questionnaire contained items enquiring staffi ng patterns of the chief intensivist, consultant intensivists, fellows and post graduate resident doctors in the PICU along with queries pertaining to quality of care in the PICU. Information regarding Level 3 PICUs in the country was sought through the National registry of accredited Level 3 PICU from the website of the College of Pediatric Critical Care (www.collegeofpediatriccriticalcare.org). The PICU directors were detailed about the purpose of the study and requested to participate in the survey through a social media based and e-mail-based questionnaire (google-docs). The survey was undertaken between August and September 2017. Strict confi dentiality of the obtained data was maintained during the

performance and analysis of the survey. Survey data was entered in a suitable custom-made database and presented descriptively using proportions, mean and standard deviation.

ResultsA total of 59 Level 3 PICUs across the country participated in the survey and responded by fi lling in the google-docs form and sending them back to our center.The intensivist staffi ng patterns along with the clinical services provided during routine and after hours in the participating PICUs were as elaborated below:

1. Consultant staffi ng patternsAll the PICUs in the survey were staffed by certifi ed pediatric intensivists. Out of these 61% PICUs were staffed with at least 2 intensivists, 18.6% PICUs were staffed with 3 intensivists and 20.3% PICUs were staffed with 4 intensivists. (Fig 1).

Fig 1: Number of Intensivists staffi ng PICUs.

2. Working hours of pediatric intensivists and clinical practice patternsThe average working hours were more than 8 hours for 66.1% intensivists, up to 8 hours for 28.8% intensivists and up to 6 hours for 5.1% intensivists.Out of these 74.6% intensivists confi rmed practicing allied pediatric specialties during regular working hours and only 25.4% Intensivists dedicated their entire time exclusively for PICUs. Of the intensivists who engaged in allied

ORIGINAL ARTICLE Clinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs)


specialties, 63.8% did it on a need basis whereas 36.2% had a protected time for the same. The allied disciplines in which pediatric intensivists were engaged are shown below in (Fig 2).

Fig 2: Allied specialties practiced by Intensivists.

3. Daytime patient servicesThe directors of the PICU were available for rounds in 98.3% of the units on working days. Out of these 74.6% conducted both morning and evening rounds in their units while direct parental counselling was done by 88.1% of the directors. Bedside emergencies during daytime were attended by 91.5% of the directors, whereas 76.3% directors performed emergency and elective procedures during daytime.Parental counselling was performed by consultants after daily rounds mandatorily in 93.2% of the PICUs and documented in patient ‘s records in 72.9% of the PICUs. In addition to fellows and postgraduates, participation of consultants in parental counselling sessions was mandatory in 69.5% of the PICUs.Consultants performed all PICU procedures in almost half (49.2%) of the units and supervised 88.1% of the other half performed by critical care fellows/postgraduates.Critical care fellows conducted parental counselling on their own in 13.6% of the PICUs. They also performed critical care transport (inter hospital and intra hospital) in 89.8% of PICUs. Protected time was reserved for teaching fellows and postgraduate residents in 64.4% PICUs.

4. Night time patient servicesIntensivists were present in the premises at night in only 32.3% of PICUs in the survey. Consultant pediatric intensivists were able to attend to patients

at short notice in the majority of the PICUs. The average time required for consultants to reach their PICU at night is depicted below in (Fig 3).

Fig 3: Average time needed for on call Intensivist to reach PICU

Consultant pediatric intensivists were required for help daily at night in only 8.5% of PICUs, whereas they were needed for help twice a week in 69.5% PICUs and four times a week in 22% PICUs. Critical care fellows or post graduate residents provided in-house cover at night for the major part of the week. These fi ndings are as shown below in (Fig 4).

Fig 4: Night time cover provided by Fellows and Residents.

Fellows and postgraduate residents also performed transport of critically ill patients from referral hospitals at night in 69.5% of PICUs in the survey.The majority of PICUs had back up of other specialists at night such as Pediatric surgery (94.9%), Radiology (84.7%), Anesthesia (86.4%), Orthopedics and Neurosurgery (78%).A greater proportion of PICUs (64.4%) reported instances of deterioration in patient condition at night due to lack of better clinical surveillance. However, instances of patient mortality at night



due to the inability of fellows or residents to establish emergent airway and vascular access in a safe and timely manner was reported from fewer PICUs (13.6%). Infection control practices were ensured during night time by means of frequent interviews of staff in 72.9% PICUs and by CCTV surveillance in the facility by 27.1% PICUs. The majority of the PICUs (79.7%) did not report any instance of fatal drug errors in their units.The frequency of non-fatal drug errors reported by participating PICUs is shown below in (Fig 5).

Fig 5: Frequency of non-fatal drug errors.

DiscussionAll the PICUs (100%) in our survey functioned as closed units with at least one intensivist which is comparable to the fi gures in United States (94%), Europe (98%), and Australia (100%) and better than those reported from developing nations like Nepal (6.25%), Turkey (30%), Pakistan (19%). 9-14However, these numbers could be falsely high as all the respondents for the survey were from accredited PICUs. The number of intensivists staffi ng the PICUs which did not participate in the survey and number of existing centers without a full time Intensivist needs further study. The average number of intensivists staffi ng each PICU in our survey was 2.5±0.8. A recent international survey involving 73 centers from 34 countries reported the mean number of intensivists staffi ng PICUs as 5.5 ± 4.3.15

The average working hours was more than 8 hours for most pediatric intensivists (66.1%) in this survey which is comparable with a similar survey performed in the United States.9 Up to 75% of intensivists in this study were also engaged in other allied disciplines

such as: General Pediatrics, Neonatology etc. In contrast, a European survey of 92 PICUs which reported up to 72% intensivists dedicating their time solely for their respective PICU.10 Our study highlights the added responsibilities pediatric intensivists share in their day to day work in India, due to fewer numbers of professionals in this fi eld, as compared to other developed countries.Close to 90% of directors of PICUs in this survey were involved in patient care services such as: clinical rounds, attending bedside emergencies and parental counselling. The corresponding fi gure from the European survey is 72%.10 This greater responsibility and workload could be explained by the shortage of qualifi ed professionals in pediatric critical care in India compared to those in Europe. The day time patient care services provided by intensivists such as - clinical rounds, managing bedside emergencies, performing procedures and parental counselling were like those provided in other countries.9, 10 Round the clock (24 hours a day and 7 days a week) coverage was provided by intensivists in 96.6% of PICUs in our survey with an in-house (onsite) coverage in 32.3% of PICUs. Most of intensivists in our survey were able to attend to patients at night within the prescribed time norms (<30min). Similar surveys from United states and Europe have found these fi gures to be 68% and 78.3% respectively, however these surveys do not clearly distinguish between the type of coverage provided by the intensivists (in house or on call from home).9,10 Such a coverage was provided by intensivists on call from home as per a survey from Turkey.13

Critical care fellows and postgraduate residents provided direct clinical in-house cover at night and carried out transport of patients from referral hospitals for majority of the PICUs in this study. A great number of PICUs provided protected teaching time for fellows and postgraduate residents. This training and teaching module was like that followed in other countries.9,10,13,16

Up to two thirds of the PICUs in the survey reported instances of deterioration in patient condition at night due to lack of better clinical surveillance and a minority also reported mortality due to inability



of fellows to manage patients appropriately and independently.The evidence from studies comparing outcomes in ICUs with 24/7 in house intensivist coverage versus those without, is mixed. Most of them have shown a reduced length of PICU stay with in-house intensivist coverage, but no difference in mortality rates.16-18

Close to three quarters of the PICUs in this study reported no fatal drug errors in patients and almost all PICUs ensured infection control practices were followed. These are encouraging fi ndings and highlight the importance of following standardized bundles and checklists for ensuring patient safety.19

Further studies are needed to estimate the actual proportion of patients affected by non-compliance with patient safety measures.A greater proportion of PICUs in the survey had the back up of other specialties such as radiology, anesthesiology, surgery, neurosurgery, orthopedics etc. thus functioning as multidisciplinary units. These estimates concur with a recent international survey evaluating availability of resources for PICUs in high income and low middle-income countries.15

This is one of the fi rst surveys reporting physician staffi ng patterns and clinical services being provided at Level 3 PICUs in the country. We had a good response rate to the survey and hence believe that this data represents the current pediatric intensive care practices across the country. Our survey details the work profi le of ICU directors and pediatric intensivists in the country, which has not been addressed before.With the present evidence, there is a need to improve pediatric intensivist staffi ng in PICUs in the country as this is one of the rapidly growing sectors of child health care. A short-term solution to the problem of understaffi ng would be to adopt a shift model of working for pediatric intensivists thereby ensuring round the clock coverage. The obvious long-term measure would be to train more critical care pediatricians through fellowship programs carefully designed to allow adequate skills acquisition and knowledge along with confi dence in functioning independently across the nation.

Conclusions from the survey1. This is probably the fi rst survey of Level 3 PICUs

across India scattered across public, semi private / charitable and private institutions on medical staffi ng patterns.

2. The majority of PICUs have the good culture of the director and consultant pediatric intensivists providing direct patient care for the most part of the day.

3. Night time coverage of all PICUs is mostly by fellows in training and postgraduates, supported by consultants as back up from home. Clinical vigilance probably needs to be addressed after hours, as instances of errors and patient deterioration have been reported in most centers.

4. Majority of pediatric intensivist are overburdened as they need to cover emergency hours also (as on call). However, most of patients at night were attended within the prescribed time norms (<30min) by them.

5. Two thirds of pediatric intensivists engage in non PICU clinical activities either of their own choice and accord or as a need in allied pediatric specialties.

6. The study has not addressed the staffi ng patterns of those PICUs which did not participate in the survey. Little is known about units manned by part time emergency care pediatricians and intensivists supported by general pediatricians

Confl ict of Interest: NoneSource of Funding: None

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patterns and clinical outcomes in critically ill patients: A systematic review. JAMA 2002; 288:2151–2162

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care units in India. Indian Pediatr. 2002; 39(1):43–55. Parshuram CS, Kirpalani H, Mehta S, et al; for the Canadian

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6. Pronovost PJ, Thompson DA, Holzmueller CG, et al: The organization of intensive care unit physician services. Crit Care Med 2007; 35:2256–2261

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8. Arias Y, Taylor DS, Marcin JP. Association between evening admissions and higher mortality rates in the pediatric intensive care unit. Pediatrics 2004; 113: 530–4.

9. Odetola FO, Clark SJ, Freed GL, Bratton SL, Davis MM. A national survey of pediatric critical care resources in the United States. Pediatrics. 2005;115(4): e382–6.

10. Nipshagen MD, Polderman KH, DeVictor D, et al: Pediatric intensive care: Result of a European survey. Intensive Care Med 2002; 28:1797–1803.

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12. A Khanal, A Sharma, S Basnet. Current state of pediatric

intensive care and high dependency care in Nepal. Pediatr Crit Care Med 2016; 17:1032–40

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How to cite this articlePrasad VSV, Parashar A. Clinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs). Crit Care Pediatr. 2018;1(2):26-31

How to cite this URLPrasad VSV, Parashar A. Clinical Service & Medical Staffi ng Patterns in Indian Pediatric Intensive Care Units (PICUs). Crit Care Pediatr. 2018;1(2):26-31Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01024.html



Original ArticleIntermittent Dose of Propofol for Parenteral sedation in Outpatient

Pediatric MRI - A single centre experienceBhaskar Saikia1, Pradeep Kumar Sharma2, Rachna Sharma3, Praveen Khilnani4

1Senior Consultant, Pediatric Intensive Care Unit, Max Super Speciality Hospital, 2Senior Consultant and Head, Pediatric Critical Care and Pulmonology, Sri Balaji Action Medical Institute, 3Senior Consultant, Pediatric Intensive Care Unit, B L Kapur Super Speciality Hospital, 4Clinical Director and Senior Consultant, Pediatric Critical Care and

Pulmonology, Rainbow Children Hospital, New Delhi, IndiaReceived:10-April-18/Accepted: 10-May-18/Published online:18-Jun-18

Corresponding authorDr Rachna Sharma, Senior Pediatric Intensive Care Unit, B L Kapur Super Speciality Hospital, New Delhi, IndiaEmail: [email protected]

ABSTRACTObjective: To study effi cacy and safety of intermittent dose of Propofol for outpatient Pediatric MRI sedation.Design: Retrospective AnalysisSetting: Outpatient MRI in pediatric age group at Tertiary care HospitalSubjects: Retrospectively 114 patients underwent MRI under parenteral sedation from April 2010 to March 2013. Complete data was available for 107 patients and subsequently analyzed.Measurement and Main Results: All patients underwent MRI sedation as per pre-formed protocol. Premedication consisted of intravenous (IV) Atropine 0.01 mg/kg. Sedation was induced with IV Propofol 2mg/kg and maintained with intermittent IV propofol 1-2 mg/kg as and when required basis with maximum permissible dose of 10mg/kg. Outcome measures were induction time, recovery time, cardio-respiratory events, cumulative dose and sedation failure. Median age was 3 years with range from 2 months to 15 years. Mean induction time was 1.45±0.6 minutes with range from 1- 3 minutes. Mean total cumulative dose was 4.36±0.9mg/kg. Mean recovery time after the procedure was 6±1.9 minutes. Two patients developed itching and macular rash and two had apnea during procedure. One procedure could not be completed due to apnea.Conclusion: Intermittent small doses of propofol are safe and effi cacious for pediatric ambulatory MRI. Our regimen of propofol alone for pediatric MRI sedation has rapid induction, recovery time and few respiratory complications.Keywords: Propofol; Parenteral Sedation; Magnetic resonance imaging; Pediatric

IntroductionA stay still period of 30 to 60 minutes or more is necessary for MRI. Children commonly require sedation for the same due to a noisy and claustrophobic environment. Due to provision of images with improved resolution, frequency of these procedures on an outpatient basis has been on the rise. The use of general anaesthesia is not ideal in this situation, due to the time involved for induction, recovery and the side effects to the patient. An effective, effi cient and

ideal sedative protocol for MRI in children is still not available. The ideal sedative agent for pediatric MRI should have a rapid onset, rapid recovery, with minimal hemodynamic effects. Propofol as sedative agent has a rapid onset, rapid recovery, minimal residual effects and less hemodynamic interaction and it has been used as a standalone sedative in adults for day care procedures. We have used this agent alone for past several years for outpatient MRI in pediatric age group at our centre.

Material and MethodsOurs is a tertiary care multispecialty centre, having


5-7 pediatric MRI’S on outpatient basis every month. We follow a pre-formed propofol based protocol for sedation. Our protocol requires patients to have minimum 4 hours of fasting. Age, weight sex and allergic history to egg and any medication were recorded. Heart rate, blood pressure and airway assessment were done prior to sedation. Premedication with atropine (0.01 mg/kg, minimum 0.2 mg, maximum 0.6 mg) was done. Atropine was given to prevent sudden transient bradycardia associated with propofol. Oxygen at 4 liters/min was administered during procedure. Induction dose of 2mg/Kg was used; subsequent doses given were 1mg/kg if required before 10 minutes and 2mg/kg if required after 10 minutes of last dose on as and when required basis. Maximum permissible cumulative dose was 10mg/kg. Heart rate and oxygen saturation were monitored during the procedure. Respiration is monitored by intensivist clinically during the procedure. Induction time, recovery time, total cumulative dose and any cardio-respiratory events were recorded. Retrospectively 114 patients underwent MRI under parenteral sedation from April 2010 to March 2013. Complete data was available for 107 patients and subsequently analyzed. The study is approved by Institutional review board via vide no BLK/IRB/SP/2014/01.

ResultsMedian age was 3 years and age ranged from 2 months to 15 years. Out of 107 cases, 65 (60.7%) were males and 42 (39.5%) were females. Out of 107 MRI, 94 were brain, 5 spine, 4 brain & spine, 2 abdomens and one each lower limb& MR angiogram brain. Mean induction time was 1.45±0.6 minutes with range from 1- 3 minutes. Mean total cumulative dose was 4.36±0.9 mg/kg. 51 (47.6%) patients required cumulative dose of 4mg/kg, 36 (33.6%) required 5mg/kg, 12 (11.2%) required 3mg/kg, 4 required 6mg/kg, 2 required 8 mg/kg and one patient required 2 mg/kg. Mean recovery time after the procedure was 6±1.9 minutes. (Table 1) Two cases developed itching and macular rash after propofol, responded to anti-histaminic however both completed the procedure. A 2-month-old child with Arnold chiari type-2 malformation had apnea immediately after fi rst dose of propofol without desaturation and bradycardia. Child received less than 2 minutes of bag and mask

ventilation for revival and procedure was carried out, however intensivist decided to use only 1mg/kg of propofol for subsequent doses. Child required 3 more dose for MRI brain and spine and no further complication was recorded. One patient aged 11 months with cerebral palsy had stridor and desaturation after induction dose, requiring bag and mask ventilation for 10 minutes. Procedure was aborted.

Table 1: Main ResultsNumber of patients 107

Male: Female 65:42Mean Induction time 1.45±0.6 minutes

Mean Cumulative dose 4.36±0.9 mg/kgRecovery time 6±1.9 minutes

Rash and itching 2(0.02%)Apnea 2(0.02%)

DiscussionThe empirical formula of propofol (2,6- diisopropylphenol) is C12H18O and it is formulated in a white, oil-in-water emulsion. Current formulations consist of 1% or 2% (w/v) propofol, 10% soya bean oil, 1.2% egg phosphatide, and 2.25% glycerol. Propofol exerts its sedative-hypnotic effects through a GABAA receptor interaction. The onset of action of propofol is within 40 seconds with a peak effect of 1 minute. Infusions of propofol in doses commonly employed for conscious sedation inhibit the normal protective respiratory refl exes including the hypoxic ventilatory drive and normal response to hypercarbia.1 Concomitant use of opioids intensifi es the inhibition of these refl exes.2 In addition, there is a dose-dependent relationship to the propensity of upper airway collapse. Effects on the respiratory system include a dose-dependent reduction in minute ventilation, tidal volume, and functional residual capacity. Propofol, like benzodiazepines, has anxiolytic effect at doses that do not induce sedation.3, 4Propofol is a poor analgesic.5 Only sedation and anxiolysis with no need of analgesia is required for MR, propofol seems to be an ideal agent in paediatrics.The most studied regimes are multi-drugs combinations. In recent propofol based sedation in MRI comprising 500 pediatric patients, the authors used midazolam, nalbuphine and propofol bolus (1mg/kg) followed by continuous propofol infusion of 5mg/kg/hr. Their

ORIGINAL ARTICLEIntermittent Dose of Propofol for Parenteral sedation in Outpatient Pediatric MRI

- A single centre experience


mean induction time was 2 min, sedation time 55 min, and recovery time 8 min. Additional sedation was necessary in 2.2% and, mild respiratory events occurred 1%.6 The induction, recovery and complication rate are comparable with our study except cumulative dose is less in our group. Hasan et al used propofol infusion in 115 children and they found total dose of propofol was 4.3 ±1.7 mg/kg body weight. The mean duration of sedation induction was 4.5 ± 3.5 mins. The recovery time was 20 ± 15 mins. No episodes of hypoxia, apnea, or a need for artifi cial airway were noted.7 An RCT compared intermittent dose versus continuous infusion of propofol in 170 children with 75 in group continuous and 95 in intermittent groups. Continuous group required a lesser dose of propofol (132 ± 54μg/kg/min) compared to intermittent group (162 ± 74 μg/kg/min). No differences were seen between the two groups about quality of the imaging study, recovery time, or incidence of complications.8 The dose used in this study for intermittent group is higher than our group. They used 2-4mg/kg as loading dose. Also, continuous infusion requires MRI compatible infusion pump and advance monitoring devices. Chen et al also found intermittent propofol to be safe and effective in 120 pediatric MRI 9. Studies comparing propofol with other agents like pentobarbital, fentanyl and midazolam showed that Propofol is more effective and effi cient and offered signifi cantly shorter sedation induction time, recovery time and total sedation time.10, 11

ConclusionIntermittent dose of propofol can be effectively and safely used for pediatric MRI, however a pre-evaluation of airway and continuous monitoring is mandatory. Our study shows that intermittent small dose of propofol is safe and effi cacious for pediatric ambulatory MRI.Confl ict of interest: no confl icts of interestFunding: NoneEthical clearance: Manuscript is cleared by

Institutional review board via vide no BLK/IRB/SP/2014/01

References1. Morgan, G.E., Mikhail, M.S., & Murray, M.J. Nonvolatile

anesthetic agents. In G.E. Morgan, Jr., M.S. Mikhail, & M.J. Murray (Eds.) Clinical anesthesiology. 4th ed.New York: Lange Medical Books/McGraw-Hill Medical Publishing Division/Mosby. 2002. pp. 200-202

2. Stoelting, R.D., & Miller R.D. Intravenous anesthetics. In R.K. Stoelting & R.D. Miller (Eds.). Basics of anesthesia. 4th ed. Philadelphia: Churchill Livingstone. 2000. pp. 58-61

3. Smith I, Monk TG, White PF, Ding Y. Propofol infusion during regional anesthesia: sedative, amnestic, and anxiolytic properties. Anesth Analg. 1994; 79(2):313-319

4. Ito H, Watanabe Y, Isshiki A, Uchino H. Neuroprotective properties of propofol and midazolam, but not pentobarbital, on neuronal damage induced by forebrain ischemia, based on the GABAA receptors. Acta Anaesthesiol Scand 1999; 43:153–162

5. Godambe SA, Eliot V, Matheny D. Comparison of propofol/fentanyl versus ketamine/midazolam for brief orthopedic procedural sedation in a pediatric emergency department. Pediatrics. 2003; 112:116-123

6. Machata AM, Willschke H, Kabon B, Kettner SC and Marhofer P. Propofol-based sedation regimen for infants and children undergoing ambulatory magnetic resonance imaging. British Journal of Anaesthesia 2008; 101 (2): 239–43

7. Hasan RA, Shayevitz JR, Patel V. Deep sedation with propofol for children undergoing ambulatory magnetic resonance imaging of the brain: experience from a pediatric intensive care unit. Pediatr Crit Care Med. 2003; 4(4):454-8

8. Hassan NE, Betz BW, Cole MR, Wincek J, Reischman D, Sanfi lippo DJ, Winterhalter-Rzeszutko KM, Kopec JS. Randomized controlled trial for intermittent versus continuous propofol sedation for pediatric brain and spine magnetic resonance imaging studies. Pediatr Crit Care Med. 2011; 12(6):e262-5

9. Chen YL, Chen CC. Intermittent small doses of propofol for sedation of pediatric patients undergoing magnetic resonance imaging. Acta Paediatr Taiwan. 2007; 48(6):305-8

10. Mallory MD, Baxter AL, Kost SI. Propofol vs pentobarbital for sedation of children undergoing magnetic resonance imaging: results from the Pediatric Sedation Research Consortium. Paediatr Anaesth. 2009; 19(6):601-11

11. Pershad J, Wan J, Anghelescu D L. Comparison of Propofol With Pentobarbital/ Midazolam/Fentanyl Sedation for Magnetic Resonance Imaging of the Brain in Children. Pediatrics 2007;120: e629-36

How to cite this articleSaikia B, Sharma PK, Sharma R, Khilnani P. Intermittent dose of Propofol for parenteral sedation in Outpatient Pediatric MRI- A single centre experience. Crit Care Pediatr. 2018;1(2):32-34

How to cite this URLSaikia B, Sharma PK, Sharma R, Khilnani P. Intermittent dose of Propofol for parenteral sedation in Outpatient Pediatric MRI- A single centre experience. Crit Care Pediatr. 2018;1(2):32-34Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01025.html

ORIGINAL ARTICLEIntermittent Dose of Propofol for Parenteral sedation in Outpatient Pediatric MRI

- A single centre experience


Original Article Nebulized 3% Hypertonic Saline with Epinephrine Vs Normal Saline

with Epinephrine in the Treatment of Acute Bronchiolitis in the Emergency Department

Karan Raheja1, Ashish Prakash2, Azay Punj3

1Consultant and In-charge Pediatric Intensive Care, 2Senior Consultant and HOD, Department of Pediatrics Yashoda Hospital, Ghaziabad, 3Professor, Department of Pediatrics, Subharti Medical College, Meerut, India


ABSTRACTObjective: To determine whether nebulized 3% hypertonic saline with epinephrine is more effective than nebulized 0.9% saline with epinephrine in the treatment of bronchiolitis in the emergency department.Methods: Randomized, double blind, control trial.Results: 120 patients were enrolled and 110 were evaluated. The two study groups had almost similar baseline characteristics. All the data for hypertonic saline & normal saline was expressed in terms of mean & SD respectively. Further, by paired t test, a signifi cant difference was observed at 5% level of signifi cance in Respiratory Distress Assessment Instrument (RDAI), SPO2, change in Respiratory rate & change in Heart rate in hypertonic & normal saline groups respectively. However, by using unpaired t test, a signifi cant difference was observed in the differences of different characteristics between two groups at 5% level of signifi cance, further a high improvement in RDAI, SPO2, Change in Respiratory Rate & change in Heart rate was observed in hypertonic saline as compared to normal saline.Conclusions: Results of this double blind randomized control trial suggest that administration of hypertonic saline (3%) with epinephrine by nebulizer in infants aged 12 months or younger presenting with acute bronchiolitis in ED causes statistically signifi cant improvement in terms of RDAI score, respiratory rate, SPO2 as compared to normal saline with epinephrine. There was no increase in heart rate in both the groups.Keywords: Acute Bronchiolitis, Hypertonic Saline, Epinephrine and Normal Saline

IntroductionAcute viral Bronchiolitis (AVB) is the most common lower respiratory tract disease in infants worldwide1. Respiratory syncytial virus (RSV) is the most important pathogen responsible for acute bronchiolitis. The morbidity and mortality due to RSV infection is greatest in infants younger than 3 months and in those with known risk factors such as prematurity, congenital heart disease and tobacco smoke exposure2. AVB is clinically characterized by an episode of respiratory distress, presence of

wheezing, crackles, signs of upper respiratory track infection, and fever (Rectal temperature>38OC). The currently accepted treatment (Adequate hydration, supplementary oxygen and aspiration of upper respiratory tract secretions) remains as non-controversial3. Nebulized epinephrine is commonly used for treatment of bronchiolitis in children having signifi cant respiratory distress. A Cochrane review and meta analysis examining the effi cacy of epinephrine in bronchiolitis concluded that there is some evidence that epinephrine may be favorable compared with salbutamol and placebo in outpatients4,

5. Nebulized hypertonic saline is another modality of treatment. Nebulized hypertonic saline has been shown to improve mucociliary clearance and sputum expectoration in patients with cystic fi brosis and

Corresponding authorDr Karan Raheja, Consultant and In- charge PICU, Yashoda Hospital, Nehru Nagar, Ghaziabad, U.PMob: 9899311517, Email: [email protected]


with mucociliary dysfunction6,7. It is hypothesized that hypertonic saline may be useful in bronchiolitis by absorbing water from the sub mucosa, thereby decreasing edema and improving mucociliary function. A study done by Grewal in 20098 showed no clinically signifi cant improvement in clinical severity with hypertonic saline with epinephrine in emergency setting compared with normal saline when a maximum of 2 doses were used. Further research is needed to determine whether hypertonic saline with epinephrine dose, in fact, have a role in the treatment of bronchiolitis in the ED setting. So, we conducted this study to compare the effi cacy of 3% NS with epinephrine versus Normal saline with epinephrine in acute bronchiolitis in ED settings.

Material and MethodsA randomized double blind clinical study involving 109 children was undertaken between Oct-2011 to March 2012 in department of Pediatrics, Subharti Medical College Meerut, to compare the Effi cacy of nebulized hypertonic saline with epinephrine and normal saline with epinephrine in acute bronchiolitis. Ethical approval for the study was taken from the ethical committee of the institute. Departmental review board approved the Protocol for study. Infant aged between 6 weeks to 12 months presenting with fi rst episode of bronchiolitis (defi ned as the fi rst episode of wheezing and clinical symptoms of a viral respiratory infections) an initial oxygen saturation of 85% or more on arrival to the emergency department (ED) and their initial respiratory distress assessment instrument (RDAI) score was 4 or higher. Infant with history suggestive of, born at ≤ 34-week gestation, Congenital heart disease, H/o of apnea with in 24 hours before presentation, chronic cardiopulmonary

disease, immune defi ciency past history of respiratory disease requiring nebulization and critical illness at presentation were excluded. Infants with a history of use of systemic or nebulized bronchodilators or nebulized hypertonic saline in last 24 hours were also excluded from study. The study medicines were epinephrine with 3% NS and epinephrine with normal saline. Physician working in the ED performed a standard history and physical examination on all infants and assessed them for study eligibility. The study was double blind and comparative in nature to assess the effects of two drugs on the above-mentioned parameters. The randomization scheme was generated by the pharmacy using the website randomization.com (http:// www.randomization.com). Our pharmacy also prepared 2.5ml aliquots of 3% hypertonic saline and 2.5ml aliquots of a second, indistinguishable solution of normal saline. The solutions were similar in appearance and smell stored in identical syringes, labeled only by a code number and place in the research cupboard with in the ED. The randomization was concealed by the pharmacy until completion of study. When the salt solution was given to the patient, the ED nurse added 0.5ml of epinephrine to the randomization solution and the total mixture of 3ml was given to patient by nebulization. Because the randomization process was determined by the pharmacy, emergency physicians, house staff, nurse, study personnel and patients remained blinded to treatment allocation throughout the study. Each group received one nebulization every 30 minutes for 4 hours of the random designated drug. The following base line clinical characteristics were recorded initially and after giving nebulization. Viz Respiratory rate (RR), Hear rate (HR), Oxygen saturation in room air (SPO2), Respiratory distress score by (RDAI)

Points maximum Variable 0 1 2 3 4 points Wheezing Expiration None End ½ ¾ All 4 Inspiration None Part All NA NA 2 Location None Segmental, ≤ of 4 lung fields Diffuse, ≥ 3 of 4 lung fields NA NA 2 Retractions Supraclavicular None Mild Moderate Marked NA 3 Intercostal None Mild Moderate Marked NA 3 Subcostal None Mild Moderate Marked NA 3

ORIGINAL ARTICLE Nebulized 3% Hypertonic Saline with Epinephrine Vs Normal Saline with Epinephrine in the Treatment of

Acute Bronchiolitis in the Emergency Department


Respiratory Distress Assessment InstrumentThe study was double blind and comparative in nature to assess the effects of two drugs on the above-mentioned parameters. A sample of size 109 patients was studied to detect the signifi cant difference between pre to post interventional study in Hypertonic saline = 54 & normal saline =55 by using formula 4σ2/E2 for qualitative data. The samples were collected randomly & RDAI, SPO2, Change in respiratory rate & change in HR was studied in normal & hypertonic saline groups. The least permissible lesson was .0231 with a power of 85% between two groups.

ResultsOf 120 patients agent 6 week to 12 months presenting in ED with acute bronchiolitis, 109 patients were

enrolled and randomized to treatment with either hypertonic or normal saline with epinephrine.Enrollment and Outcomes

Allocated to Epinephrine with Hypertonic saline (n=54)

Analyzed (n=54) Analyzed (n=55)

Allocated to Epinephrine with normal saline (n=55)

120 patients Assessed for eligibility (n=120)

Randomized (n=109)

Excluded (n=11)Ineligible (n=10) d/t CHD, prematurityConsent was not given (n=1)

Table 1: Presentation of Mean & S.D., signifi cant difference b/w pre-& post treatment (By paired “t” test) and their P- values for different characteristics in Hypertonic SalineS. No.

Characteristics Hypertonic Saline (Mean ± S.D.) Difference (Mean ± S.D.)

Probability of Paired- t TestPre-Treatment Post Treatment

1 R.D.A.I. 11.9074± .9763 6.1296± .7017 5.7777±1.3552 .0000*2 SPO2 92.0926±1.5451 97±1.1655 -4.9074±.9570 .0000*3 Change in respiratory Rate 61.2407±2.8479 54.9444±2.1841 6.2963±1.5373 .0000*4 Change in heart Rate 114.8704±4.5143 117.6481±4.5315 -2.7777±.9648 .0000*

*P<.05 shows a signifi cant difference at .05 level of signifi cance.

Table 2: Presentation of Mean & S.D., signifi cant difference b/w pre-& post treatment (paired “t” test) and their P- values for different characteristics in Normal SalineS. No.

Characteristics Normal Saline (Mean ± S.D.) Difference (Mean ± S.D.)

Probability of Paired-t TestPre- treatment Post treatment

1 R.D.A.I. 12.1091±.7116 9.5272±.92004 2.5818±.6580 .00002 SPO2 91.7636±1.4913 94.9273±.8336 -3.1636±1.1828 .00003 Change in respiratory Rate 61.1091±2.4012 58.4±2.3381 2.7091±.8959 .0000

4 Change in heart Rate 117.9815±1.9569 121.6296±2.8701 -3.6482±1.1518 .0000*P<.05 shows a signifi cant difference at .05 level of signifi cance.

Table 3: Signifi cant difference (By unpaired “t” test) B/W the differences in HYPERTONIC & NORMAL SALINE for different characteristicsS. No.

Characteristic Difference in Hypertonic Saline

Difference in Normal Saline

Probability of “t” (unpaired)

1 R.D.A.I. 5.7777±1.3552 2.5818±.6580 .00002 SPO2 -4.9074±.9570 -3.1636±1.1828 .00003 Change in respiratory Rate 6.2963±1.5373 2.7091±.8959 .00004 Change in heart Rate -2.7777±.9648 -3.6482±1.1518 .0000





Table 4: Percentage Changes (improvement/ decrement) from pre to post observations in different characteristicsS. No.

Characteristics % Improvement in hypertonic saline (pre- post)

% Improvement in normal saline (pre-post)

1 R.D.A.I. 48.52% 21.32%2 SPO2 -5.33% -3.45%3 Change in respiratory Rate 10.28% 4.43%4 Change in heart Rate -2.418% -3.09%

Table 5: Base Line Profi le of Different Patients (N=109) Enrolled in The StudyS. No. Characteristics Hypertonic Saline (Group 1) Normal Saline ( Group 2) P-value*1 Age (Months) 5-6 5-6 .1528.2

SexMale 58% 60% .3581Female 42% 40% .2581

3 Duration of Illness Before Admission (Days)

3±2.1 3.4±21 .1284

4 Family History of Asthma 5% 7% .08745 Active Smoking 2% 1% .0623.6 Previous E D Visit .2% .1% .09827 Infants Treated with Antibiotics Before

Study Entry5% 4% .2343


All the data for hypertonic saline & normal saline was expressed in terms of mean & SD respectively (Table 1 & 2). Further, by paired t test, a signifi cant difference was observed at 5% level of signifi cance in RDAI, SPO2, change in Respiratory rate & change in Heart rate in hypertonic & normal saline groups respectively. However, by using unpaired t test, a signifi cant difference was observed in the differences of different characteristics between two groups at 5% level of signifi cance (Table 3) further a high improvement in RDAI, SPO2, Change in Respiratory Rate & change in Heart rate was observed in hypertonic saline as compared to normal saline (Table 4).

DiscussionEpinephrine has a theoretical effect on acute bronchiolitis because it contains alpha-adrenergic properties, which lead to vasoconstriction and reduction of airway edema.9 However, a recent Cochrane Review showed that nebulized epinephrine for acute bronchiolitis results in a modest short-term improvement in outpatients, but not among inpatients.10 Hypertonic saline solution has been shown to increase mucociliary clearance in normal

patients, in asthma, bronchiectasis, cystic fi brosis and sinonasal diseases.11-14 Such benefi ts would also be expected in infants with acute bronchiolitis.15 The postulated mechanisms of benefi t are as follows: 1) hypertonic saline induces and osmotic fl ow of water into the mucus layer, rehydrating the airway surface liquid and improving mucus clearance15; 2) hypertonic saline breaks the ionic bonds within the mucus gel, thereby reducing the degree of cross linking and entanglements and lowering the viscosity and elasticity of the mucus secretion16; 3) hypertonic saline stimulates clinical beat via the release of prostaglandin E2.17 Moreover, by absorbing water from the mucosa and sub mucosa. Hypertonic saline solution can theoretically reduce edema of the airway wall in infants with acute bronchiolitis.15 Hypertonic saline inhalation can also cause sputum outside of the bronchi and thus improve airway obstruction. The above-mentioned theoretical benefi ts provide the rationale for the treatment of acute bronchiolitis with nebulized hypertonic saline solution. Results of this double blind randomized trial suggest that administration of Hypertonic saline (3%) with epinephrine by nebulizer in infants aged 12 months or younger presenting with acute bronchiolitis in ED causes statistically signifi cant improvement in terms




of RDAI score, R.R., SPO2 as compared to normal saline with epinephrine. There was no increase in heart rate in both the groups. To our knowledge, this is the positive study examining the role of hypertonic saline with epinephrine in treatment of bronchiolitis in the ED setting. Prior to this only one study Grewal et al 2009 was done which showed no clinically signifi cant improvement in clinical severity with hypertonic saline with epinephrine in the emergency setting compared with normal saline with epinephrine. When a maximum of 2 dose were used however, there seemed to be trend toward decreased rates of hospitalization in the hypertonic saline group. Our results differ from Grewal study (2009), it may be because of small number of participants, the small number of inhalation (up to two doses) and short monitoring time (up to 120 minutes post inhalation) in Grewal study. Another study published in 201418 of treatment of bronchiolitis with hypertonic saline, hospitalized patients were randomized to receive repeated dose of either hypertonic saline or normal saline in addition to routine bronchodilator therapy approximately 5 times a day in addition to the study solution. Authors found a clinically relevant reduction in length of hospital study in the hypertonic saline group that resembles to our study. The other studies19-21 also points toward the benefi ts of 3% Normal saline. There was approximately a one-day reduction in the duration of hospitalization. The pooled results from these four trials demonstrate that nebulized 3% saline could produce reduction of 1.16 day in the mean length of hospital stay. This represents a 24.1% reduction from the mean length of hospitalization in the normal saline group. This reduction may be considered clinically relevant. Another study example published in 2016, showed use of hypertonic saline treatment in bronchiolitis in inpatient and ED was better in comparison to normal saline22. Clinical score is generally considered a relatively objective measure to assess the severity of illness. There are two clinical severity-scoring systems more commonly used by randomized trials involving infants with viral bronchiolitis. One is a Respiratory Distress Assessment Instrument (RDAI) which assesses chest retractions and auscultatory fi ndings, and provides a score ranging from 0 to 17, with a higher score indication more severe

respiratory distress.23 The other scoring system, initially described by Wang, assesses respiratory rate, wheezing, retraction and general condition, providing a score ranging from 0 to 12, with increased severity receiving a higher score.24 The pooled results from these trials demonstrate a statistically signifi cant lower mean post-inhalation score among infants treated with 3% saline inhalation compared to those treated with 0.9% saline inhalation in the fi rst three days of treatment. The magnitude of reduction in the severity score produced by 3% saline inhalation may be considered clinically relevant because it represents a reduction of up to 30% from the mean clinical score in the 0.9% saline group. The benefi ts of nebulized 3% saline in improving clinical score are observed in both outpatients and inpatients. These all four studies also favor our results although present study was done in ED setting.In our study there were no apparent adverse effects attributable to the use of HS with a bronchodilator, although the numbers were insuffi cient to allow further exploration of this issue. Adverse effects encountered with the use of hypertonic saline are rare and infrequent. Wark and McDonald described and excellent safety profi le for hypertonic saline after studying 143 patients with severe cystic fi brosis who were treated with hypertonic saline solution inhalations. There is a reported risk of bronchospasm and of decreased ciliary beat frequency; however, these are usually only seen with higher concentrations of hypertonic saline (>7%). In our study, we used a 3% hypertonic saline solution to decrease the risk of the above adverse effects. In addition by giving the hypertonic saline with epinephrine, a bronchodilator any additional bronchoconstriction effect secondary to the hypertonic saline was avoided.Confl ict of Interest: NoneSource of Funding: None

References1. Phelan PD, Olinsky A, Robertson CF, Respiratory Illness in

children Oxford, England: Blackwell Scientifi c; 1994:71-77.2. Simoes EAF, Carbonell-Estrany X. Impact of severe disease

caused by respiratory syncytial virus in children living in developed countries. Ped Inf Dis J. 2003;22(2) (Suppl): S13-S20.




3. American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. Diagnosis and management of bronchiolitis Pediatrics 2006; 118:1774-93.

4. Hartling L, Wlebe N, Russell K, Patel H, Klassen TP. A meta-analysis of randomized controlled trials evaluating the effi cacy of epinephrine for the for the treatment of acute viral bronchiolitis. Arch Peditr Adolesc Med. 2003;157(10):957-964.

5. Hartling L, Wiebe N, Russell K, Patel H, Klassen TP. Epinephrine for bronchillitis. Cochrane Database Syst Rev. 2004;(1):CD003123.

6. Daviskas E, Robinson M, Anderson SD, Bye PT. Osmotic Stimuli increase clearance of mucus in patients with mucociliary dysfunction. J Aerosol Med. 2002;15(3):331-341.

7. Wark PA, McDonald V. Nebulized hypertonic saline for cystic fi brosis, Cochrane Database Syst Rev. 2003;(1):CD001506.

8. Grewal S, Ali S, McConnell DW, Vandermeer B, Klassen TP. A randomized trial of nebulized 3% hypertonic saline with epinephrine in the treatment of acute bronchiolitis in the emergency department. Archives of Pediatrics & Adolescent Medicine 2009;163(11):1007–12.

9. Wohl MEB, Chernick V. State of the art: bronchiolitis. American Review of Respiratory Diseases 1978; 118:759–81.

10. Hartling L, Wiebe N, Russell K, Patel H, Klassen TP. Epinephrine for bronchiolitis. Cochrane Database of Systematic Reviews 2004;1:CD003123

11. Daviskas E, Anderson SD, Gonda I, Eberl S, Meikle S, Seale JP, et al. Inhalation of hypertonic saline aerosol enhances mucociliary clearance in asthmatic and healthy subjects. European Respiratory Journal 1996;9(4):725–32.

12. Kellett F, Redfern J, Niven RM. Evaluation of nebulised hypertonic saline (7%) as an adjunct to physiotherapy in patients with stable bronchiectasis. Respiratory Medicine 2005;99(1):27–31.

13. Shoseyov D, Bibi H, Shai P, Ahoseyov N, Shazberg G, Hurvitz H. Treatment with hypertonic saline versus normal saline nasal wash of pediatric chronic sinusitis. Journal of Allergy and Clinical Immunology 1998;101 (5):602–5.

14. Wark PAB, McDonald V, Jones AP. Nebulised hypertonic saline for cystic fi brosis. Cochrane Database of Systematic Reviews 2007:4:CD001506

15. Mandelberg A, Amirav I. Hypertonic saline or high volume normal saline for viral bronchiolitis: Mechanisms and rationale. Pediatr Pulmonol 2010; 45:36–40.

16. Ziment I. Respiratory pharmacology and therapeutics. Philadelphia, PA: WB Saunders, 1978:60-104

17. Assouline G, Leibson V, Danon A. Stimulation of prostaglandin output from rat stomach by hypertonic solution. European J of Pharmacol 1977; 44:271–3.

18. Wu S, Baker C, Lang ME, Schrager SM, Liley FF, Papa C, Mira V, Balkian A, Mason WH et al. Nebulized hypertonic saline in the treatment of viral bronchiolitis in infants. JAMA Pediatr 2014; 168(10):971-75.

19. Luo Z, Liu E, Luo J, Li S, Zeng F, Yang X, et al.Nebulized hypertonic saline/salbutamol solution treatment in hospitalized children with mild to moderate bronchiolitis. Pediatr International 2010;52: 199–202.

20. Mandelberg A, Tal G, Witzling M, Someck E, Houri S, Balin A, et al.Nebulized 3% hypertonic saline solution treatment in hospitalized infants with viral bronchiolitis. Chest 2003; 123:481–7.

21. Tal G, Cesar K, Oron A, Houri S, Ballin A, Mandelberg A. Hypertonic saline/epinephrine treatment in hospitalized infants with viral bronchiolitis reduces hospitalization stay: 2 years experience. Israel Med Asso J 2006; 8:169–73.

22. Hypertonic Saline for the Treatment of Bronchiolitis in Infants and Young Children: A Critical Review of the Literature. Jeffrey Baron and Glagys El-Chaar J Pediatr Ther.2016; 21(1):7-26.

23. Lowell DI, Lister G, Von Kloss H, McCarthy P. Wheezing in infants: the response to epinephrine. Pediatrics 1987; 87:939–45.

24. Wang EE, Milner RA, Navas L, Maj H. Observer agreement for respiratory signs and oximetry in infants hospitalized with lower respiratory infections. American Rev of Resp Dis 1992; 145(1):106–9.

How to cite this articleRaheja K, Prakash A, Punj A. Nebulized 3% hypertonic saline with Epinephrine Vs normal saline with Epinephrine in the Treatment of Acute bronchiolitis in the Emergency Department. Crit Care Pediatr. 2018;1(2):35-40

How to cite this URLRaheja K, Prakash A, Punj A. Nebulized 3% hypertonic saline with Epinephrine Vs normal saline with Epinephrine in the Treatment of Acute bronchiolitis in the Emergency Department. Crit Care Pediatr. 2018;1(2):35-40Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01026.html




IntroductionAlexander Fleming, during his Nobel Prize acceptance speech, spoke of the potential organisms to develop resistance to penicillin due to overuse and under dosing. Since Fleming’s lecture in 1945, almost as a prediction, antimicrobial resistance evolved slowly and now has attained an alarming speed.1 Methicillin resistant Staphylococcus aureus(MRSA) emerged in hospitals and the community in the 1990’s. Around the same time Vancomycin resistant enterococcus (VRE) was reported. In the late 1980s extended-spectrum beta-lactamases (ESBLs) appeared, although third generation cephalosporins (e.g. ceftriaxone, ceftazidime) had only been introduced nine years earlier. The increased use of carbapenems (e.g. meropenem, imipenem) during the 2000s resulted in the development of carbapenem resistant Enterobacteriaceae (CRE). Thus, every few years there are reports of antibiotic resistant microbes that prompt a series of predictions about “the end of antibiotics”.2-4

Multidrug resistant organisms (MDRO) are defi ned as

bacteria that have become resistant to more than one class of antimicrobial agents, complicating treatment of illnesses they cause. Currently, two-thirds of all health-care-associated infections (HAIs) are caused by just six MDRO referred to by the acronym ESKAPE: Enterococcus species (vancomycin resistant, VRE), Staphylococcus aureus (methicillin resistant, MRSA; intermittent or resistant to vancomycin, VISA/VRSA), Klebsiella pneumoniae and Enterobacter species (extended-spectrum beta-lactamase-producing gram-negative bacilli, ESBLs and fl uoroquinolone-resistant (P.aeruginosa).4-6

One of the reasons for antibiotics losing their effectiveness is because of their inappropriate use. Studies have shown, repeatedly, that up to 50% on antibiotic prescriptions are either unnecessary or inappropriate. In addition to reducing antibiotic overuse, it is important to prevent the transmission of resistant organisms through the implementation of effective infection prevention and control (IPC) measures. IPC and antibiotic stewardship (AS) programs need to be inseparable sides of the same coin in the battle against MDROs.

Infection PreventionThe traditional IPC practices are optimal if practised

Review ArticleSynergy of Antimicrobial Stewardship and Infection Prevention and Control

Aparna Chakravarty1, Chandrasekhar Singha2

1Assistant Professor, Department of Pediatrics, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi, India, 2Senior Consultant, Madhukar Rainbow Children’s Hospital, Malviya Nagar, New Delhi, India


ABSTRACTThe emergence of multidrug resistant organisms (MDROs) have become a major public health threat. With a dry antibiotic pipeline and rising resistance, existing antimicrobials need to be used very cautiously. In addition to reducing antibiotic overuse, it is important to prevent the transmission of resistant organisms through the implementation of effective infection prevention and control (IPC) measures. Antimicrobial Stewardship (AS) is an inter-professional effort to optimise the use of antimicrobials for the best clinical outcome and have an impact on minimising antimicrobial resistance (AMR). Leveraging the synergy of IPC and antimicrobial stewardship (AS) programs has become key strategy in the battle against MDROs.Keywords: Multidrug resistant organisms; Infection prevention and control; Antimicrobial stewardship; Antimicrobial resistance

Corresponding authorDr. Aparna Chakravarty, Assistant Professor, Department of Pediatrics, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi. Mob: +919910995545, Email: [email protected]


robustly. The basic IPC paradigm (Figure 1) is intrinsically simple. The effective application of interventions to broadly prevent pathogen transmission have proven to be challenging.

HCW Hands Patient Environment

MDRO’s in Patients

Exposed Patients

ISOLATION

DISINFECTION HAND

HYGIENE

Fig 1. Optimizing infection control in healthcare settings.

The following infection control practices should be integrated for a good outcome.7

1. IsolationSince ancient times the intrinsic value of isolation practice has been recognized. Patients with highly transmissible or epidemiologically important pathogens need to be identifi ed and isolated along with standard precautions.Standard Precautions: Applied to all patients always, regardless of diagnosis and infection status. Essential for protection of patient, health care workers and visitors which include• Hand hygiene• Use of personnel protective equipment (PPE)• Appropriate handling of patient care equipment

and soiled linen• Prevention of needlestick and/ sharp injuries• Environmental cleaning and spills management• Appropriate handling of waste.1.1. Transmission-based precautions: Specifi c

to the mode of transmission which include• Airborne precautions• Droplet precautions• Contact precautions1.1a. Airborne precautions

Airborne transmission occurs when droplet nuclei <5 micron in size are disseminated in the air and remain

suspended for long periods of time. Diseases which spread by this mode include active pulmonary tuberculosis, measles, chickenpox, pulmonary plague and hemorrhagic fever with pneumonia. Airborne precautions are designed to reduce the transmission of airborne diseases include• Standard precautions,• Patient in single room with negative

airfl ow pressure (“negative pressure room”)

• Anyone entering the room must wear a special, high fi ltration particulate respirator (e.g. N95) mask.

1.1b Droplet precautionsDiseases, which are transmitted by this route, include pneumonias, pertussis, diphtheria, infl uenza type B, mumps and meningitis. Droplet transmission occurs when there is adequate contact between the mucous membranes of the nose and mouth or conjunctivae of a susceptible person and large particle droplet (>5microns). Droplets are usually generated during coughing, sneezing and talking. The following precautions need to be taken• Standard precautions• Place patient in a single room or

cohort with a patient with similar illness

• Wear surgical mask when working within 1-2 metres of the patient.

1.1c. Contact precautionsDiseases which are transmitted by this route include colonization or infection with multiple antibiotic resistant organisms, enteric infections and skin infections. Precautions measures include• Standard precautions• Place patient in a single room or

cohort with patients infected with the same pathogens.

REVIEW ARTICLE Synergy of Antimicrobial Stewardship and Infection Prevention and Control


• Wear a clean, non-sterile gown when entering the room if substantial contact with the patient or patient environment is anticipated.

2. Hand hygiene2.1 Proven benefi ts

After centuries of knowledge, it is now known that Semmelweis was right, and that hand-washing is an effective way to prevent HAIs. All the modern technologies and other intricate tools used to prevent HAIs can be nullifi ed if healthcare workers (HCWs) do not wash their hands. The fi ve moments of hand hygiene outlined by WHO are: Before patient contact, before aseptic task, after bodily fl uid exposure, after patient contact and after contact with patient surroundings.8

2.2 Lack of compliance and changing habits:Despite these guidelines and good awareness of hand hygiene among HCWs, the adherence to hand hygiene is usually around 50-60%. One potential reason for low compliance is that the target is invisible. HCWs do not realize that they are carrying pathogen in their hands because they are invisible. Another potential excuse for lack of compliance is the cost of time for HCWs. A very potent reason is cited that HCWs never develop a habit for hand hygiene. The act of hand hygiene needs to be “hardwired’ so that one does it on a subconscious level.

2.3 Objective monitoringThe gold standard in monitoring hand hygiene compliance is direct observation by different observers on rotating basis. Even though the reliability of this method to measure actual compliance is questionable, direct observation still has a benefi t. Direct observation reminds people to wash hands and over time, this reinforcement has an impact on the number of people who do hand hygiene.9,10

3. Environmental disinfectionEnvironmental decontamination has emerged as an important, evidence-based strategy to

decrease infection and improve patient safety. The role of surfaces in the transmission of many HAIs (MRSA, VRE, C. diffi cile, Acinetobacter, Pseudomonas, and others) and many viral pathogens (norovirus, rotavirus, adenovirus, infl uenza virus) raises the possibility that disinfection of near-patient surfaces can favorably impact HAI transmission. Although MDRO are resistant to many antibiotics, they are sensitive to properly used disinfectants. Moreover, no data are available that show that antibiotic-resistant bacteria are less sensitive to liquid chemical germicides than the antibiotic-sensitive bacteria at currently used germicide contact conditions and concentrations.11 Detergents /disinfectants that best meet the overall needs of the healthcare facility for routine cleaning and disinfection should be selected.12,13 These products which include sodium hypochlorite and quaternary ammonium chloride disinfectants must always be used as recommended by the manufacturer with particular attention being paid to compliance with directions for dilution and contact time with the surface to be disinfected.During a suspected or proven MDRO outbreak where an environmental reservoir is suspected the following steps should be taken:a. Routine cleaning procedures should be

reviewed along with assessment for need for additional trained cleaning staff.

b. Adherence should be monitored and reinforced to assure consistent and correct cleaning is performed.

c. Room cleaning of patients on contact precautions should be prioritized.

The following briefl y summarizes the infection prevention practices for optimal results.

1. Identify, monitor and report MDRO trends: look for newly emerging Gram-negative resistance.

2. Analyze and report HAIs.3. Partner with healthcare personnel to achieve

highly compliant standard and transmission-based precautions practices aimed at preventing cross transmission of pathogens.

4. Promote compulsive hand hygiene.



5. Implement care bundle checklists to reduce the risk of developing device or surgical procedure-associated infections.

6. Promote adoption of clinical treatment guidelines7. Incorporate stewardship activities into the annual

infection prevention risk assessment, based on the facility antibiogram, outbreak investigations, and antimicrobial/microbe focus reviews

8. Leverage on electronic surveillance system for timely data and reporting.

Antimicrobial Stewardship

Defi nitionAntimicrobial Stewardship (AS) is an inter-professional effort, across the continuum of care which involves timely and optimal selection, dose and duration of an antimicrobial for the best clinical outcome for the treatment or prevention of infection with minimal toxicity to the patient with minimal impact on resistance and other ecological adverse effect such as C.diffi cile.14 According to CDC, AS is the right antibiotic for the right patient, at the right time, with the right dose and the right route, causing the least harm to the patient and future patients.The need for implementing antimicrobial stewardship in hospitals1. Antimicrobial use (misuse and overuse)

With the misuse through use without a prescription and overuse for self-limiting infections, bacterial resistance has appeared and is growing fast. Antibiotic use in hospitals and the community is common and up to 50% of antimicrobial use is inappropriate. 15-17

2. Antimicrobial resistanceWorld Health Organisation has identifi ed antimicrobial resistance as a major public health threat. This is due to the lack of new antibiotics in the development pipeline and infections caused by the MDROs becoming diffi cult to treat.

Goals of antimicrobial stewardshipThe major goals of having antimicrobial stewardship programs in hospitals have been outlined as:1. Improve Patient Outcome and Safety

• Improving infection cure rates and reducing surgical site infection rates

• Overall reduce mortality and morbidity• Minimize adverse effects of antimicrobials• Reduce antimicrobial use, without increasing

mortality or hospital-acquired infections.18

2. Reduce MDROs• Restricting relevant agents can reduce

colonization or infection with Gram-positive or Gram-negative resistant bacteria.

3. Reduce Healthcare Cost• Reducing antibiotic costs can achieve savings

greater than the cost of the intervention.

Implementation of Antimicrobial Stewardship Programs (ASP)The key elements identifi ed for implementing ASP in hospitals include1. Leadership and accountability

The program must be supported by the hospital administration, who takes the leadership in implementation and are accountable for the outcomes. The ASP team members must possess expertise, credibility and leadership. The team should promote the culture of optimal antibiotic use within the facility.

2. Institution-based needAnalyse individual situation and problems to be addressed. Implementation will depend on local needs/issues, available skills/expertise and other resources. Easier and less costly approaches include- Simple clinical algorithms- Prescribing guidance for treatment, surgical

prophylaxis- Promoting intravenous (IV) to oral conversion- Provision of microbiological support- Restricting availability of certain antibiotics

(formulary restriction)- Promoting education19

3. Set up a structured teamA multidisciplinary AS team with core members being- an Infectious diseases physician or a lead



physician- a clinical microbiologist- a clinical pharmacist with expertise in infectionOther members should be infection prevention nurses, quality improvement/patient safety managers, clinicians with an interest in infection and drugs and therapeutics committee.

4. Well-defi ned priorities and measurement frameworkThe objectives of the ASP and how they are going to be achieved need to be agreed by all the key stakeholders and communicated clearly. Producing a Driver Diagram can help to achieve this goal. Example of an ASP Driver Diagram is available at www.cdc.gov/getsmart/healthcare.

5. Customize effective interventionsIn the Infectious Diseases Society of America (IDSA) guidelines 18 many stewardship interventions have been reviewed. It is best to start with the core strategies before adding some of the supplementary strategies. Strategies with strong evidence of benefi ts include- Formulary restrictions and preauthorization

(Front-end strategy)- Prospective audit with intervention and

feedback (Back-end strategy)- Streamlining and timely de-escalation of

therapy- Dose optimization- Parenteral to oral conversion19

- Guidelines and clinical pathwaysOther supplementary strategies include- Antibiotic order forms- Education- Laboratory surveillance and feedback- Antibiotic cycling- Using computer-based surveillance

6. Measurements for feedback and improvement“If you cannot measure it, you cannot improve it- Lord Kelvin”.Audit and feedback on antimicrobial prescribing should be provided regularly to prescribers in

the critical care setting areas of high quality antimicrobial use.Another way of evaluating prescribing within a unit or hospital is through regular point prevalence surveys (PPS).20,21 Regular surveillance of antimicrobial use and resistance over a period of time and monitoring trends in a single-ward can help defi ne targeted interventions. Hospital wide antimicrobial expenditure and the rate of intravenous antimicrobial use can be measured to estimate the healthcare cost.

7. Regular education and trainingThe key component of any ASP is education. Education of all healthcare professionals from all care settings as well as patients and public are required.Teaching should be included in the undergraduate curriculum, internship training, postgraduate education and training of the nursing staff.The content of education should include• Basic knowledge of infection control and

prevention• Basic microbiology• Importance of rational antimicrobial prescribing• Best practices for prescribing, administration

and monitoring of antimicrobial therapy.The training should be followed by competency assessment.

8. Communication skillsSimple and clear communication with core clinical messages should show the goals and benefi ts of the program. The importance of using data for communicating, sharing and learning is also useful. Face-to-face meetings with prescribers, to refl ect on their prescribing practices or attending multi-disciplinary teams are important in promoting learning about prudent prescribing.

9. InnovationThe need to change the core elements of ASP with more innovative strategies suited for the healthcare setting. Ensuring early and short-term gains and then consolidating the win and progressing forward with changes remains key to success of the program.



Synergy of Infection Prevention and Control (IPC) and Antimicrobial Stewardship (AS) ProgramsIPC and AS share a common goal- patient safety and improved patient outcome. AS is an important synergistic HAI prevention and control strategy. AS programs have been shown to improve patient outcomes, reduce antimicrobial agents-related adverse events, and decrease AMR.21 Furthermore, AS programs, when implemented alongside IPC measures, especially hand hygiene interventions, were more effective. Therefore, a well-functioning IPC program is fundamental to a successful organizational AS program. 21-26 IPC and AS programs are not independent of each other. There is a need for deliberate strategic relationship-building of IPC and AS program leaders. This could help achieve the larger purpose of keeping patients safe from infections along with saving effective antibiotic therapy for future generations.Confl ict of Interest: No confl icts of interestFunding: None

References1. “Sir Alexander Fleming - Nobel Lecture: Penicillin”.

Nobelprize.org. Nobel Media AB 2014. Available from: http://www.nobelprize.org/nobel_prizes/medicine/laureates/1945/fl eming-lecture.html. Accessed on 20 March 2018.

2. Raygada J L, Levine D. P. Methicillin-Resistant Staphylococcus aureus: A Growing Risk in the Hospital and in the Community. American Health & Drug Benefi ts. 2009;2(2):86–95.

3. Cetinkaya Y, Falk P, Mayhall C G. Vancomycin-Resistant Enterococci. Clinical Microbiology Reviews. 2000;13(4): 686–707.

4. Paterson, D. L, Bonomo, R A. Extended-Spectrum ß-Lactamases: A Clinical Update. Clinical Microbiology Reviews. 2005;18(4):657–686.

5. Hidron, A, Edwards J, Patel J, Horan T, Sievert D, Pollock, D et al. Antimicrobial-Resistant Pathogens Associated with Healthcare-Associated Infections: Annual Summary of Data Reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007. Infect Control & Hosp Epidemiol. 2008;29(11):996-1011.

6. Perez F, Van Duin, D. Carbapenem-resistant Enterobacteriaceae: A menace to our most vulnerable patients. Cleveland Clin J Med. 2013;80(4):225–233.

7. Michael JS, Paul H, Veeraraghavan B. Components of Infection Control Practice in Healthcare Settings. Hospital Infection Control Guidelines. Indian Council of Medical Research (ICMR) 2016: Pages 1-25.

8. WHO Guidelines on Hand Hygiene. Available from: http://www.whqlibdoc.who.int/publications/2009. Accessed on 20 March 2018.

9. Magill S, Edwards JR, Wendy B, Beldavs Z G, Dumyati G, Kainer MA et al. Multistate Point-Prevalence Survey of Health Care- Associated Infections N Engl J Med. 2014; 370:1198-1208.

10. Pineles L, Morgan D J, Limper H M, Weber S G, Thorn KA, Perencevich EN et al. Accuracy of a Radiofrequency Indentifi cation (RFID) badge System to Monitor Hand Hygiene behavior during routine clinical activities. Am J Infect Control. 2014; 42:144-147.

11. William A. Rutala, Ph.D., M.P.H., David J. Weber, M.D., M.P.H. and the Healthcare Infection Control Practices Advisory Committee (HICPAC), CDC Guideline for Disinfection and Sterilization in health care facilities 2008. Available from: http://www.cdc.gov/hicpac/pdf/guidelines/Disinfection_Nov_2008.pdf . Accessed on 20 March 2018.

12. Guidelines for Environmental Infection Control in Health-Care Facilities. Recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee (HICPAC). MMWR 2003;52 (RR10):1-42.

13. Rutala WA, Weber DJ. Disinfection and sterilization in health care facilities: What clinicians need to know. Clin Infect Dis 2004;39(5):702-9.

14. Nathwani D. Antimicrobial stewardship. In: Hospital epidemiology and infection Control; Ed: C.Glen Mayhall; 4th Edition, Philadelphia, Lippincott, Williams and Wilkins, 2012.

15. Hoffman JM, Shah ND, Vermuelen LC. Projecting future drug expenditures. Am J Health Syst Pharm 2007;64:298-314.

16. John JF, Fishman NO. Programmatic role of the infectious diseases physician in controllingantimicrobial costs in the hospital. Clin Infect Dis 1997;24:471-485.

17. Wise R, Hart T, Cars O, Streulens M, Helmuth R, Huovinen P, et al. Antimicrobial resistance is a major threat to public health. BMJ 1998;317:609–610.

18. Dellit TH, Owens RC, McGowan JE Jr., Gerding DN, Weinstein RA, Burke JP et al. Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America Guidelines for Developing an Institutional Program to Enhance Antimicrobial Stewardship. Clin Infect Dis. 2007;44:159-77.

19. Goff DA, Bauer KA, Reed EE, Stevenson KB, Taylor JJ, West JE. Is the “Low-Hanging Fruit” Worth Picking for Antimicrobial Stewardship Programs? Clin Infect Dis. 2012;55:587–92.

20. Ansari F, Erntell M, Goossens H, Davey P. The European Surveillance of Antimicrobial Consumption (ESAC) point prevalence survey of antibacterial use in 20 European hospitals in 2006. Clin Infect Dis. 2009;49:1496-504.

21. Seaton RA, Nathwani D, Burton P, McLaughlin C, MacKenzie AR, Dundas S et al. Point prevalence survey of antibiotic use in Scottish hospitals utilising the Glasgow Antimicrobial Audit Tool (GAAT). Int J Antimicrob Agents 2007; 29:693-9.



22. Septimus E, Weinstein RA, Perl T, Goldmann DA, Yokoe DS. Approaches for preventing healthcare-associated infections: go long or go wide? Infect Control Hosp Epidemiol 2014;35:797–801.

23. Baur D, Gladstone BP, Burkert F, Carrara E, Foschi F, Döbele S et al. Effect of antibiotic stewardship on the incidence of infection and colonisation with antibiotic-resistant bacteria and Clostridium diffi cile infection: a systematic review and meta-analysis. Lancet Infect Dis 2017;17: 990–1001.

24. Valiquette L, Cossette B, Garant M-P, Diab H, Pepin J. Impact of a reduction in the use of high-risk antibiotics on

the course of anepidemic of Clostridium diffi cile–associated disease caused by the hypervirulent NAP1/027 strain. Clin Infect Dis 2007;45:S112–S121.

25. Dodds Ashley ES, Keye KS, DePestel DD, Hermsen ED. Antimicrobial stewardship: philosophy versus practice. Clin Infect Dis 2014;59:S112–S121.

26. Kelly AA, Jones MM, Echevarria KL, Kralovic SM, Samore MH, Goetz MB, et al. A report of the efforts of the Veterans Health Administration national antimicrobial stewardship initiative. Infect Control Hosp Epidemiol 2017;38:513–520

How to cite this articleChakravarty A, Singha C. Synergy of Antimicrobial Stewardship and Infection Prevention and Control. Crit Care Pediatr. 2018;1(2):41-47

How to cite this URLChakravarty A, Singha C. Synergy of Antimicrobial Stewardship and Infection Prevention and Control. Crit Care Pediatr. 2018;1(2):41-47Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01027.html



Case Report and Review of LiteratureNegative Pressure Pulmonary Edema

in a Case of Adeno-tonsillectomyManish Kori1, Krishan Chugh2, Vikas Taneja3

1Associate Consultant, Pediatric Intensive Care, 2Director and Head, Department of Pediatrics, Fortis Memorial Research Institute, Gurugram, Haryana, India 3Senior Consultant, Pediatrics and PICU,

Manipal Hospitals Dwarka, New Delhi, IndiaReceived:10-April-18/Accepted: 26-May-18/Published online:18 -Jun-18

ABSTRACTNegative Pressure Pulmonary Edema (NPPE) is an important cause of acute pulmonary edema in cases associated with correction of upper airway obstruction due to various causes. We describe a case of NPPE in a 2-year-old boy who developed sudden onset pulmonary edema post adenotonsillectomy and required mechanical ventilation. We review the relevant literature and discuss implications for Pediatric Intensivists.Keywords: Negative Pressure Pulmonary Edema; Neurogenic Pulmonary Edema, PEEP; ARDS; Noninvasive Ventilation.

Corresponding authorDr Krishan Chugh, Department of Pediatrics, Fortis Memorial Research Institute, Sector -44, Opposite HUDA City Centre, Gurugram, Haryana-122002.Email: [email protected]

IntroductionNegative pressure pulmonary edema (NPPE), also known as Post Obstructive Pulmonary Edema (POPE), is a rare but important cause of sudden onset pulmonary edema in certain cases of severe upper airway obstruction (type 1 NPPE) or rapid relief of chronic upper airway obstruction.1 Understanding the pathophysiology of NPPE and anticipating its occurrence could help to avoid prolonged ventilation and complications in certain high-risk situations. We describe a case of negative pressure pulmonary edema in the immediate post-operative course requiring positive pressure ventilation and review the literature.

Case ReportA 2 year 3-month-old child, weight 10 kg, height 85 cm, presented with tonsillar hypertrophy and noisy breathing at rest and sleep disturbance for 6 months. He had bilateral kissing tonsils on examination. He underwent adenotonsillectomy under general anesthesia (induction with sevofl urane and

maintenance on fentanyl and dexmedetomidine). His pre-surgery hemoglobin was 12.9 and chest X ray was normal, while lateral neck x ray showed gross narrowing of airway because of enlarged adenoids. He was ventilated during surgery on volume control ventilation with rate-26, tidal volume (Vt)-100 ml, positive end expiratory pressure (PEEP) 4, and fraction of inspired oxygen (FiO2-0.5. Reversal was done with neostigmine and glycopyrrolate. He was extubated in the operation theater. He immediately developed suprasternal and subcostal retractions and was started on oxygen by face mask of 5 L/min with initial saturations of 100 %. He also developed stridor in the observation room which gradually increased. He was shifted to Pediatric Intensive Care Unit (PICU) in view of the non-resolving respiratory distress. He was started on injection dexamethasone and epinephrine nebulisation. In view of the fall in SpO2 and increasing work of breathing he was intubated with modifi ed rapid sequence intubation and started on pressure control mode of ventilation with 100 % FiO2, rate 30, Peak Inspiratory pressure (PIP) 15, PEEP 5, inspiratory time 0.8 seconds. His blood gas pre-intubation had a pH of 7.002, pCO2 118, pO2 67, HCO3 27.9 with lactate 1.4. His pressure requirement gradually increased in the fi rst hour after intubation. He had an episode of endotracheal bleed after 1 hour, after which settings were increased to


PIP of 18 with a PEEP of 10. His chest radiograph was suggestive of pulmonary edema (Figure 1.a). He also developed hypotension, which was managed by intravenous fl uids and dopamine infusion. Sedation was optimized, and intermittent muscle relaxation was added in view of the pulmonary bleed. There were 3 episodes of fresh bloody secretion in endotracheal tube in the fi rst 2 hours. In view of the chest x ray suggestive of pulmonary edema, furosemide was added after 5 hours as an infusion. There was gradual decline in the pressure requirement. Chest radiograph at 16 hours showed marked improvement. (Figure 1.b) There was rapid improvement in oxygenation and FiO2 was tapered from 1 to 0.6 followed by reduction in PEEP from 10 to 5 over next 24 hours. There was no further episode of pulmonary bleed. Furosemide was continued for 24 hours. Sedation was tapered off on day 2. It was planned to do fl exible bronchoscopy before extubation to evaluate for any preexisting trachea-bronchomalacia and laryngeal inlet obstruction. A 2.8 mm ID bronchoscope was passed through the endotracheal tube (ET). There was no signifi cant tracheomalacia and mucosa appeared healthy. He was extubated in the bronchoscopy suite for evaluation of subglottic area. He developed immediate desaturation with suprasternal and subcostal retractions with reduced air entry bilaterally. Following extubation, there was severe subglottic edema on bronchoscopic evaluation. He was reintubated with 3.5 mm cuffed tube and started on ventilation again. Intravenous steroids were continued. Mechanical ventilation was given for 2 days. He was re-evaluated by fl exible bronchoscopy which showed resolution of edema in the subglottic region. Chest X ray pre-extubation was normal. (Figure1.c) He was extubated in the bronchoscopy suite which he tolerated well. He was observed in PICU for 1 day followed by transfer to wards. Our patient had a history of snoring and sleep disturbance since approximately 6 months. He was evaluated for pulmonary issues preoperatively and was not found to have any pulmonary issues. No preoperative blood gas was available. Our initial bicarbonate level was 27.9, suggesting absence of chronic respiratory acidosis in our patient.

Fig 1.a. Post intubation X ray showing pulmonary edema

Fig 1.b. Chest X ray at 16 hours post intubation, resolution of pulmonary edema

Fig 1.c. Chest X ray pre-extubation, further clearing of lung fi elds

Discussion

HistoryNegative pressure pulmonary edema was fi rst described in 1927 by Moore et al in an animal experiment where inspiratory obstruction was noted to cause pulmonary congestion.2 Warren et al. described the pathophysiology in 1942.3 Capitanio et al. (1973) reported acute onset pulmonary edema in two children with croup and epiglottitis.4 Oswalt et al (1977) described perhaps the fi rst clinical incidence of NPPE in 3 adult patients who experienced acute onset pulmonary edema after acute severe upper airway obstruction.5 In the adult population it has mostly been reported by anesthesiologists, common association being with acute laryngospasm (type 1 NPPE).6, 7 In a retrospective review of 27 consecutive

CASE REPORT AND REVIEW OF LITERATURE Negative Pressure Pulmonary Edema in a Case of Adeno-tonsillectomy


adult patients, 3 (11 %) were found to have developed NPPE. No specifi c factors related to NPPE within this population were found.8 In a retrospective study on 30 adult surgical patients, the incidence of NPPE was found to be nearly 0.1%.9 This condition may be underreported in view of lack of identifi cation and misdiagnosis.10 NPPE is of two types. Type 1 NPPE is associated with acute severe airway obstruction like laryngospasm, croup, epiglottitis, strangulation, endotracheal tube obstruction etc. Type 2 NPPE is associated with precipitous relief of chronic airway obstruction from various causes like tonsillar-adenoidectomy, upper airway tumor, choanal stenosis etc. (Table 1)

Table 1: Common causes of NPPE based on typesType 1 NPPE Type 2 NPPEAcute airway obstruction Precipitous relief of chronic

airway obstructionEpiglottitisCroupLaryngospasmForeign body aspirationStrangulationHangingEndotracheal tube obstructionLaryngeal tumorNear drowningPost-operative vocal cord paralysis

Post tonsillectomy/adenoidectomyPost removal of upper airway tumorPost relief of Choanal StenosisPost repair of hypertrophic uvula

PathophysiologyNPPE develops with a forceful inspiration against upper airway obstruction e.g. laryngospasm. This is a type of Muller’s maneuver.11 NPPE is a type of Non-cardiogenic pulmonary edema. Sudden increase in negative intrathoracic pressure to the magnitude of -50 to-100 cmH2O against normal intrathoracic pressure of -5 to -10 cm H2O causes a sudden increase in venous return to the right ventricle and the pulmonary circulation, increased negative intrathoracic pressure also causes fall in extramural hydrostatic pressure. This creates a pressure gradient and fl uid now moves from a higher to a lower pressure area hence out of the pulmonary capillaries and into the lung interstitial space.12 Hypoxia leads to increased pulmonary vascular resistance. These changes lead to right ventricle dilatation, which causes the interventricular septum to shift to

left causing left ventricular diastolic dysfunction resulting in increased microvascular intramural hydrostatic pressure. The negative transmural pressure also increases left ventricular afterload. Left ventricular dysfunction causes rise in left ventricular end diastolic pressure, which results in increased left atrial and pulmonary pressures, further increasing the hydrostatic pressures in the pulmonary capillaries. Thus, collected extra fl uid does not clear even after the removal of the pressure gradient and relief of obstruction. After a point, alveolar fl uid accumulation occurs.13 The resulting hypoxemia if uncorrected by increasing inspired oxygen and PEEP, leads to increase in pre and post capillary pulmonary vascular resistance and pulmonary capillary pressures.4,14,15 Also, various authors have described the molecular mechanisms of altered pulmonary endothelial cell permeability in response to wall stress (linear stress) and oxidative stress causing increased permeability pulmonary edema in NPPE.9,10 Type 1 NPPE is most commonly associated with acute airway obstruction as already described. However, Siddik-Sayyid et al reported a case of NPPE in a 35-year-old patient on reversal of neuromuscular blockade.16 They postulate that the reason for development of NPPE was a functional airway obstruction due to patient ventilator asynchrony. This creates a physiology like acute upper airway obstruction cases with similar cardiorespiratory interactions.9 A similar case was reported by Hyeon Lee et al. 17 Derks et al reported occurrence of NPPE in case of hanging in a 16-year-old girl. They described the development of NPPE after initial resuscitation and after mechanical ventilation for 4 days.18 The main differential diagnosis in such cases is Neurogenic Pulmonary Edema (NPE). Early onset of Neurogenic pulmonary edema (NPE) also presents with acute onset hypoxemia with pink frothy sputum and bilateral infi ltrates on chest radiograph. There is resolution of symptoms within 24 to 48 hours. NPE may persist with delayed resolution in patients with ongoing brain injury.19 Neurogenic pulmonary edema is because of an intense central sympathetic discharge which causes severe generalized vasoconstriction leading to acutely increased systemic vascular resistance. There is a similar hyperadrenergic state in cases of



NPPE as well.9 There is movement of fl uid into the pulmonary circulation from the systemic side. There is some hydrostatic component also because of the increased blood volume in the pulmonary circulation. The increased intravascular pressure also causes increased permeability across the alveolar-capillary membrane.18

The pathophysiology of type 2 NPPE is less well described. It is postulated that because of the chronic airway obstruction, there is development of a certain level of auto PEEP with some occult pulmonary interstitial fl uid. As the obstruction is relieved acutely, the auto PEEP is removed, and lung volumes and pressure return to normal, creating a negative intrapulmonary pressure, which if severe enough may lead to transudation of fl uids into the lung interstitium and alveoli. This type of NPPE is less common.20,21 NPPE is more common in young adults and adolescent population. The possible explanation is the ability to generate higher negative intrathoracic pressures.10 NPPE has been reported to cause a rare reversible cardiomyopathy syndrome like acute coronary syndrome in adults.22 Goldenberg et al reported an association of cardiac anomalies with the development of NPPE in 1997.23 The onset of pulmonary edema after extubation is usually relatively rapid (minutes) although it may be delayed in certain cases. The reason for the delayed manifestation may be the positive pressure effect of expiration against closed glottis which prevents fl uid accumulation.24 It is therefore important to observe high risk patients closely in the post-operative course.

Clinical manifestationsInitially symptoms and signs are suggestive of increased work of breathing, including suprasternal and subcostal retractions, tachypnea, increase in oxygen requirement to maintain SpO2, bilateral crackles and wheeze. There is worsening of hypoxemia as NPPE develops. There is a transition from agitation to lethargy as respiratory status worsens. In severe cases there is onset of pink frothy sputum or tracheal secretions, and increased PEEP and FiO2 requirement to correct the hypoxemia. Hypotension may develop in view of left ventricular systolic dysfunction and decreased venous return. As was seen in our case, there is usually relatively

rapid resolution of the symptoms on appropriate management, as compared to acute respiratory distress syndrome (ARDS), as the alveolar capillary membrane is believed to be intact, unlike in ARDS.25

DiagnosisRapid onset of hypoxemia with development of frothy bloody pulmonary secretions and development of bilateral infi ltrates in the lung fi elds requiring positive pressure ventilation in a high-risk situation usually clinches the diagnosis. Other possibilities to be considered in the post-operative setting are Transfusion Associated Lung Injury (TRALI) and pulmonary edema due to other causes like anaphylaxis, lymphatic insuffi ciency in cases like post lung transplant.26 Differentiating between hydrostatic and increased permeability pulmonary edema requires measurement of pulmonary edema fl uid protein to plasma protein concentration ratio. Cases of NPPE have been mostly associated with an edema fl uid/ plasma protein ratio of < 0.65, which is suggestive of hydrostatic pulmonary edema. A ratio between 0.65-0.75 can have a mixed cause. A ratio of >0.75 is usually associated with high permeability edema. It is important that the samples are collected before resolution of the pulmonary edema begins. Hydrostatic pulmonary edema fl uid usually contains erythrocytes along with some monocytes. Increased permeability pulmonary edema fl uid usually has greater neutrophil concentration than hydrostatic pulmonary edema.27 Some authors postulate a role of high permeability edema as the high negative intrathoracic pressure may lead to disruption of alveolar-capillary membrane. Ruling out one of the two mechanisms is diffi cult and probably etiology may be multifactorial with hydrostatic pulmonary edema having more signifi cant contribution.9 Chest radiograph reveals diffuse interstitial and alveolar infi ltrates. Radiological features common in NPPE are septal lines, peribronchial cuffi ng and central alveolar edema.28 The distribution of the infi ltrates is more central and in the nondependent regions in contrast to the more dependent distribution in ARDS. The postulated reason for this distribution is the more negative gradient of the pleural and interstitial pressures. Radiological features of hydrostatic and increased permeability are similar



except for presence of more patchy and peripheral distribution in increased permeability edema.29Chest Computed Tomography (CT) is usually not needed for diagnosis.1

Another similar condition is re-expansion pulmonary edema. It is more common in cases where pleural effusion is associated with pneumothorax and in cases with spontaneous pneumothorax. Various authors have reported the occurrence of rapid hypoxemia with bilateral infi ltrates needing oxygen, noninvasive ventilation (NIV) and invasive ventilation in some cases.30-32 Pathophysiology of this entity is also related to the preexisting negative pleural pressures. Although hydrostatic mechanisms predominate, stress induced basement membrane dysfunction produces high permeability edema also.33

ManagementManagement involves anticipation of the condition. Patients may develop rapid hypoxemia and desaturation. Ongoing obstruction must be relieved depending upon the cause (laryngospasm/ laryngeal edema may need further intubation, surgical removal in cases of upper airway structural obstruction or tracheostomy). Baseline heart ailments need to be ruled out ideally in all patients as coexisting heart condition like hypertrophic cardiomyopathy or valvular regurgitation may contribute to development of NPPE.23 All high-risk cases should ideally be extubated under controlled conditions and preferably monitored in PICU. It is advised that extubation should be done in an awake patient, without stimulating the patient or removing the tube in a deep plane to avoid risk of laryngospasm. Use of topical or intravenous laryngeal anesthesia (2 % lidocaine) has been recommended to prevent laryngospasm.34 Early reversal of neuromuscular blockade by agents like sugammadex may lead to generation of early high negative intrathoracic pressures contributing to NPPE, as reported by Ji Hyeon Lee et al.17 A trial of NIV may be given if the condition is identifi ed early with intact sensorium and respiratory drive in the patient. Oxygen supplementation should begin preferably with a high concentration non- rebreathing mask. Blood gas helps to quantify the degree of hypoxemia and hypercapnia. High PEEP

requirement and high negative intrathoracic pressures may cause hypotension in the post intubation period which is managed by fl uids and vasoactive agents as needed. Diuretics must be added once the patient is hemodynamically stable for a reasonable duration of time. Diuretics have a marked benefi cial response. As the alveolar-capillary membrane dysfunction is not developed and the alveolar fl uid clearing mechanisms are intact, the resolution is fast.25 Patients can be weaned off the high settings as the oxygenation improves. Steroids may be given for prevention of post extubation stridor and upper airway edema, they are not needed for NPPE as the resolution is fast.10

ConclusionAwareness of NPPE is crucial to prevent complications in high risk cases. Pre-operative checkup should be thorough. Anesthesiologists should be careful in the immediate post extubation period and frequent reassessment should be done. Pediatric Intensivists should be made aware of high-risk cases and should be involved as soon as possible in cases of sudden development of features of NPPE. Topical laryngeal anesthesia should be used to prevent acute laryngospasm. Identifi cation of NPPE can prevent harm from more aggressive treatment modalities as it is self-resolving over 24-48 hours. Coordination between the anesthesia and PICU teams is essential to prepare for possible development of NPPE in high risk cases.7


References1. Mehta KK, Ahmad SQ, Shah V, Lee H. Post obstructive

pulmonary edema after biopsy of a nasopharyngeal mass. Respir Med Case Rep. 2015; 16:166-8.

2. Richmond L. Moore and Carl A. L. Binger.The response to respiratory resistance a comparison of the effects produced by partial obstruction in the inspiratory and expiratory phases of respiration. J Exp Med1927; 45(6): 1065–1080.

3. Warren, M.F., Peterson, D.K., Drinker, C.K. The effects of heightened negative pressure in the chest, together with further experiments upon anoxia in increasing the fl ow of lung lymph. Am J Physiol. 1942; 137:641–648.

4. Capitanio MA, Kirkpatrick JA. Obstructions of the upper airway in children as refl ected on the chest radiograph. Radiology. 1973; 107:159–61



5. Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. JAMA. 1977;1833-5.

6. Halow KD, Ford EG. Pulmonary edema following post-operative laryngospasm: a case report and review of the literature. Am Surg.1993; 4:443-7.

7. Lorch DG, Sahn SA. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk? Chest. 1986; 90(6):802-5.

8. Tami TA, Chu F, Wildes TO, Kaplan M. Pulmonary edema and acute upper airway obstruction. Laryngoscope. 1986;96(5):506-9.

9. Deepika K, Kenaan CA, Barrocas AM, Fonseca JJ, Bikazi GB. Negative pressure pulmonary edema after acute upper airway obstruction. J Clin Anesth. 1997;9(5):403-8.

10. Malcolm Lemyze and Jihad Mallat. Understanding negative pressure pulmonary edema Intensive Care Med. 2014; 40(8): 1140–1143.

11. Travis Kenneth W, Atlee John L. Postobstruction Pulmonary Edema. In: Atlee, J. (2007). Complications in anesthesia. 2nd ed. Philadelphia: Elsevier/Saunders, pp.213-215.

12. Buda AJ, Pinsky MR, Ingels NB Jr, Daughters GT 2nd, Stinson EB, Alderman EL. Effect of intrathoracic pressure on left ventricular performance. N Engl J Med.1979;301(9):453-9.

13. Matthay MA, Folkesson HG, Clerici C. Lung epithelial fl uid transport and the resolution of pulmonary edema. Physiol Rev. 2002;82(3):569-600.

14. Lang SA, Duncan PG, Shephard DA, Ha HC. Pulmonary oedema associated with airway obstruction. Can J Anaesth. 1990;37(2):210-8.

15. Birukov KG, Jacobson JR, Flores AA, Ye SQ, Birukova AA, Verin AD et al. Magnitude-dependent regulation of pulmonary endothelial cell barrier function by cyclic stretch. Am J Physiol Lung Cell Mol Physiol. 2003;285(4): L785-97.

16. Siddik-Sayyid SM, AlFahel W, El-Khatib MF. Patient-ventilation asynchrony causing negative pressure pulmonary edema in an intubated obese patient. Middle East J Anaesthesiol. 2016;23(4):495-8.

17. JiHyeon Lee, Jae Ho Lee, Min Hyun Lee, Hyun Oh Cho, and Soon Eun Park. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report Korean J Anesthesiol. 2017; 70(1): 95–99.

18. Lucia Derks MD, Walker Plash MD, Elizabeth Powell MD, Peter V.R. Tilney. 16-Year-Old Female Near Hanging with Negative Pressure Pulmonary Edema. Air Med J. 2017; 36:5-7.

19. Danielle L Davison, Megan Terek and Lakhmir S Chawla. Neurogenic pulmonary edema. Crit Care. 2012; 16(2): 212.

20. Lang SA, Duncan PG, Shephard DA, Ha HC. Pulmonary

oedema associated with airway obstruction. Can J Anaesth. 1990; 37(2):210-8.

21. Mark A.Van Kooy, M.D. and Richard F. Gargiulo, M.D. Postobstructive Pulmonary Edema. Am Fam Physician. 2000;62(2):401-404

22. Bharathi KS, Kulkarni S, Sadananda KS, Gurudatt CL. Takotsubo cardiomyopathy precipitated by negative pressure pulmonary oedema following total thyroidectomy. Indian J Anaesth. 2016;60(3):202-5

23. Goldenberg JD, Portugal LG, Wenig BL, Weingarten RT. Negative pressure pulmonary edema in the otolaryngology patient. Otolaryngol Head Neck Surg. 1997;117(1):62-6.

24. Balu Bhaskar and John F. Fraser. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3): 308–313

25. Fremont RD,Kallet RH, Matthay MA, Ware LB. Postobstructive pulmonary edema: a case for hydrostatic mechanisms. Chest. 2007;131(6):1742-6.

26. Krodel DJ,Bittner EA, Abdulnour R, Brown R, Eikermann M. Case scenario: acute postoperative negative pressure pulmonary edema. Anesthesiology. 2010;113(1):200-7.

27. Matthay MA. Resolution of pulmonary edema-New insights. West J Med 1991; 154:315-321.

28. Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, Chiolero R, Vock P, Wicky S. Clinical and radiologic features of pulmonary edema. Radiographics.1999;19(6):1507-31

29. Cascade PN, Alexander GD, Mackie DS. Negative-pressure pulmonary edema after endotracheal intubation. Radiology. 1993;186(3):671-5.

30. Taira N, Kawabata T, Ichi T, Yohena T, Kawasaki H, Ishikawa K. An analysis of and new risk factors for reexpansion pulmonary edema following spontaneous pneumothorax. J Thorac Dis. 2014;6(9):1187-92.

31. OlíviaMeira Dias, Lisete Ribeiro Teixeira, and Francisco S Vargas. Reexpansion pulmonary edema after therapeutic thoracentesis. Clinics (Sao Paulo). 2010; 65(12): 1387–1389.

32. Yoon JS, Suh JH, Choi SY, Kwon JB, Lee BY, Lee SH, et al. Risk factors for the development of reexpansion pulmonary edema in patients with spontaneous pneumothorax. J Cardiothorac Surg. 2013; 8:164

33. Meeker JW, Jaeger AL, Tillis WP. An uncommon complication of a common clinical scenario: exploring reexpansion pulmonary edema with a case report and literature review. Journal of Community Hospital Internal Medicine Perspectives. 2016;6(3):10.3402/jchimp.v6.32257. doi:10.3402/jchimp.v6.32257.

34. Hobaika AB, Lorentz MN. Laryngospasm. Rev Bras Anestesiol 2009; 59: 487-95.

How to cite this articleKori M, Chugh K, Taneja V. Negative Pressure Pulmonary Edema in a case of Adeno-tonsillectomy. Crit Care Pediatr. 2018;1(2):48-53

How to cite this URLKori M, Chugh K, Taneja V. Negative Pressure Pulmonary Edema in a case of Adeno-tonsillectomy. Crit Care Pediatr. 2018;1(2):48-53Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01028 .html



Case ReportExchange Transfusion as a Treatment Strategy in Severe Pertussis

with Hyperleukocytosis in an Infant - A case reportAbdul Rauf1, Anil Sachdev2, Dhiren Gupta3

1FNB Resident, 2Director, 3Senior Consultant, Department of Pediatric Intensive care, Sir Ganga Ram hospital, New Delhi, Delhi 110060

Received:7-April-18/Accepted: 17-May-18/Published online:18-Jun-18

ABSTRACTHyperleukocytosis in pertussis has a correlation with disease severity. We describe a 5-week-old infant with severe pertussis and hyperleukocytosis requiring mechanical ventilation. Baby developed refractory hypoxemia. Two cycles of exchange transfusion were done on different occasions. Exchange transfusion resulted in signifi cant improvement in oxygenation and hemodynamic parameters. Exchange transfusion is a viable treatment option in pertussis hyperleukocytosis complicated by refractory hypoxemia or persistent features of Systemic Infl ammatory Response Syndrome.Keywords: Pertussis; Hyperleukocytosis; Exchange transfusion

Corresponding authorDr Anil Sachdev, Director, Department of Pediatric Intensive care and Pulmonology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi-110060. Email: [email protected]

IntroductionHyperleukocytosis is a common laboratory fi nding in pertussis, especially in young children.1 It is traditionally called as Lymphoid-leukemoid reaction due to the lymphocytic predominance. Hyperleukocytosis has been found to have correlation with disease severity and outcome.2 It causes pulmonary leukostasis, leading to impairment in gas exchange and an increased the risk of cerebral vascular thrombosis and haemorrhage. Role of leukoreduction by exchange transfusion in pertussis hyperleukocytosis is not clearly established. Here we describe a case of severe pertussis with hyperleukocytosis in a young infant where Exchange Transfusion (ET) resulted in signifi cant improvement in hemodynamic and oxygenation paramteres.

Case ReportA 5-weeks-old male infant (weight -3.9 kg) presented with history of paroxysmal cough and fever for 5 days followed by progressive breathlessness and one episode of generalized seizure. In emergency

room, child was intubated in view of respiratory failure and was shifted to the pediatric intensive care unit (PICU). At admission, his heart rate (HR) was 180/min, sinus rhythm, peripheral pulses were good volume, capillary fi ll time<3 seconds and non-invasive blood pressure 80/52 mm Hg. Child was ventilated with pressure regulated volume control mode to maintain oxygen saturation> 92%. Chest-X ray showed non-homogenous opacity with air bronchogram suggestive of consolidation in right upper zone. Other investigations revealed markedly high total leukocyte count (TLC) of 110× 109/L with 84% lymphocytes. Possibility of pertussis with pneumonia was considered and ceftriaxone and oral azithromycin were started. The nasopharyngeal swab sent at admission was reported positive for Bordetella Pertussis (using Respiratory biofi re test - Multiplex PCR for respiratory viruses and bacteria, BioMerieux, USA). At 6 hours of hospital stay, baby developed persistent tachycardia (HR 220/min) without signifi cant change in any other hemodynamic parameter. There was no improvement in heart rate with temperature control and adequate sedation and analgesia. There was no clinical or bedside ultrasonographic evidence of hypovolemia or fl uid responsiveness and ECG showed sinus rhythm. Ejection Fraction was 45% and there was no evidence of pulmonary arterial hypertension


on echocardiography. Child also developed severe hypoxemia (PaO2-64 mmHg, PaO2/FiO2 ratio- 98) and metabolic acidosis with increased serum lactate (lactate - 3.5 mmol/L). Possibility of impaired gas exchange due to pulmonary leukostasis was considered. Double volume blood ET with 480 mL whole blood was done at 10 hrs of admission. Blood was drained through right radial arterial catheter and administered through right femoral central venous line in aliquots of 10 mL each. Post ET, tachycardia improved, fever settled and there was remarkable improvement in oxygenation and ventilation (Table 1). There was a fall in TLC to 32 × 109/L. Subsequently, child had another worsening of hemodynamic, oxygenation and ventilation parameters on day 3 with rapid increase in TLC to 70 × 109/L for which another cycle of ET was done. Baby again showed improvement in hemodynamics and oxygenation after this cycle of ET. Unfortunately, baby had secondary deterioration on day 5 in form of hypotension with features suggestive of septic shock. Antibiotics were upgraded and inotropes were initiated. Laboratory parameters showed elevated infl ammatory markers (CRP-70 mg/L, Procalcitonin-35 ng/mL) without signifi cant change in TLC. Clinical condition deteriorated rapidly, and baby succumbed on day 6 due to refractory shock. Blood culture report which was collected later was

positive for Burkholderia Cepacia. Clinical course suggested that the deterioration was probably due to the secondary bacterial sepsis rather than pertussis.

DiscussionPertussis resurgence has been a concern for last few years. As per WHO EPI factsheet, there were 37274 cases of pertussis reported from India in 2016.3 Pertussis related mortality commonly occur in smaller children. Severe pertussis or critical pertussis, which occur only in a small proportion of patients is characterized by refractory hypoxemia, pulmonary hypertension and cardiogenic shock.4 In a study by Murray et al in 31 children with severe pertussis admitted in PICU, TLC count >30 × 109/L was a consistent feature in all cases.5 Hyperleukocytosis is a common fi nding in pertussis and is related to mortality. Mechanisms proposed for hyperleukocytosis include Pertussis toxin mediated prevention of leukocyte extravasation from blood vessels and the increased release of leukocytes from bone marrow and spleen. Adverse effects of hyperleukocytosis are pulmonary leukostasis causing impairment of gas exchange, pulmonary hypertension, cardiogenic shock and risk of cerebral vascular thrombus and hemorrage.6 As reviewed by Kuperman et al, there has been around 47 cases reported in world literature where ET was done in pertussis hyperleukocytosis.7 In general, ET resulted in decreased TLC count, decreased fever and improvement in cardiorespiratory status in these patients. We could observe similar benefi ts in our case also. Rowlands et al found a mortality reduction from 44% to 10% after addition of leukodepletion by ET in the intensive care of infants with critical pertussis.8 Benefi t of leukoreduction in this setting can be due to two mechanisms- reducing leukostasis or lowering the toxaemia by the resultant plasma exchange. Leukoreduction can also be done by leukoapharesis, but ET has been found to be equally effective and is technically easy and can be performed even in non-tertiary care centres. There has been no consensus on the cut off value in pertussis for considering ET. Kuperman et al suggested HR> 170/min, respiratory rates >70/min, TLC > 30 × 109 TLCs/L, development of pulmonary hypertension, as cut off levels for ET in severe pertussis. Based on

Table 1: Vital parameters, Blood counts and Arterial Blood Gas reports before and after exchange transfusion Parameters Pre Exchange

TransfusionPost-Exchange

TransfusionVital Parameters HR (/min) BP (mmHg) SpO2 Temp

Blood count Hb (gm/dL) TLC (× 109/L) DLC % (N/L) Platelet (×109/L)

Arterial blood gas Ph PO2 (mm Hg) PCO2 (mm Hg) HCO3 Lactate (mmol/L)

22274/33/46

9039.3°C

11.5110

16/84140

7.156458223.5

18278/34/47

9438°C

11.032

11/74120

7.247850242.7

CASE REPORT AND REVIEW OF LITERATUREExchange Transfusion as a Treatment Strategy in Severe

Pertussis with Hyperleukocytosis in an Infant - A case report


our case report and available literature, it seems that ET should be considered in cases of severe pertussis with refractory hypoxemia or persistent features of Systemic Infl ammatory Response Syndrome like tachycardia, with a high or rapidly increasing TLC. Our case was just 5 weeks old, 1 week due for his fi rst DPT immunisation. He might have acquired infection from susceptible adults who didn’t receive booster doses of pertussis vaccines. Two strategies have been proposed to safeguard such infants. Cocoon vaccination strategy is where all household contacts of the infant are immunised, but such an approach is diffi cult to implement. Maternal immunisation strategy, where mother is given Tdap booster in place of routine TT vaccination during pregnancy has been advocated by WHO and is gaining importance among obstetric societies all over world.9 Unfortunately, this practice is still not followed in tropical countries like India. There is a need to create awareness among physicians to follow this policy.10


References1. Heininger U, Klich K, Stehr K, Cherry JD. Clinical fi ndings

in Bordetella pertussis infections: results of a prospective multicenter surveillance study. Pediatrics. 1997;100: E10.

2. Pierce C, Klein N, Peters M. Is leukocytosis a predictor of mortality in severe pertussis infection? Intensive Care Med. 2000; 26:1512-4.

3. World Health Organization EPI factsheet 2017. Available from: http://www.searo.who.int/immunization/data/india_2017.pdf. Accessed January 16, 2018.

4. Namachivayam P, Shimuzu K, Butt W. Pertussis: severe clinical presentation in pediatric intensive care and its relation to outcome. Pediatr Crit Care Med. 2007;8:207-11.

5. Murray E, Nieves D, Bradley JS. Characteristics of severe Bordetella pertussis infection among Infants ≤90 days of age admitted to pediatrics intensive care units—Southern California, September 2009-June 2011. J Pediatr Infect Dis. 2013;2:187-8.

6. Carbonetti N.H. Pertussis leukocytosis: Mechanisms, clinical relevance and treatment. Pathog Dis. 2016;74:pii:ftw087.

7. Kuperman A, Hoffmann Y, Glikman D, Dabbah H, Zonis Zl. Severe pertussis and hyperleukocytosis: is it time to change for exchange? Transfusion. 2014;54:1630-3.

8. Rowlands HE, Goldman AP, Harrington K, Karimova A, Brierly J, Cross N. Impact of rapid leukoreduction on the outcome of severe clinical pertussis in young infants. Pediatrics. 2010;126:816-27.

9. Summary of the Pertussis Vaccines: WHO position paper – September 2015. Available from: http://www.who.int/immunization/documents/pertussis_pp_2015_summary.pdf. Accessed January 16, 2018.

10. Healy CM. Pertussis vaccination in pregnancy. Human Vaccines & Immunotherapeutics. 2016;12:1972-81.

How to cite this articleRauf A, Sachdev A, Gupta D. Exchange transfusion as a treatment strategy in Severe Pertussis with Hyperleukocytosis in an infant -A Case Report. Crit care Pediatr. 2018;1(2):54-56

How to cite this URLRauf A, Sachdev A, Gupta D. Exchange transfusion as a treatment strategy in Severe Pertussis with Hyperleukocytosis in an infant - A Case Report. Crit care Pediatr. 2018;1(2):54-56Available from: : http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP01029.html

CASE REPORT AND REVIEW OF LITERATUREExchange Transfusion as a Treatment Strategy in Severe

Pertussis with Hyperleukocytosis in an Infant - A case report


Letter to EditorSpontaneous Retrograde Coiling of Central Venous Catheter into the

Ipsilateral Internal Jugular Vein - Can it happen?Ankur Khandelwal1, Surya K. Dube2, Gyaninder P. Singh3

1Senior Resident, 2Assistant Professor, 3Associate Professor, Department of Neuro-anaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi-110029, India


Corresponding authorDr Surya Kumar Dube, Assistant Professor, Department of Neuro-anaesthesiology and Critical Care, 7th Floor, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India, 110029Mob: (0091)9013172155, Email: [email protected]

Central venous catheters (CVC) malposition is not an uncommon and post procedure chest X-ray gives information about the catheter location. However, daily chest X-ray is not advisable to follow up the position of CVC. With this practice we may miss the CVC malposition occurring after a correct placement. We report one such case of spontaneous malposition of CVC on 5th day post insertion.A 5.5 Fr triple lumen CVC (Certifi x Trio® B. Braun, Melsungen AG) was inserted under direct ultrasound visualisation in second attempt into the right internal jugular vein (IJV) of a 9-years-old female child posted for right fronto-parieto-temporal craniectomy. There was no thoracoabdominal/neck injury in the child. The CVC was found to be in correct position post operatively (Figure 1 A). No further chest X- rays were done since the patient apparently did not have any lung pathology. On 5th day, there were erroneous readings of central venous pressure (CVP) which did not correlate with the patient’s clinical state. In addition, free fl ow of blood could not be obtained from any of the CVC ports. A chest X-ray was done which showed retrogradely coiled CVC into the ipsilateral IJV (Figure 1 B). The catheter was subsequently removed, and a new triple lumen CVC was inserted into the left IJV.A mal-positioned CVC can lead to erratic readings of CVP, formation of coagulum, catheter erosion and thrombophlebitis.1 Manoeuvre described to prevent misplacement of CVC into ipsilateral IJV during subclavian vein cannulation2 may not prevent coiling of the CVC inside ipsilateral IJV. Moreover, CVC

that are inserted successfully can coil subsequently during the course of treatment. The most important factor leading to retrograde coiling is the reversal of venous blood fl ow secondary to IJV valve incompetence.3 Incompetence of IJV valve can occur in patients with history of previous cannulation or it can be due to trauma to the IJV valve by multiple attempts at the time of cannulation. Factors like chronic obstructive pulmonary disease (COPD), pulmonary hypertension and high intrathoracic or intraabdominal pressures increase chances of the IJV valve malfunction and hence allow retrograde fl ow into the IJV there by leading to coiling of the CVC. The most probable explanation for the retrograde coiling of CVC in our case is IJV valve malfunction (caused by IJV valve injury at the time of cannulation) leading to retrograde fl ow of blood into IJV due to transient rise of intrathoracic pressure anytime during to mechanical ventilation.Presence of valve in IJV is quite common and it is mostly located in the distal portion of the IJV, just proximal to the jugular bulb in the retro-clavicular space.5 This position might make the ultrasound assessment of the valve diffi cult during routine cannulation, leading to its injury. With this report we want to emphasise that spontaneous retrograde coiling of CVC can happen days after the IJV cannulation due to IJV valve malfunction and rise in intrathoracic or intraabdominal pressure. The possible way to prevent it is to avoid IJV valve injury during cannulation and to prevent the factors aggravating the retrograde blood fl ow into IJV. A high index of suspicion is required to detect retrograde coiling of CVC into IJV especially in cases where multiple attempts were made during cannulation and daily /frequent chest X-ray is not done. In cases of retrograde coiling of CVC into IJV we suggest removal of CVC and insertion of CVC into another site.


Fig 1 A: Chest X-ray shows CVC in right IJV. (1st day of ICU)

Fig 1 B: Retrograde Coiled CVC (5th day of ICU).

References1. Ruesch S, Walder B, Tramer MR. Complications of central

venous catheters: internal jugular versus subclavian access –a systematic review. Crit Care Med 2002; 30:454-60.

2. Ambesh SP, Dubey PK, Matreja P, Tripathi M, Singh S. Manual occlusion of the internal jugular vein during subclavian vein catheterization: A maneuver to prevent misplacement of catheter into internal jugular vein. Anesthesiology. 2002; 97:528–9.

3. Wu X, Studer W, Erb T, Skarvan K, Seeberger MD. Competence of the internal jugular vein valve is damaged by cannulation and catheterization of the internal jugular vein. Anesthesiology 2000; 93(2):319-24.

4. Samra T, Saini V. Coiling of central venous catheter in right internal jugular vein. Indian J Crit Care Med. 2014; 18:830-1.

5. Fukazawa K, Aguina L, Pretto EA Jr. Internal jugular valve and central catheter placement. Anesthesiology 2010; 112:979.

How to cite this articleKhandelwal A, Dube S K, Singh G P. Spontaneous retrograde coiling of central venous catheter into the ipsilateral internal jugular vein – Can it happen? Crit Care Pediatr. 2018;1(2):57-58

How to cite this URLKhandelwal A, Dube S K, Singh G P. Spontaneous retrograde coiling of central venous catheter into the ipsilateral internal jugular vein – Can it happen? Crit Care Pediatr. 2018;1(2):57-58Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP010210.html

LETTER TO EDITORSpontaneous Retrograde Coiling of Central Venous Catheter

into the Ipsilateral Internal Jugular Vein - Can it happen?


Best EvidenceJournal Scan

Naresh Lal, Rachna SharmaConsultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India

Received:29-May-18/Accepted: 3-June-18/Published online:18 -Jun-18

Corresponding authorDr Naresh Lal. Consultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India Mob: +91-9176792892, Email: [email protected],

Articles Reviewed1. Hypofi brinogenemia Is Associated with Poor

Outcome and Secondary Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome in Pediatric Severe Sepsis.Signoff J, Fitzgerald J, Teachey D, Balamuth F, Weiss S. Pediatr Crit Care Med 2018;19(5):397-405.

ObjectivesSome children with sepsis exhibit a sustained hyperinfl ammatory response that can trigger secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome. Although hypofi brinogenemia is a shared feature of sepsis and hemophagocytic lymphohistiocytosis, there are no data about fi brinogen as a biomarker to identify children with sepsis/secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome overlap. We hypothesized that hypofi brinogenemia is associated with poor outcomes and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome and has utility as a screening biomarker for this sepsis phenotype.

DesignA retrospective cohort study of patients less than or equal to 21 years treated for severe sepsis from January 2012 to December 2014.

SettingEmergency department and PICU at a single academic children’s hospital.

PatientsConsecutive patients with greater than or equal to one episode of hypofi brinogenemia (serum

fi brinogen < 150 mg/dL) within 7 days of sepsis were compared with a random sample of patients without hypofi brinogenemia using an a priori sample size target of 190. Thirty-eight patients with hypofi brinogenemia were compared with 154 without hypofi brinogenemia.

InterventionsNone

Measurements and Main ResultsThe primary outcome was “complicated course” (composite of 28-d mortality or ≥ two organ failures at 7 d). Secondary outcomes were 28-day mortality and fulfi llment of diagnostic criteria for secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome. We used Wilcoxon rank-sum, Fisher exact test, and multivariable logistic regression to compare patients with versus without hypofi brinogenemia. Patients with hypofi brinogenemia were more likely to have a complicated course (73.7% vs 29.2%; p < 0.001), 28-day mortality (26.3% vs 7.1%, p = 0.002), and meet diagnostic criteria for secondary hemophagocytic lymphohistiocytosis/ macrophage activation syndrome (21.1% vs 1.3%; p < 0.001). After controlling for confounders, hypofi brinogenemia remained associated with complicated course (adjusted odds ratio, 8.8; 95% CI, 3.5–22.4), mortality (adjusted odds ratio, 6.0; 95% CI, 2.0–18.1), and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome (adjusted odds ratio, 27.6; 95% CI, 4.4–173).

ConclusionsHypofi brinogenemia was independently associated with poor outcome and secondary hemophagocytic lymphohistiocytosis/ macrophage activation syndrome in pediatric sepsis. Measurement of fi brinogen may provide a pragmatic biomarker to identify children with possible sepsis/secondary


hemophagocytic lymphohistiocytosis/ macrophage activation syndrome overlap for whom further diagnostic testing and consideration of adjunctive immunomodulatory therapies should be considered.

Reviewer’s CommentsLack of specifi c biomarkers impedes early detection and management of pediatric septic shock. Sepsis is sometimes complicated by development of secondary HLH of which hyperferritinemia and hypofi brinogenemia are characteristic fi ndings. This retrospective observational cohort study used hypofi brinogenemia as a biomarker for recognition of sepsis associated HLH/MAS for whom further diagnostic testing and consideration of adjunctive immuno-modulatory therapies could be considered early. The hypofi brinogenemia was defi ned as fi brinogen level less than or equal to 150 mg/dl within 2 days before through 7 days following sepsis recognition. Patients were further divided into very low (50–100 mg/dL), low (101–150 mg/dL), normal (151–471 mg/dL), and high (> 471 mg/dL) fi brinogen groups as per the lab values. Hypofi brinogenemia within the fi rst 2 days of sepsis recognition was independently signifi cantly associated with a complicated PICU course, (73.7% vs 29.2%; p < 0.001), 28-day hospital mortality (26.3% vs 7.1%; p = 0.002) and to meet diagnostic criteria for sHLH/MAS (21.1% vs 1.3%; p < 0.001). Complication was defi ned as mortality at 28 days and persistent of 2 or more organ dysfunction at 7 days following recognition of sepsis. Incidence of fungal infection and culture-negative sepsis were more common in patients with versus without hypofi brinogenemia (8% vs 1% and 53% vs 36%, respectively). DIC was more common as was hepatic and haematological dysfunction (coagulopathy) in hypofi brinogenic patients than in normal fi brinogen group. Limitation of the study was that it was a single centre study and a small sample size. Correlation of fi brinogen with ferritin was not done which is a stronger marker of sepsis as shown in various studies. Relying on a single indice rather than a composite score may not be the solution for a variable and complex problem like sepsis associated with HLH. DIC can alter the fi brinogen level which fortunately is less common in sepsis.

2. Low-Dose Epinephrine Boluses for Acute Hypotension in the PICUReiter P, Roth J, Wathen B, LaVelle J, Ridall L (Pediatr Crit Care Med 2018;19(4):281-286.

ObjectivesTo describe the use of low-dose bolus epinephrine in critically ill children during an acute hypotensive episode or prearrest condition.

DesignInstitutional Review Board approved, single-center, retrospective medical chart review.

SettingLarge medical-surgical PICU within a freestanding, tertiary care children’s hospital.

PatientsPatients admitted to the PICU between June 1, 2015, and June 1, 2016, who received low-dose (≤ 5 μg/kg) IV bolus epinephrine.

InterventionsNone

Measurement and Main ResultsTwenty-four resuscitation episodes (63 doses; 19 patients) were analyzed. Median age and weight of patients were 9 years (interquartile range, 1–15 yr) and 38.5 kg (interquartile range, 12–54.8 kg). Median Pediatric Risk of Mortality III score was 17 (interquartile range, 10–27). Mean epinephrine dose was 1.3 ± 1.1μg/kg. Median number of doses per patient was two. If more than one dose was provided, median dosing interval was 6.5 minutes. Heart rate and mean arterial blood pressure were compared at the time of epinephrine administration and 1–4 minutes (median = 1 min) following administration. Heart rate changed from 130 ± 41 to 150 ± 33 beats/ min (p < 0.05), and mean arterial blood pressure changed from 51 ± 17 to 75 ± 27 mm Hg (p < 0.001). Variability in mean arterial blood pressure response was observed; nonresponders required extracorporeal membrane oxygenation; 66% of doses resulted in up to 100% mean arterial blood pressure increase, and

BEST EVIDENCE Journal Scan


21% of doses resulted in greater than 100% mean arterial blood pressure increase. Doses below 1 μg/kg were associated with a lower mean arterial blood pressure increase than doses between 1 and 5 μg/kg (mean percent change in mean arterial blood pressure = 6.6% vs 60%, respectively). Children less than or equal to 2 years old had the greatest percentage increase in heart rate and mean arterial blood pressure.

ConclusionsProvision of low-dose bolus epinephrine during periods of acute hypotension can result in a signifi cant increase in mean arterial blood pressure and heart rate. This dosing strategy may provide temporary stabilization while other therapies are added or adjusted, but further research is needed.

Reviewer’s CommentsEpinephrine is a potent sympathomimetic agent with alpha- and beta-receptor activity. In addition to its vasopressor effects, epinephrine is also an inotropic and chronotropic agent, increasing cardiac output, heart rate (HR), and systemic vascular resistance, which can markedly improve perfusion during acute decompensated events. Vasopressor boluses especially ephedrine and phenylephrine have been used more frequently by anaesthetists than Epinephrine in post medical and surgical procedure for hypotension in adults. These ‘push-dose pressors’ are the perfect solution to short-lived hypotension, e.g., post intubation or during procedural sedation, which if not dealt timely can cause hemodynamic collapse. In children, Epinephrine boluses have been used in pre-arrest condition albeit in high doses. Epinephrine infusion is used to maintain stable hemodynamics post procedures and in peri-intubation period in pediatric cardiogenic shock, but this may be time consuming in the emergency room with requirement of trained nursing staff. Fluid administration may not feasible in some patients (eg myocarditis) and only inopressors may help. Also, absence of central line may impede administration of vasopressors, so the peripheral use of low dose epinephrine boluses can help us to tide over the acute crisis. Its safety has also been shown by Weingart et al (Clin Exp Emerg Med. 2015; 2: 131–132). The present study used low-dose epinephrine

boluses (defi ned as ≤5μg/kg/dose) in management of acute hypotension in children. The study defi ned dose and hemodynamic effects of bolus epinephrine on heart rate (HR) and mean arterial pressure (MAP). This study was done in medical and surgical PICU and excluded post cardiac surgical patients. Age groups were defi ned (<2yr;2-12yr;>12yr), dose response relationship was identifi ed and number of children requiring full resuscitation doses(0.01mg/kg) was noted. Effect of concomitant vasopressor infusions was also studied. The most common etiology for acute decompensation was septic shock followed by tracheal intubation and post arrest hypotension. Epinephrine boluses were used in 19 patients. 15 received single dose and 4 required more than one dose (range 1-7). The mean dose of epinephrine administered was 1.3 ± 1.1μg/kg (range 0.2–5 μg/kg). Though there was signifi cant change (p<0.05) in HR at 1 min of dosing, the percentage changes were not signifi cant in subgroup of age defi ned. 67% of doses caused expected rise in MAP but doses less than 1 μg/kg were associated with a smaller change in MAP than those greater than or equal to 1 μg/kg exhibiting a dose effect relationship. Also, changes in MAP were more evident in younger age group (< 2yr) as compared to the other 2 groups. Overall, changes in MAP were more variable than HR with no response in some (3 patients) and exaggerated response in others causing hypertension (19% of doses). This effect was seen even in patients given multiple epinephrine boluses. Changes in MAP were not signifi cant when child was on multiple vasopressors and low dose epinephrine was used. Three children (16%) progressed to cardiac arrest, and three other children required extracorporeal membrane oxygenation.Major limitation of this study was that it was a single centre study and the use of concomitant vasoactive infusion therapy may have affected outcomes. Though epinephrine boluses is a useful concept it raises some concerns too. Arrhythmias in already hypoxic and stunned myocardium are a possibility. Its usefulness will also be limited in vasodilatory warm septic shock. Prospective studies will be required to further assess the safety of epinephrine in patients of cardiac etiology.



3. Survival and Long-Term functional outcomes for children with cardiac arrest treated With Extracorporeal Cardiopulmonary Resuscitation.Torres F, Fink L, Bell M, Sharma M, Yablonsky E, Toledo J. Pediatr Crit Care Med 2018;19(5):451-458.

ObjectivesTo identify patient- and disease-related factors related to survival and favorable outcomes for children who underwent extracorporeal cardiopulmonary resuscitation after a refractory cardiac arrest.

DesignRetrospective observational study with prospective assessment of long-term functional outcome.

PatientsFifty-six consecutive children undergoing extracorporeal cardiopulmonary resuscitation at our institution from 2007 to 2015. Median age at arrest was 3.5 months (interquartile range, 1–53).

SettingTertiary pediatric university hospital with a referral heart center. Interventions: Health-related quality of life and family functioning assessment with the Pediatric Quality of Life Inventory and the McMaster Family Assessment Device.

Measurements and Main ResultsFifty - eight consecutive extracorporeal cardiopulmonary resuscitation episodes were included, with 46 (79.3%) related to primary cardiac conditions. Initial cannulation site was central in 19 (32.8%) and peripheral in 39 (67.2%). Survival to decannulation was 77.6% with survival at hospital discharge and at the end of the follow-up period being 65.5% and 62.1%, respectively. Time to follow-up was 38 months (interquartile range, 19–52). Patients who survived tended to be younger (3.5 mo [1 mo to 2 yr] vs 7 mo [1.25 mo to 17 yr]; p = 0.3) with decreased extracorporeal cardiopulmonary resuscitation times (28 min [15–47 min] vs 37.5 min [28.5–55 min]; p = 0.04). Those who received therapeutic hypothermia

tended to have higher hospital survival (21/28 [75%] vs 16/29 [55%]; p = 0.08). Follow-up assessments of survivors demonstrated good quality of life and family functioning (Pediatric Quality of Life Inventory, 84 [76–89.5]; McMaster Family Assessment Device, 1.62 [1.33–1.83]).

ConclusionsIn this series, extracorporeal cardiopulmonary resuscitation was associated with relatively high survival rates and a good health-related quality of life and family functioning. Larger series are needed to assess whether this technique should be more broadly available in the pediatric critical care community.

Reviewer’s CommentsThere is an increasing trend of ECMO CPR (ECPR) for sudden and refractory cardiopulmonary arrest in children. This was a retrospective observational study to assess functional and neurologic outcomes of children undergoing ECPR. Though there is substantial data for adult ECMO survivors there is relatively little long-term functional outcome data for pediatric ECMO patients. The CESAR trial in adults demonstrated no difference in severe disability of any measure of health care quality between patients randomized to the ECMO group versus the control group. In the present study in children the functional assessment scores (PedsQL and MMFAD) revealed a good quality of life and good family functioning among ECPR survivors. Cashen et al (Pediatr Crit Care Med 2017) reported 95% survival rate without severe functional abnormalities in his study (2012-2014) on ECPR. The study population with neurological complications also had lower survival.More than 50% population had abnormal brain imaging (infarct and haemorrhage) after ECMO in this study but no statistical differences were found between survivors and non-survivors. Thiagarajan et al (Circulation 2007) reported infarction and haemorrhage to be more common in non-survivors than survivors in their study. Further, children with better imaging had higher values of physical health and total scores on the PedsQL evaluation but psychosocial fi eld (including language evaluation) was not affected. They also had good performance at



school and home. Hamric et al (Pediatrics 2003) and Lequier et al (J Thorac Cardiovasc Surg 2008) found 50% incidence of moderate to severe cognitive delay and 12%-25% incidence of neuromotor delay among long term survivors of post cardiac ECMO in their study. Huang et al (Resuscitation 2012), Prodhan et al (Resuscitation 2009) and Kane et al (Circulation 2010) reported post ECPR normal or mild cerebral disability in 75% of their study patients using different scores (Pediatric Cerebral Performance Category (PCPC) and Pediatric Outcome Performance Category (POPC) scores). A review article by Mehta et al (World J Crit Care Med 2010) reported grossly normal survival even after prolonged (> 60 min) CPR in few of their patients. Post cardiac surgery had better survival as compared to non-cardiac surgery cases but it was not signifi cant in the study. Joffe et al (ASAIO J 2012) and Raymond et al (Pediatr Crit Care Med 2010) also reported poor survival in non-cardiac patients undergoing ECPR. Present study showed a higher hospital survival of ECPR of 65.5% as compared with ELSO registry which have reported survival rates from 39% to 41% probably due to higher number of infant population in this study for which ECMO has been found to be superior to adults. Out of hospital cardiac arrest (OHCA) had less than 50% survival as compared to intra hospital cardiac arrest (IHCA) in the study. Patients who survived had shorter ECPR duration in the study. More than one ECPR session and high lactates post ECPR were associated with higher mortality. Cashen et al (Pediatr Crit Care Med 2017) study also echoed similar fi nding and Mehta et al (World J Crit Care Med 2010) also reported no correlation between duration of CPR and survival. Demography had no signifi cant factors affecting mortality. In a literature review including 17 ECPR studies (2000 to 2011) Joffe et al (ASAIO J 2012) found non-cardiac etiology, renal dysfunction, lowest pH, and neurologic complications while on ECMO being the most consistent predictors of mortality. Cashen et al (Pediatr Crit Care Med 2017) also revealed multiorgan failure as the cause of mortality. The study had limitations as it was single centre study and functional outcomes were based on assessment by telephonic interviews accuracy of which can be

questionable.In conclusion, this study supports the use of ECPR as a life-saving strategy for children with refractory IHCA allowing survival in those with expected mortality. As more and more centres are doing ECMO better outcomes are expected and hence acceptance will increase with the growing evidence. Further prospective studies are required to study the functional outcomes in children.

4. Association between fl uid balance and Outcomes in Critically Ill Children – A Systematic Review and Meta-analysis.Alobaidi R, Morgan C, Basu R, Stenson E; Feathers R, Majumdar S, Bagshaw S. JAMA Pediatr. 2018;172(3):257-268.

ImportanceAfter initial resuscitation, critically ill children may accumulate fl uid and develop fl uid overload. Accruing evidence suggests that fl uid over load contributes to greater complexity of care and worse outcomes.

ObjectiveTo describe the methods to measure fl uid balance, defi ne fl uid overload, and evaluate the association between fl uid balance and outcomes in critically ill children.

Data SourcesSystematic search of MEDLINE, EMBASE, Cochrane Library, trial registries, and selected grey literature from inception to March 2017.

Study SelectionStudies of children admitted to pediatric intensive care units that described fl uid balance or fl uid overload and reported outcomes of interest were included. No language restrictions were applied.

Data Extraction and SynthesisAll stages were conducted independently by 2 reviewers. Data extracted included study characteristics, population, fl uid metrics, and



outcomes. Risk of bias was assessed using the Newcastle-Ottawa Scale. Narrative description of fl uid assessment methods and fl uid overload defi nitions was done. When feasible, pooled analyses were performed using random-effects models.

Main Outcomes and MeasuresMortality was the primary outcome. Secondary outcomes included treatment intensity, organ failure, and resource use.

ResultsA total of 44 studies (7507 children) were included in this systematic review and meta-analysis. Of those, 27 (61%) were retrospective cohort studies, 13(30%) were prospective cohort studies, 3(7%) were case-control studies, and 1 study (2%) was a secondary analysis of a randomized trial. The proportion of children with fl uid overload varied by case mix and fl uid overload defi nition (median, 33%; range, 10%-83%). Fluid overload, however defi ned, was associated with increased in-hospital mortality (17studies [n=2853]; oddsratio [OR], 4.34 [95% CI, 3.01-6.26]; I2=61%). Survivors had lower percentage fl uid overload than non-survivors (22 studies [n=2848]; mean difference, −5.62 [95% CI, −7.28 to −3.97]; I2 =76%). After adjustment for illness severity, there was a 6% increase in odds of mortality for every 1% increase in percentage fl uid overload (11 studies [n=3200]; adjusted OR, 1.06 [95% CI,1.03-1.10]; I2 =66%). Fluid overload was associated with increased risk for prolonged mechanical ventilation (>48 hours) (3 studies [n=631]; OR, 2.14 [95% CI,1.25-3.66]; I2=0% and acute kidney injury (7studies [n=1833]; OR, 2.36 [95% CI,1.27-4.38]; I2 =78%).

Conclusions and RelevanceFluid overload is common and is associated with substantial morbidity and mortality in critically ill children. Additional research should now ideally focus on interventions aimed to mitigate the potential for harm associated with fl uid overload

Reviewers CommentsThere is a growing body of evidence against

excessive fl uid administration in shock resuscitation with increased incidence of mortality and morbidity shown in various studies. In a recent meta-analysis by Zhang et al (Jour of Crit Care, August 2015) fl uid overload was shown to be associated with mortality and delayed kidney recovery in patients with acute kidney injury in critically ill adults. Similar analysis was lacking in children. This meta-analysis summarises the evidence voiced in various studies about fl uid overload and its outcomes. Aim of this study was to describe the methods used to assess fl uid balance, discuss the defi nitions for fl uid overload, and evaluate the association between fl uid balance and outcomes in critically ill children. 44 studies including 7507 children were included in the meta-analysis. Predominantly weight based, and fl uid intake output methods have been used as a method to quantify fl uid overload with later being a more accepted method. Discrepancies arise due to the weight that was being considered. PICU admission weight is better marker than hospital admission weight or OPD admission weight but overall a good correlation occurred between the two methods. Percentage fl uid overload (FO) and day of maximum fl uid overload was also varied in the study. 4 thresholds of FO were accepted. Cumulative FO of 5% over fi rst 24 hours, peak percentage FO exceeding 10 % during PICU stay, 10% and 20 % FO before CRRT initiation. Despite this heterogeneity the fi ndings were in tune with growing evidence of negative association between fl uid accumulation and outcomes in adult critically ill populations, including ARDS, sepsis, AKI and in perioperative settings. Patient with fl uid overload has increased incidence of renal failure and worst outcome on respiratory parameters. They had less ventilator free days and consequently more PICU length of stay. Consequently, more mortality was seen in fl uid overloaded patients. Conservative fl uid management strategies are the current norm of management of sick children. The FEAST trial highlighted the ill effects of unmonitored fl uid boluses outside the realm of modern PICUs and reported increased mortality. Previous studies (FACTT trial) and the more recent trials (ProCESS, ProMISe and ARISE) in adults have given us more insights into benefi ts of early haemodynamically guided resuscitation fl uid



management and hence more conservative approach with lesser mortality than the fi rst cult study by Rivers et al in 2001. A similar study in children known as SQUEEZE trial to determine whether septic shock reversal is quicker in pediatric patients randomized to an early goal-directed fl uid-sparing strategy vs usual care is underway, and results are still pending.Limitations of the study are in the retrospective and observational nature of the studies included which are prone to selection bias. Also, heterogeneity in defi nitions and thresholds of fl uid overload also compounds the issue. Further it was diffi cult to classify fl uid overload in the sub groups of pediatric populations with trauma and burns so generalizability of these fi ndings in this population is limited and fi nally, many studies did not consider the pre PICU fl uid status of the child as patient may have received fl uid in the ER or general ward. In conclusion, a fl uid overload is common among critically ill children and exerts a strong negative association with outcomes. Active de-resuscitation after initial fl uid management and preventing further fl uid overload will improve outcomes. Use of CRRT especially in the setting of renal failure with fl uid overload seems justifi ed and further studies are required to evaluate active strategies to prevent fl uid overload in children are desirable. USG assessment of fl uid overload is an important tool and more studies are required to validate it.

5. Cardiac Index changes with Fluid Bolus Therapy in children with sepsis—An Observational Study.Long E, Babl F, Oakley E, Sheridan B, Duke T, on behalf of the Pediatric Research in Emergency Departments International Collaborative (PREDICT). Pediatr Crit Care Med 2018; DOI: 10.1097/PCC.0000000000001534

ObjectivesFluid bolus therapy is the initial recommended treatment for acute circulatory failure in sepsis, yet it is unknown whether this has the intended effect of increasing cardiac index. We aimed to describe the effect of fl uid bolus therapy on cardiac index in children with sepsis.

DesignA prospective observational cohort study. Setting: The Emergency Department of The Royal Children’s Hospital, Melbourne, VIC, Australia. Patients: A convenience sample of children meeting international consensus criteria for sepsis with acute circulatory failure.

InterventionTreating clinician decision to administer fl uid bolus therapy.

Measurements and Main ResultsTransthoracic echocardiography was recorded immediately before, 5 minutes after, and 60 minutes after fl uid bolus therapy. Cardiac index was calculated by a pediatric cardiologist blinded to the timing of the echocardiogram. Cardiac index was calculated for 49 fl uid boluses in 41 children. The median change in cardiac index 5 minutes after a fl uid bolus therapy was +18.0% (interquartile range, 8.6–28.1%) and after 60 minutes was –6.0% (interquartile range, –15.2% to 3.0%) relative to baseline. Thirty-one of 49 fl uid boluses (63%) resulted in an increase in cardiac index of greater than 10% at 5 minutes, and these participants were considered fl uid responsive. This was sustained in four of 31 (14%) at 60 minutes. No association between change in cardiac index at 5 or 60 minutes and age, baseline mean arterial blood pressure, fl uid bolus volume, and prior volume of fl uid bolus therapy was found on linear regression.

ConclusionsFluid bolus therapy for pediatric sepsis is associated with a transient increase in cardiac index. Fluid responsiveness is variable and, when present, not sustained. The effi cacy of fl uid bolus therapy for achieving a sustained increase in cardiac index in children with sepsis is limited.

Reviewer’s CommentsFluid resuscitation is initial prime management in septic shock patients, but a targeted end point variable still eludes us. Fluid overload kills the patients as shown in studies and recent meta-analysis in children (Alobaidi et al 2018). To know who may be



harmed by fl uid bolus therapy in the initial treatment of sepsis is therefore a current research area.The physiologic rationale for administering fl uid bolus therapy in sepsis is to increase cardiac index (CI), with the intention of increasing end-organ perfusion and oxygen delivery. Clinical examination and vital signs are unreliable predictors of the response to a fl uid challenge. An increase in CI of greater than 10% following fl uid bolus therapy is considered “fl uid responsiveness as shown by Marik et al (CCM 2016). The effect of fl uid bolus therapy on CI in children with sepsis has not been described. This was a prospective observational cohort study and the primary aim of this study was to measure changes in cardiac index after a fl uid bolus and its sustained effect after 5 min and 60 min of resuscitation. 41 patients were included in the study. Of 63% who were fl uid responsive to fl uid bolus at 5 min less than 5% remained fl uid responsive at 60 min showing a transient increase only in CI which was unexpected. CI returned to baseline after 1 hour. Prior volume of fl uid bolus therapy and the amount of fl uid bolus (10 or 20 ml/kg) volume did not correlate with the

change in CI at 5 or 60 minutes though the number of patients with 10ml/kg were less. Smaller volumes may be insuffi cient to fi ll the tank to show a change in CI while previous boluses would also affect the fl uid responsiveness. These results are more prominent in sepsis patients probably due to capillary leakage. FACTT trial and Nunes et al (Ann Intensive Care. 2014) also corroborated this fact and showed unsustained responses to crystalloids 60-90 minutes after fl uid resuscitation. Furthermore, changes in HR and MAP were not signifi cantly correlated with changes in CVP.Important limitations of this study were that it was a single centre study and it was carried out in septic shock patients. The implications of the study results may not be valid in other scenarios. Also, results may be affected by inotropes and in patients receiving multiple fl uid boluses where aortic diameter may not be constant and hence calculated values of LVOT may differ. Long term implications of these result beyond the fi rst hour of resuscitation and in reducing mortality is uncertain.

How to cite this articleLal N, Sharma R. Best Evidence-Journal Scan. Crit Care Pediatr. 2018;1(2):59-66

How to cite this URLLal N, Sharma R. Best Evidence-Journal Scan. Crit Care Pediatr. 2018;1(2):59-66Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP010211.html



Critical Th inkingPICU Quiz

Naresh Lal, Rachna SharmaConsultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India

Received:29-May-18/Accepted: 3-June-18/Published online:18 -Jun-18

Corresponding authorDr Naresh Lal. Consultant, Pediatric Intensive Care Unit, BLK Superspeciality Hospital, New Delhi, India Mob+91-9176792892, Email: [email protected]

1. A 5-year-old child with muscular dystrophy is scheduled to undergo muscle biopsy for diagnosis. Anesthesia is induced using sevoflurane and you start injecting succinylcholine in preparation for intubation. Child develops masseter spasm immediately and temperature rises to 41 degrees Celsius. After immediate discontinuation of inhaled anesthesia and succinylcholine, which one of the following steps is the most appropriate?A. Start normal saline bolusB. Intravenous injection of dantroleneC. Arrange bed in PICUD. Start 100% oxygen with high fl ow rate to

wash out residual sevofl uraneE. Paralyze and intubate the child with another

agent.

2. An 18-month-old boy with type I spinal muscular atrophy is in the pediatric intensive care unit with respiratory syncytial virus (RSV) bronchiolitis which presented as fever and copious secretions. He has an RR of 56 breaths/min with deep subcostal retractions and is started on non-invasive positive-pressure ventilation with inspiratory pressure of 15 cm H2O and expiratory pressure of 5 cm H2O. After a while, his retractions are much improved, and RR is 30 breaths/min. However, saturations are only 92% on 40% oxygen, and the chest radiograph reveals basilar atelectasis. Which one of the following treatment plans will best recruit her collapsed lung?A. Increase expiratory pressures to 10 cm of

H2O and inspiratory pressures to 20 cm H2OB. Just Increase expiratory pressjure to 10 cm of

H2O

C. Give Glycopyrolate to decrease secretionsD. Intubation and mechanical ventilationE. Chest physiotherapy with mechanical

insuffl ation-exsuffl ation

3. A 4-year-old boy is being treated for pneumococcal pneumonia and sepsis. You have noticed decreased breath sounds on the right side along with increased ventilatory settings. He has become more oedematous, has decreased urine output, and has oozing around his central and arterial lines. His blood workup shows thrombocytopenia, elevated liver enzymes, coagulopathy, and worsening renal function. His chest radiograph shows a new right-sided pleural effusion. You decide to place a right-sided chest tube to evacuate the effusion. He is receiving a fentanyl drip and intermittent benzodiazepine for sedation. Which one of the following options would be the most appropriate next step in management of this patient?A. Use Rocuronium for paralysis and start

diuretics to help decrease pleural effusion.B. Use Cisatracurium for paralysis, insert the

ICD in fi fth ICS in right mid axillary line.C. Use Cisatracurium for paralysis, insert the

ICD in second ICS in right mid clavicular line.

D. Use rocuronium for paralysis, insert the ICD in fi fth ICS in right mid axillary line.

E. Use rocuronium for paralysis, insert the ICD in second ICS in right mid clavicular line

4. A 2-month-old girl developed poor feeding and irritability early this morning. She was brought to ED due to respiratory distress. On examination, she looks mottled and has weak pulses. Her rhythm strip in lead II showed the following rhythm. Emergency physician tried cardioversion with 0.5 J/kg but rhythm on the monitor did not change.Which one of the following options is the next


most appropriate intervention?

A. Synchronized Cardioversion with 0.25 J/KgB. 25 mg/kg of IV magnesium sulphateC. Defi brillation with 2 J/kgD. Synchronized cardioversion with 2 J/kgE. 0.1 mg/kg of iv adenosine

5. A 2-year-old infant is brought to the emergency department after his mother found him drinking an unknown substance from a soda bottle in the family’s pool house. You suspect that the substance was an acidic pool cleaner. Physical examination of the child’s lips, tongue, and oropharynx reveals no abnormalities. Of the following, the MOST appropriate next step in management is:A. Emergent upper gastrointestinal radiographic

seriesB. Initiation of oral antibiotic therapy.C. Parental reassurance and patient discharge.D. Placement of a nasogastric tube for lavage.E. Referral for emergency esophagoscopy.

6. A 10-year-old girl was admitted in PICU with history of injury over the right ankle 1 week back. Child had features of sepsis with septic shock and was ventilated for a duration of 48 hours. Diagnosis of MRSA septicaemia was made, and she had responded well to intravenous vancomycin. Child was extubated on to nasal prong oxygen and showed significant clinical improvement. After 10 hours of extubation you get a call from ICU, that the child had sudden deterioration in the form of increased respiratory distress, tachycardia and hypotension. What are the possibilities you consider and intervention?A. Tension pneumothorax and needs an

emergency ICD insertionB. Seizure and needs intravenous midazolamC. Bronchospasm and needs intravenous steroid

and nebulisationsD. Cardiac Tamponade secondary to pericardial

effusion leading to obstructive shock and needs urgent ECHO and drainage

E. Septic shock and needs fl uid bolus

7. A child presents with elevated serum free calcium but PTH is in normal range. What is the best conclusion?A. PTH is normal, therefore problem does not lie

in parathyroid gland.B. PTH should be low if the parathyroid is

functioning normally, thus the problem is in the parathyroid gland.

C. Child is excessively sensitive to PTH, since normal levels are stimulating excessive calcium mobilization from bone.

D. You need a parathyroid scan to make a conclusion.

8. Which is/are correct statements regarding the inspiratory time (Ti)A. At the end-inspiratory time, the expiration

phase always starts.B. If Ti is set by the Inspiration:Expiration

ratio, the Ti is independent ofventilator frequency.

C. If Ti is directly set, the expiratory time decreases with increasing ventilatorfrequency.

D. Normal Ti is in the range of 3–4 seconds.

9. Causes of right ventricular failure include/s:A. Acute pulmonary embolusB. ProtamineC. ARDSD. Obstructive sleep apneaE. All of the above.

10. Regarding prone position ventilation which is correct:A. The PROSEVA study group showed

no mortality benefi t at 28 daysin severe acute respiratory distress syndrome (ARDS).

B. Alveolar recruitment is affected as drainage of secretions gets impaired.

C. A more homogenous ventilation distribution is achieved, due tofavourable changes in thoraco-abdominal compliance.

D. Proning increases extravascular lung water.E. The optimal duration of prone positioning is

24 hours.

CRITICAL THINKING PICU Quiz


Answers1. D: Start 100% oxygen with high fl ow rate to wash

out residual sevofl uraneRationale: Child has features of malignant hyperthermia. Patients with muscular dystrophy are at increased risk of malignant hyperthermia when exposed to inhalational anesthetic agents like halothane, sevofl urane, isofl urane, and/or succinylcholine. Features of malignant hyperthermia are muscle rigidity, fever, increased carbon dioxide production, acidosis, and tachycardia. It is a fatal condition and immediate intervention in order of sequence includes discontinuation of offending agents, oxygenation with 100% oxygen to wash out the offending inhalational agent, intravenous injection of dantrolene, use of cold normal saline if temperature is above 30 degrees Celsius. Avoid paralysis and intubation in this patient.)

2. E: Chest physiotherapy with mechanical insuffl ation-exsuffl ationRationale: The child will need frequent breaks from ventilator to remove secretions. He will need assistance in the form of chest physiotherapy and cough assist. Use of these methods improves strength of cough and helps resolve atelectasis. Increasing pressures might help temporarily but will fail in due course.

3. B: Use Cisatracurium for paralysis, insert the ICD in fi fth ICS in right mid axillary line.Rationale: Patient has features of multiorgan dysfunction. Cisatracurium is eliminated by hofmann elimination, which is spontaneous degradation of the medication at physiological pH and temperature. Usual site for thoracentesis or chest tube placement is fourth or fi fth ICS in anterior or mid clavicular line. Rocuronium is not the ideal choice for paralysis in children with renal failure, as kidneys mostly eliminate it. Diuretics are not going to be effective to decrease pleural effusion.

4. D: Synchronized cardioversion with 2 J/kgRationale: This is a child with unstable ventricular tachycardia. Rhythm strip shows monophasic ventricular tachycardia. In this scenario, electrical cardioversion is recommended. If lower energy fails to convert or break ventricular tachycardia synchronized cardioversion with higher energy should be tried.

5. E: Referral for emergency esophagoscopy.Rationale: Upper endoscopy under anaesthesia should be performed within the fi rst 48 hours of caustic ingestion to determine the extent of the oesophageal injury. The objective of the endoscopy is to establish the presence or absence of an oesophageal lesion and to determine the extent of the injury.

6. D: Cardiac Tamponade secondary to pericardial effusion leading to obstructive shock and needs urgent ECHO and drainageRationale: MRSA septicaemia can lead to collection in the pericardial space which if left unnoticed and monitored can lead to increase and cause obstructive shock. Urgent Echo and relieving the tamponade can be lifesaving. Tension pneumothorax is unlikely if child remained stable for over 10 hours post extubation and with no PPV. Other options don’t fi t in.

7. C: Child is excessively sensitive to PTH, since normal levels are stimulating excessive calcium mobilization from bone.

8. C: If Ti is directly set, the expiratory time decreases with increasing ventilator frequency

9. E: All of the above.10.C: A more homogenous ventilation distribution is

achieved, due to favourable changes in thoraco-abdominal compliance.

How to cite this articleLal N, Sharma R. Critical Thinking: PICU Quiz. Crit Care Pediatr. 2018;1(2):67-69

How to cite this URLLal N, Sharma R. Critical Thinking: PICU Quiz. Crit Care Pediatr. 2018;1(2):67-69Available from: http://www.criticalcarepediatrics.in/userfi les/2018/0102-ccp-apr-jun-2018/CCP010212.html

CRITICAL THINKING PICU Quiz


Indian Diploma in Pediatric Critical Care MedicineBrief InformationIndian Diploma in Pediatric Critical Care Medicine (IDPCCM) is a one year course (for MD / DNB) and 2 year course for DCH candidates. The course is currently being run in accredited centers in India. Eligibility is MD / DNB / DCH in Pediatrics (MCI approved). The candidates can check the centers where the course are being run on this website and apply directly to the Directors of the center. The selection of the candidate and remuneration is as per each institutional policy and college is not involved in their internal decisions. Registration for the course, each year, needs to be done usually by 30th November (to check with director / contact office for updated information); for the exam which will be conducted in subsequent year (Register 1 year in advance). Curriculum for this course is displayed on this website. Exam pattern consists of MCQ based (100 marks question paper- 3 hours), and passing is strictly 60% and above. Those who pass this theory exam, are then allowed to appear for practical exam which consists of case based viva (Long or Short) along with OSCE (Observed structured clinical examination). Thus the exam has 3-4 components (heads), and for passing minimum average 60% is required with minimum 50% in each head. Exam forms are sent to the registered candidates 2 months prior to examination. Registrations forms available on this website.

Indian Fellowship in Pediatric Critical Care Medicine

Brief InformationIndian Fellowship in Pediatric Critical Care Medicine is a two-year course for MD / DNB and three years

course for DCH candidates. The course is currently being run in accredited centers in India. Eligibility is MD / DNB /DCH in Pediatrics (MCI approved). The candidates can check the centers (or contact office) where the course are being run on this website and apply directly to the Directors of the center. The selection of the candidate and remuneration is as per each institutional policy and college is not involved in their internal decisions. Registration for the course, each year, needs to be done by 30th of June (Register 2 years in advance) and is permitted to be done till 30th Sept in special circumstances; and also will be allowed to appear along with other candidates registered before 30th June. However, results of late joining candidates will be declared after completing 2 year tenure.Exam pattern consists of MCQ based (100 marks theory paper- 3 hours) with additional descriptive question paper, and passing is strictly 60% and above. Those who pass this theory exam, are then allowed to appear for practical exam which consists of case based viva (Long or Short), bedside viva along with OSCE (Observed structured clinical examination). Thus the exam has 3-4 components (heads), and for passing, minimum average 60% is required with minimum 50% in each head. Exam forms are sent to the registered candidates 2 months prior to examination.

Indian Diploma in Pediatric Critical Care NursingBrief InformationIndian Diploma in Pediatric Critical Care Nursing is a one-year course. The course is currently being run in all the accredited centers across India. Eligibility is graduation in nursing course from authorized body. The exam is in the form of theory and practical- viva. Passing is for 50%.Currently there are 29 training centers accredited by

InformationCollege of Pediatric Critical Care

Training Courses and Accredited Centres


the College of Pediatric Critical Care. Accreditation goes through a systematic process to ensure adequate opportunities for trainees in terms of number of patients, case mix, procedures, mechanical ventilations, and accredited teachers. Following

is the list of training centers accredited (updated in November 2017). Candidates aspiring to do fellowship can themselves apply to any center below addressing the directors of each unit.

INFORMATION College of Pediatric Critical Care Training Courses and Accredited Centres

Training CentresSr. No Name of the Training Center Name of the Director Associate Faculty1 Bai Jerbai Wadia Hospital for Children,

Acharya Dhonde Marg, Parel, Mumbai – 400012Dr. Lakshmi [email protected]

Dr. Rekha SolomonDr. Mahesh Mohite

2 Max Super Speciality Hospital, Patpar Ganj, L-60 Kalka JI, New Delhi-110019

Dr. Rajiv [email protected]

Ravi Shankar Nagraj

3 K.E.M. Hospital & Research Centre,Dept. of Pediatrics, TDH Ground Floor, KEM Hospital, Rasta Peth, Pune 411 011

Dr. Madhumati [email protected]

Dr. Manoj Patil

4 Kanchi Kamakoti Childs Trust Hospital,PICU, 12A, Nageswara Road, Nungambakkam, Madras-600034

Dr. Bala [email protected]@hotmail.com

Dr. Sajith KesavanDr. Ravikumar Krupanandam

5 Sir Ganga Ram Hospital,Dept of Pediatrics, Institute Child Health, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi

Dr. Anil [email protected]

Dr. Dhiren GuptaDr. Suresh Gupta

6 Apollo Childrens Hospital,No-15, Shafi Mohammed Road, Thousand Heights, Chennai- 06

Dr. Suchitra [email protected]

Dr. Indira JaykumarDr. RajeshwariDr. Satishkumar

7 Rainbow Childrens Hospital, Plot#22, Rd#10, Banjara Hills, Hyderabad-34

Dr. Dinesh [email protected]@gmail.com

Dr. Farhan Shaikh

8 Apollo Hospital,Sarita Vihar, Mathura Road, New Delhi – 76

Dr. Anita [email protected]@yahoo.co.uk

Dr. Nameet Jerath

9 Christian Medical College & Hospital,Vellore-S 632004

Dr. Ebor Jacobpicu@[email protected]

Dr. Kala Ebenezer

10 Manipal Hospital,No. 98 Rustam Bagh ,Old Airport Road, Bangalore -560017

Dr. Shiva [email protected]

Dr Ashwath Ram

11 BLK Superspecialty Hospital, Pus Road, New Delhi Dr. Rachana [email protected]

Dr Naresh Lal

12 Sri Ramachandra Medical Centre, Porur,Chennai-600116.

Dr. S. [email protected]@gmail.com

Dr. Rajakumar PS

13 Lotus Children Hospital, #6-2-29, Lakdipul,Hyderabad, 500004

Dr. V.S.V. [email protected]

14 Dayanand Medical College and Hospital, 9/25, P.A.U. Campus, Ludhiana 141004

Dr. Puneet A [email protected]

Dr. Siddharth

15 Nirmal Hospital Pvt Ltd, Ring Road, Surat – 395002 Dr. Nirmal [email protected]

Dr. Jignesh PatelDr. Jigesh Vaidhya

16 Rainbow Children’s Hospital, Matharhalli, Bangluru Dr. Rakshay [email protected]

Dr Sujatha Thygarajan



17 Rainbow Childrens Hospital Benarghatta,Bengaluru

Dr [email protected]@hotmail.com

Dr Prakash

18 Medanta The Medicity, Sector 38, Gurugram, Delhi NCR

Dr. Sunit [email protected]

Dr Maninder Dhaliwal

19 Narayana Hrudayalaya, Bengaluru Dr Rajiv [email protected]

Dr. Sagar Hiremath

20 Fortis Hospital Mulund, Mumbai Dr Jesal [email protected]

Dr.Sameer Sadavarte

21 Regency Hospital Kanpur, Kanpur Dr Rashmi [email protected]

22 Action Balaji Medical Institute, Delhi Dr Pradeep [email protected]

Dr. Nikhil Vinayak

23 Rangadore Memorial Hospital, Bangaluru Dr Meera [email protected]

24 Rainbow Children’s Hospital, Vikram Puri Dr Preetham [email protected]

25 Sparsh Multispeciality Hospital, Bhilai, Chattisgarh Dr Satyen D [email protected]

26 Rainbow Children’s Hospital, Vijay wada Dr [email protected]

27 People Tree Hospital, Bengaluru Dr Supraja [email protected]

Dr. Gurudutt

28 Fortis Memorial Research Institute, Gurgaon Dr Krishan [email protected]

29 SPS Hospital, Ludhiana Dr Vikas [email protected]

30 St Johns Hospital, Bengaluru Dr Lalitha [email protected]

31 Dr Mehta,s Hospital Dr [email protected]

32 MAX Superspeciality Hospital, Saket Dr. Bhaskar [email protected]

Dr. Preeti Anand

List of Accredited TeachersSr. No Name Institute1 Dr. Anil Sachdev

[email protected] Ganga Ram Hospital, New Delhi

2 Dr. Anita [email protected]

Apollo Indraprastha Hospital, New Delhi

3 Dr. Anitha [email protected]

MIOT International Hospital, Chennai

4 Dr. Anjul [email protected]

Continental Hospitals, Gachibowli, Hyderabad

5 Dr. Arun [email protected]

PGIMER, Chandigarh

6 Dr. Arun K [email protected]

PGIMER, Chandigarh


7 Dr. Ashok [email protected]

Wayne State University, Detroit, USA

8 Dr. Bala [email protected]

Kanchi Kamakoti Childs Trust Hospital, Chennai

9 Dr. Banani [email protected]

Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow

10 Dr. Bhaskar [email protected]

MAX Superspeciality Hospital, New Delhi

11 Dr. Deepika [email protected]

SRM Institute for Medical Sciences (SIMS), Chennai

12 Dr. [email protected]

Central India’s CHILD Hospital, Nagpur

13 Dr. Dhiren [email protected]

Sir Ganga Ram Hospital, New Delhi

14 Dr. Dinesh [email protected]

Rainbow Children’s Hospital, Hyderabad

15 Dr. Ebor [email protected]

Christian Medical College & Hospital, Vellore

16 Dr. Farhan [email protected]

Rainbow Children’s Hospital, Hyderabad

17 Dr. Girish [email protected]

KR Hospital, Bangalore

18 Dr. Gnanam [email protected]

Manipal Hospital, Bangalore

19 Dr. Indira [email protected]

Apollo Children Hospitals, Chennai

20 Dr. Jesal [email protected]

Fortis hospital, Mulund, Mumbai

21 Dr. Kala [email protected]


22 Dr. Karnam Ravi [email protected]

Childs Trust Hospital, Chennai

23 Dr. Krishan [email protected]

Fortis Memorial Research Institute, Gurgaon NCR

24 Dr. Kundan [email protected]

B. D. Sharma, PGIMS, Rohtak

25 Dr. Lakshmi [email protected]

Bai Jerbai Wadia Children’s Hospital

26 Dr. Lalitha [email protected]

St. John Hospital, Bangaluru

27 Dr. M. [email protected]

PGIMER, Chandigarh

28 Dr. Madhumati [email protected]

KEM Hospital, Pune

29 Dr. Mahesh A. [email protected]

Sai Child Care, Panvel, BJWC Hospital, Mumbai

30 Dr. Maniva [email protected]


31 Dr. Manoj [email protected]

D.Y. Patil Hospital & Research



32 Dr. Mohan [email protected]

Omaha Childrens Hospital, USA

33 Dr. N. [email protected]


34 Dr. Nameet [email protected]

Apollo Indraprastha Hospital, New Delhi

35 Dr. Natesan [email protected]

U S

36 Dr. Nirmal [email protected]

Nirmal Hospital Private Limited, Surat

37 Dr. Parag [email protected]

Rainbow Hospital, Hyderabad

38 Dr. Parthasarathi [email protected]

Apollo Gleneagles Hospitals, Kolkata

39 Dr. Prabhat [email protected]

Artemis Hospitals, Gurgaon NCR

40 Dr. Praveen [email protected]

Rainbow Children’s Hospital, Delhi

41 Dr. Preetha [email protected]

Kokilaben Hospital, Mumbai

42 Dr. Punit [email protected]

Dayanand Medical College & Hospital, Ludhiana

43 Dr. Rachna [email protected]

BLK Superspecialty Hospital, Delhi

44 Dr. Rajakumar [email protected]

Sri Ramachandra Medical Centre, Chennai

45 Dr. Rajeshwari [email protected]


46 Dr. Rajiv [email protected]

Narayana Hrudayalaya, Bangalore

47 Dr. Rajiv [email protected]

MAX Superspeciality Hospital, New Delhi

48 Dr. Rakesh [email protected]

AIIMS, New Delhi

49 Dr. Rakshay [email protected]

Rainbow Children Hospital, Banglore

50 Dr. Ramakrishnan Meera [email protected]

Rangadore Memorial Hospital, Bangalore

51 Dr. Rashmi [email protected]

Regency Hospital, Kanpur

52 Dr. Ravi Shankar [email protected]

UK

53 Dr. Rekha [email protected]

Bai Jerbai Wadia Children’s Hospital

54 Dr. S. [email protected]

Sri Ramachandra Medical Centre, Chennai

55 Dr. S.C [email protected]

Choithram Hospital, Indore

56 Dr. Sachin [email protected]

Surya Mother and Child Superspeciality Hospital, Pune



57 Dr. Sajith [email protected]

Kanchi Kamakoti CHILDS Trust Hospital, Chennai

58 Dr. Sathishkumar [email protected]


59 Dr. Shiva Kumar [email protected]

Manipal Hospital, Bangalore

60 Dr. Shrishu [email protected]

SRM Institute for Medical Sciences (SIMS), Chennai

61 Dr. Siddharth [email protected]

Dayanand Medical College & Hospital, Ludhiana

62 Dr. Soonu [email protected]

SRCC Children’s Hospital (NH), Mumbai

63 Dr. Suchitra [email protected]


64 Dr. Sunil [email protected]

Abu Dhabi Mafreq

65 Dr. Sunit [email protected]

Medanta (Medicity) Hospital, Delhi

66 Dr. Suresh [email protected]

Paramitha Childrens Hospital, Hyderabad

67 Dr. Thangavelu [email protected]

Dr. Mehta’s Hospital, Chennai

68 Dr. Uma Sankari [email protected]

Lilawati Hospital, Mumbai

69 Dr. Urmilla [email protected]

Maulana Azad Medical College, New Delhi

70 Dr. Venkataraman [email protected]

Children’s Hospital of Pittsburgh, USA

71 Dr. Vikas [email protected]

Fortis Memorial Research Institute, Gurgaon NCR

72 Dr. Vinay [email protected]

Kokilaben Hospital, Mumbai

73 Dr. Vishram [email protected]

Central India’s CHILD Hospital, Nagpur

74 Dr. VSV [email protected]

Lotus Children’s Hospital, Hyderabad

75 Dr. Vikram [email protected]

Genesis Hospital, New Delhi

76 Dr. [email protected]

Dr. Mehta’s Hospital, Chennai

77 Dr. Jignesh [email protected]

Nirmal Hospital, Surat

78 Dr. Naresh [email protected]

BLK Superspeciality Hosptal, Delhi

79 Dr Neeraj [email protected]

SGRH, Delhi

80 Dr Sujatha [email protected]

Rainbow Children’s Hospital, Bengaluru

81 Dr [email protected]

Rainbow Children’s Hospital, Vijay Wada




Rainbow Childrens Hospital, Bannerghatta Road Bangalore

83 Dr Deepika [email protected]

MAX Suprspeciality Hospital, Vaishali

84 Dr Maninder S [email protected]

Medanta the Medicity,Gurgaon

85 Dr Sameer [email protected]

Fortis Hospital, Mulund

86 Dr Supraja [email protected]

Peoples Tree Hospital, Bengaluru

87 Dr Neil [email protected]

Surya Hospital, Mumbai

88 Dr Rajappan [email protected]

Aster Medicity, Kochi


People Tree Hospital, Bengaluru

90 Dr Vikas [email protected]

SPS Hospital Ludhiana

91 Dr Satyen D [email protected]

Sparsh Multispeciality Hospital Bhilai, Chattisgarh

92 Dr Veena [email protected]

Medanta, The Medicity, Gurgaon

93 Dr Shipra [email protected]

MAX Superspeciality Hospital, Patpar Ganj, Delhi

94 Dr Ramesh Kumar [email protected]

DM, Institution is JIPMER Pondicherry

95 Dr Pradeep Kumar [email protected]

Sri Balaji Action Medical Institue, Delhi

96 Romit [email protected]

MAX Superspeciality Hospital Shalimar Bagh, Delhi

97 Dr Preeti [email protected]

MAX Superspeciality Hospital, Saket, New Delhi

98 Ashwath [email protected]

Manipal Hospital, Bengaluru


Rainbow Childrens Hospital, Vikram puri

100 Dr Chandrashekhar [email protected]

Rainbow Childrens Hospital, Delhi

101 Dr Vasanth [email protected]

Apollo Children’s Hospital, Chennai

102 Dr Ankur [email protected]

Kailash Hospital, Noida

103 Dr Sarvanan [email protected]


104 Priyavarthini [email protected]




Fundamental Pediatric Intensive Care Course FPICCThis is a two day course, designed to initiate, y

For more information: Contact Offi ce

introduce, and impart basic skills to a practicing pediatrician or to postgraduate students. The comprehensive course consists of didactics and hands on experience that takes one through basics of identifi cation of a sick child to managing shock, neurological emergencies, basic skills of mechanical ventilation, blood gas interpretation etc. The skill stations with smaller groups makes this uniquely interactive. This has been updated in March 2018.

Advanced Pediatric Intensive Care Course APICCThis is a two day course, designed to update the knowledge of a practicing pediatric intensivist. This comprehensive course consists of didactics on recent advances and hands on experience that takes one through advanced ventilation, diffi cult airway management, renal replacement therapy including CRRT, extra corporeal membrane oxygenation to name a few.

Advanced Pediatric Intensive Care Course

For more information: Contact Offi ce

Basic Pediatric Critical Care Nursing Course BPCCNCThis is a one day course for pediatric critical care nursing course, more useful for those who do have some exposure to PICU nursing, but also for beginners, and involved lectures and skill stations. Identifying a sick baby, monitoring, infection control, trouble shootingetc are some of the important part of this course.For more information: Contact Offi ce

For more information: Contact Offi ceOffi ce e-mail: [email protected]: www.collegeofpediatriccriticalcare.orgDr. Praveen Khilnani, MD FICCM FAAP MCCM(USA)Tel: 9810159466E mail: [email protected]

Chancellor College of Pediatric Critical CareFellowship in Pediatric Critical Care: Harvard Medical School American Board Certifi cation in Pediatrics and Pediatric Critical Care MedicineClinical Director and Senior Consultant Pediatric Critical Care and PulmonologyRainbow Childrens HospitalGitanjali (near malviyanagar metro station)New Delhi - 110017



Guidelines• All abstracts submitted should be in English• Abstracts must be submitted to: [email protected]• The submission process is as for any standard journal• Hard copies will not be accepted• Submission of more than one abstract by the same fi rst author

is permitted• Authors can submit their abstracts indicating their preference

as e-poster or oral presentation, however the fi nal decision will rest with the Abstract selection committee

Format• Abstracts are restricted to 400 words• Abstracts should not include any tables or graphs• References in the text have to be cited at the end of the abstract

(they are excluded from the word count)• All content of the abstract is in the sole responsibility of the

author(s) of the abstract

Process• You need to have registered for the conference to be able to

submit an Abstract• The deadline for Submission of Abstracts is 15th August,

2018• Intimation on acceptance of Abstract will be issued on 15th

September 2018• On approval, you will be invited to either present an Oral

Presentation or a Poster• Oral presentation and Poster presentation guidelines will be

intimated along with the approval email• For submission &queries, please write to journalccp@gmail.

com or [email protected]

RequirementsAbstracts will be chosen to be presented as either oral paper

International Pediatric Critical CareConference of India - IPCCCI 2018

AbstractsRequirement and guidance for submitting abstracts

presentations or a poster presentation. This year we give you the opportunity to submit your scientifi c work under the following categories• Neurocritical Care• Respiratory Critical Care• Cardiac Critical Care• Infectious Diseases• Nutritional and Gastrointestinal Critical Care• Renal, Endocrine and Metabolic• Oncological, Immunological and Hematological Critical Care• Epidemiology• Quality and Safety• Miscellaneous

AwardsCollege of Pediatric Critical care is proud to announce Awards for Scientifi c Paper Presentations to recognize the research work done in the fi eld of Pediatric Critical Care.

The Award categories are as follows1. CPCC Award for Oral Paper2. CPCC Award for Poster Presentation

• A structured ABSTRACT with the following subheadingso Backgroundo Objectiveso Methodso Resultso Conclusion

• Word count of abstract should not exceed 400 words• Abstract should not contain any tables, graphs, images or

illustrations• Clearly identify the person who will present the paper

(who will be the lead author andcontact person by default)and the said person must be a registered delegate at theConference


For Conference details: www.collegeofpediatriccriticalcare.org



th stDate: 20 & 21 October, 2018, Venue: (HICC) Hyderabad, Workshop/Courses : Date: 22nd & 23rd October, 2018

Registration Form

College ofPediatric Critical Care



After July - 6000/-15th Spot - 7500/- Before 15th July

PGs and Fellows - 3500/- Foreign Delegate USD 150/-

For PGs and Fellows a covering letter for their teaching institute will be required.

Registration Fee for Conference

5000/-

Conference Secretariat : Dr Dinesh K Chirla. Rainbow Children’s Hospital

Road No.2, Banjara Hills, Near L.V. Prasad Eye Institute. Hyderabad - 500034.

[email protected],Email: [email protected], praveenkhilnani [email protected]

Advisors :

Organizing Chairperson :

Organizing Secretary :

Co-Organizing Secretary :Scientific Committee :

Workshop Co-Chair :

Dr Soonu Udani, Dr Krishan Chugh,

Dr Praveen Khilnani (Mobile : + 91 9810159466)

Dr Dinesh Chirla (Mobile: + 91 9849790003)

Dr Farhan Shaikh

Dr Suchitra Ranjit, Dr Rajiv Uttam, Dr Anil SachdevDr VSV Prasad, Dr Nameet Jerath

Organizing Committee

Make your Payments at..

Fundamental Pediatric Critical Care (FPICC)

Advanced Pediatric Critical Care (APICC)

2 Days Dr Rajiv Uttam, Dr Anjul Dayal, Dr Rakshay Shetty

2 Days Dr Dinesh Chirla, Dr Farhan Shaikh, Dr Rajeshwari

Critical Care Ultrasound Dr Dhiren Gupta, Dr Nameet Jerath, 1 Day Dr Vikas Taneja

Pediatric Ventilation

Non Invasive Ventilation

(Two-days Courses : 22nd & 23rd / One-day workshop : 22nd Oct)

Dr V S V Prasad, Dr Praveen Khilnani1 Day Dr Anil Sachdev,

Dr Nand Kishore, Dr Manu S1 Day Dr Bala Ramachandran,

3000/-

3000/-

2000/-

2000/-

2000/-

After registration of the Course / Workshop, please share your payment details with:

Dr Farhan Shaikh - +91 9866007602, Mr. Mateen - +91 9701443111 / Mr. Srinivas - +91 7989393920 / 9949622702

or Email: [email protected] / [email protected]

Courses/Workshops

Name: ......................................................................................................................................................................................

Institution: ...............................................................................................................................................................................

Address: ...................................................................................................................................................................................

..................................................................................................................................................................................................

Email: .................................................................................... Tel No.: .....................................................................................

If you also wish to attend Course/workshop, then please mention your first three choices in order of preferences...

Preference # 1 : ........................................................................................................................................................................

Preference # 2 :.........................................................................................................................................................................

Preference # 3 :........................................................................................................................................................................

(Note: 40 seats are allotted per workshop and if your first preference if full, we shall offer your next preference)

Total amount (Conference with or without Workshop) paid : .................................................................................................

Your payment details (DD No/Online transaction ID / Cheque No./ Cash. Etc)........................................................................

.

Mode of Payment : DD/Cheques Payable to “ ”

Transfer Details : AXIS Bank Saket New Delhi. 110017. A/C No.: . IFSC:

SWIFT NO : AXISINBB160 for international wire

college of pediatric critical care A/c conference 2018

918010049712697 UTIB0000160

Pediatric Critical Care Nursing (PCCN) Dr Nirmal Choraria, Dr Rachna Sharma, Br. Sreejith 1 Day 500/-

PICU Procedures & Transports Dr Suresh Panuganti, Dr Hemkumar, Dr Chetan M.1 Day 2000/-

(22nd & 23rd Oct.)

(22nd & 23rd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

Pradeep

Inserted Text

Co-Organizing Secretary: Dr Farhan Shaikh


International

Pediatric

Critical Care


International

Pediatric

Critical Care

Conference of India - IPCCCI 2018Theme : Do it Now, Do it Right...

Organized by College of Pediatric Critical Care

Main Conference 20th and 21st October 2018 ,

Workshops / CME : 22nd & 23rd October 2018

A unique opportunity for practicing pediatricians, trainees, emergency

physicians and Intensivists for this customized event with academic excellence.

To download registration form or for On-line registration,

please log on to:www.collegeofpediatriccriticalcare.org

Invitation for Sponsorship




Dear Industry Partner,

It is our great pleasure to invite you to participate in the 1st International Pediatric Critical Care Conference of India

(IPCCI-2018)which will be held from October 20th-23rd, 2018 at HICC, Hyderabad.

This innovative conference will include presentations and discussions on promoting, learning and collaboration for

the care we provide to children with critical illness and their families.

National and International domain experts from across the globe will lead academic deliberations and represent

their point of views.

You will benefit from outstanding advantages linked to your supporter category.

We humbly invite to participate in this great effort by becoming the sponsors for the conference in various categories.

Industry support is vital to the success of this conference and demonstrates your commitment to improving

patient care

You will be given a support category status dependent upon the total amount of your support contribution. The total

contribution will consist of items such as advertisements, sponsored sessions and exhibition space.

DIAMOND 30 Lac Logo Recognition on Conference Website and on the sponsorship page.

Logo recognition on the Conference banners and Standies

Logo recognition on conference promo material inside the delegate kits.

One complementary exhibit “premier stalls” & Two Normal stalls

Full colour inside page advertisement in the conference book of abstracts

GOLDGOLD SILVER 10 Lac BRONZE 5 Lac

Logo recognition on the

Conference banners and Standees

Logo recognition on conference

promo material inside the

delegate kits.

One complementary exhibit

“premier stalls” & One Normal stall

Half-page coloured

advertisement in the conference

book of abstracts / Journal

Logo recognition on conference

promo material inside the

delegate kits.

Two complementary exhibit

“Normal stall”

Half-page coloured



One complementary exhibit

“Normal stall”

1/4th page coloured



BRONZE20 Lac20 Lac 10 Lac 5 Lac

Mode of Payment : DD/Cheques Payable to “ ”

Transfer Details : AXIS Bank, Saket, New Delhi. 110017. A/C No.: . IFSC:

SWIFT NO : AXISINBB160 for International wire


918010049712697 UTIB0000160

For a normal Stall 1.5 Lakh INRsFor Sponsorhip of a session 2.5 Lakh INRs For Premium Stall 2 Lakh INRs

Dates: 20th - 23rd October, 2018Scientific Highlights: (for more details log on to www.collegeofpediatriccriticalcare.org)

Hands-on Courses/Workshops

(Two-days Courses : 22nd & 23rd / One-day workshop : 22nd Oct)

National Faculty includes..

All Renowned Pediatric Intensivist from the Country

Dr Soonu Udani, Mumbai

Dr Krishan Chugh, Delhi

Dr Praveen Khilnani, Delhi

Dr Suchitra Ranjit, Chennai

Dr Anil Sachdev, Delhi

Dr Rajiv Uttam, Delhi

Dr Bala Ramachandran, Chennai

Dr Deepika Chennai

Dr Madhumati Otiv, Pune

...and more to join....

International Faculty includes..

Dr Mohan Mysore, Dr Utpal Bhalala

Dr Peter Cox, Dr Bhushan Katira

Dr Shekhar Venkatraman

Dr Akaash Deep, Dr Gayathri Subramanian

Dr Mehak Bansal

Dr Rahul joshi

Dr Manu Sundaram

Dr Satoshi Nakagawa

Abstract submission for Posters/Oral presentations

Submits Abstracts at : [email protected], For Further details contact

Dr Pradeep Sharma , E : [email protected]. +91 9868797049Last date for abstract submission :

15th August 2018

Scientific discussion on hot topics in pediatric critical care and emergency medicine

Exciting workshops covering all dimensions of pediatric critical care

Research Poster / Oral presentations and hunt for the “Young Talent”

Annual convocation for the teachers and fellows of College of Pediatric Critical Care

Fundamental Pediatric Critical Care (FPICC) 2 Days Dr Rajiv Uttam, Dr Anjul Dayal, Dr Rakshay Shetty 3000/- Venue: Continental Hospital, Gachibowli, Hyderabad.

Advanced Pediatric Critical Care (APICC) 2 Days Dr Dinesh Chirla, Dr Farhan Shaikh, Dr Rajeshwari 3000/-

Venue: Rainbow Children’s Hospital, Banjara Hills, Hyderabad.

Critical Care Ultrasound Dr Dhiren Gupta, Dr Nameet Jerath, 1 Day Dr Vikas Taneja 2000/-

Venue: Aditya Hospital, Hyderabad

Venue: Lotus Children’s Hospital, Hyderabad

Pediatric Ventilation Dr V S V Prasad, Dr Praveen Khilnani1 Day Dr Anil Sachdev, 2000/-

Non Invasive Ventilation Dr Nand Kishore, Dr Manu S1 Day Dr Bala Ramachandran,

Venue: Krishna Institute of Medical Sciences (KIMS), Hyderabad

2000/-

Venue: Nice Children’s Hospital, Hyderabad

Pediatric Intensive Care Procedures

& Transports

Dr Suresh Panuganti, Dr Hemkumar, Dr Chetan Mundada 1 Day 2000/-

Pediatric Critical Care Nursing (PCCN) Dr Nirmal Choraria, Dr Rachna Sharma, Br. Sreejith 1 Day 500/-

Venue:

Workshops & Courses

After registration for the Course / Workshop, please share your choice with:

Dr Farhan Shaikh - +91 9866007602 or Mr. Mateen- + 91 9701443111 or Mr. Srinivas- + 91 7989393920 / 9949622702

or Email: [email protected] / [email protected]

Dr Dinesh Chirla, Hyderabad

Dr VSV Prasad, Hyderabad

Dr Dhiren Gupta, Delhi

Dr Nameet Jerath, Delhi

Dr Farhan Shaikh, Hyderabad

Dr Anjul Dayal, Hyderabad

Dr Parag Dekate, Hyderabad

Dr Rakshay Shetty, Bangalore

(22nd & 23rd Oct.)

(22nd & 23rd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

(22nd Oct.)

After July - 6000/-15th Spot - 7500/- Before 15th July

PGs and Fellows - 3500/- Foreign Delegate USD 150/-

For PGs and Fellows a covering letter for their teaching institute will be required.

Registration Fee for Conference

5000/-

PROGRAMME SCHEDULE

Duration Time Module

08:00am – 09:00am

30 min 09:00am – 09:30am

DAY - 1

Emergency Room Guidelines and Algorithms:

Diving Deep: Ventilation

Care of patient on ECMO: Challenges and Trouble-shooting

PLENARY 2 : The thin line between success and failure in PICU09:30am – 10:00am 30 min

APRV: the new workhorse in the armamentarium against ARDS10:10am – 10:30am

Ventilator asynchrony: Tips &tricks to succeed

10:30am – 10:50am 20 min Smooth weans and successful extubations: How do I get it right? 10:50am – 11:10am 20 min

11:10am – 11:20am 10 minTEA BREAK

Let’s put it to Practice – Refractory hypoxemia case scenario11:20am – 11:40am

20 min 11:40am – 12:00pm

• Zero medical error – achievable or fantasy?• Choosing the right quality indicators• Cost containment and quality – can they go together?

Quality meets Safety: Indian scenario

12:00pm – 12:40pm 40 min

Corticosteroids in Critical Illness:

It’s All About the Right Dose, Right Time, and Right Duration 12:40pm – 01:00pm 20 min

60 minLUNCH BREAK

01:00pm – 02:00pm

• Septic shock: How I integrate hemodynamic variables at the bedside • Overlooked causes of refractory shock – Diastolic / RV failure• The numbers look good, but patient not great: Remember the microcirculation

Bedside Rounds in Septic shock: Help! My patient is still in shock after the initial fluid bolus

60 min 02:00pm – 03:00pm

PRO-CON debate: Adrenaline vs noradrenaline as a first line agent in septic shock03:00pm – 03:20pm 20 min

PICU related delirium - what do we really know? 03:40pm – 04:00pm 20 min

• How I prescribe Antibiotics in order to maximize efficacy and minimize drug resistance• Severe community-acquired MRSA infections• Combating serious Gram-Negative infections in PICU

Panel Discussion : Smart antibiotic prescriptions in the ICU

60 min 04:00pm – 05:00pm

PICU QUIZ

05:00pm – 05:40pm 40 min

PLENARY 1 : Understanding Stress and strain in Ventilator induced Lung Injury (VILI)

10:30am – 11:20am

11:20am – 11:40am 20 min Fact or fiction?Surviving acute liver failure without transplant

20 min 11:40am – 12:00pm When drugs don’t work:Remembering principles of PK / PD in the critically ill

60 min 12:00am – 01:00pm Free papers

01:00pm – 02:00pm LUNCH BREAK60 min

60 min

20 min

20 min

DAY - 2


60 min 08:00am – 09:00am

30 min 09:00am – 09:30am

Dandi march at Sunrise Case based panel-discussion: Sodium disorders

Half-a-dozen myths in neurocritical CareTiered approach to ICP managementNIRS and cEEG in the neuro-critical care patient

Need a Heads-Up? Unravelling the Neural network

Plenary 3 : Growth of Pediatric Intensive Care in India: Views from near and afar

09:30am – 09:45am

09:45am – 10:00am 15 min

15 min

Take the drama out of trauma: Damage control Resuscitation10:00am – 10:20am 20 min

10 min 10:20am – 10:30am TEA BREAK

The Art of Medicine: Making difficult conversations better(10 minutes each)

• The Language of Caring – what you say and how you say it matters• Disclosure Training – conveying medical missteps to families• Medicolegal aspects of consent and documentation • Brain death certification: current certification• Legality of DAMA/ DNR

50 min

02:00pm – 02:30pm 30 min PRO-CON: Closed vs Open ICU: what is best for the patient?

60 min 02:30pm – 03:30pm Landmark papers that changed my practice- Session 1(6 papers from various Teaching Units)

15 min 03:30pm – 03:45pm Organ cross-talk and therapeutic conflict: When mechanical lung meets artificial kidney

15 min 03:45pm – 04:00pm PICU Game-changer:Goal Directed Sedation

15 min 04:15pm – 04:30pm More than 50 shades of Grey: Deciphering TAMOF/TTP/HUS

55 min 04:35pm – 05:30pm • Transitioning into the Real World: Viewpoint of two Recent Graduates • Winners of Young Talent Hunt

Training Our Trainees: How are we doing?

IPCCCI- Scientific Programme DIVING DEEP: Day 1 & 2College of

Pediatric Critical Care

www.rainbowhospitals.in

60 min 08:00am – 09:00am 30 min 09:00am – 09:30am

Emergency Room Guidelines and Algorithms: (COMMON to both Halls) Understanding Stress and strain in Ventilator induced Lung Injury (VILI) (COMMON)PLENARY 1 :

PLENARY 2 : The thin line between success and failure in PICU(COMMON to both Halls)30 min 09:30am – 10:00am

1. NIV and HFNC- A gentle way to avoid intubation2. Safe intubation practice in the critically ill child3. pARDS: An algorithmic approach 4. Lung recruitment and proning5. Prevention of ventilator associated pneumonia6. Fast track weaning and Liberation (ABCDE approach)7. QA

From Start to Finish : Smart Strategies in Airway and Ventilation10:00am – 10:15am 10:15am – 10:30am 10:30am – 10:45am 10:45am – 11:00am 11:00am – 11:15am 11:15am – 11:30am 11:30am – 11:45am

15 minEach

12:00pm – 12:20pm 12:20pm – 12:40pm 12:40pm – 01:00pm

20 minEach

LUNCH BREAK

01:00pm – 02:00pm 60 min20 min 02:00pm – 02:20pm PRO-CON debate:Midazolam-fentanyl is the best sedative combo for PICU ventilation

Learn the Art and Craftof Infection Control from the expertsPanel discussion: Infection control and antibiotic stewardship

02:20pm – 03:20pm

Septic shock management- Step by Step

1.Precision management of septic shock using ECHO2.Rise and fall of the legend-Dopamine3.De-resuscitation in septic shock

50 min

03:30pm – 04:15pm

Less is MORE- Choosing wisely ( 10 mins each)

• Transfusion practice in ICU• Cross referrals in critically ill• Ordering Investigations • Buying a new ventilator

45 min

04:15pm – 05:00pm 45 min

05:00pm – 05:40pm 40 min PICU QUIZ(COMMON to both Halls)

PROGRAMME SCHEDULE


DAY - 1

PICU Potpourri

Top Pearls in burns management for the Intensivist How to optimise nutrition in critically ill: Do's and don'ts Stings and bites – practical aspects in countering the sting operation

Yeh Dil Maange More

• How I decide on my choice of RRT: PD vs SLEDD vs CRRT • Acute Encephalitis syndromes including auto-immune encephalitis and Acute

Necrotizing Encephalitis

09:30am – 09:45am 09:45am – 10:00am

15 min

Pro-con debate: Kal Aaj aur KalCVP is useful for fluid management decisions in my ICU

12:00pm – 01:00pm Free paper session (2)60 min

02:00pm – 02:20pm 20 min

02:30pm – 03:30pm 60 min Landmark papers that changed my practice (6 papers from various Teaching Units)

Difficult management decisions : Managing a child with severedengue in the ICU

Fluid management in severe dengue Pitfalls in management of complicated dengue How I treat Hyper-ferritinemia with multi-organ failure

03:30pm – 03:50pm

03:50pm – 04:10pm

04:10pm – 04:30pm

20 minEach

60 min Transitioning into the Real World: Viewpoint of two recent graduates Winners of Young Talent Hunt (2 speakers)

Training Our Trainees: How are we doing?(COMMON to both Halls)


DAY - 2

60 min 08:00am – 09:00am

30 min

Dandi march at Sunrise Case based panel discussion: Sodium disorders (COMMON to both Halls)Plenary 3: Growth of Pediatric Intensive Care in India: Views from far and near (COMMON to both Halls)

09:00am – 09:30am

Each

How I do it : Clinical Conundrums

DKA – Algorithmic approach Optimising aerosol delivery in NIV and ventilated patients Pitfalls in Haematological emergencies

11:20am – 11:40am 11:40am – 12:00pm

20 minEach

04:30pm – 05:30pm

IPCCCI- Scientific Programme (Hall B)DAY -1 & 2: Basic to Advanced PICU College of

Pediatric Critical Care

Organizing Committee

Hyderabad, INDIAHICC Hyderabad, INDIA

DD/Cheques Payable to “ ”

Transfer Details : AXIS Bank, Saket, New Delhi. 110017. A/C No.: . IFSC:

SWIFT NO : AXISINBB160 for International wire


918010049712697 UTIB0000160

Mode of Payment

Conference Venue : HICC HyderabadConference Secretariat : Dr Dinesh K Chirla. Rainbow Children’s Hospital

Road No.2, Banjara Hills, Near L.V. Prasad Eye Institute. Hyderabad - 500034.


Advisors :

Organizing Chairperson :

Organizing Secretary :

Co-Organizing Secretary : Scientific Committee :

Workshop Co-Chair :

Dr Soonu Udani, Dr Krishan Chugh,

Dr Praveen Khilnani (Mobile : + 91 9810159466) Dr Dinesh Chirla (Mobile: + 91 9849790003)

Dr Farhan ShaikhDr Suchitra Ranjit, Dr Rajiv Uttam, Dr Anil Sachdev

Dr VSV Prasad, Dr Nameet Jerath

Finance Committee

Dr Bala Ramachandran,

Dr Dinesh Chirla, Dr VSV Prasad,

Dr Farhan Shaikh, Dr Nirmal Choraria

Dr Anjul Dayal, Dr Madhumati Otiv,

Dr Vikas Taneja, Dr Preetham Reddy

Dr Anil Sachdev

Organizing Committee Hyderabad : Dr Nandkishore, Dr Pritesh, Dr Suresh Panda, Dr Parag Dekate, Dr Chetan M, Dr Suresh Panuganti

Dr Anupama Yerra, Dr Kishore Jaishi, Dr Amer Altaf, Dr Avash Pani, Dr Anupama Bahe, Dr Paritosh, Dr Akheel Rizwan,

Dr Chandrashekhar K, Dr Satyanarayana,

To download registration form or for On-line registration,

please log on to:www.collegeofpediatriccriticalcare.org

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Pradeep

Inserted Text

Co-Organizing Secretary: Dr Farhan Shaikh

Pradeep

Sticky Note

Unmarked set by Pradeep

Conference Secretariat: Dr Dinesh K Chirla, Rainbow Children’s HospitalRoad No.2, Banjara Hills, Near L. V. Prasad Eye Institute, Hyderabad - 500034.


Fundamental Pediatric Critical Care (FPICC) 2 Days Dr Rajiv Uttam, Dr Anjul Dayal, Dr Rakshay Shetty ` 3000/-

Advanced Pediatric Critical Care (APICC) 2 Days Dr Dinesh Chirla, Dr Farhan Shaikh, Dr Rajeshwari ` 3000/-

Critical Care Ultrasound 1 Day Dr Dhiren Gupta, 1 Day Dr Nameet Jerath, Dr Vikas Taneja ` 2000/-

Pediatric Ventilation 1 Day Dr V S V Prasad, Dr Anil Sachdev, Dr Praveen Khilnani ` 2000/-

Non Invasive Ventilation 1 Day Dr Bala Ramachandran, Dr Nand Kishore, Dr Manu S ` 2000/-

PICU Procedures & Transports 1 Day Dr Suresh Panuganti, Dr Hemkumar, Dr Chetan M ` 2000/-

Pediatric Critical Care Nursing (PCCN) 1 Day Dr Nirmal Choraria, Dr Rachna Sharma, Br. Sreejith ` 500/-

International Pediatric Critical CareConference of India - IPCCCI 2018

Organized by College of Pediatric Critical CareTheme: Do it Now, Do it Right...

Main Conference: 20th and 21st October, 2018 | Workshops/CME : 22nd & 23rd October, 2018

Venue : HICC Hyderabad, India

A unique opportunity for practicing pediatricians, trainees, emergency physicians and Intensivists for this customized event with academic excellence.

Conference Highlights:

(for more details log on to www.collegeofpediatriccriticalcare.org)

Conference Registration

Courses/Workshops

Courses/Workshops

International Faculty includes..

` 5000/- After 15th July - ` 6000/- Spot - ` 7500/-

PGs and Fellows - ` 5000/- Foreign Delegate USD 150/-

Dr Shekhar VenkatramanDr Mohan MysoreDr Utpal Bhalala

Dr Akaash DeepDr Gayathri SubramanianDr Mehak Bansal

Dr Manu Sundaram Dr Satoshi Nakagawa

Dr Rahul JoshiDr Peter CoxDr Bhushan Katira

(Two-days Courses : 22nd & 23rd / One-day workshop : 22nd October)

Advisors: Dr Soonu Udani, Dr Krishan ChughOrganizing Chairperson: Dr Praveen Khilnani (Mobile: + 91 9810159466)Organizing Secretary: Dr Dinesh Chirla (Mobile: + 91 9849790003)Co-Organizing Secretary: Dr Farhan ShaikhScientifi c Committee: Dr Suchitra Ranjit, Dr Rajiv Uttam, Dr Anil SachdevWorkshop Co-Chair: Dr VSV Prasad, Dr Nameet Jerath

Abstract submission for Posters/Oral presentations

Submits Abstracts at: [email protected] Further details contact

Dr Pradeep Sharma

Email: [email protected] | M: +91 9868797049

Last date for abstract submission: 15th August, 2018

After registration for the Course / Workshop, please share your choice with:

Dr Farhan Shaikh - +91 9866007602 orMr. Mateen - +91 9701443111 orMr. Srinivas - +91 7989393920 / 9949622702or Email: [email protected] / [email protected]

Finance Committee

Dr Bala Ramachandran, Dr Anil SachdevDr Dinesh Chirla, Dr V S V PrasadDr Farhan Shaikh, Dr Nirmal ChorariaDr Anjul Dayal, Dr Madhumati Otiv,Dr Vikas Taneja, Dr Preetham Reddy

Mode of Payment: DD/Cheques Payable to “college of pediatric critical care A/c conference 2018”Transfer Details: AXIS Bank Saket New Delhi. 110017 | A/C No.: 918010049712697 | IFSC: UTIB0000160 | SWIFT No: AXISINBB160 for international wire

• Renowned National and International Faculty • Research Poster / Oral presentations and hunt for the “Young Talent”• Scientifi c discussion on hot topics in pediatric critical care and

emergency medicine• Annual convocation for the teachers and fellows of College of

Pediatric Critical Care• Exciting workshops covering all dimensions of pediatric critical care


critical care pediatricscollegeofpediatriccriticalcare.org/wp-content/uploads/2018/06/ccp... ·...

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