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KONIKA XIX Proceeding Book Rev 120225

The document outlines the 19th National Congress of the Indonesian Pediatric Society (KONIKA XIX) scheduled for September 27 to October 1, 2024, in Semarang and Solo, with the theme 'Ensuring Equal Access of Childcare in the Era of Society 5.0.' It includes details about workshops, organization meetings, and a scientific congress aimed at improving child healthcare through technological advancements. The congress aims to address disparities in healthcare access for children in Indonesia and promote better health outcomes through collaboration among pediatric professionals.

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0% found this document useful (0 votes)
553 views182 pages

KONIKA XIX Proceeding Book Rev 120225

The document outlines the 19th National Congress of the Indonesian Pediatric Society (KONIKA XIX) scheduled for September 27 to October 1, 2024, in Semarang and Solo, with the theme 'Ensuring Equal Access of Childcare in the Era of Society 5.0.' It includes details about workshops, organization meetings, and a scientific congress aimed at improving child healthcare through technological advancements. The congress aims to address disparities in healthcare access for children in Indonesia and promote better health outcomes through collaboration among pediatric professionals.

Uploaded by

justmokhtar
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter


supported by
Indonesian Pediatric Society

PROCEEDING BOOK

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG
Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

SEKRETARIAT
IKATAN DOKTER ANAK INDONESIA – CABANG LAMPUNG Indonesian Pediatric Society
– Central Java Chapter
Gedung Alamanda Lantai 4 (Ruang KSM / Bagian Ilmu Kesehatan Anak)
RSUD dr. H. Abdul Moeloek Provinsi Lampung Jl. Kyai Saleh 15 (Gergaji), Semarang -50231
Jl. dr. A. Rivai No. 6 Penengahan, Bandar Lampung
Email: [email protected] Cabang Jawa Tengah Email: [email protected]
PIC: dr. Songgot Nauli BR Girsang, Sp.A +6282144796717
Kurnia Ari Ningtyas +6281272224638

PROCEEDING BOOK KONIKA XIX


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

PROCEEDING BOOK

The 19th National Congress of Indonesian Pediatric Society

(KONIKA XIX)

Semarang – Solo 2024

“Ensuring Equal Access of Childcare in the Era of Society 5.0”

Editor:
Dr. dr. Mexitalia Setiawati E.M, Sp.A(K)
Dr. dr. Agustini Utari, Sp.A(K)
dr. M. Supriatna, Sp.A(K)
dr. Vianandra Renani, Sp.A

Reviewer:
dr. Tartila, Sp.A(K)
dr. Lies Dewi Nurmalia, Sp.A(K)
dr. Nina Dwi Putri, Sp.A(K), M.Sc(TropPaed)

Hak Cipta Dilindungi Undang-Undang

Dilarang memperbanyak, mencetak, dan menerbitkan sebagian atau seluruh isi buku ini
dengan cara dan bentuk apapun juga tanpa seizing penulis dan penerbit

Diterbitkan oleh

Badan Penerbit Ikatan Dokter Anak Indonesia

PROCEEDING BOOK KONIKA XIX


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

FOREWORD
President of Indonesian Pediatric Society

Assalamualaikum wr.wb.

Greetings to all of us. Praise to God Almighty, for by His protection, all of us, fellow General Practitioners and
Pediatricians will gather once again at the 19th National Congress of Indonesian Pediatrics Society (KONIKA XIX)
in Semarang-Solo 2024.

As we are aware, this year's KONIKA theme is "Ensuring Equal Access of Childcare in The Era of Society 5.0". The
Society 5.0 era is an era when technologies such as the internet, big data, and artificial intelligence are leveraged
to enhance the quality of human life and solve social problems. In the realm of child healthcare, aimed at improving
children's health and well-being, we should integrate technology to provide smarter, more humane, and sustainable
healthcare services.

In recent years, Indonesia has made progress in various fields, but there are still some areas where healthcare
access remains unequal. According to UNICEF statistics in 2018, around 12 % of Indonesian children live below
the poverty line. This disparity results in inadequate sanitation facilities, incomplete immunizations, lack of health
insurance, malnutrition, limited access to basic education, and barriers to adequate healthcare services. To address
these challenges, we must leverage technological advancements to overcome barriers to healthcare access.
For instance, utilizing telemedicine, maximizing social media for disseminating crucial knowledge, particularly to
expectant mothers, emphasizing the importance of preventive behaviors such as complete routine immunizations
for children, exclusive breastfeeding for the first six months, regular visits to integrated health posts (Posyandu),
providing nutritious and protein-rich complementary feeding for infants over six months. Aside from that, we must also
ensure a comprehensive immunization coverage nationwide, good newborn screening practices, non-communicable
disease management, and so forth. The ultimate goal is to cultivate long-term health among Indonesian children to
ensure they become exceptional human resources in the future.

Hopefully the 19th National Congress of Indonesian Pediatric Society (KONIKA XIX Semarang-Solo 2024) brings
forth advancements to empower us as General Practitioners and Pediatricians. Our role is crucial in enhancing child
healthcare quality for their optimal growth and development.

I personally extend my gratitude to all participants who have actively engaged in the KONIKA XIX Semarang-Solo
2024. Hopefully, this event serves as a valuable platform for both Pediatricians and General Practitioners to expand
their knowledge in child healthcare. Let us work together to ensure excellent healthcare services for our children.

Wassalamualaikum, Wr Wb

President of Indonesia Pediatric Society


dr. Piprim Basarah Yanuarso, Sp.A(K)

ii PROCEEDING BOOK KONIKA XIX


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

FOREWORD
Chairman of Indonesian Pediatric Society – Central Java Chapter

Assalamu’alaikum Wr.Wb.

Dear Colleagues,

The 3rd KONIKA in Central Java is being held this time after it was first held in 1968 and the 9th in 1993. IDAI Central
Java Branch is a branch of IDAI that has two Pediatric Specialist Education Institutes (IPDSA) located in Solo and
Semarang. We deliberately held the pre-congress activities in Solo at the same time as the congress activities in
Semarang with the hope that all IDAI members could learn more about the cultural and culinary diversity that exists
in the Central Java region so that they could have a pleasant experience during the conference.

Bringing the theme "Ensuring Equal Access to Child Care in the Era of Society 5.0" really challenges us as the
pediatrician profession to be able to transform health services in line with technological advances. In today's rapidly
evolving world, where technological advances are revolutionizing every aspect of our lives, it is important that we
leverage these innovations to create positive change in healthcare delivery. One of the most pressing challenges
we face as a nation is the high infant and child mortality rate, which can be significantly reduced with targeted
interventions and increased access to quality health services.

We have the power to change the health conditions of the nation's children and pave the way to a brighter and
healthier future for future generations. It is hoped that the 19th KONIKA will provide benefits and enthusiasm to
start this transformative journey together, with mutual synergy, determination and a shared vision for a healthier
Indonesia for all.

We, all members of IDAI Central Java Branch, are very enthusiastic about welcoming the 19th KONIKA activities.

Ke Solo beli serabi, Ke semarang makan lumpia


Ayo datang bersilaturahmi, bersama keluarga kita ke KONIKA

Wassalamu’alaikum wr. Wb.

Chairman of Indonesian Pediatric Society - Central Java Chapter


Dr. dr. Fitri Hartanto. Sp.A(K)

PROCEEDING BOOK KONIKA XIX iii


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

FOREWORD
Chairman of KONIKA XIX

It is a great honour and pleasure to welcome you to this prestigious 19th Indonesian Congress of Pediatrics
(KONIKA) 2024, organized by the Indonesian Pediatric Society - Central Java Branch, mandated by the
National Board of the Indonesian Pediatric Society. The congress will be held from September 27th to October
1st, 2024, at the Harris & Swiss-Belinn Saripetojo Hotel, in Solo and the Padma Hotel in Semarang Central
Java

The theme of the 19th congress is "Ensuring Equal Access to Childcare in the Era of Society 5.0." We offer pre-
congress workshop, keynote speeches, plenary sessions, plenary symposia, parallel symposia, breakthrough
symposia, lunch symposia, meet-the-experts sessions, free paper symposia, and poster sessions. This
scientific congress provides pediatric professionals with a platform to advance their understanding of pediatric
healthcare. We believe that all participants will be inspired to apply what they have learned in their daily
practices.

We do hope that your visit to Solo and Semarang will be an unforgettable experience for you. Solo and
Semarang offer various historically significant tourist destinations such as the Surakarta Palace, batik craft
centers, Borobudur Temple, Gedong Songo, Sampoo Kong, and the Old Town of Semarang, also known as
Little Netherlands. Additionally, there is a wide variety of delicious local cuisine in Solo and Semarang that is
sure to tantalize your taste buds. It goes without saying that Solo and Semarang are rich in traditional culture,
batik craftsmanship, Jepara teakwood carvings, and more.

On behalf of the Committee, I extend my best wishes for a fruitful and enjoyable congress. We eagerly
anticipate your participation.

Warm regards,

Chairman of the Organizing Committee


dr. Mohamad Supriatna TS, Sp.A(K)

iv PROCEEDING BOOK KONIKA XIX


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

ORGANIZING COMMITTEE
COMMITTEE PATRON

• Governor of Central Java


• Mayor of Semarang District
• President of Indonesian Medical Association

ADVISORY BOARD

• Rector of Diponegoro University, Semarang


• Dean of Faculty of Medicine Diponegoro University, Semarang
• Director of Dr. Kariadi General Hospital
• Chairman of Indonesian Medical Association of Central Java

STEERING COMMITTEE

• President of Indonesian Pediatric Society


• President of The Indonesian College of Pediatric
• Chairman I of Indonesian Pediatric Society
• Chairman II of Indonesian Pediatric Society
• Chairman III of Indonesian Pediatric Society
• Chairman of Ethics Board Indonesian Pediatric Society
• Chairman of Indonesian Pediatric Society, Central Java Chapter

ORGANIZING COMMITTEE

• Chairman : dr. M. Supriatna TS, Sp.A(K)


• Vice Chairman : Dr. dr. Hari Wahyu Nugroho, Sp.A(K)., M.Kes
• Secretary : dr. Ariawan, Sp.A
dr. Juwita Pratiwi, Sp.A
dr. Nisa Alifia, Sp.A
dr. Gerin Orviyanti, Sp.A
• Vice Secretary : Dr. dr. Hikari Ambara Sjakti, Sp.A(K)
Dr. dr. Putri Maharani Tristanita Marsubrin, Sp.A(K)
• Treasurer I : dr. Nahwa Arkhaesi, M.Si.Med., SpA
• Treasurer II : dr. Stephanie Adelia, Sp.A
• Treasurer III : dr. Rosalia Dewi Roeslani, Sp.A(K)

1st DIVISION: ORGANIZATION

• Field Advisory Board : dr. Bambang Sudarmanto, Sp.A(K)., MARS


• Coordinator : Dr. dr. MS Anam, M.Si.Med., Sp.A
• IDAI Meeting Session : dr. Abdul Hakam, Sp.A
Dr.dr. Qodri Santosa, Sp.A
dr. Hery Susanto, Sp.A
dr. Lilia Dewiyanti, Sp.A
dr. Krisna Adhi Nugraha, Sp.A
• Collegium Meeting : Dr. dr. M. Heru Muryawan, Sp.A(K)
Session Dr. dr. Hendriani Selina, Sp.A(K)
• Professional Credit : dr. Rosalia Desi Susanto, Sp.A
Certification (SKP)

PROCEEDING BOOK KONIKA XIX v


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

2ND DIVISION : EXHIBITION AND VENUE

• Field Advisory Board : Dr. dr. M. Heru Muryawan, Sp.A(K)


• Coordinator : dr. Setya Dipayana, Sp.A
• Technology, Information : dr. Tun Paksi Sareharto, M.Si.Med., Sp.A(K)
& Publication dr. Akhad Kartika, Sp.A
dr. David Anggara Putra,Sp.A
dr. Rekno Widati, Sp.A
• Funding & Partnership : dr. Bambang Sudarmanto, Sp.A(K)., MARS
dr. Gatot Irawan, Sp.A(K)
Dr. dr. Moedrik Tamam, Sp.A(K)
Dr. dr. Fitri Hartanto, Sp.A(K)
• Venue’s Equipment : dr. Setya Dipayana, Sp.A
Dr. dr. Muh. Riza, Sp.A(K)., M.Kes
dr. Bagus Artiko, Sp.A(K)., M.Kes
dr. Susilo Adi Nugroho, Sp.A
• Event Planning : dr. Adhie Nur Radityo, M.Si.Med., Sp.A(K)
dr. Farid Agung Rahmadi, M.Si.Med., Sp.A(K)
dr. Sri Martuti, Sp.A(K)., M.Kes
Dr. dr. Dwi Hidayah,Sp.A(K)., M.Kes
dr. Erna Mirani, Sp.A
dr. Anna Mariska, Sp.A
dr. Rio Gasa Handriyo
dr. Wahyu Adhitya Prawirasatra
dr. Dody Eka Setiawan
dr. Melisa Berlian
dr. Albertus Febrianto Slamet Riyono
dr. Risa Haryati Tambunan
dr. Yesita Novia Hertina
dr. Evelyn Meiliani Panji Putri
• Registration : dr. Astra Parahita, Sp.A
Dr. dr. Ismiranti Andarini, Sp.A(K)., M.Kes
dr. Pitra Sekar Handini,Sp.A
3RD DIVISION : SCIENTIFIC

• Field Advisory Board : Prof. Dr. dr. Harsono Salimo, Sp.A(K)


dr. Nina Dwi Putri, Sp.A(K)., M.Sc.TropPaed
dr. Lies Dewi Nurmalia, Sp.A(K)
• Coordinator : Dr. dr. Mexitalia Setiawati E.M, Sp.A(K)
• Pre Congress Workshop : Dr.dr. Annang Giri Moelyo, Sp.A(K)., M.Kes
dr. Rina Pratiwi, MSi.Med, Sp.A(K)
dr. Arsita Eka Rini, MSi.Med, Sp.A(K)
dr. Septin Widiretnani, Sp.A(K)., M.Kes
dr. Dewinda Candrarukmi, Sp.A
dr. Gloria Sheila Ratna Utari
dr. Dyota Sulia Mutiari
• Symposium session : Dr. dr. Omega Mellyana, Sp.A(K)
Dr. dr. Ninung Rose Diana K, Sp.A(K)
dr. Mulyono, Sp.A
dr. Anna Mariska, Sp.A
dr. Maria Septiani N. P. Nasution
dr. Ajrina Luthfita Bayu Putri
dr. Novia Khoerunnisa
dr. Adinda Ratna Puspita
• Lunch and Break Symposium :
dr. Yusrina Istanti, MSi.Med., Sp.A(K)
dr. Rr. Retno Suminar
vi
PROCEEDING BOOK KONIKA XIX dr. Irwan Nuryadin
Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

Free paper : dr. Wistiani, M.Si.Med, Sp.A(K)


Dr. dr. Anindita Soetadji, Sp.A(K)
dr. Galuh Hardaningrum, M.Si.Med., Sp.A(K)
dr. Samuel Raditya Wibawa
dr. Yohannes Kurniawan Soeparno
dr. Prabha Vignesvari Sasongko
Best Research award (and Collegium session) :
dr. Yetty Movieta Nency, Sp.A(K)
dr. Randy Renaldo Witara
dr. Priskila Tania Damitrias
dr. Jeslyn Tengkawan
Scientific Publication : Dr. dr. Agustini Utari, M.Si.Med., Sp.A(K)
Dr. dr. Annang Giri Moelyo, Sp.A(K)., M.Kes
dr. Vianandra Retnani, Sp.A
dr. Ardana Windriy
dr. Stefhani Gista Luvika

4TH DIVISION : HEALTH & SUPPORT


Field Advisory Board : Dr. dr. Alifiani Hikmah Putranti, Sp.A(K)
Coordinator : dr. Dimas Tri Anantyo, Sp.A
Accommodation & : dr. Ricky Wibisono, Sp.A
Transport dr. Andrew Hartono, Sp.A
Dr. dr. Fadhilah Tia Nur, Sp.A(K)., M.Kes
Non Scientific : dr. Agus Saptanto, Sp.A
Committee dr. Hartono, Sp.A
dr. Endang Sulistyowati, Sp.A
dr. Rivai Koesen, Sp.A
dr. Marcella Trixie, Sp.A
dr. Patricia Vaness Antolis, Sp.A
dr. Monica Katherina, Sp.A
dr. Afriliana Mulyani, Sp.A
Food & Beverage : dr. Dewi Ratih, M.Si.Med., Sp.A(K)
dr. Dian Emiria, Sp.A
dr. Ratna Ardiana, Sp.A
dr. Fitri Amalia, Sp.A
dr. Pridania Vidya Ayuningtyas, Sp.A
dr. Husnia Auliyatul Umna, Sp.A., M.Kes
Health & Medicine : dr. Helmia Farida, M.Kes., Sp.A(K)., Ph.D
dr. Jati Kusuma Wardhani, Sp.A
dr. Masayu Lubna Anniazi, Sp.A
Security & Permission : dr. Puni Oktisari, Sp.A
dr. Winres Sp.A
dr. Agustina Wulandari, Sp.A(K)., M.Kes
Documentation : dr. Vira Ari Nindya Dewi, Sp.A
dr. Evi Rokhayati, Sp.A(K)., M.Kes
Family Program : Ibu Nadiya Tun Paksi Sareharto
Ibu Vembyanti Adhie Nur Radityo
Ibu Uswatun Anam
Ibu Dyah Ratih Fitri Hartanto

PROCEEDING BOOK KONIKA XIX vii


Volume 19, 2024 p-ISSN-3089-1132

Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

LIST OF CONTRIBUTORS
Aditiawati Muchammad Fahrul Udin

Agustina Wulandari Olga Rasiyanti Siregar

Andi Dwi Bahagia Febriani Pandu Caesaria Lestari

Anggraini Alam Retno Palupi-Baroto

Antonius Hocky Pudjiadi Rini Sekartini

Aryono Hendarto Ririe Fachrina Malisie

Astrid Kristina Kardani Saptadi Yuliarto

Conny Tanjung Satrio Wibowo

Diah Asri Wulandari Siska Mayasari Lubis

Dwi Kisworo Setyowireni Susanto Nugroho

Dyahris Koentartiwi Tjhin Wiguna

Eddy Fadlyana Wistiani

Edy Novery Mexitalia Setiawati EM

Hesti Lestari Eddy Supriyadi

Himawan Aulia Rahmana Rinawati Rohsiswatmo

I Gusti Lanang Sidiartha Rizqi Amalia

I Nyoman Budi Hartawan Suryadi N. N. Tatura

Jufitriani Ismy Tunjung Wibowo

Klara Yuliarti Titis Prawitasari


Meita Dhamayanti Irawan Mangunatmadja

Mohammad Sjaifullah Noer

viii PROCEEDING BOOK KONIKA XIX


Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

TABLE OF CONTENT
Foreword from the President of Indonesian Pediatric Society��������������������������������������������� ii
Foreword from the Chairman of Indonesian Pediatric Society – Central Java Chapter�������iii
Foreword from the Chairman of KONIKA XIX��������������������������������������������������������������������� iv
Organizing Committee���������������������������������������������������������������������������������������������������������� v
List of Contributors�������������������������������������������������������������������������������������������������������������viii
Table of Content������������������������������������������������������������������������������������������������������������������ ix

Teaching Professionalism in Medicine


dr. Aditiawati, Sp. A(K)���������������������������������������������������������������������������������������������������������� 1

When do We be Aware that a Kidney may be Involved in a Child with Joint Pain?
dr. Agustina Wulandari, Sp.A(K), M.Kes������������������������������������������������������������������������������� 4

Blood Product Transfusion in Neonates: When Should It Be Given?


dr. Andi Dwi Bahagia, Ph.D, Sp.A(K)������������������������������������������������������������������������������������ 9

Non-antibiotics Strategies for Sepsis: Is Antibiotics the Only Solution?


Dr. dr. Anggraini Alam, Sp.A(K)������������������������������������������������������������������������������������������ 13

The Application of Phoenix Score in Pediatric Sepsis: New but Old?


Prof. Dr. dr. Antonius H. Pudjiadi, Sp.A(K)������������������������������������������������������������������������� 17

Professionalism With Physician Colleagues and Other Health Professionals


Prof. Dr. dr. Aryono Hendarto, Sp.A(K), MPH, SH, MH������������������������������������������������������ 22

Update on Diagnosis and Management of Pediatric Acute Kidney Injury


dr. Astrid Kristina Kardani, Sp.A (K), M.Biomed����������������������������������������������������������������� 26

Principles for the Implementation of Personalized Nutrition Approach in Paediatric


Dr. dr. Conny Tanjung, Sp.A(K)������������������������������������������������������������������������������������������ 29

Recognizing Extrapulmonary TB in Adolescence


dr. Diah Asri Wulandari, Sp.A(K)���������������������������������������������������������������������������������������� 31

Coughing: Allergic or Infection


dr. Dwi Kisworo Setyowireni, Sp.A(K)�������������������������������������������������������������������������������� 39

New Concept of Management Rheumatic Heart Disease


in Adolescents
dr. Dyahris Koentartiwi, Sp.A(K)����������������������������������������������������������������������������������������� 43

The Future Impact of Stunting: How to Prevent


Dr. dr. Eddy Fadlyana, Sp.A(K), M.Kes������������������������������������������������������������������������������ 46

PROCEEDING BOOK KONIKA XIX ix


Indonesian Pediatric Society – Central Java Chapter

27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

Recent Update in Medication of Paediatric Rheumatology


dr. Edy Novery, Sp.A(K), M.Kes����������������������������������������������������������������������������������������� 54

Internet Addiction in Children: How to Detect and Prevent


Dr. dr. Hesti Lestari, Sp.A(K)���������������������������������������������������������������������������������������������� 56

Diagnostic Approach and Management in Pediatric Gastrointestinal Bleeding


dr. Himawan Aulia Rahman, Sp.A(K)��������������������������������������������������������������������������������� 60

Diagnosis and Management of Stunting in Children


Dr. dr. I Gusti Lanang Sidiartha, Sp.A(K)���������������������������������������������������������������������������� 63

Fluid Management in Pediatric Shock: How Low Can We Go


Dr. dr. I Nyoman Budi Hartawan, M.Sc., Sp.A(K)��������������������������������������������������������������� 68

Motor Problems Related Nutritional Problems


Dr. dr. Jufitriani Ismy, Sp.A(K), M.Kes, M. Ked.(Ped)��������������������������������������������������������� 70

Testing Strategy for Inborn Error of Metabolism in the Newborn


dr. Klara Yuliarti, Sp.A(K)���������������������������������������������������������������������������������������������������� 73

Empowering Parents in The Early Detection and Intervention of Children With ASD
Prof. Dr. dr. Meita Dhamayanti, M.Kes., Sp.A(K)��������������������������������������������������������������� 75

The Expanding Role of Telemedicine in the Management of Chronic Kidney Disease


(CKD) and Dialysis Care for Indonesian Children
Prof. dr. Mohammad Sjaifullah Noer, Sp.A(K)�������������������������������������������������������������������� 79

Emergency In Children with Pneumonia: Community-Acquired Pneumonia, How to


Treat in Hospital Setting
dr. Muchammad Fahrul Udin, Sp.A (K) M.Kes������������������������������������������������������������������� 82

Coagulation Disorders in Neonates


dr. Olga Rasiyanti Siregar M.Ked (Ped)., Sp.A(K)�������������������������������������������������������������� 86

Tips and Pitfalls in The Screening, Diagnosis, and Management of Autism Spectrum
Disorder
dr. Pandu Caesaria Lestari, Sp.A(K)���������������������������������������������������������������������������������� 90

How to Manage Fluid and Electrolyte in Pediatric Kidney Diseases


dr. Retno Palupi-Baroto, B.Med.Sc.M.Epid, M.Sc, Sp.A(K)����������������������������������������������� 94

Quality of Life in Adolescents with Tuberculosis and the Challenges


Prof. Dr. dr. Rini Sekartini, Sp.A(K)������������������������������������������������������������������������������������ 97

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Cardiorespiratory Failure in Patients Hospitalized with Pneumonia


Dr. dr. Ririe Fachrina Malisie, Sp.A(K)������������������������������������������������������������������������������ 101

Pitfalls of Crystalloid Leading to Pediatric Acute Kidney Injury


dr. Saptadi Yuliarto, Sp.A(K)., M.Kes�������������������������������������������������������������������������������� 104

Pediatric Inflammatory Bowel Disease


dr. Satrio Wibowo, Sp.A(K)., M.Si.Med���������������������������������������������������������������������������� 108

Management of Adrenal Insufficiency in Children


Dr. dr. Siska Mayasari Lubis, M.Ked.(Ped), Sp.A(K)�������������������������������������������������������� 112

Blood Product Transfusion in Sepsis: When It is Not Too Late?


dr. Susanto Nugroho, Sp. A(K)����������������������������������������������������������������������������������������� 116

Cognitive Function in Children with Autism


Prof. Dr. dr. Tjhin Wiguna, SpKJ(K)���������������������������������������������������������������������������������� 119

Concerning Social Interaction Problems in the “Z” Generation


Prof. Dr. dr. Tjhin Wiguna, SpKJ(K)���������������������������������������������������������������������������������� 122

Management of Cough-Related Allergy


dr. Wistiani, Sp. A(K), M.Si.Med.�������������������������������������������������������������������������������������� 125

Disorders of Gut-Brain-Interaction: Understanding Food as Triggers and


Therapeutic Agents
Dr. dr. Mexitalia Setiawati EM, Sp.A(K)���������������������������������������������������������������������������� 129

NCCP iCAYA: The Journey of Developing the Pediatric National Cancer Control
Plan: A Better Future for Indonesian Children
dr. Eddy Supriyadi, Sp.A(K), Ph.D������������������������������������������������������������������������������������ 137

Indonesian Neonatal Registry: What Can We Learn from it to Improve Neonatal


Outcome
Prof. Dr. dr. Rinawati Rohsiswatmo, Sp.A(K)������������������������������������������������������������������� 142

Indonesian Preterm Baby Screening


Prof. Dr. dr. Rinawati Rohsiswatmo, Sp.A(K)������������������������������������������������������������������� 144

When to Suspect Immunodeficiency in Mycobacterium Infection


dr. Rizqi Amalia, Sp.A(K)�������������������������������������������������������������������������������������������������� 147

Cough: Do We Need Antibiotic?


Dr. dr. Suryadi N. N. Tatura, Sp.A(K)�������������������������������������������������������������������������������� 153

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Early Recognition in Neonate with Critical Congenital Heart Disease: Clinical Point
of View
Dr. dr. Tunjung Wibowo, M.Kes., MPH., Sp.A(K)������������������������������������������������������������� 156

Artificial Intelligence and Big Data in Nutrition and Metabolic Disease Care: Ethical,
Privacy, Security, and Bias Issues
Dr. dr. Titis Prawitasari, Sp.A(K)��������������������������������������������������������������������������������������� 158

The Use of Digital Technology in the Diagnosis and Management of Neurological


Disorders in Indonesian Children
Prof. Dr. dr. Irawan Mangunatmadja, Sp.A(K)������������������������������������������������������������������ 163

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Teaching Professionalism in Medicine


Aditiawati
Department of Child Health University of Sriwijaya, Palembang, Indonesia
E-mail: [email protected]

Professionalism in medicine is more than just about ethical codes or mastering technical
skills; it is the symbol of values, behaviors, and attitudes that support patients' trust in their
healthcare providers. Teaching professionalism is integral to medical education as it shapes
the morals and ethics of future healthcare professionals, ensuring that they deliver care with
compassion, integrity, and respect.
At the heart of teaching professionalism in medicine lies the commitment to patient welfare.
Medical professionals are often faced with complex situations that demand not only clinical
expertise but also ethical judgment. Teaching these principles involves more than just
theoretical instruction; it requires role modeling by experienced clinicians, reflective practice,
and continuous assessment to ensure that students internalize these values.
One effective approach to teaching professionalism is through the use of real-life scenarios
and case-based learning. By engaging students in discussions about ethical dilemmas and
challenging situations, educators can help them develop critical thinking skills and moral
reasoning. For instance, scenarios involving informed consent, end-of-life care, or conflicts
of interest provide rich opportunities for students to explore the nuances of professional
behavior. These discussions not only highlight the importance of ethical decision-making
but also encourage students to consider the impact of their actions on patients, colleagues,
and society at large.
Another crucial aspect of teaching professionalism is the emphasis on communication skills.
Effective communication is essential for building trust and rapport with patients, as well as for
collaborating with colleagues in a multidisciplinary healthcare environment. Medical students
must be trained to communicate clearly, empathetically, and respectfully, whether they are
delivering difficult news to a patient or working as part of a team. Simulation exercises, role-
playing, and feedback from peers and instructors can be valuable tools in helping students
refine their communication skills and understand the importance of professionalism in every
interaction.
Professionalism in medicine extends beyond individual behavior to encompass larger
responsibilities, such as advocacy and leadership. Physicians are often seen as leaders in
healthcare settings, and they must be prepared to advocate for their patients, communities,
and the profession itself. Teaching professionalism, therefore, involves encouraging

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students to take an active role in promoting health equity, addressing social determinants of
health, and participating in healthcare policy discussions. By encouraging a sense of social
responsibility, medical educators can inspire students to become not only skilled clinicians
but also advocates for positive change in the healthcare system.
Continuous reflection and self-assessment are also vital components of teaching
professionalism. Encouraging students to regularly reflect on their experiences, challenges,
and personal growth helps them develop a deeper understanding of their professional
identity. Reflective practice allows students to recognize areas for improvement, celebrate
successes, and maintain a lifelong commitment to professional development. Incorporating
reflective exercises into the curriculum, such as journaling or debriefing sessions, can reinforce
the importance of self-awareness and ongoing learning in maintaining professionalism
throughout one’s career.
In conclusion, teaching professionalism in medicine is a multifaceted process that requires
a comprehensive approach, combining theoretical knowledge with practical experience. By
introducing the values of compassion, integrity, and social responsibility, medical educators
can prepare students to navigate the complexities of modern healthcare with professionalism
at the core of their practice. As the medical field continues to evolve, the commitment to
teaching and supporting professionalism will remain a basis of quality healthcare and the
foundation of the patient-physician relationship.

Keywords: Teaching, Professionalism, medicine

Reference:
1. Cruess, R. L., Cruess, S. R., & Steinert, Y. (2008). "Role modeling—making the most
of a powerful teaching strategy." BMJ, 336(7646), 718-721.
2. Epstein, R. M., & Hundert, E. M. (2002). "Defining and assessing professional
competence." JAMA, 287(2), 226-235.
3. Swick, H. M. (2000). "Toward a normative definition of medical professionalism." Academic
Medicine, 75(6), 612-616.
4. "Professionalism—The next wave." New England Journal of Medicine, 355(20),
Hafferty, F. W. (2006). 2151-2152.
5. Wear, D., & Kuczewski, M. G. (2004). "The professionalism movement: Can we
pause?" The American Journal of Bioethics, 4(2), 1-10.
6. Birden, H., Glass, N., Wilson, I., Harrison, M., Usherwood, T., & Nass, D. (2013). "Teaching
professionalism in medical education: A Best Evidence Medical Education (BEME)
systematic review." Medical Teacher, 35(7), e1252-e1266.

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7. Wong, B. M., Goguen, J., & Shojania, K. G. (2013). "Building capacity for quality: A pilot
co-learning curriculum in quality improvement for faculty and resident learners." Journal
of Graduate Medical Education, 5(4), 689-693.
8. Lucey, C. R., & Souba, W. W. (2010). "Perspective: The problem with the problem of
professionalism." Academic Medicine, 85(6), 1018-1024.

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When do We be Aware that a Kidney may be Involved in a Child with


Joint Pain?
Agustina Wulandaria
Division of Nephrology and Hypertension, Department of Child Health, Faculty of Medicine
Dr. Moewardi Hospitala
Universitas Sebelas Maret, Surakarta, Indonesiab
E-mail: [email protected]

Multi-systemic inflammatory diseases that affect infants and adolescents are collectively
referred to as pediatric rheumatological diseases. Numerous rheumatological conditions
involve the kidneys as a target organ during the acute presentation and life course. In
contrast to adults who may have pre-existing renal disease, children are more susceptible to
a transient, potentially reversible inflammatory process that necessitates early intervention
(1). This article aims to review pediatric rheumatic diseases that frequently affect the kidney,
including childhood-onset systemic lupus erythematosus (cSLE), IgA vasculitis, ANCA-
associated vasculitis (AAV), and polyarteritis nodosa (PAN).
Lupus nephritis (LN), a kidney symptom of cSLE can vary from acute kidney failure to the
frequency of microscopic urine abnormalities (2). The induction and maintenance phases
of lupus nephritis are treated with immunosuppressive agents, primarily intravenous
glucocorticoids, followed by oral prednisone which is tapered to the lowest effective dose.
Steroid-sparing agents, such as mycophenolate mofetil, azathioprine, or cyclophosphamide,
are also used (3). Other treatments were supportive, including hydroxychloroquine,
hypertension medications, angiotensin-converting enzyme (ACE) inhibitors, and lowering
thrombotic risk to achieve full remission (4).
Henoch-Schönlein purpura (HSP) or immunoglobulin-A vasculitis (IgAV) can present as
IgAV nephritis (IgAVN), which is the primary cause of morbidity in IgAV patients (5). It may
manifest as microscopic hematuria, either with or without proteinuria, or as the more severe
and uncommon acute nephrotic or nephritic syndrome (6). The clinical severity of IgAVN,
as well as the histological features, are the determining factors in the management of the
disease. This includes proteinuria and kidney function. Oral corticosteroids are typically
administered in conjunction with a disease-modifying antirheumatic drug (DMARD), as well
as an ACE-I or ARB, to manage proteinuria (6).
Multi-systemic small and medium-vessel vasculitides, including granulomatosis with
polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with
polyangiitis (EGPA), are collectively referred to as anti-neutrophil cytoplasmic antibody

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(ANCA)—associated vasculitis (AAVs) (7). This group of vasculitides is distinguished by


kidney manifestations that are extremely prevalent and substantially contribute to morbidity
and mortality. Hematuria, proteinuria, hypertension, and edema are among the clinical
characteristics of nephritis in children with AAV. In certain cases, acutely deteriorating
kidney function is accompanied by swiftly progressive glomerulonephritis (8). To achieve
rapid remission for a severe, life-threatening, or refractory disease with kidney involvement,
rituximab, IV cyclophosphamide, plasma exchange, and/or intravenous immunoglobulin
(IVIG) should be considered following IV methylprednisolone (8,9).
The disruption to tiny and medium-sized arteries is the cause of polyarteritis nodosa (PAN),
an uncommon form of vasculitis. Hypertension, proteinuria, hematuria, and impaired kidney
function are the hallmarks of PAN in the kidneys (10). The initial management of PANs typically
involves the use of corticosteroids and either mycophenolate mofetil or cyclophosphamide
(11).
The aorta and its primary tributaries are the primary sites of Takayasu arteritis (TA), a
large-vessel vasculitis. The most common kidney complication of TA in children is renal
artery stenosis, which leads to renovascular hypertension. Despite their rarity, renal artery
aneurysms can rupture and result in life-threatening hemorrhage (12). Despite the absence
of a current consensus on treatment, antiplatelet therapy and a variety of prospective agents,
such as TNFα, IL-6, and JAK inhibitors, may be considered. Interventional revascularization
procedures, such as percutaneous transluminal renal angioplasty (PTRA), kidney auto-
transplantation, and surgical bypass, may be undertaken in the context of renal artery
stenosis (13).
The involvement of internal organs and blood vessels, as well as cutaneous sclerosis, are
the distinguishing features of juvenile-onset systemic sclerosis (jSSc). The symptoms that
patients present with include severe hypertension, reduced eGFR, hemolytic anemia, and
hematuria. A kidney biopsy is conducted to verify the diagnosis. Scleroderma renal crisis is
a rare but severe complication of SSc that can lead to a rapid diminution in kidney function
(14).
Originating during childhood Sjogren syndrome (cSS) is a chronic systemic autoimmune
disease that is characterized by the chronic infiltration of the exocrine glands by lymphocytes.
The involvement of the kidney in cSS is rare and typically presents as tubular interstitial
nephritis (TIN) as a result of lymphocytic infiltration and tubular dysfunction (15). Renal
tubular acidosis (RTA), which is typically distal, hypokalemia, nephrocalcinosis, or renal
Fanconi syndrome may result from this (16).
The hallmark of IgG4-related disease (IgG4-RD), an uncommon fibro-inflammatory condition,

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is tumor-like lymphoplasmacytic infiltrations. It is uncommon for minors to experience kidney


manifestations, which are typically characterized by TIN, membranous glomerulonephritis,
or obstructive acute kidney injury as a consequence of retroperitoneal fibrosis (17).
Children should, at the very least, undergo a baseline urinalysis and blood pressure exam
in diseases where kidney involvement is a recognized complication. A summary of other
kidney-specific investigations is also included in Table 1 (18). The kidney is a target organ
in a wide range of rheumatological diseases that affect young people, so rapid screening of
renal function and precise diagnosis should always be made in these conditions.
Urinalysis Hematology Immunology Imaging Other
Urine dipstick FBC Immunoglobulins Abdominal USS Blood pressure
with Doppler measurement
measurements

UA:UC ratio or ESR and CRP Complement Height to calculate


UP:UC ratio (C3 and C4) eGFR

Urine Clotting ± and Anti-streptolysin Skin biopsy with IgA


microscopy for prothrombotic O antibody titer immunofluorescence
quantification screen (ASOT)
of haematuria
and evidence
of active
sediment
U&Es, bone ANA Renal biopsy
profile, and LFTs

CPK and LDH Anti-dsDNA


ANCA and APS
antibodies

Anti-GBM antibody

Anti-PR3 and
MPO titres if
ANCA positive

Keywords: acute kidney injury; arthritis; chronic kidney disease; pediatric; rheumatology.

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References:
1. Alobaidi S, Alotaibi M, Al-Zahrani N, Al-Dhaheri F. Renal system and rheumatology.
Skills in rheumatology. 2021;309–28.
2. Bankole AA, Nwaonu JN. The Shifting Landscape of Lupus Nephritis Management: A
Review. Cureus. 2022 Jan;14(1):e20950.
3. Musa R, Brent LH, Qurie A. Lupus Nephritis. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2024 [cited 2024 Aug 24]. Available from: http://www.ncbi.
nlm.nih.gov/books/NBK499817/
4. Groot N, de Graeff N, Marks SD, Brogan P, Avcin T, Bader-Meunier B, et al. European
evidence-based recommendations for the diagnosis and treatment of childhood-onset
lupus nephritis: the SHARE initiative. Ann Rheum Dis. 2017 Dec;76(12):1965–73.
5. Chen JY, Mao JH. Henoch-Schönlein purpura nephritis in children: incidence,
pathogenesis and management. World J Pediatr. 2015 Feb;11(1):29–34.
6. Ozen S, Marks SD, Brogan P, Groot N, de Graeff N, Avcin T, et al. European consensus-
based recommendations for diagnosis and treatment of immunoglobulin A vasculitis-
the SHARE initiative. Rheumatology (Oxford). 2019 Sep 1;58(9):1607–16.
7. Calatroni M, Oliva E, Gianfreda D, Gregorini G, Allinovi M, Ramirez GA, et al. ANCA-
associated vasculitis in childhood: recent advances. Ital J Pediatr. 2017 May 5;43(1):46.
8. Plumb LA, Oni L, Marks SD, Tullus K. Paediatric anti-neutrophil cytoplasmic antibody
(ANCA)-associated vasculitis: an update on renal management. Pediatr Nephrol. 2018
Jan;33(1):25–39.
9. de Graeff N, Groot N, Brogan P, Ozen S, Avcin T, Bader-Meunier B, et al. European
consensus-based recommendations for the diagnosis and treatment of rare paediatric
vasculitides – the SHARE initiative. Rheumatology. 2019 Apr 1;58(4):656–71.
10. Eleftheriou D, Dillon MJ, Tullus K, Marks SD, Pilkington CA, Roebuck DJ, et al. Systemic
polyarteritis nodosa in the young: a single-center experience over thirty-two years.
Arthritis Rheum. 2013 Sep;65(9):2476–85.
11. Brogan PA, Arch B, Hickey H, Anton J, Iglesias E, Baildam E, et al. Mycophenolate Mofetil
Versus Cyclophosphamide for Remission Induction in Childhood Polyarteritis Nodosa:
An Open-Label, Randomized, Bayesian Noninferiority Trial. Arthritis Rheumatol. 2021
Sep;73(9):1673–82.
12. Aeschlimann FA, Twilt M, Yeung RSM. Childhood-onset Takayasu Arteritis. Eur J
Rheumatol. 2020 Feb;7(Suppl1):S58–66.
13. Aeschlimann FA, Yeung RSM, Laxer RM. An Update on Childhood-Onset Takayasu
Arteritis. Front Pediatr. 2022;10:872313.

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14. Foeldvari I, Klotsche J, Torok KS, Kasapcopur O, Adrovic A, Stanevicha V, et al. Are
diffuse and limited juvenile systemic sclerosis different in clinical presentation? Clinical
characteristics of a juvenile systemic sclerosis cohort. J Scleroderma Relat Disord.
2019 Feb;4(1):49–61.
15. Basiaga ML, Stern SM, Mehta JJ, Edens C, Randell RL, Pomorska A, et al. Childhood
Sjögren syndrome: features of an international cohort and application of the 2016 ACR/
EULAR classification criteria. Rheumatology (Oxford). 2021 Jul 1;60(7):3144–55.
16. Bogdanović R, Basta-Jovanović G, Putnik J, Stajić N, Paripović A. Renal involvement
in primary Sjogren syndrome of childhood: case report and literature review. Mod
Rheumatol. 2013 Jan;23(1):182–9.
17. Capecchi R, Giannese D, Moriconi D, Bonadio AG, Pratesi F, Croia C, et al. Renal
Involvement in IgG4-Related Disease: From Sunlight to Twilight. Front Med (Lausanne).
2021;8:635706.
18. Patel A, Marro J, McCann L, Oni L. Kidney Manifestations of Rheumatological Diseases
in Children. Curr Treat Options Peds. 2023 Dec 1;9(4):338–55.

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Blood Product Transfusion in Neonates: When Should It Be Given?


Andi Dwi Bahagia Febriani
Department of Child Health, Faculty of Medicine, Hasanudin University, Makassar
Indonesia
E-mail: [email protected]

Introduction
Blood transfusions are an important intervention and are often carried out in the NICU. In
neonates, especially premature or critically ill infants, transfusions are often necessary to
address problems such as anemia, blood loss, or coagulopathy. Given the delicate nature of
neonates, the process must be carefully managed to minimize risks and optimize outcomes
A framework for safe and efficient blood product transfusions in newborns is provided by
several guidelines. Institution-specific protocols differ but often involve rigorous blood type
matching, pre-transfusion testing, and reaction monitoring.
The need for blood product transfusions in neonates arises from a variety of clinical situations:
1. Anemia: Due to decreased red blood cell formation and increased red blood cell
breakdown, neonates especially preterm infants are susceptible to anemia. Transfusions
are frequently necessary for conditions like anemia of prematurity (AAP) when hemoglobin
levels fall below tolerable criteria.
2. Hemorrhage: Transfusions may be required in cases of acute blood loss after surgeries,
trauma, or difficult deliveries. To preserve hemodynamic stability, neonates experiencing
substantial bleeding require prompt treatment. (Levy et al., 2020).
3. Coagulation Disorders: Transfusions of clotting factors or fresh frozen plasma may be
necessary for infants with congenital or acquired coagulopathies to prevent or treat
bleeding episodes.
4. Neonatal Sepsis: Transfusions may be necessary to treat severe anemia or coagulopathy
that might result from sepsis.
Red Blood Cells (RBCs): When hemoglobin levels fall below 7-8 g/dL, transfusion is usually
considered; however, the precise threshold may differ depending on the clinical situation and
the infant's general health. RBC transfusions at a dose of 10 to 15 mL/kg, with a maximum
of 20 mL/kg, for 1 to 2 hours.
Platelets: When platelet count falls below 30,000/µL or falls below 10,000/µL in an
asymptomatic newborn with a high risk of bleeding, platelet transfusion becomes necessary.
The usual dose for platelet transfusions is 10 mL/kg, which should transiently increase the
platelet count by 50–100 x 109/L over 30–60 minutes.

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Fresh Frozen Plasma (FFP): FFP is given to treat coagulopathy when there is severe
bleeding or aberrant clotting patterns, particularly when liver disease or disseminated
intravascular coagulation (DIC) is present. The usual dose is 10–15 mL/kg, administered
over 30–60 minutes.
Acute reactions that can occur immediately after a blood transfusion in neonates include:
y Febrile Non-Hemolytic Transfusion Reactions (FNHTR): These reactions are
characterized by a mild increase in body temperature (less than 2°C) and are often due
to inflammatory cytokines released from white blood cells during storage or preformed
recipient antibodies reacting with WBCs in the infused component. FNHTR is more
common in neonates and can be managed with supportive care and possibly pre-storage
leukoreduction of RBCs and platelets
y Acute Hemolytic Transfusion Reactions (AHTR) are characterized by increased
plasma free hemoglobin, hemoglobinuria, increased potassium concentration, and
lowered pH, which can occur in newborns, however, it is uncommon. Although the
symptoms might not be as severe as in adults, supportive care is still necessary to keep
blood pressure and kidney perfusion stable.
y Transfusion-Related Acute Lung Injury (TRALI): Although rare, Acute respiratory
distress following transfusion is a defining feature of TRALI, which can occur. (Dzik,
2020). This is a serious complication characterized by acute onset of hypoxemia
with bilateral infiltrates on chest radiographs within 6 hours of transfusion. It is often
unrecognized but can be treated with oxygen support and mechanical ventilation.
y Transfusion-Associated Circulatory Overload (TACO): Neonates have a small
blood volume, making them susceptible to volume overload from transfusions. This can
lead to cardiac and respiratory complications and is a significant concern in neonatal
transfusions. Heart failure can result from overloading the circulatory system, especially
in premature or critically sick infants.
y Infections: The risk of spreading illnesses like CMV, HIV, and hepatitis B or C is still
present, even though it is reduced by thorough screening and testing.
y Allergic Reactions: Transfusion-related allergic responses can range from minor
rashes to life-threatening anaphylactic events.

Potential long-term consequences, such as:


y Iron Overload: Over time, excessive iron buildup from repeated transfusions may harm
organs.

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y Immune Sensitization: Alloimmunization, a condition where a newborn develops


antibodies against transfused blood components, might result after several transfusions
and complicate subsequent transfusions.
y Transfusion-Related Graft-Versus-Host Disease (TA-GVHD), although rare, can
happen. It is characterized by the recipient's tissues being attacked by the donor's
immune cells.
Special considerations for all blood products:
y Leukocyte depletion: to reduce the risk of adverse reactions and infections
y Irradiation to prevent TA-GVHD
y ABO compatible with the infant’s red cell antigens to prevent hemolytic reactions
y Risk assessment: the risk of transfusion must be weighed against its risks, including the
potential for adverse outcomes.

Conclusions
Transfusions of blood products are essential for the treatment of newborns suffering from a
range of ailments. Despite the important advantages they provide, it is imperative to adhere
to established rules and procedures to reduce risk and complications. Improved safety
procedures and ongoing developments in transfusion medicine are intended to improve the
prognosis for these susceptible patients.
The prevention of anemia of prematurity, and the use of restrictive transfusion protocols
and strategies are the best approaches. For platelet transfusion, bleeding risk assessment,
clinical manifestations, and laboratory features should be considered. Fresh frozen plasma
is recommended in neonates with coagulopathy and active bleeding, with disseminated
intravascular coagulation, or with congenital factor deficiency for which no specific treatment
is available. All blood products have side effects that guarantee a personalized and thorough
assessment of the need for transfusions.
Keywords: Blood products; Neonates; Management.

References
1. Boix H, Sánchez-Redondo MD, Cernada M, Espinosa Fernández MG, González-
Pacheco N, Martín A, et al. Recomendaciones para la transfusión de hemoderivados en
neonatología. An Pediatr (Barc). 2022;97:60.

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2. Christensen, R. D., Bahr, T. M., Davenport, P., C., M., Ohls, R. K., Ilstrup, S. J., & Kelley, W.
E. (2024). Implementing evidence-based restrictive neonatal intensive care unit platelet
transfusion guidelines. Journal of Perinatology, 1-8. https://doi.org/10.1038/s41372-024-
02050-x
3. Deschmann E, Dame C, Sola-Visner MC, et al. Clinical Practice Guideline for
Red Blood Cell Transfusion Thresholds in Very Preterm Neonates. JAMA Netw
Open. 2024;7(6):e2417431. doi:10.1001/jamanetworkopen.2024.17431
4. Goel R and Josephson CD. Recent advances in transfusions in neonates/infants [version
1; peer review: 2 approved]. F1000Research 2018, 7(F1000 Faculty Rev):609 (https://
doi.org/10.12688/f1000research.13979.1)
5. Kirpalani H, Bell EF, Hintz SR, et al. Higher or lower hemoglobin transfusion thresholds
for preterm infants. N Engl J Med. 2020;383 (27):2639–2651
6. Klanderman RB, Bosboom JJ, Migdady Y, Veelo DP, Geerts BF, Murphy MF, Vlaar APJ.
Transfusion-associated circulatory overload-a systematic review of diagnostic biomarkers.
Transfusion. 2019 Feb;59(2):795-805. doi: 10.1111/trf.15068. Epub 2018 Nov 29. PMID:
30488959; PMCID: PMC7379706.
7. Moiseiwitsch N, Brown AC. Neonatal coagulopathies: A review of established and
emerging treatments. Exp Biol Med (Maywood). 2021 Jun;246(12):1447-1457.
doi: 10.1177/15353702211006046. Epub 2021 Apr 15. PMID: 33858204; PMCID:
PMC8243218.
8. Shah, F.T., Porter, J.B., Sadasivam, N., Kaya, B., Moon, J.C., Velangi, M., Ako, E. and
Pancham, S. (2022), Guidelines for the monitoring and management of iron overload
in patients with haemoglobinopathies and rare anaemias. Br J Haematol, 196: 336-
350. https://doi.org/10.1111/bjh.17839
9. Wang P, Wang X, Deng H, Li L, Chong W, et al. (2021) Restrictive versus liberal transfusion
thresholds in very low birth weight infants: A systematic review with meta-analysis. PLOS
ONE 16(8): e0256810. https://doi.org/10.1371/journal.pone.0256810
10. Zerra PE, Josephson CD. Transfusion in Neonatal Patients: Review of Evidence-Based
Guidelines. Clin Lab Med. 2021 Mar;41(1):15-34. doi: 10.1016/j.cll.2020.10.002. Epub
2020 Dec 23. PMID: 33494882; PMCID: PMC9015674.

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Non-antibiotics Strategies for Sepsis:


Is Antibiotics the Only Solution?
Anggraini Alam
Divisi Infeksi dan Penyakit Tropis KSM/Dep. IK Anak FK Universitas Padjadjaran
E-mail: [email protected]

Background
In the 21st century, sepsis remains a major cause of morbidity and mortality in childhood and
adolescence. Prevention and timely and adequate therapy are major goals to improve clinical
results. Antibiotics are mandatory to treat sepsis, but indiscriminate use and resistance
development can lead to higher medical costs, drug side effects, and increased mortality.1
Sepsis is a life-threatening emergency condition of global public health concern with substantial
mortality and financial costs. The future of sepsis management lies in personalizing all our
therapies to individual patients.2
The treatment of sepsis includes three components: infection control; organ support, in
particular restoring and maintaining an adequate hemodynamic status; and modulation of
the host response.3
We need to be able to better identify the right patients for any given intervention at the right
time. Patients with sepsis are highly heterogeneous in terms of individual characteristics
(age, sex, comorbidities), infection-related factors (causative microorganism, source of
infection, antimicrobial susceptibilities), patterns of organ dysfunction, and degree of immune
response, which, importantly, will alter during sepsis.4
Developing cutting-edge novel therapies and medicines is a step in the right direction, holding
promising outcomes. Researchers have investigated various immunomodulatory drugs and
targeted therapies to disrupt the complicated mechanisms that drive the advancement of
sepsis.5

Future Directions in Research and Therapeutics of Non-antibiotic for Sepsis


Sepsis is a complicated disruption of immunologic equilibrium, highlighting its complexity and
the intricate link between immune function and clinical symptoms. The mortality, morbidity, and
economic impact of sepsis are global concerns. Non-target-specific antibiotic therapy, misuse
or abuse of antibiotic therapy, polypharmacy, and inadequate empiric antibiotic therapy may
favor the emergence of multidrug resistance organisms (MDROs). Antimicrobial resistance
determines treatment ineffectiveness in clinical settings, leading to rapid advancement to

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sepsis and septic shock. Multidisciplinary strategies for timely diagnosis and application
of appropriate antimicrobial treatment are critical in managing septic patients and limiting
sepsis-related complications. Therefore, there is an urgent need for early administration of
antimicrobials and organ support due to the time-dependent nature and severity of sepsis.5
Therapies used in the treatment of infectious diseases involve modulating the host's
inflammatory response to infection. Systemic corticosteroids thought to act by decreasing
the deleterious effects of the host inflammatory response, have been found beneficial when
used in conjunction with antimicrobial therapy for the treatment of bacterial meningitis,
tuberculous meningitis, and pneumocystis pneumonia in patients with AIDS. Temporary
discontinuation or dose reduction of immunosuppressive agents is often required for the
successful treatment of infections in organ transplant recipients or patients with rheumatologic
disorders. Intravenous immunoglobulin therapy, which acts to neutralize toxins produced
by the bacteria, can be used in addition to surgical debridement and antimicrobial therapy
in the treatment of necrotizing fasciitis caused by group A streptococci and severe toxic
shock syndrome. Some of these interventions lack a strong evidence base but are often
recommended by experts based on clinical experience.1
Identifying better and more effective alternatives to antibiotics, such as phage therapy,
immune-based therapies involving monoclonal and polyclonal antibodies, and precision
medicine.6
The use of nanoparticles and immune-based therapeutics, in combination with precision
medicine, is an important field of research for healthcare providers, including physicians,
pharmacists, and microbiologists. Furthermore, addressing the challenges associated with
antimicrobial resistance (AMR) is essential to ensure effective treatment and minimize
adverse effects.7
Despite many years of research, no agents have been developed that act directly on the host
response and have been shown to consistently improve outcomes. Given the complexity of
the immune response, it is unlikely that an agent working against a single mediator will be
effective in all patients, and agents with more global or multiple modes of action may be
more effective.4

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Table 1. Immunomodulatory strategies.4


Non-specific interventions
• Hydrocortisone (in severe shock)
• Vasopressin
• Gamma-globulins
• Thrombomodulin
• Vitamin C
• Extracorporeal removal
Immunostimulatory
• granulocyte-macrophage colony-stimulating factor (GM-CSF)
• interferon-gamma (IFN- )
• interleukin (IL)-7
• anti-programmed cell death protein 1 (PD1) antibodies
• anti-PD1 ligand antibodies
Currently employed or in phase III clinical trials.4

Other Non-antibiotic Strategies for Sepsis


Antimicrobial therapy is usually, but not always, the most important therapy for infectious
diseases; however, there are many “non-antimicrobial therapies” that may avoid treatment
failure. The best-recognized example of non-antimicrobial therapy in the treatment of infection
is “source control”, namely the use of operative drainage or debridement. This procedure is
useful when the organism burden is very high or in the management of abscesses, for which
the penetration and activity of antimicrobial agents are often inadequate.9
There are very few studies that adequately addressed the role of source control in reducing
the infectious inoculum (i.e. drainage, surgical debridement, removal of devices and/or
catheters) in critically ill patients. However, an adequate source control, in particular for
intra-abdominal or soft tissue infections, could be even more relevant to patients’ outcomes
than the use of antibiotics.8 As an example, many cases of biliary tract or intra-abdominal
infections could evolve towards a rapid clinical response when the inoculum is drained,
even when the pathogens are resistant to the prescribed antibiotic therapy. On the opposite,
without focus sanitation, a clinical response will be probably poor, no matter how optimized
the antibiotic therapy is. As such, in patients with persistent shock, inadequate source control
should be suspected, and the initial diagnosis or discussed for further investigations (i.e. CT-
scan to detect a deep abdominal collection or a pulmonary empyema).8

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Conclusion
Management of sepsis remains a challenge and consists of infection control, hemodynamic
and other organ support, and modulation of the host response. While the search for new
drugs must continue and improve. In this context, “sepsis teams” should be established
to facilitate the rapid investigation and timely management of patients with sepsis. The
future of sepsis management lies in personalizing all our therapies to individual patients.
Personalized medicine will help improve patient management by enabling therapies to be
targeted more appropriately at individual patients. We need to be able to better identify the
right patients for any given intervention at the right time.

References:
1. Mau LB and Bain V. Antimicrobial Therapy in Pediatric Sepsis: What Is the Best Strategy?
Front. Pediatr. 2022;10: p.830276.
2. Vincent JL. The coming era of precision medicine for intensive care. Crit Care. 2017;21:
p.31.
3. Vincent JL, Mongkolpun W. Non-antibiotic therapies for sepsis: an update. Expert Rev
Anti Infect Ther. 2019 Mar;17(3): p.169–75.
4. Cohen J. Non-antibiotic strategies for sepsis. Clin Microbiol Infect. 2009 Apr;15(4): p.302–
7.
5. Seymour, C.W.; Kennedy, J.N.;Wang, S.; Chang, C.H.; Elliott, C.F.; Xu, Z.; Berry, S.;
Clermont, G.; Cooper, G.; Gomez, H.; et al.Derivation, Validation, and Potential Treatment
Implications of Novel Clinical Phenotypes for Sepsis. JAMA. 2019;321: p.2003–17
6. Peters van Ton, A.M.; Kox, M.; Abdo, W.F.; Pickkers, P. Precision Immunotherapy for
Sepsis. Front. Immunol. 2018;9: p.1926
7. Kumar NR, Balraj TA, Kempegowda SN, Prashant A. Multidrug-Resistant Sepsis: A
Critical Healthcare Challenge. Antibiotics (Basel). 2024 Jan 4;13(1): p.46.
8. Filippo Annoni, David Grimaldi & Fabio Silvio Taccone (2019): Individualized antibiotic
therapy in the treatment of severe infections, Expert Review of Anti-infective Therapy,
DOI: 10.1080/14787210.2020.1696192
9. Bassetti M, Montero JG, Paiva JA. When antibiotic treatment fails. Intensive Care Med.
2018 Jan;44(1): p.73–5.

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The Application of Phoenix Score in Pediatric Sepsis: New but Old?


Antonius Hocky Pudjiadi
Department of Child Health, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
E-mail: [email protected]

Infection and infectious diseases have been documented since around 2000 years ago.
In the last few decades of the 20th Century, intensive care medicine has grown across
many hospitals. This emerging medical specialty identified a high mortality rate associated
with severe infectious disease, which often presented with similar symptoms, such as
inflammation, respiratory failure, shock, and other organ failures. In 1991 experts developed
the first consensus definition of sepsis, which is described as a systemic inflammatory
response syndrome (SIRS) caused by infections (Figure 1).1 This definition laid the
foundation for numerous clinical trials and therapeutic interventions. However, despite its
usefulness, this definition also introduced a new syndrome associated with extremely high
mortality. To address this, a second consensus conference was held in 2001 to provide
a practical framework for this progressive process that leads to organ failures.2 The first
generation of sepsis and organ dysfunction definition in pediatrics was adapted from the
sepsis definition for adults by the International Pediatric Sepsis Consensus Conference.3 In
2002, the International Sepsis Forum was launched at the European Society of Intensive
Care Medicine annual meeting in Barcelona. This initiative convened to develop guidelines
to reduce sepsis mortality. The first edition of Surviving Sepsis Campaign guidelines was
subsequently published in 2004.4 Based on the same principle, a clinical practice guideline
for hemodynamic support in pediatric and neonatal septic shock was published in 2009.5
This evidence-based guideline has effectively reduced sepsis mortality in developed
countries. However, the SIRS-based definition has limitations, as its criteria are too loose
and inadequately describe the diverse course of the disease.

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Figure 1. Interrelationships among systemic inflammatory response syndrome (SIRS),


sepsis, and infection (adapted from American College of Chest Physicians/Society of Critical
Care Medicine Consensus Conference)1
The art of medicine has created the need for a re-evaluation of sepsis definition. In 2014,
the Society of Critical Care Medicine and the European Society of Intensive Care Medicine
re-examined the "old" sepsis definition. This effort resulted in a new understanding that
sepsis is a life-threatening condition resulting from tissue injury due to the body's response
to infection. In 2015, the definition was established as Sepsis-3, describing sepsis as a life-
threatening organ dysfunction caused by dysregulated host response to infection.6 According
to this definition, sepsis is diagnosed based on the presence of suspected or documented
infection and an acute increase of ≥2 SOFA (Sequential Organ Failure Assessment) points
(a proxy for organ dysfunction). In 2019, the Society of Critical Care Medicine Pediatric
Sepsis Definition Task Force was established to update the pediatric sepsis definition and
criteria. The task force adopted the conceptual definition of Sepsis-3 to develop criteria
applicable across various resource settings, resulting in the creation of the Phoenix Sepsis
Score (Table 1).7 The new criteria defined pediatric sepsis as a Phoenix Sepsis Score of ≥2
in children with suspected infection. Meanwhile, septic shock is described as sepsis with 1
or more cardiovascular points.
The classification of illness severity in critically ill patients has been used since the early days
of the intensive care unit. Therapeutic Intervention Scoring System (TISS) was developed to
provide a quantitative comparison of patient care while also offering insight into the degree
of illness.8 Currently, methods to predict mortality based on intervention are still commonly
done using tools such as Therapeutic Intervention Scoring System (TISS-28) or Vasoactive
Inotropic Score (VIS).9-11

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Table 1. The Phoenix Sepsis Score (adapted from Sanchez-Pinto et al.) 7


0 Points 1 Points 2 Points 3 Points

PaO­2:FiO2 < 400 and PaO­2:FiO2 PaO­2:FiO2 <


PaO­2:FiO2 ≥ 400
Respiration any respiratory support 100 – 200 or 100 and IMV
or SpO2:FiO2 ≥
(0-3 points) or SpO2:FiO2 < 292 and SpO2:FiO2 148 or SpO2:FiO2 <
292
any respiratory support -220 and IMV 148 and IMV
2 points (up
to 6) for:
1 point each (up to 3)
≥ 2 vasoactive
Cardiovascular No vasoactive for:
medications
(0-6 points) medications 1 vasoactive medication
Lactate ≥ 11
Lactate < 5 Lactate 5 – 10.9 mmol/L
mmol/L
mmol/L
Mean arterial
pressure by
age, mmHg
< 1 mo > 30 17 – 30 < 17
1 – 11 mo > 38 25 – 38 < 25
1–<2y > 43 31 – 43 < 31
2– <5y > 44 32 – 44 < 32
5 – < 12 y > 48 36 – 48 < 36
< 38
12 – 17 y > 51 38 – 51

1 point each
Platelets >
(maximum of 2 points)
100x103 / µL
for:
INR ≤ 1.3
Coagulation Platelets < 100 x 103 / µL
D-dimer ≤ 2
(0 – 2 points) INR > 1.3
mg//L FEU
D-dimer > 2
Fibrinogen ≥ 100
mg//L FEU
mg/dL
Fibrinogen < 100 mg/dL

Glasgow Coma
Neurologic Glasgow Coma Scale Fixed pupils
Scale score > 10;
(0-2 points) score ≤ 10 bilaterally
pupils reactive

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Another way to assess the severity of acute illness is by measuring the degree of physiological
abnormalities. The Physiologic Stability Index (PSI) was the earliest method to evaluate the severity
of illness using this approach in critically ill infants and children.12 The Pediatric Risk of Mortality
(PRISM) score, a tool for estimating Pediatric Intensive Care Unit mortality risk, was developed
based on PSI.13
In developing countries with limited resources, it is more important to prioritize early intervention of
infection and the management of existing medical emergencies. These approaches are essential
as they prevent further disease progression, which impacts morbidity, mortality, and the overall
disease burden of sepsis. Based on this understanding, the definition of sepsis should enable the
earliest possible detection of suspected cases. Therefore, the previous definition is more suitable
to be implemented in primary healthcare facilities. Sophisticated definitions such as the Phoenix
Sepsis Score will only be useful in a very limited number of pediatric intensive care units (PICU) if
such units exist.

Keywords: Children; Phoenix Score; Sepsis Definition

References
1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference:
Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in
sepsis. Critical Care Medicine. 1992;20(6):864-74.
2. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/
ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003;31(4):1250-
6. DOI: 10.1097/01.CCM.0000050454.01978.3B.
3. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference:
definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):2-
8. DOI: 10.1097/01.PCC.0000149131.72248.E6.
4. Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, et al. Surviving Sepsis
Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med.
2004;32(3):858-73. DOI: 10.1097/01.ccm.0000117317.18092.e4.
5. Brierley J, Carcillo JA, Choong K, Cornell T, Decaen A, Deymann A, et al. Clinical practice
parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update
from the American College of Critical Care Medicine. Crit Care Med. 2009;37(2):666-88. DOI:
10.1097/CCM.0b013e31819323c6.
6. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The
Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA.
2016;315(8):801-10. DOI: 10.1001/jama.2016.0287.

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7. Sanchez-Pinto LN, Bennett TD, DeWitt PE, Russell S, Rebull MN, Martin B, et al.
Development and Validation of the Phoenix Criteria for Pediatric Sepsis and Septic
Shock. JAMA. 2024. DOI: 10.1001/jama.2024.0196.
8. Cullen DJ, Civetta JM, Briggs BA, Ferrara LC. Therapeutic intervention scoring system:
a method for quantitative comparison of patient care. Crit Care Med. 1974;2(2):57-60.
9. Pudjiadi AH, Pramesti DL, Pardede SO, Djer MM, Rohsiswatmo R, Kaswandani N.
Validation of the vasoactive-inotropic score in predicting pediatric septic shock mortality:
A retrospective cohort study. Int J Crit Illn Inj Sci. 2021;11(3):117-22. DOI: 10.4103/
IJCIIS.IJCIIS_98_20.
10. Sandrio S, Krebs J, Leonardy E, Thiel M, Schoettler JJ. Vasoactive Inotropic Score as
a Prognostic Factor during (Cardio-) Respiratory ECMO. J Clin Med. 2022;11(9). DOI:
10.3390/jcm11092390.
11. Vivanco-Allende A, Rey C, Concha A, Martínez-Camblor P, Medina A, Mayordomo-
Colunga J. Validation of a Therapeutic Intervention Scoring System (TISS-28) in critically
ill children. Anales de Pediatría (English Edition). 2020;92(6):339-44. DOI: 10.1016/j.
anpede.2019.10.007.
12. Yeh TS, Pollack MM, Ruttimann UE, Holbrook PR, Fields AI. Validation of a physiologic
stability index for use in critically ill infants and children. Pediatr Res. 1984;18(5):445-51.
DOI: 10.1203/00006450-198405000-00011.
13. Pollack MM, Ruttimann UE, Getson PR. Pediatric risk of mortality (PRISM) score. Crit
Care Med. 1988;16(11):1110-6. DOI: 10.1097/00003246-198811000-00006.

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Professionalism With Physician Colleagues and Other Health


Professionals
Aryono Hendartoa
The Indonesian Collegium of Pediatrics, Department of Pediatrics, Faculty of Medicine,
Universitas Indonesiaa
Cipto Mangunkusumo Hospital (RSCM)b
E-mail: [email protected]

Introduction
Professionalism, as defined by the Indonesian Dictionary (KBBI), encompasses the
qualities, standards, and behaviors intrinsic to a profession.1 Physicians are regarded as one
of the most trusted professions by society and their peers. Professional competence entails
the adept application of communication, knowledge, technical skills, clinical reasoning,
emotions, values, and reflection in practice to benefit individuals and communities.2
The continuum of professionalism begins with education and training, progressing
through credentialing and ongoing quality improvement to meet societal needs.3 Its
importance is underscored by its role in ensuring patient safety, which is achieved through
effective communication, honesty, respect, confidentiality, and accountability in healthcare
delivery.

Medical Professionalism in the Modern Era


Historically, medical professionalism was linked to virtues like compassion, respect,
and trustworthiness. By the late 20th century, the focus shifted to a behavioral model
emphasizing measurable competencies, addressing the shortcomings of virtue-based
approaches in ensuring consistent professional conduct. In this framework, a competent
physician exhibits specific behaviors and skills.4
In the past decade, professional identity formation has emerged as a third model,
responding to concerns about the reductionist nature of the behavioral model. This
approach emphasizes the integration of values and aspirations into a physician's identity,
where good physicians internalize the values of their professional community. Each model—
virtue-based, behavioral, and identity-based—offers unique contributions to understanding
professionalism.
Generational differences also affect professionalism, with variations in lifestyle and
work styles influencing ethical values among students, residents, faculty, and practitioners.

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Contemporary professionalism faces threats from self-interest, power, prestige, profit, pride,
and negative traits such as irresponsibility and greed, which can foster unprofessional
behavior.5,6

Components of Professionalism
The American Board of Internal Medicine (ABIM) defines six core dimensions of
professionalism: altruism, accountability, excellence, duty, integrity, and respect. Factors
that erode professionalism include abuse of power, sexual harassment, conflicts of interest,
arrogance, physician health violations, and research fraud.7
According to the American Board of Pediatrics, eight aspects comprise professionalism:
honesty/integrity, reliability/accountability, respect for others, compassion/empathy, self-
Improvement, self-awareness/knowledge of limitations, communication/collaboration,
altruism/advocacy.8

Professionalism Among Physicians and Other Healthcare Professionals


Collegiality is a core element of professionalism in healthcare, representing a
collaborative relationship aimed at achieving shared goals. It is characterized by mutual
respect, trust, and cooperation among healthcare professionals, which enhances clinical
outcomes, patient safety, and the overall quality of care. Key aspects of collegiality include
commitment to shared objectives, respectful collaboration, constructive feedback, and
positive interactions. To foster collegiality, professionals engage in specific behaviors:
maintaining composure during challenges, valuing input from colleagues, clarifying team
roles, offering help when needed, and sharing knowledge. They take personal responsibility
for mistakes, acknowledge others' contributions, and advocate for their peers. Awareness
of power dynamics, support for colleagues in distress, and adherence to professional
boundaries further strengthen collegial relationships.8
Professionalism among physicians and other healthcare professionals is anchored in
two key principles:
1. Commitment to Improving Quality of Care: Physicians must collaborate in
interdisciplinary teams to enhance patient safety and reduce errors. This involves
valuing team dynamics, continuously assessing care systems, and accepting
accountability for shortcomings. Emphasizing patient safety and promptly reporting
potential incidents are crucial for optimal outcomes.

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2. Commitment to Professional Responsibility: Physicians, as vital members of


healthcare teams, must effectively fulfill their roles while leveraging others' expertise.
This fosters a culture of mutual respect, ensuring a safe patient care environment
and promoting continuous improvement. Professionalism in interdisciplinary teams
encompasses collaboration, respect, cooperation, and information sharing for optimal
patient outcomes. Leaders should exemplify professionalism and avoid power misuse.
Physicians are accountable to peers, supporting colleagues, meeting deadlines,
seeking assistance, and respecting all providers. Addressing unprofessional behavior
is essential for maintaining standards, with self-regulation key to preventing and
rectifying misconduct.8
Physicians should demonstrate professionalism by adhering to policies, collaborating
effectively, demonstrating self-awareness, accepting feedback, participating in training,
respecting colleagues, teaching peers, and providing constructive feedback while avoiding
neglecting self-reflection, ignoring feedback, evading patient input, lacking leadership,
shrinking conflict resolution, overlooking team expertise, and displaying disrespect toward
colleagues.

Professional Behavior Learning


Professional competence involves a commitment to excellence through the integration
of evolving knowledge, skills, and behaviors. This mindset fosters continuous growth via
self-development and lifelong learning. Emotional intelligence often holds greater societal
relevance than mere knowledge, making strong motivation for achievement essential.9
Professionalism education should start early in medical training, addressing
the fundamentals of the profession, medical ethics, and professional skills. Methods
include lectures, lab practice, and simulations, while community engagement enhances
understanding of public health dynamics.10-12 Implicitly, professionalism can be conveyed
through a hidden curriculum, where role models effectively instill professional values.13

Keywords: Healthcare professionals; physicians; professionalism.

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References:
1. Badan Pengembangan dan Pembinaan Bahasa, Kementerian Pendidikan,
Kebudayaan, Riset, dan Teknologi Republik Indonesia. Kamus Besar Bahasa
Indonesia; edisi-6.Balai Pustaka;2023.
2. Epstein RM, Hundert EM. Defining and assessing professional competence.
JAMA.2002;287(2):226-35.
3. Pengurus Besar Ikatan Dokter Indonesia. Kode Etik Kedokteran Indonesia.
Jakarta:2012.
4. Rosenberg AA, Yolanda H. Wimberly YH. Professionalism with Physician Colleagues
and Other Health Professionals. American Board of Pediatrics. Proc (Bay Univ Med
Cent). 2007;201`3-6.
5. Byyny RL. Medical professionalism in the modern era.Pharos.2018:1-11.
6. Akabayshi A. Modern Medical Professionalism. Bioethics Across the Globe.2020;89-97.
7. ABIM foundation. American Board of Internal Medicine, ACP-ASIM Foundation.
American College of Physicians-American Society of Internal Medicine, European
Federation of Internal Medicine. Medical professionalism in the new millennium: A
physician charter. Ann Intern Med. 2002;136:243-6.
8. American Board of Pediatrics. Education and Training Committee. Teaching,
Promoting and Assessing Professionalism Across the Continuum: A Medical
Educator's Guide;2017.
9. Desai MK, Kapadia JD. Medical Professionalism and Ethics. Journal of Pharmacology
and Pharmacotherapeutics.2022;13: 113-8.
10. Purnamasari CB, Claramita M, Prabandari YS. Pembelajaran profesionalisme
kedokteran dalam persepsi intruktur dan mahasiswa. Jurnal Pendidikan Kedokteran
Indonesia.2015;4:21-7.
11. Jha V, Bekker HL, Duffy SR, Roberts TE. Perceptions of professionalism in medicine:
a qualitative study. Medical education. 2006;40(10):1027-36.
12. Gliatto PM dan Stern DT. Professionalism. In: Dent J, dan Harden RM, editors. A
practical guide for medical teachers. London: Elsevier; 2009.
13. Hafferty FW, Franks R. The hidden curriculum, ethics teaching, and the structure of
medical education. Acad Med. 1994 Nov 1;69(11):861-71.

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Update on Diagnosis and Management of Pediatric Acute Kidney Injury


Astrid Kristina Kardania
Nephrology Division, Department of Pediatric, Dr. Saiful Anwar General Hospitala
Faculty of Medicine, Brawijaya University, Malang, East Java, Indonesiab
Email: [email protected]

Acute kidney injury (AKI) is linked with high morbidity and mortality, impacting approximately
5% of non-critically ill children and 27% of those who are critically ill. In Indonesia, nearly
half of the ICU patients were at risk of developing AKI, and among those who did, 48.5%
experienced severe AKI, classified as stage 3. The International Society of Nephrology (ISN),
using the 0 by 25 campaign, is aiming for 0 deaths from untreated or preventable AKI in
limited resource settings including Indonesia in 2025. Therefore, prompt management of AKI
including prevention, recognition, treatment, and prevention of its long-term complications
is important.1,2
Acute kidney injury is a syndrome marked by a sudden decrease in kidney function,
leading to an impaired ability to regulate fluid, electrolytes, acid-base balance, and waste
elimination. The causes of acute kidney injury in pediatric patients are varied, with sepsis
as the leading cause of AKI in Indonesia. The Kidney Disease: Improving Global Outcomes
(KDIGO) guidelines provide a standardized classification system for AKI, which is crucial
for consistent diagnosis and management. Acute kidney disease is a recently introduced
concept in kidney disease terminology, aimed at more accurately defining the transition
period between AKI and CKD. Initially defined by ADQI in 2017 as persistent stage 1 AKI
or higher lasting 7 days or more and classified based on the degree of serum creatinine
elevation from baseline, the definition of AKD was later extended by KDIGO in 2021. This
expanded definition includes functional criteria for AKI and minor variations in eGFR and
creatinine that do not necessarily fulfill the diagnostic criteria for AKI. Acute kidney disease
can also be divided into AKD with AKI and AKD without AKI. This encompasses patients who
do not meet the creatinine or urine output thresholds for AKI but still qualify under the criteria
for AKD. Although the prevalence data in the pediatric population is scarce due to limited
studies, AKD has been linked to an elevated risk of developing CKD and higher 1-year
mortality rates in adulthood.3
Accurate and timely diagnosis of AKI is critical for improving outcomes in pediatric patients.
Acute kidney injury prediction, risk stratification, and diagnostic work-up become the pillars
in the diagnosis and management of AKI. Traditional diagnostics such as serum creatinine
levels and urine output have several limitations including delayed elevation after kidney
injury and variability due to factors unrelated to kidney function. Emerging biomarkers

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such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, and kidney injury


molecule-1 (KIM-1), are showing promise in detecting AKI earlier and more accurately.
These biomarkers can provide a more sensitive and specific indication of kidney injury,
allowing for prompt intervention. Imaging studies, including renal ultrasound, can be useful
in diagnosing AKI, particularly in identifying obstructive causes. However, the use of contrast
agents should be carefully considered due to their nephrotoxic potential.4,5
Management of AKI in pediatric patients involves addressing the underlying cause, supporting
kidney function, and preventing complications. Key strategies for the management of
AKI include fluid and hemodynamic management, medication management, and renal
replacement therapy (RRT). Patients at all stages of AKI require careful monitoring of their
fluid balance, appropriate fluid management should be done without causing fluid overload
which leads to worsening kidney function. Avoidance of nephrotoxic drugs and dose
adjustment should be done to avoid further kidney damage. Recent advancements in AKI
management include the development of continuous renal replacement therapy (CRRT),
which offers more precise control of fluid and electrolyte balance in critically ill children.
Research into novel pharmacological agents and protective strategies, such as antioxidants
and anti-inflammatory drugs, is ongoing and holds promise for reducing the incidence and
severity of AKI. In pediatrics, nutritional support also becomes an important factor to meet
metabolic needs and avoid a developmental problem.6,7
Long-term follow-up is essential for children who have experienced AKI, as they are at
increased risk for developing CKD. Several biomarkers such as KIM-1, IL-18, NGAL, and
Liver-type fatty acid binding protein (L-FABP) are used to detect the progression of AKI
into CKD. Regular monitoring of blood pressure, kidney function, and growth parameters is
recommended. Early detection and management of CKD can improve long-term outcomes
and quality of life, preserve kidney function, and prevent further kidney damage.4,5

Keywords: Acute Kidney Injury; Diagnosis; Management; Pediatric

References
1. Patel M, & Gbadegesin RA. Update on prognosis driven classification of pediatric AKI.
Front Pediatr. 2022;10:1039024.
2. Jonny J, Hasyim M, Angelia V, Jahya AN, Hilman LP, Kusumaningrum VF, & Srisawat N.
Incidence of acute kidney injury and use of renal replacement therapy in intensive care
unit patients in Indonesia. BMC Nephrol. 2020 May;21(1):191.
3. Grilli BA, & Webb TG. KDIGO Clinical Practice Guideline for Acute Kidney Injury (AKI)
and Acute Kidney Disease (AKD) Update 2023. Strateg Sourc Public Sect. 2023;75–88.

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4. Schuermans A, Van den Eynde J, Mekahli D, & Vlasselaers D. Long-term outcomes of


acute kidney injury in children. Curr Opin Pediatr. 2023 Apr;35(2):259–67.
5. Bazargani B, & Moghtaderi M. New Biomarkers in Early Diagnosis of Acute Kidney Injury
in Children. Avicenna J Med Biotechnol. 2022;14(4):264–9.
6. Sethi SK, Bunchman T, Chakraborty R, & Raina R. Pediatric acute kidney injury: new
advances in the last decade. Kidney Res Clin Pract. 2021 Mar;40(1):40–51.
7. Krishnasamy S, Sinha A, & Bagga A. Management of Acute Kidney Injury in Critically Ill
Children. Indian J Pediatr [Internet]. 2023;90(5):481–91.

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Principles for the Implementation of Personalized Nutrition Approach in


Pediatric
Conny Tanjung
Department of Postgraduate School, Hasanuddin University
Email: [email protected]

Advances in genomic sciences are contributing to a better understanding of the role of genetic
variants and epigenetic signatures as well as gene expression patterns and microbiota in the
development of diverse chronic conditions and how they may modify intervention responses.
In the field of nutrition, these approaches are recognized as personalized nutrition (PN)
although there are no authoritative or universal definitions for PN. It plays a significant role in
modern nutrition interventions as it attempts to take relevant information from the individual
into account as it is more appropriate than a generalized ‘one-size-fits-all’ approach as it is
more biologically relevant to the individual. It has been shown to help drive behavior change
and positively influence health outcomes. This has led to an increase in the development
of commercially available PN programs, which utilize various forms of individual-level
information to provide services and products for consumers. By this, we must have a strong
and in-depth understanding of PN so that we can choose the suitable and best services.
In this article, we present a clear example of PN on docosahexaenoic acid (DHA) and
arachidonic acid (ARA) based on our genetic signatures. Both DHA and ARA play a crucial
role in infant development and immune systems. Impact of genetic variability common
variants in the fatty acid desaturase (FADS) gene cluster modify the activity of PUFA
desaturation and the composition of human blood and tissue lipids. FADS polymorphisms
show large effect sizes on plasma and tissue concentrations of ARA and small effects on
DHA. Infants with genetic FADS variants predicting a low activity of the 5 and 6 desaturase
enzymes comprise two-thirds of our infants in Indonesia. In these infants with genetically
determined low desaturase activity, ARA synthesis is ineffective, therefore they developed
particularly low plasma AA concentrations without a dietary supply of preformed ARA.
Studies on variations in the FADS gene cluster provide impressive indications for marked
gene-diet interactions in the modulation of complex phenotypes such as eczema, asthma,
and cognition, with some studies indicating that breastfeeding providing both preformed
AA and DHA reduced asthma risk and improved cognitive outcomes in those infants with a
genetically determined low formation of LC-PUFA.
By looking at these data, it is clear that PN can be translated for individual advice and might
influence the government regulatory judgment, while also aligning with the well-accepted
population-based guidance currently in place as long as we have a clear guiding principle
for the implementation of PN.
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Keywords: Personalized nutrition, Nutrigenetic, Nutrigenomic, Epigenetic, Guiding


principles, Behaviour Change

References:
1. Tanjung C, Rzehak P, Sudoyo H, Mansyur M, Munasir Z, Immanuel S, et al. The effect
of fatty acid desaturase gene polymorphisms on long chain polyunsaturated fatty acid
composition in Indonesian infants. Am J Clin Nutr 2018;108(5):1135–44.
2. Koletzko B, Bergmann K, Brenna T, Calder PC, Campoy, Clandinin MT, et al. Should
formula for infants provide arachidonic acid along with DHA? A position paper of the
European Academy of Paediatrics and the Child Health Foundation. Am J Clin Nutr
2020;111:10–16.
3. Touniana P, Bellaı¨cheb M, Legrandc P. Review article ARA or no ARA in infant formulae,
that is the question. Archives de Pe´diatrie 2021; 28: 69–74.
4. Ramos-Lopez O, Milagro F I, Allayee H, Chmurzynska A, Choi MS, Curi R, et al. Guide
for Current Nutrigenetic, Nutrigenomic, and Nutriepigenetic Approaches for Precision
Nutrition Involving the Prevention and Management of Chronic Diseases Associated
with Obesity. J Nutrigenet Nutrigenomics 2017;10:43–62.
5. Wilson-Barnes S, Gymnopoulos L P, Dimitropoulos K, Solachidis V, Rouskas K, et al.
EMERGING RESEARCH : Personalised nutrition for healthy living: The PROTEIN
project. Nutrition Bulletin. 2021; 46: 77–87.
6. Adams SH, Anthony JC, Carvajal R, Chae L, Khoo CS, Latulippe ME, et al. Perspective:
Guiding Principles for the Implementation of Personalized Nutrition Approaches That
Benefit Health and Function. Adv Nutr 2020;11:25- 34.

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Recognizing Extrapulmonary TB in Adolescence


Diah Asri Wulandaria
KSM Ilmu Kesehatan Anak RSUP Dr. Hasan Sadikina
FK Universitas Padjadjaran Bandungb
E-mail: [email protected]

Introduction
The 1.3 billion adolescents in the world today represent more than one-sixth of the global
population.1 The definition of an adolescent according to the World Health Organization
(WHO) is a person who is 10-19 years old.1,2 Despite this right, adolescents suffer a high
burden of disease from preventable causes, including tuberculosis.1 In high tuberculosis (TB)
transmission settings, the incidence of tuberculosis increases rapidly during adolescence and
peaks in early adulthood.3-5 Approximately 15–25% of TB infections involve extrapulmonary
sites and cause extrapulmonary TB (EPTB) through hematogenous and lymphatic
dissemination of M. tuberculosis.6 Extrapulmonary TB refers to any bacteriologically
confirmed or clinically diagnosed case of TB involving organs other than the lungs (e.g.
pleura, peripheral lymph nodes, abdomen, genitourinary tract, skin, joints and bones, central
nervous system).2
1. Tuberculous lymphadenitis
The most common extrapulmonary tuberculosis (TB) is tuberculous lymphadenitis (TBLA).7,8
The lymph nodes usually are unilateral, painless, non-tender lymph node enlargement (often
>2 cm) for >1 month and do not respond to other treatments. The most common site is the
cervical nodes.2,8 Histologic diagnosis is based on identifying granulomatous inflammation
commonly characterized by aggregates of epithelioid histiocytes, multinucleated giant cells
(Langhans giant cells), and central necrosis is distinctly present in necrotizing granulomas.
The sensitivity of histology was reported 59-88%.8,9 Acid Fast Bacilli (AFB) identification in
the specimen can also help to diagnose TBL. The fine-needle aspiration culture (FNAC) has
a specificity of 88–96%, while the smear has 34.6–66.0% sensitivity and 87.5% specificity
in diagnosing TBL.8 In 2017, WHO endorsed the next-generation Xpert MTB/RIF ultra with
improved detection and sensitivity similar to solid culture.9 The ultrasonic signs of hilus
absence, short-to-long axis (S/L) ratio ≥0.5, unclear edge, necrosis, echogenic thin layer,
strong echoes, and capsular or peripheral vascularity may aid in the diagnosis of tuberculous
lymphadenitis.10
2. Tuberculous pleural effusions
Tuberculous pleura effusion (TPE) results from Mycobacterium tuberculosis (MTB) infection
of the pleura and is characterized by an intense chronic accumulation of fluid and inflammatory

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cells in the pleural space.11 TPE is commonly found in adolescents.8 Symptoms of pleural
tuberculosis have an acute to subacute onset, with non-productive cough and pleuritic pain,
febrile, and dyspnea occur if the effusion is large.11-13 Physical examinations reveal dullness
on percussion and reduced breath sounds.2 Chest radiography findings are unilateral pleural
effusions vary in size and pleural wall thickening.8,11-13 The findings of ultrasound include free-
flowing anechoic effusions, complex echogenic effusions, and effusions with septations/
loculations.12 Tuberculous effusions are straw-colored exudates. The nucleated cell count is
typically 1000–6000/ml and has >50% lymphocytes. Elevated lactate dehydrogenase (LDH)
levels are present in 75% and often >500 IU/L, while a protein level >30 g/L is present in
55–77% of cases.12 AFB staining is rarely positive in TPE as TPE is mostly a hypersensitivity
reaction. MTB culture positivity rates were <20%, and liquid media (BACTEC 13A) increased
the yield to about 45%. A Cochrane review found that the pooled sensitivity and specificity
of pleural fluid X-pert MTB/RIF were 51% and 99%, respectively.13 Adenosine deaminase
(ADA) is present in high concentrations in tuberculous effusions, with a value of >40 IU/L in a
lymphocyte-predominant exudate that carries a positive predictive value (PPV) of 98%.2,12,13
3. Abdominal tuberculosis
Abdominal tuberculosis (ATB) is classified into four major patterns of involvement: peritoneal,
luminal, visceral, or lymph nodal.8,14,15 The clinical features vary according to the site of
ATB. Intestinal tuberculosis may be associated with abdominal pain, nausea, vomiting,
diarrhea, fever, weight loss, and lack of appetite. Peritoneal tuberculosis is characterized
by abdominal pain, abdominal distension, and fever. Abdominal ultrasonography may
show ascites, lymphadenopathy, peritoneal and omental changes, and mural thickening
of the bowel wall.8,14,15 The findings on computed tomography (CT) may include ascites,
lymphadenopathy (hypodense center, calcifications), peritoneal involvement (thickening,
nodularity, enhancement), omental involvement (omental thickening, nodularity, masses),
mural thickening (asymmetric, mural enhancement), and bowel stricture.8,14 ADA levels (36–
40 U/L) were used to diagnose peritoneal TB with 100% sensitivity and 97% specificity.8 The
sensitivity of Xpert MTB/RIF for the diagnosis of peritoneal TB was 64% and the specificity
was 97%, with the sensitivity and specificity of Xpert MTB/RIF using the intestinal tissue
being 23% and 100%, respectively.16 Stool Xpert was positive in 20% of cases, with a
sensitivity of 39.1% and a specificity of 85.7%, with a positive and negative predictive value
of 45% and 82.5% respectively.17
4. Tuberculous pericarditis
Tuberculous pericarditis (TBP) has three clinical forms: pericardial effusion, constrictive
pericarditis, and a combination of effusion and constriction. TBP is characterized by fever,
weight loss, night sweats, cough, chest pain, and breathlessness in moderate to high

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pericardial effusion. Constrictive pericarditis is seen with thick fibrinous fluid around the
heart.2 On physical examination reveals signs of cardiac failure, distant or muffled heart
sounds, and apex beat difficult to palpate.2 Chest X-ray and echocardiogram showing
effusion >1 cm are essential for diagnosing pericarditis.8,18 A typical finding from the aspirated
fluid is a protein-rich lymphocytic exudate.18 The definitive diagnosis involves the presence
of AFB on smear or culture of pericardial fluid or caseating granulomatous lesions in the
histopathology of pericardium samples. Diagnosis using pericardial ADA levels >40 U/L had
87–93% sensitivity and 89–97% specificity.8,18 Xpert MTB/RIF in TBP showed a sensitivity of
63.8% with high specificity (100%).18
5. Musculoskeletal Tuberculosis
Musculoskeletal TB (MSTB) is a common form of EPTB including skeletal, muscular, and
musculoskeletal components.8 Any bone, joint, or bursa can be infected, the major weight-
bearing bones, such as the spine, hip, and knee, are the most prevalent infection sites,
representing 70-80% of tuberculous arthritis cases.8,19 Spinal TB (tuberculous spondylitis
or Pott’s disease) is the most predominant form of MSTB, with an incidence of 1–2% of
all TB cases. The clinical manifestations include fever, malaise, loss of body weight, back
pain, spinal deformity, paraplegia, kyphosis with varying degrees, paraspinal abscesses,
and neurologic deficits.8 Collapse of the anterior spinal elements results in a kyphotic
deformity, giving the hunchback appearance and Gibbus deformity.19 The clinical symptoms
of tuberculous arthritis include slow progressive painful swelling, range of motion pain,
synovial hypertrophy, and effusion.8,19 Imaging of the affected area is performed using
conventional X-rays, CT, or magnetic resonance imaging (MRI) to assess the damage. MRI
helps provide diagnostic clues, as it may easily demonstrate anterior corner destruction, the
relative preservation of the intervertebral disk, multilevel involvement with or without skip
lesions, and a large soft tissue abscess. The synovial fluid ADA levels can be helpful in TB
diagnosis with a cut-off value of ≥31 U/L. The sensitivity and specificity for the ADA test have
been indicated at 83.3% and 96.7%, respectively for TB arthritis. Xpert MTB/RIF and Ultra
synovial fluid samples have a sensitivity of 97% and 96% with a specificity of 94% and 97%,
respectively.8
6. Cutaneous Tuberculosis
Cutaneous or skin tuberculosis (CTB) constitutes 1–1.5% of all EPTB.8,20 Exogenous
CTB includes tuberculous chancre and TB verrucosa cutis. Endogenous CTB includes
scrofuloderma and TB orificialis.20 Scrofuloderma occurs on the skin as a contiguous
extension of underlying TB, usually lymphadenitis or bone or joint TB. This lesion appears
as a subcutaneous swelling or nodule attached to the overlying skin and eventually
develops draining sinus tracts that drain watery, purulent, or caseous material or cutaneous
abscesses.8,20 Scrofuloderma involves granulomatous inflammation with caseous necrosis
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and acid-fast bacilli. The gold standard for CTB diagnosis is a mycobacterial culture of skin
biopsy specimens.20
7. Genitourinary Tuberculosis
Kidneys are the primary organ affected in genitourinary tuberculosis (GUTB), where the
disease progresses slowly and is mostly asymptomatic but can be highly destructive to the
organ, and lead to renal dysfunction and renal failure.8 Constitutional symptoms, including
fever, weight loss, and sweating, are observed along with urologic symptoms, such as
flank pain, dysuria, pyuria, hematuria, urinary frequency, and urinary incontinence.8,21,22
Radiographic imaging, intravenous urography, ultrasonography, and CT should be performed
to assess abnormalities such as fibrosis, calcification or thickening, or possible ulceration.8
CT urography reveals parenchymal granulomas and parenchymal lesions can sometimes
manifest as cystic masses, calcifications, perirenal stranding, thickening of the pararenal
fascia, moth-eaten calyx sign, papillary necrosis, pelvic-infundibular strictures/stenosis, and
hydroureteronephrosis.23 Histology studies of fine-needle aspiration or biopsy samples show
classical epithelioid cell granuloma with caseating necrosis.8,21 A previous report showed
a pooled sensitivity and specificity of 87% and 91% (respectively) for Xpert MTB/RIF in
detecting GUTB using urine samples.8 The culture-based for urine or tissue biopsy specimens
is the gold standard with a sensitivity of 80–90% and a specificity of roughly 100%.21
8. Central nervous system tuberculosis
Central nervous system (CNS) TB accounts for 1–10% of all TB cases, and it has the
highest mortality and morbidity among all TB infections. Tuberculous meningitis (TBM) is
the most common of CNS TB. The onset is usually insidious with fever, malaise, weight loss,
and anorexia, followed by headache, photophobia, and meningism. If untreated, the illness
progresses to a vasculitis phase, with focal neurological deficits like cranial nerve palsies
and hemiparesis often accompanied by seizures with worsening sensorium and coma.24
Disturbance of CSF circulation with subsequent hydrocephalus is common.25 Choroid
tubercles, seen in TBM associated with miliary tuberculosis, are pathognomonic but seen
only in 10% of cases.24 TBM staging according to the modified British Medical Research
Council grading system are stage I, GCS 15 without focal neurologic deficit; stage II, GCS
11–14, or 15 with focal neurologic deficit; and stage III, GCS <10.26-27 Cerebrospinal Fluid
(CSF) should be examined for tuberculous meningitis, including cell count, biochemical
parameters, acid-fast staining, culture, and nucleic acid amplification tests. Most cases have
lymphocytic pleocytosis with a total count of 50–500 cells/mm, and elevated protein (100–
500 mg/dL) with 10% greater than 500 mg/dL. If CSF is allowed to stand at room temperature
for 6–12 hours, a "cobweb" coagulum is formed. Moderately low glucose and about 80%
of cases have values less than 45 mg/dL. The yield of smear examination by routine

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Ziehl-Neelsen and Kinyoun stains is very low in TBM. The gold standard is MTB culture.24
Systematic review and meta-analysis study of Xpert MTB/RIF for tuberculous meningitis
reveals that Xpert MTB/RIF sensitivity was 85% and specificity was 98%.28 Marais S et al in
2010, developed a scoring system for diagnostic criteria of tuberculous meningitis. Patients
with no cranial imaging: criteria probable if total score ≥10 and possible if total score 6-9; and
patients with cranial CT/MRI: criteria probable if total score ≥12 and possible if total score
6-11.29 Both MRI and CT contrast scans reveal basal enhancing exudates, leptomeningeal
enhancement along Sylvian fissures, with enlargement of ventricles is helpful for diagnosis.
On CT/MRI, tuberculomas appear as round or irregular nodules (disc or ring enhancement)
with moderate to marked edema. Complications like hydrocephalus can be seen.24,25,29
9. Miliary Tuberculosis
Miliary tuberculosis (MiliTB) is a fatal form of disseminated TB developed by hematogenous
spread from a primary focus. The common symptoms of MiliTB are fever, malaise,
anorexia, weight loss, and cough with septicemia. Specific disease symptoms are also
observed depending on the organ involvement.8,30 TBM is more frequently seen in children
and adolescents with miliary TB (20%–40%). Careful physical examination should focus
on identifying organ system involvement. Fundus examination for detecting choroid
tubercles can help in early diagnosis as their presence is pathognomonic of miliary TB. The
miliary pattern in chest X-ray has been defined as “a collection of tiny discrete pulmonary
opacities (2 mm or less in diameter) that are generally uniform in size and widespread in
distribution.30 High-resolution CT imaging identifies miliary nodules, ground-glass opacities,
and interlobular septal thickening. Diagnostic imaging, including ultrasound, MRI, positron
emission tomography-CT (PET-CT), or echocardiography, is recommended to assess the
extent of organ damage. Sputum, bronchoalveolar lavage (BAL), or other fluids (pleural,
peritoneal, pericardial, ascitic, CSF), and biopsy specimens are used for biochemical,
microbiological, histopathological, and molecular testing of MiliTB. AFB smear and bacterial
culture are generally positive for mycobacteria in MiliTB. Histopathology shows caseating
granuloma with necrosis. Molecular methods such as Xpert MTB/RIF can rapidly diagnose
MiliTB cases.8,30
Clinical assessment in all presumed cases of EPTB should consider: •) history of TB contact;
•) collection of appropriate specimens from an affected site (including CSF, lymph node
aspirate, lymph node biopsy, pleural fluid, peritoneal fluid, pericardial fluid, synovial fluid
or urine specimens) for confirmatory tests, including molecular WHO recommended rapid
diagnostic tests (mWRDs), and histology where appropriate and available; •) collection of
respiratory samples (stool, expectorated or induced sputum, gastric aspirate or NPA sample)
to evaluate for PTB (as the child may have both PTB and EPTB); •) CXR and other imaging,
depending on the affected site; •) HIV testing.2 x
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Treatment
Children and adolescents with forms of drug-susceptible EPTB other than TBM, milliary
(disseminated), and osteoarticular TB should be treated with a 6-month treatment regimen
of 2HRZE/4HR. Children and adolescents with milliary (disseminated) and osteoarticular
TB should be treated with 2HRZE/10HR. Children and adolescents with TBM should be
treated with 2HRZE/10HR or the newly recommended alternative short intensive treatment
regimen composed of 6 months of isoniazid, rifampicin, pyrazinamide, and ethionamide
(6HRZEto). WHO recommends using corticosteroids for forms of EPTB disease for TBM
and tuberculous pericarditis.2
Adolescents were a risk factor for associated factors of mortality and loss to follow-up (LTFU),
especially for TBM and milliary TB.31

References
1. World Health Organization. Global Accelerated Action for the Health of Adolescents (AA-
HA!): guidance to support country implementation. Geneva, Switzerland: WHO, 2023.
Available at: https://www.who.int/publications/i/item/9789240081765.
2. World Health Organization. WHO operational handbook on Tuberculosis: Module 5:
management of tuberculosis in children and adolescents. 2022. Available at: https://
www.who.int/publications/i/item/9789240046832.
3. Loftian F, Loftian G, Bolursaz MR, Tabarsi P, Velayati A. Comparison between
pulmonary and extrapulmonary tuberculosis in adolescents. Arch Pediatr Infect Dis.
2017;5(3):e57253.
4. Snow KF, Sismanidis C, Denholm J, Sawyer SM, Graham SM. The incidence of
tuberculosis among adolescents and young adults; a global estimate. Eur Respir J.
2018;51:1702352.
5. Snow KJ, Cruz AT, Seddon JA, Ferrand RA, Chiang SS, Hughes JA, et al. Adolescent
tuberculosis. Lancet Child Adolesc Health. 2020;4(1):68-79.
6. Fang Y, Zhou Q, Li L, Zhou Y, Sha W (2022). Epidemiological characteristics of
extrapulmonary tuberculosis patients with or without pulmonary tuberculosis.
Epidemiology and Infection. 2022;150(e158):1–5. Available at: https://doi.org/10.1017/
S0950268822001236.
7. Sivaratnam L, Nawi AM, Manaf MRA. An Evidence Based Clinical Pathway for the
Diagnosis of Tuberculous Lymphadenitis: A Systematic Review. Int J Mycobacteriol
2020;9:107-15.

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8. Gopalaswamy R, Dusthackeer VNA, Kannayan S, Subbian S. Extrapulmonary


Tuberculosis—An Update on the Diagnosis, Treatment and Drug Resistance. J. Respir.
2021;1:141–164.
9. Tahseen S, Ambreen A, Ishtiaq S, Khanzada FM, Safdar N, Sviland L. The value of
histological examination in the diagnosis of tuberculous lymphadenitis in the era of
rapid molecular diagnosis. Scientific Reports. 2022;12:8949. Available at: https://doi.
org/10.1038/s41598-022-12660-0.
10. Yu TZ, Zhang Y, Zhang WZ, Yang GY. Role of ultrasound in the diagnosis of cervical
tuberculous lymphadenitis in children. World Journal of Pediatrics. 2021;17: 544–550.
11. Zhai K, Lu Y, Shi HZ. Tuberculous pleural effusion. J Thorac Dis 2016;8(7):E486-494.
12. Shaw JAA, Diacon AH, Koegelenberg CFN. Tuberculous pleural effusion. Respirology.
2019;24:962–971.
13. Lo Cascio CM, Kaul V, Dhooria S, Agrawal A, Chaddha U. Diagnosis of tuberculous
pleural effusions: A review. Respiratory Medicine. 2021;188: 106607. Available at: https://
doi.org/10.1016/j.rmed.2021.106607.
14. Dawra S, Harshal S Mandavdhare HS, Singh H, Sharma V. Abdominal Tuberculosis:
Diagnosis and Management in 2018. JIACM. 2017; 18(4): 271-74.
15. Jha DK, Pathiyil MM, Sharma V. Evidence-based approach to diagnosis and management
of abdominal tuberculosis. Indian J Gastroenterol. 2023;42(1):17–31.
16. Sharma V, Soni H, Kumar P, Dawra S, Mishra S, Mandavdhare HS, et al. Diagnostic
accuracy of the Xpert MTB/RIF assay for abdominal tuberculosis: a systematic review
and meta-analysis. Expert Rev Anti Infect Ther. 2021;19(2):253-265.
17. Talib A, Bhatty S, Mehmood K, Naim H, Haider I, Lal H, et al. GeneXpert in stool: Diagnostic
yield in Intestinal Tuberculosis. J Clin Tuberc Other Mycobact Dis. 2019;100131. Available
at: https://doi.org/10.1016/j.jctube.2019.100131
18. Isiguzo G, Du Bruyn E, Howlett P, Ntsekhe M. Diagnosis and Management of Tuberculous
Pericarditis: What Is New? Current Cardiology Reports. 2020;22(2):1-8.
19. Leonard JM. Central Nervous System Tuberculosis. Microbiol Spectrum 2017;5(2):TNMI7-
0044-2017.
20. Nguyen KH, Alcantara CA, Glassman I, May N, Mundra A, Mukundan A, et al. Cutaneous
Manifestations of Mycobacterium tuberculosis: A Literature Review. Pathogens. 2023,
12, 920.
21. Mantica G, Ambrosini F, Riccardi N, Vecchio E, Rigatti L, De Rose AF, et al. Genitourinary
Tuberculosis: A Comprehensive Review of a Neglected Manifestation in Low-Endemic
Countries. Antibiotics. 2021;10:1399.
22. Muneer A, Macrae B, Krishnamoorthy S, Zumla A. Urogenital tuberculosis epidemiology,
pathogenesis and clinical features. Nat Rev Urol. 2019;16:573–598.

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23. Naeem M, Zulfiqar M, Siddiqui MA, Shetty AS, Haq A, Varela C, et al. Imaging
Manifestations of Genitourinary Tuberculosis. RadioGraphics. 2021;41:1123–1143.
24. Kunju PAM, James J. Central Nervous System Tuberculosis in Children. Pediatr Inf Dis
2019;1(1):23-29.
25. Schaller MA, Wicke F, Foerch C, Weidauer S. Central Nervous System Tuberculosis:
Etiology, Clinical Manifestations and Neuroradiological Features. Clin Neuroradiol.
2019;29:3-18.
26. Nataprawira HM, Gafar F, Risan NA, Wulandari DA, Sudarwati S, Marais BJ. Treatment
Outcomes of Childhood Tuberculous Meningitis in a Real-World Retrospective Cohort,
Bandung, Indonesia. Emerg Infect Dis. 2022;28(3):660-671.
27. Abdella A, Deginet E, Weldegebreal F, Ketema I, Eshetu B, Desalew A. Tuberculous
Meningitis in Children: Treatment Outcomes at Discharge and Its Associated Factors
in Eastern Ethiopia: A Five Years Retrospective Study. Infection and Drug Resistance
2022;15:2743–2751.
28. Hernandez AV, de Laurentis L, Souza I, Pessanha M, Thota P, Roman YM, et al.
Diagnostic accuracy of Xpert MTB/RIF for tuberculous meningitis: a systematic review
and meta-analysis. Trop Med Int Health. 2021;26(2):122–132.
29. Marais S, Thwaites G, Schoeman JF, Török ME, Misra UK, Prasad K, et al. Tuberculous
meningitis: a uniform case definition for use in clinical research. Lancet Infect Dis.
2010;10:803–12.
30. Sharma SK, Mohan A, Sharma A. Journal of Clinical Tuberculosis and Other Mycobacterial
Diseases. 2016;3:13–27.
31. Gafar F, van’t Boveneind-Vrubleuskaya N, Akkerman OW, Bob Wilffert B, and Alffenaar
JWC. Nationwide analysis of treatment outcomes in children and adolescents routinely
treated for tuberculosis in the Netherlands. Eur Respir J. 2019;54:1901402

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Coughing: Allergic or Infection


Dwi Kisworo Setyowireni
Department of Child Health, Faculty of Medicine, Public Health & Nursing,
Universitas Gadjah Mada, Yogyakarta, Indonesia
E-mail: [email protected]

Cough during childhood is very common and is one of the most frequent reasons for
consultation in daily pediatric practice. Cough can be classified based on its duration (acute,
sub-acute, chronic/persistent) and its quality (sound, wet/dry).
Most cases of acute and sub-acute cough in children are associated with viral upper
respiratory tract infections that do not require specific diagnosis evaluation. Between 35%
and 40% of school-age children continue to cough 10 days after the onset of a common cold,
and 10% of preschool children continue to cough 25 days after a respiratory tract infection.1
The most common cause of chronic cough in children found was persistent bacterial
bronchitis (40%), spontaneously resolving prolonged or overlapping upper respiratory tract
infection (URTI) and the rest were asthma and GERD (10%).2 Viral respiratory infections are
the major cause of acute asthma exacerbations and may contribute to asthma inception in
high-risk young children with susceptible genetic backgrounds.3
Children with chronic coughs without cough pointers can be safely managed using the
watchful waiting approach.4 Conversely, in the presence of cough pointers or persistence of
cough, the patient needs to have further investigations and treatments based on the etiology,
aiming to intercept the underlying disease, prevent potentially irreversible tissue damage,
and improve the general health of patients affected by chronic cough, as well as the quality
of life of patients and their family.5 Children with non-specific cough are commonly treated
with a variety of medications to treat the symptoms of cough. Careful assessment of children
with chronic cough is important to identify any underlying disease.
Based on the quality of the cough, chronic cough can be differentiated from wet or dry
cough. A wet cough indicates an underlying cause of mucous hypersecretion or impaired
mucociliary clearance, whereas a dry cough indicates an underlying cause of airway
irritation or inflammation or a non-airway cause.5 The common cause of wet chronic cough
is protracted bacterial bronchitis (PBB), a bacterial infection of the lower airways leading to
a chronic wet cough. The limitation of flexible bronchoscopy for confirming the diagnosis,
based on the clinical trial recommends giving empiric antibiotics without bronchoscopy and
lavage. The distinction between dry and wet cough can be valid in directing the differential
diagnosis of the cough. Clinicians should be aware that a dry cough can be converted to a
wet cough when airway secretion increases.
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Cough that is caused by respiratory infection and allergies sometimes is difficult to differentiate.
Some research has found that respiratory viral infection has the potential role play in the
inception of asthma. Epidemiological studies have shown an increased risk of asthma with
lower respiratory infection (LRI) caused by human rhinovirus (HRV). Childhood asthma
studies have also found that respiratory syncytial virus (RSV) and HRV are associated with
increased asthma risk at age six years.6 There appears to be a synergistic interaction between
viral infection and allergic sensitization. These provide strategies for the primary prevention
of asthma by prevention of either allergic sensitization or LRI in high-risk children.3
Cough caused by allergic sensitization may be associated with previous respiratory viral
infection in children. Therefore, acute or subacute cough in children may continue to cough
for more than 10 days (chronic cough) and may be caused by infection as well as allergic
(asthma). Identification of the type of cough in children is difficult but important. Cough
frequency, duration, and qualitative features historically have relied on patient/family reports.
More objective measures of cough duration and characteristics would be useful to determine
the management of cough.
The treatment of cough should be based on the etiology. In some cases of nonspecific
chronic cough, in which no underlying condition can be found, empirical treatment based on
the cough characteristics may be useful. There is no scientific evidence to justify the use of
over-the-counter cough remedies (antitussives, mucolytics, and/or antihistamines), as they
could have potentially serious side effects, and thus should not be prescribed in children.7

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Figure 1. Clinical algorithm for the evaluation and management of chronic cough in children

Keywords: Cough; Pediatric; Allergic; Infection.

References
1. Hay AD, Wilson A, Fahey T, Peters TJ. The duration of acute cough in pre-school children
presenting to primary care: a prospective cohort study. Fam Pract [Internet]. 2003 Dec
1;20(6):696–705. Available from: https://doi.org/10.1093/fampra/cmg613
2. Marchant JM, Masters IB, Taylor SM, Cox NC, Seymour GJ, Chang AB. Evaluation and
Outcome of Young Children With Chronic Cough. Chest [Internet]. 2006;129(5):1132–41.
Available from: https://www.sciencedirect.com/science/article/pii/S0012369215506909
3. Ahanchian H, Jones CM, Chen Y sheng, Sly PD. Respiratory viral infections in children with
asthma: do they matter and can we prevent them? BMC Pediatr [Internet]. 2012;12(1):1.
Available from: BMC Pediatrics
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4. Chang AB, Van Asperen PP, Glasgow N, Robertson CF, Mellis CM, Masters IB, et
al. Children with chronic cough: When is watchful waiting appropriate? Development
of likelihood ratios for assessing children with chronic cough. Chest [Internet].
2015;147(3):745–53. Available from: http://dx.doi.org/10.1378/chest.14-2155
5. Marseglia GL, Manti S, Chiappini E, Brambilla I, Caffarelli C, Calvani M, et al. Chronic
cough in children and adolescents: A systematic review and a practical algorithm by
the Italian Society of Pediatric Allergy and Immunology. Allergol Immunopathol (Madr).
2021;49(2):133–54.
6. Jackson DJ, Gangnon RE, Evans MD, Roberg KA, Anderson EL, Pappas TE, et al.
Wheezing rhinovirus illnesses in early life predict asthma development in high-risk
children. Am J Respir Crit Care Med. 2008;178(7):667–72.
7. Lamas A, Ruiz de Valbuena M, Máiz L. Cough in children. Arch Bronconeumol.
2014;50(7):294–300.

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New Concept of Management Rheumatic Heart Disease


in Adolescents
Dyahris Koentartiwi
Department of Child Health, Universitas Brawijaya, Malang, Indonesia
E-mail:[email protected]

Rheumatic heart disease is an acquired heart disease characterized by heart valve disorders
following acute rheumatic fever or post-infectious sequel of acute rheumatic fever resulting
from an abnormal immune response to streptococcal pharyngitis or Group A Streptococcus
(GAS) that triggers valvular damage.1,2
Recent data from the Global Burden of Disease (GBD) showed that RHD affects 400,000
people globally, with approximately 310,000 deaths in 2019. Despite being preventable,
RHD remains a significant health issue, especially in low-income countries, with South Asia
accounting for over 50% of RHD-related deaths. The disease primarily affects individuals
under 50, with the highest incidence in children aged 0-14 and peak prevalence in adults
aged 20-34. Women are disproportionately affected, leading to high maternal and fetal
mortality rates.2-6
Diagnosing RHD in adolescents is crucial as it remains a leading cause of death among
non-communicable diseases. Echocardiography, including handheld and artificial intelligent
assisted methods, can confirm diagnoses even in asymptomatic cases, classified as definite
or borderline per World Heart Federation criteria. A study in New Caledonia found RHD
prevalence at age 16 was four times higher than in children aged 9-10. Another study
identified a significant correlation between NT-pro BNP levels and the severity of mitral
regurgitation (MR) and left ventricular dilatation in RHD, suggesting a cut-off value for NT-
pro BNP could be used for screening severe MR beyond echocardiography.7-11
Adolescence is a critical phase of development between childhood and adulthood.
Adolescents with RHD form a unique population with specific needs to maintain health
into adulthood. They face not only emotional and psychological challenges but also issues
related to the progression of their illness, relationships, and future planning. Conditions like
mitral valve prolapse and aortic regurgitation can lead to heart failure at a young age. They
must also prepare for potential complications such as infective endocarditis, atrial fibrillation,
stroke, and even death.4,12-14
Managing RHD requires a comprehensive approach involving four levels of intervention.
Primordial prevention addresses social determinants of health to reduce GAS transmission.
Primary prevention focuses on the timely diagnosis and treatment of GAS infections with

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penicillin to prevent rheumatic fever (RF). Secondary prevention includes ongoing benzathine
penicillin prophylaxis to prevent RF recurrence and early detection and management of
RHD to avoid complications. Tertiary interventions involve heart surgery, catheter-based
procedures, and chronic medical treatment for managing long-term RHD.15
A study on patients with congenital heart disease and RHD concluded that an Adolescent
Transition Psycho-Educational Program should be developed to help adolescents with
moderate to severe heart disease manage emotional and psychological issues, cope with
the lifestyle impacts of disease progression, and prepare for the future. This program should
include support groups and psychosocial support. However, our institution lacks a specific
transitional program to assist adolescents transitioning to adult care. While many support
groups exist in our country, none fully address the psychological needs of adolescents with
RHD.14

Keywords: adolescent, rheumatic heart disease, RHD prevention, psychological need

References
1. Park MK, Salamat M. Park’s pediatric cardiology for practitioners. 2021.
2. Marijon E, Mocumbi A, Narayanan K, Celermajer DS. Persisting burden and challenges
of rheumatic heart disease. 2021;3338–48.
3. Shi L, Bao C, Wen Y, Liu X, You G. Analysis and comparison of the trends in burden of
rheumatic heart disease in China and worldwide from 1990 to 2019. 2023;1–12.
4. Zühlke L, Engel ME, Karthikeyan G, Rangarajan S, Mackie P, Cupido B, et al.
Characteristics, complications, and gaps in evidence-based interventions in rheumatic
heart disease: The Global Rheumatic Heart Disease Registry (the REMEDY study).
Eur Heart J. 2015;36(18):1115–22.
5. Argyriou A V., Polykretis C, Teeuw RM, Papadopoulos N. Geoinformatic Analysis
of Rainfall-Triggered Landslides in Crete (Greece) Based on Spatial Detection and
Hazard Mapping. Sustain. 2022;14(7).
6. Naseeb K, Khan MN, Soomro NA, Hameed A, Chand G, Ram J, et al. Temporal Trends
and Burden of Rheumatic Heart Disease in South Asia: A Comprehensive Analysis of
Three Decades from Global Burden of Disease Study. Glob Heart. 2024;19(1).
7. Chatard J claude, Dubois T, Espinosa F, Kamblock J. Screening Rheumatic Heart
Disease in. 2020;1–9.
8. Reméanyi B, Wilson N, Steer A, Ferreira B, Kado J, Kumar K, et al. World Heart
Federation criteria for echocardiographic diagnosis of rheumatic heart disease-an
evidence-based guideline. Nat Rev Cardiol. 2012;9(5):297–309.

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9. Rwebembera J, Marangou J, Mwita JC, Mocumbi AO, Mota C, Okello E, et al. 2023
World Heart Federation guidelines for the echocardiographic diagnosis of rheumatic
heart disease. Nat Rev Cardiol. 2024;21(4):250–63.
10. Koentartiwi D, Kadafi KT, Hikmah FIN, Khalasha T, Ramadhanti A, Suwarniaty R.
Predictor of mitral valve regurgitation severity and left ventricular dilatation using amino-
terminal pro-brain natriuretic peptide marker in pediatric rheumatic heart disease. Int J
Crit Illn Inj Sci. 2024;14(1):43–50.
11. Brown K, Roshanitabrizi P, Rwebembera J, Okello E, Beaton A, Linguraru MG, et al.
Using Artificial Intelligence for Rheumatic Heart Disease Detection by Echocardiography:
Focus on Mitral Regurgitation. J Am Heart Assoc. 2024;13(2):1–10.
12. Ralph AP, Currie BJ. Therapeutics for rheumatic fever and rheumatic heart disease.
Aust Prescr. 2022;45(4):104–12.
13. The Promise of Adolescence. The Promise of Adolescence. 2019.
14. Tye SK. Challenges for Adolescents With Congenital Heart Defects / Chronic
Rheumatic Heart Disease and What They Need : Perspectives From Patients, Parents
and Health Care Providers at the Institut Jantung Negara ( National Heart Institute ),.
2021;11(January):1–9.
15. Shimanda PP. Preventive Interventions to Reduce the Burden of Rheumatic Heart
Disease in Populations at Risk : A Systematic Review. 2024;

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The Future Impact of Stunting: How to Prevent


Eddy Fadlyanaa
Division of Growth and Development - Social Pediatrics, Child Health Department,
Universitas Padjadjarana
Dr. Hasan Sadikin Hospital, Bandungb
E-mail: [email protected]

Introduction
Stunting is a pressing global public health issue, particularly in low-and middle-income
countries. Data show that 25% of stunted children are from low-income countries, 66%
from middle-income countries, and 8% from high-income countries. In Indonesia, 30.8% of
children under five are stunted, as per the 2018 Riskesdas data, down from 37.2% in 2013.
Regional disparities are significant, with prevalence ranging from 11.9% in Maluku to 2.8%
in Bali. Indonesia ranks fifth globally in stunting prevalence and is among the 17 countries
identified by the 2014 Global Nutrition Report as facing major malnutrition issues, including
stunting, wasting, and obesity.1,2,3,4
Despite multi-sectoral efforts since 2017, including the National Strategy to Accelerate
Stunting Prevention, progress remains insufficient. The Indonesian government aims to
address this issue with ambitious targets to reduce stunting and wasting.5,6,7 This paper will
explore the stunting problem in Indonesia, and its long-term impacts, and evaluate current
and proposed strategies, including early interventions and the provision of animal-based
protein.

The Problem of Stunting in Indonesia


Stunting is defined as the percentage of children whose height-for-age is below minus two
standard deviations of the 2006 WHO Child Growth Standards impacts both physical and
cognitive development. In Indonesia, 21.6% of children under five were affected in 2022,
down from 31.8% in 2020 but still above global averages and WHO thresholds. Despite
progress from 41.5% in 2000 to 30.8% in 2021, further action is needed to meet global targets.
Socio-economic factors such as parental education, sanitation, and economic conditions
significantly influence stunting rates. Lower educational levels are linked to higher stunting
risks, and inadequate sanitation exacerbates malnutrition. The COVID-19 pandemic has
further worsened economic conditions, increasing food insecurity.8-19
The Indonesian government’s National Strategy for the Acceleration of Stunting Prevention
allocates approximately $3.9 billion annually and involves 23 ministries. Community-based

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programs focus on improving health infrastructure, providing nutritional counseling, and


distributing micronutrient supplements. However, inconsistent service delivery and socio-
economic inequalities pose challenges. Achieving the ambitious target of reducing stunting
to 14% by 2024 requires effective collaboration between government entities, NGOs, and
local communities to ensure successful implementation and resource utilization.20,21,22,23

Long-Term Consequences of Stunting


A multi-country cohort study showed early-onset persistent stunting was associated with
lower cognitive development in children at 5 years of age. Several studies in Indonesia
regarding the long-term impacts of stunting include a meta-analysis study Effects of Stunting
on Child Development conducted by Rosyidah M (2021) concluded that Stunting increases
the risk of abnormal development in children (aOR=3.71; 95%CI=2.35 to 5.86; p=0.760).24,25,26
Stunting, a result of chronic malnutrition, impairs cognitive and motor skills in early childhood,
as observed by Mustakim et al. (2022), leads to lower IQ and academic achievement in the
medium term, corroborated by Suryawan et al. (2019) and Prado et al. (2019), and results
in reduced productivity and higher health risks in adulthood, as highlighted by Akbar et al.
(2023) and Huriah & Nurjannah (2020), underscoring the urgent need for early nutritional
interventions to mitigate these extensive and enduring impacts. Addressing stunting through
targeted environmental interventions can significantly improve long-term developmental and
health outcomes.24,25,26,27,28

How to Prevent Stunting?


To prevent stunting, it is essential to meet children's basic needs, which are influenced by
both genetic and environmental factors, with interventions primarily targeting environmental
issues. Education is vital in preventing stunting by raising awareness about nutrition and
empowering communities to make healthier choices. Despite various efforts, results have
been mixed, indicating the need for more innovations and tailored programs. For instance,
in Ethiopia, intensive behavior change interventions improved dietary diversity and reduced
stunting prevalence. Conversely, in Guatemala, micronutrient supplementation had no
significant impact on growth. In Uganda, different formulations of lipid-based nutrient
supplements did not significantly affect developmental outcomes, although there was a slight
increase in head circumference. These mixed results highlight the importance of context-
specific interventions.29,30,31
In Indonesia, the Baduta project integrated nutrition-specific and sensitive interventions to
improve breastfeeding and complementary feeding. Community-based trials in Madagascar

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and the Philippines also yielded varied results. Studies in Pakistan indicated that locally
produced supplementary foods and lipid-based nutrient supplements could reduce stunting,
especially among younger children. However, micronutrient powders did not significantly
reduce stunting. These findings emphasize the need for targeted, context-specific approaches
and consistent delivery of successful interventions to effectively combat stunting. (Table 1)32-
38

Conclusion
Addressing stunting in Indonesia demands a comprehensive approach that includes behavior
change interventions, micronutrient supplementation, and integrated nutrition programs,
while also addressing socio-economic determinants such as education, sanitation, and
economic conditions. The long-term consequences of stunting underscore the urgency
for sustained and effective interventions. Collaborative efforts among government entities,
NGOs, and local communities are essential, ensuring consistent delivery of interventions
and tackling socio-economic inequalities.

Acknowledgments: We would like to express our sincere gratitude to Muhammad Gilang


Dwi Putra and Alvira Dwilestarie Putri for their invaluable contributions to this paper.

Table 1. The Preventive Measures for Stunting in Children


Study Statistical Findings on Significant
Intervention Age Group Methods Interpretation
Location Analysis Stunting Results
Odds ratios Significant Higher odds of
Multi-platform
Alive & Thrive’s for dietary improvements meeting dietary Effective in
intervention (mass
intensive Infants diversity and in dietary diversity and improving
media, community
Ethiopia 29 behaviour and young meal frequency diversity and meal frequency CF practices
mobilization,
change children standards, reductions standards, better and reducing
interpersonal
interventions height-for-age in stunting height-for-age stunting
communication)
z-scores prevalence z-scores
Comparison
No significant Similar rates of
of growth and Questions the
Long-term Randomized impact on zinc deficiency
micronutrient effectiveness
micronutrient 6-72 controlled trial growth, stunting and no iron
Guatemala 30 status between of large-scale
supplementation months (Chispuditos® vs. prevalence, or deficiency
intervention micronutrient
(Chispuditos®) lactose-free milk) micronutrient anemia in both
and control supplementation
status groups
groups
No significant
Randomized, double- Analysis of impact on Neither dairy in
Lipid-based No
blind, community- developmental developmental LNS nor LNS
nutrient improvements in
Uganda31 1-5 years based trial (different outcomes domains, a itself improved
supplements developmental
LNS formulations vs. and head slight increase developmental
(LNS) outcomes
no supplementation) circumference in head outcomes
circumference

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Analysis
of stunting
No significant Higher odds
The Baduta prevalence, Improved
improvements of achieving
project (nutrition- iron-folic breastfeeding
Under 2 Cluster-randomized in linear growth minimum dietary
Indonesia32 specific and acid pill and
years controlled trial or reductions diversity and
nutrition-sensitive consumption, complementary
in anemia acceptable diet
interventions) exclusive feeding practices
prevalence scores
breastfeeding
rates
Higher length-
for-age
Analysis of
LNS and home z-scores and No main effects
length-for- Importance of
visits integrated Under 6 Community-based lower stunting on child growth
Madagascar 33
age z-scores starting LNS at 6
into an existing months trial prevalence for or development
and stunting months
nutrition program children under in the full sample
prevalence
6 months at
baseline
Low-intensity None of the
Adjusted Adjusted odds
School- health interventions
School WaSH Cluster-randomized odds ratios ratio for stunting
Philippines34 aged education improved overall
intervention controlled trial for stunting reduction with
children reduces height-for-age
reduction LIHE was 0.95
stunting z-scores
Analysis
Community- of stunting
No significant
driven prevalence, Modest
impacts on Implementing
development iron-folic improvements
General Cluster-randomized stunting or multifaceted
Indonesia35 grants, health acid pill in maternal and
population controlled trial long-term interventions is
provider training, consumption, child nutrition
undernutrition complex
and sanitation exclusive practices
outcomes
training breastfeeding
rates
Significant
Length-for- The control
increase in
age z-scores, group had a 1.7 Effective in
Pakistan Locally produced 6-18 length-for-age
Longitudinal study incidence rate times higher preventing
(Kurram)36 RUSF months z-scores and
of stunting, likelihood of stunting
lower incidence
hazard ratios stunting
rate of stunting
Risk ratios Effective in
Lipid-based
for stunting Significantly RR = 0.91, 95% reducing
Pakistan nutrient 6-23 Cluster-randomized
reduction, reduced risk of CI 0.88-0.94, stunting among
(Sindh)37 supplement months controlled trial
subgroup stunting p<0.001 food-insecure
(Wawamum)
analysis by age children
Analysis
of plasma
micronutrient
levels, Improved
No significant
Locally produced hemoglobin, plasma Not sufficient to
Pakistan 24-48 Community-based change in
micronutrient weight- micronutrient combat stunting
(Kurram)38 months trial height-for-age
powder for-height, levels and in young children
z-score
weight-for- hemoglobin
age z-scores,
height-for-age
z-scores

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Keywords: Stunting, Long-Term Impact, Nutritional Interventions, Socio-Economic Factors,


Child Development, Prevention Strategies

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using additive quantile regression. PloS one. 2013 Nov 4;8(11):e78692.

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13. Vaivada T, Akseer N, Akseer S, Somaskandan A, Stefopulos M, Bhutta ZA. Stunting in


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25. Suryawan A, Jalaludin MY, Poh BK, et al. Malnutrition in early life and its
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34. Sangalang SO, Lemence AL, Ottong ZJ, Valencia JC, Olaguera M, Canja RJ, Mariano
SM, Prado NO, Ocaña RM, Singson PA, Cumagun ML. School water, sanitation, and
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35. Beatty A, Borkum E, Leith W, Null C, Suriastini W. A cluster randomized controlled trial
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36. Fazid S, Haq ZU, Gillani BH, Khan AJ, Khan MN, Khan A, Garzon C, Habib I, Tanimoune
M, Ihtesham Y, Heald AH. Effectiveness of locally produced ready-to-use supplementary
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37. Khan GN, Kureishy S, Ariff S, Rizvi A, Sajid M, Garzon C, Khan AA, De Pee S, Soofi SB,
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38. Khan A, Ul-Haq Z, Fatima S, Ahmed J, Alobaid HM, Fazid S, Muhammad N, Garzon
C, Ihtesham Y, Habib I, Tanimoune M. Long-term impact of multiple micronutrient
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Recent Update in Medication of Paediatric Rheumatology


Edy Noverya
Allergy-Immunology Division, Department of Child Health, Mohammad Hoesin Hospitala
Faculty of Medicine, Sriwijaya University, Palembang, Indonesiab
E-mail: [email protected]

The recent update in medication of pediatric rheumatology has made a lot of progress.
However, we know that medication in pediatric rheumatology is always behind adults. Part
of the reason for the delay is that clinical trials in children can only begin after studies
in adult patients have reached phase 3. Management of children's rheumatism varies
depending on the underlying disease. The use of steroids, non-steroidal anti-inflammatory
drugs (NSAIDs), other immunosuppressants, and biologic agents is very diverse. However,
what we need to be aware of is that apart from being a pillar for treatment, these various
drugs must be properly considered regarding the side effects that arise. Biologic agents and
small molecule agents have been very developed and provide better outcomes compared
to previous conventional therapies. The development of biological and small molecule agent
therapy has progressed significantly over the last 5 years. Some guidelines recommend the
use of biological agents even at the start of diagnosis. Of course, this is a challenge in itself
for countries with all the shortcomings and limitations both in terms of funding for treatment
and the availability of these drugs. Organ damage in pediatric rheumatology diseases
does not only occur due to the rheumatological disease. This condition can also be caused
by side effects arising from the use of the drug itself. Choosing medications for pediatric
rheumatology diseases must be very careful and oriented towards the therapeutic target.
Several drugs that were previously considered to have many benefits are now considered to
be used due to side effects or complicating the long-term prognosis. Pediatric rheumatology
diseases are the main focus in the era of the development of autoimmune diseases because
a recent update in medication is expected to improve the quality of life and also improve the
long-term prognosis.

Acknowledgments: We would like to thank members of the Allergy Immunology Working


Group of the Indonesia Pediatric Society for sharing knowledge and information about
pediatric rheumatology cases.

Keywords: Recent Update; Medication; Rheumatology; Paediatric.

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References
1. Katarzyna PB, Wiktor S, Ewa D, Piotr L. Current treatment of systemic lupus
erythematosus: a clinician’s perspective. Rheumatol Int. 2023;43:1395–407.
2. Correl CK, Klein-Gitelman MS, Henrickson M, Battafarano DF, Orr CJ, Leonard Mb,
et al. Child Health Needs and the Pediatric Rheumatology Workforce: 2020-2040.
Pediatrics. 2024;153: e2023063678R.
3. Maggio MC, Miniaci A, Gallizzi R, Civino A. Neuroimmunoendocrinology in children
with rheumatic glucorticoids are the orchestra director. Int J Mol Sci. 2023;24:1–21.
4. Evolution of understanding of pediatric rheumatologic diseases as captured by
paediatrics over 75 years. Pediatrics. 2023;11:1–12.

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Internet Addiction in Children: How to Detect and Prevent


Hesti Lestari
Department of Child Health, Faculty of Medicine, Sam Ratulangi University, Manado,
Indonesia
E-mail: [email protected]

The Internet has become an integral part of modern society, with user populations continuing
to grow across all age groups. Healthy internet use refers to the use of the internet for a
specific purpose at an appropriate time, without any cognitive or behavioural impairment.
Maladaptive use of the Internet can be conceptualized as a behavioural addiction. The
concept of “Internet addiction” has been proposed as an explanation for the uncontrollable,
damaging use of technology to access the Internet. Symptoms are compared to the criteria
used to diagnose other addictions. It has been referred to by various terms, including
compulsive internet use, internet dependence, pathological internet use, and problematic
internet use (PIU). The terms have been used as an umbrella term that refers to the
problematic or compulsive use of activities related to the Internet, including but not limited
to, online gaming, gambling, buying, and pornography viewing, as well as social networking
and cyberbullying.1
Internet addiction (IA) refers to behaviour characterized by excessive and prolonged use of
the internet; reactions of anger, frustration, or panic when unable to use; and unsuccessful
attempts to reduce the time spent on them. It consists of three main factors, which include
obsession (e.g. obsessive thoughts about checking social media), neglect (failing to complete
homework due to internet use), and lack of control (unable to stop online activity).1,2
Recent estimates of IA prevalence have ranged from 0.7 to 20.0%, depending on the year
of study, location, measurement, and/or sample population. The more recent the studies,
the higher the prevalence rate, which matched the increasing trend of time spent on the
Internet over the past 10 years. Furthermore, the addictive use of smartphones and other
Internet-enabled devices appears to affect all generations due to the rapid dissemination
of smartphones and other information technologies across all ages, especially adolescents
and youths. Adolescents (12-17 years) seem particularly vulnerable since they access the
internet more than other age groups and they are at risk due to the slow maturation of areas
in the brain involved in behavioural control. Internet abuse in young people is associated
with living outside the family home, low self-esteem, and a higher prevalence of problems
with other behavioural addictions or substance use.1-3
In many studies, the associations between PIU and physical and psychological health have
been carried out. Empirical evidence has suggested an association between excessive use of

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the Internet and physical health problems such as obesity, vision problems, musculoskeletal
problems, hearing impairments, and sleep deprivation. Numerous studies have shown
indulging in the use of the Internet is associated with a variety of psychological problems,
such as increased addictive personal habits of smoking, drinking alcohol or coffee, and
taking drugs, high levels of depressive symptoms, interpersonal problems, and aggressive
behaviours. Psychosomatic symptoms might be important signals of mental health and this
should be taken seriously. Regardless, the overall problem size appears comparable with
the problem size of other major mental disorders.1-3
Internet addiction is associated with various risk factors, including sociodemographic
variables (including male gender, younger age, and higher family income), Internet use
variables (including time spent online, using social and gaming applications), psychosocial
factors (including impulsivity, neuroticism, and loneliness), and comorbid symptoms (including
depression, anxiety, and psychopathology in general), suggesting these factors contribute
to an increased vulnerability for developing Internet-use related problems. Gaming and
gambling addictions were usually more severe problems compared to generalized Internet
addiction. In addition, gambling appears to be more severe than gaming.1,3
To measure PIU or IA symptoms, some questionnaires were used. The Internet Addiction Test
(IAT) developed by Young4 was the first test scale developed to measure the level of Internet
addiction. The test has 20-item attempts to establish whether a respondent suffers from
Internet addiction, all measured on a 5-point Likert scale. The questions are scored from 1 to
5, with a score of 1 for the answer ‘‘rarely’’ and 5 for the answer ‘‘always.’’ Summative scores
ranging from 20 to 49 are considered ‘‘average’’ online users. Scores ranging from 50 to 79
are considered to be Internet users experiencing occasional to frequent problems due to the
Internet. Scores ranging from 80 to 100 are considered to be users suffering from significant
problems due to their Internet usage.2 The factors measured by the IAT are ‘‘withdrawal and
social problems,’’ ‘‘time management and performance,’’ and ‘‘reality substitute’’. The other
questionnaire was Kuesioner Diagnostik Adiksi Internet (KDAI), developed in Indonesia by
Siste.5 The tool is self-administered, and consists of 7 subscales, namely, “withdrawal”, ‘loss
of control’, ‘priority enhancement’, ‘negative consequences’, ‘mood modification’, ‘salience’,
and ‘impairment’. Each statement is scored with a 7-point Likert scale. A score of ≥108
indicates IA (out of 264 maximum).
To prevent Internet addiction and the subsequent development of other psychopathologies
among children, it is crucial to explore how parents influence children’s development, and
how they can be helpful in risk identification in this context. Prevention will be successfully
implemented in the interaction of family, educational organizations, and adolescent society.2,6

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Health education, including education on IA, may promote more health behaviours. However,
more targeted strategies may be needed for IA prevention. Organizations and schools need
tools to be able to screen for Internet-related activities to know what problems to prevent.
Prevention programs that deter overall Internet use may not be sustainable in a modern
world where we communicate using the Internet and homework/work requires the use of the
Internet. Instead, prevention and harm reduction of PIU could explore helping users make
educated choices, build resilience, and shape a culture of safe Internet-related activity use.2,6
The following options are preventive actions that can be introduced:7
• To encourage alternative motivations, engagement in alternative entertainment
behaviours (also those including Internet use), new coping skills, cognitive and emotional
skills, and healthy attachment styles to reduce the risk of Internet use-related problems
and to reduce Internet usage, if needed (e.g., through alerts and notifications) and to
provide alternative options of relaxation (e.g., reading, meeting people, and engaging in
physical activities).
• To detect the risk of experiencing other comorbidities or problems and address them
with professional support and the support of significant others (e.g., caregivers in the
case of adolescents), and to embrace systemic approaches.
• If a problem with Internet usage is present, all Internet use-related addictions should be
simultaneously assessed, especially gaming and gambling addiction.
• Enhanced family, partner, and peer communication and caretaking (e.g., through
parents, siblings, partners, or friends) can prevent the problems from emerging when
risk indicators appear and develop progressively (e.g., excessive time spent playing
online games, lack of sleep due to a constant online connection, irritability, and mood
changes when disconnecting, neglecting school or relationships). Thus, ‘keeping an
eye’ on time spent and having conversations about online uses can be the first measure
of prevention in families and friendship groups.
• Information should also be available for users’ environments (e.g., for families, schools,
and communities) about the risks of habitually engaging in online role-playing games
or online gambling applications which can be out of control and cause negative health
consequences (i.e., functional impairment and distress) or financial problems (i.e., online
gambling).
Prevention strategies should be careful not to pathologize and stigmatize Internet use in
general but to focus on safe use while preventing possible harm from various Internet-related
activities. Young individuals should be engaged in conversations and activities concerning

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offline and online health, potential positive and negative implications of excessive online
behaviors, and provided with information on alternative pastime activities and alternative
coping strategies not involving Internet use.

Keywords: Internet; Addiction; Children.

References:
1. Wang j, Hao QH, Tu Y, Peng W, Wang Y, Li H, et al. Assessing the Association Between
Internet Addiction Disorder and Health Risk Behaviors Among Adolescents and Young
Adults: A Systematic Review and Meta-Analysis. Front. Public Health 2022; 10. https://
doi.org/10.3389/fpubh.2022.809232
2. Romero SSM, Van den Broucke S, Chau C. The effectiveness of prevention programs
for problematic Internet use in adolescents and youths: A systematic review and meta-
analysis. Cyberpsychology: Journal of Psychosocial Research on Cyberspace 2021.
15(2). https://doi.org/10.5817/CP2021-2-10
3. Rosenthal A, Cha YJ, Clark MA. The Internet Addiction Test in a Young Adult U.S.
Population. Cyberpsychology, Behavior, and Social Networking 2018: 21;10. https://doi.
org/10.1089/cyber.2018.0143
4. Young, K.S. Psychology of computer use: XL. Addictive use of the Internet: A case that
breaks the stereotype. Psychol. Rep. 1996, 79, 899–902.
5. Siste K. Development of kuesioner diagnostik adiksi Internet for adolescents: Brain
functional connectivity through fMRI BOLD, study of prevalence, risk factors, and
protective factors. [Dissertation]. Universitas Indonesia: Indonesia (2019).
6. Shi J, Van der Maas M, Yu L, Jiang QL, Agasee S, Turber NE. Current prevention
strategies and future directions for problem Internet use. Current Opinion in Behavioral
Sciences 2022, 48:101231. https://doi.org/10.1016/j.cobeha.2022.101231
7. Lopez-Fernandez O, Kuss DJ. Preventing Harmful Internet Use-Related Addiction
Problems in Europe: A Literature Review and Policy Options. Int. J. Environ. Res. Public
Health 2020, 17(11), 3797. https://doi.org/10.3390/ijerph17113797

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Diagnostic Approach and Management in Pediatric Gastrointestinal


Bleeding
Himawan Aulia Rahmana
Gastrohepatology Division, Department of Child Health, Faculty of Medicine Universitas
Indonesiaa
Dr. Cipto Mangunkusumo Hospital, Jakarta, Indonesiab
E-mail: [email protected]

Gastrointestinal bleeding in children can be divided based on the location of the source of
the bleeding: upper gastrointestinal bleeding (UGIB) originating proximally from the ligament
of Treitz and lower gastrointestinal bleeding (LGIB) originating distally from the ligament of
Treitz. Upper gastrointestinal bleeding usually manifests as blood vomits (hematemesis) or
black tarry stools (melena), while lower gastrointestinal bleeding usually manifests as bloody
stools (hematochezia). Gastrointestinal bleeding can also occur in small amounts (occult) if
positive fecal occult blood is found or there is recurrent anemia of unknown etiology.

Upper gastrointestinal bleeding


The management approach for upper gastrointestinal bleeding includes stabilization,
seeking etiology, and specific management. In the stabilization step, determining the primary
survey that includes airway, breathing, and circulation is essential to do first. Often, initial
management requires fluid resuscitation or blood product transfusion. The severity of upper
gastrointestinal bleeding can also be assessed using the Sheffield score, a scoring system
that considers various clinical parameters to determine the severity of bleeding.1
The etiology of UGIB can be confidently predicted based on the patient's age, source of
bleeding, and symptoms other than bleeding. Etiology can be predicted based on the patient's
age group, i.e., neonates, infants, and children or adolescents. For example, bleeding due
to cow's milk protein allergy (CMPA) is usually found in neonates or young infants.2 Second,
UGIB can also be divided based on its source: variceal or non-variceal bleeding. The
presence of signs of portal hypertension and splenomegaly leads to suspicion of variceal
bleeding, while in non-variceal, there are usually no such signs. Third, symptoms other than
bleeding can lead to a specific etiology. For example, the presence of epigastric pain or
heartburn can lead to gastritis, stress ulcers, or esophagitis. Symptoms of hematemesis can
also be caused by swallowing maternal blood (in neonates) or epistaxis.
After stabilization, some specific management of UGIB includes gastric lavage to ensure
whether the bleeding is still ongoing or has stopped, administration of proton pump inhibitors
(PPIs), use of somatostatin analogs such as octreotide to reduce portal system flow
(especially in variceal bleeding), and diagnostic or therapeutic endoscopy (hemostatic) using

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ligation, sclerotherapy, clipping, or argon plasma coagulation (APC).3 Specifically for the
management of variceal bleeding, the use of primary and secondary prophylaxis to prevent
recurrent bleeding is also known.4 Antibiotics may also be helpful to prevent bacteremia in
variceal bleeding by reducing the risk of infection from the gastrointestinal tract.5

Lower gastrointestinal bleeding


The management approach for lower gastrointestinal bleeding is as thorough as for
upper
gastrointestinal bleeding: stabilization, seeking etiology, and specific management.
Sometimes, we have difficulty determining whether what is in the black/red-colored stool
is blood or whether the source of the bleeding is from the lower gastrointestinal tract or the
upper gastrointestinal tract. Some medications, such as iron supplementation or rifampicin,
can cause stools to appear colored as if there is gastrointestinal bleeding. Therefore, a stool
occult blood (guaiac) examination can be performed if we are unsure about gastrointestinal
bleeding.
The etiology of LGIB can also be predicted based on the patient's age group and the
presence of symptoms other than bleeding. For example, LGIB due to intussusception is
usually experienced by children aged around 1-2 years, while inflammatory bowel disease
(IBD) is usually suffered by school-age children and adolescents.6 Sometimes, the presence
or absence of accompanying symptoms can also be a clue to a particular etiology. For
example, in Meckel's diverticulum, there is usually massive LGIB, but there are no other
symptoms. While if there are symptoms of constipation, it is likely that the bleeding comes
from an anal fissure.
Indications for colonoscopy in LGIB depend on the suspected diagnosis. However, a
colonoscopy is usually needed if blood occurs repeatedly or continuously in the stool. In
cases of gastrointestinal bleeding accompanied by acute abdominal symptoms or suspected
Meckel's diverticulum, immediate surgical consultation is necessary. If the source of bleeding
is not found after upper and lower gastrointestinal endoscopy, other examinations to check
for bleeding in the small intestine, such as enteroscopy, capsule endoscopy, nuclear
scintigraphy, or angiography, may help find the etiology.7

Keywords: gastrointestinal hemorrhage, infant, child, adolescent

References:
1. Thomson MA, Leton N, Belsha D. Acute upper gastrointestinal bleeding in childhood:
development of the Sheffield scoring system to predict need for endoscopic therapy. J
Pediatr Gastroenterol Nutr. 2015;60(5):632-6.

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2. Gilger MA, Buren KWV. Upper gastrointestinal bleeding. In: Kleinman RE, Goulet O-J,
Mieli-Vergani G, Sanderson IR, Sherman PM, Shneider BL, editors. Walker’s pediatric
gastrointestinal disease. 6 ed. Raleigh: People’s Medical Publishing House; 2018. p.
1853-62.
3. Romano C, Oliva S, Martellossi S, Miele E, Arrigo S, Graziani MG, et al. Pediatric
gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric
Gastroenterology. World J Gastroenterol. 2017;23(8):1328-37.
4. Abd ElRahim AY, Fouad R, Khairy M, Elsharkawy A, Fathalah W, Khatamish H, et
al. Efficacy of carvedilol versus propranolol versus variceal band ligation for primary
prevention of variceal bleeding. Hepatol Int. 2018;12(1):75-82.
5. Castillo L, Prachuapthunyachart S, Hall M, Shelby S, Quiros-Tejeira RE, Vo HD. Antibiotic
use in cirrhotic children with acute upper gastrointestinal bleeding: A retrospective study
using the pediatric health information system (PHIS) database. Medicine (Baltimore).
2019;98(29):e16505.
6. Turck D, Michaud L. Lower gastrointestinal bleeding. In: Kleinman RE, Goulet O-J,
Mieli-Vergani G, Sanderson IR, Sherman PM, Shneider BL, editors. Walker’s pediatric
gastrointestinal disease. 6 ed. Raleigh: People’s Medical Publishing House; 2018. p.
1887-904.
7. Tringali A, Thomson M, Dumonceau JM, Tavares M, Tabbers MM, Furlano R, et al.
Pediatric gastrointestinal endoscopy: European Society of Gastrointestinal Endoscopy
(ESGE) and European Society for Paediatric Gastroenterology Hepatology and Nutrition
(ESPGHAN) Guideline Executive summary. Endoscopy. 2017;49(1):83-91.

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Diagnosis and Management of Stunting in Children


I Gusti Lanang Sidiartha
Department of Child Health, Faculty of Medicine, University of Udayana, Bali, Indonesia
E-mail: [email protected]

Stunting in children is still high in Indonesia. Based on the data of Survei Status Gizi Indonesia
(SSGI) year 2022, the prevalence of stunting in children under five is 21.6%, highest than
wasting, underweight, and overweight are 7.7%, 17.1%, and 3.5%, respectively.1 In children
with specific diseases such as congenital heart disease and neurologic infection, the
prevalence of stunting was higher that was 51% and 48.1%, respectively.2,3
Stunting in early life hurts children’s health later. It increased morbidity and mortality, reduced
physical, neurodevelopmental, and economic capacity, and an elevated risk of metabolic
disease into adulthood.4 Women who were themselves stunted in childhood tend to have
stunted offspring, creating an intergenerational cycle of poverty and reduced human capital
that is difficult to break.5
Michael Golden divided a child’s response to a nutrient deficiency into two types: type 1
and type 2. In type 1, he or she can continue growing, consume the body stores, and then
have a reduction in specific bodily functions. In type 2, he or she can stop growing and,
if necessary, lose weight to make the nutrient internally available and thus maintain the
nutrient concentration in the tissue. According to this response, type 2 nutrient deficiency is
responsible for stunting. Type 2 nutrients include protein (essential amino acids), potassium,
sodium, magnesium, zinc, phosphorous, and oxygen.6
A cross-sectional study, including 313 children aged 12-59 months in rural southern Malawi,
reported children with stunting had lower serum concentrations of all nine essential amino
acids compared with no stunted children. In addition, stunted children also had lower serum
concentrations of conditionally essential and non-essential amino acids.7 Another study in
Klungkung, Bali, reported that stunted children had lower serum zinc concentrations and
lower calorie intake.8 A study in our hospital reported that stunting in children was associated
with inadequate intake of energy and protein.9
Globally, around 70% of stunting in children under five was found to be due to faltering
during the first 1000 days of life, including 20% prenatally. Then around 30% was due to
continued increases in faltering from age 2 to 5 years.10 So, the current global programmatic
momentum is to focus on the first 1000 days of life to prevent stunting in children and its
consequences throughout the lifecycle.10

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Families and health workers often fail to recognize stunting in children because linear growth
is not routinely measured as part of community health programs and lack of awareness
of stunting’s devastating health consequences.11 In communities where short stature is
so common, childhood stunting is often considered normal.11 Assessment of linear growth
(children’s length up to 24 months or height from 24 months onwards) is essential for
determining or diagnosing whether a child is stunting or not. It was impossible to distinguish
which child was stunted merely by observing them play and interact with each other.
For example, two girls from the Maldives of identical height (86 cm). While one of the girls,
at 2 years and 2 months, is growing adequately, the other, who is 4 years and 4 months old,
is severely stunted (Fig. a and Fig. b). After height measurements and plotting to the WHO
Child Growth Standards, we know which one is stunting and normal.

Figure. (a) Two girls with identical height (86 cm) cannot be distinguished by observing
them play and interact with each other. (b) Height-for-age measurements of two girls plotted
to the WHO Child Growth Standards.11

Assessing linear growth requires adherence to key principles and attention to detail. The
accuracy and reliability of length and height measurements are highly dependent on the
robustness, precision, maintenance, and calibration of the anthropometric equipment, the
measurement techniques, and the establishment of data quality procedures.12 The influences
of variability in length and height measurements, including the behaviour and cooperation
of the child, the setting where measurements are taken, the accuracy and precision of the
instruments, the anthropometrism’s technical capability, and data recording methods.12
Besides anthropometric measurements, there are two points that should be considered in
diagnosing stunting.13 First, there are growth-inhibiting conditions, such as poverty, neglect,
or unknowing about how to give adequate nutrition. In addition, there is sometimes recurrent

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infection, such as diarrhea, upper respiratory tract infection, or pneumonia. The latter is
called secondary undernutrition which causes stunting. Second, a reduction in linear growth
velocity below the median or 50th percentile (length deceleration), resulting in that length
crossing downward the growth percentile lines.13
If a diagnosis of stunting is made, appropriate guidance for catch-up growth should be
made.13,14 Age-appropriate nutritional counseling should be provided to parents. For breastfed
infants, recommending breastfeeding more often, ensuring lactation support, or discussing
formula supplementation until catch-up growth is achieved may be helpful. For formula-fed
infants, may be instructed on how to make energy-dense formula by concentrating the ratio
of formula to water or by using oral nutrition supplement (ONS) during periods of catch-up
growth.14,15
Toddlers should avoid excessive juice because this can interfere with proper nutrition.
Nutritional supplements may be given until catch-up growth is achieved. Catch-up growth
in humans is defined as height velocity above the statistical limits of normal (more than
2 standard deviations above the mean) for age and/or maturity during a defined period,
following a transient period of growth inhibition.16 During a period of catch-up growth, parents
may also instructed to provide calorie-dense foods and priority consume animal protein food
sources with a protein-energy ratio of more than 10%.
Close follow-up should be performed, including evaluation of height or length and weight.
Multidisciplinary interventions, including home visits, should be considered to improve weight
and length gains, parent-child relationships, and cognitive development.14 When a disease
or medical condition is identified, the correct management may include instituting specific
treatment of the condition or seeking consultation from a subspecialist or other health care
professional for further evaluation and management recommendations.14
There is consensus that severe or prolonged malnutrition including stunting can negatively
affect a child’s health and cognitive development. Recognizing these consequences, the
global community has responded by setting targets to reduce the prevalence of child
stunting as a main international nutrition goal. The most effective strategy to reduce stunting
is through programs that prevent rather than treat linear growth retardation during the first
1000 days of life.13

Keywords: Catch-up growth, Early life nutrition, Stunting

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References
1 Kementerian Kesehatan Republik Indonesia. Buku Saku Hasil Studi Status Gizi
Indonesia (SSGI) Tahun 2022. Kemenkes RI 2022; : 1–14.
2 Agustini W, Yantie NPVK, Gunawijaya E, Sidiartha GL, Pratiwi GAE. Underweight,
Stunted, and Wasted among Children with Congenital Heart Disease: Acyanotic versus
Cyanotic. Open Access Maced J Med Sci 2022; 10: 610–613.
3 Ayu Diah Perdana Paramita, I Gusti Ngurah Made Suwarba, Dewi Sutriani Mahalini, I
Gusti Lanang Sidiartha. Prevalence and Associated Factors of Malnutrition in Patients
with Intracranial Infections at Sanglah Hospital Denpasar. GSC Adv Res Rev 2021; 9:
044–050.
4 Dewey KG, Begum K. Long-term consequences of stunting in early life. Matern Child
Nutr 2011; 7: 5–18.
5 Prendergast AJ, Humphrey JH. The stunting syndrome in developing countries. Paediatr
Int Child Health 2014; 34: 250–265.
6 Golden MHN. Specific deficiencies versus growth failure: Type I and type II nutrients. J
Nutr Environ Med 1996; 6: 301–308.
7 Semba RD, Shardell M, Sakr Ashour FA, Moaddel R, Trehan I, Maleta KM et al. Child
Stunting is Associated with Low Circulating Essential Amino Acids. EBioMedicine 2016;
6: 246–252.
8 Mardewi KW, Sidiartha IGL, Gunawijaya E. Low serum zinc and short stature in children.
Paediatr Indones 2016; 56: 171.
9 Yuliana; Sidiartha IGL. ASSOCIATION BETWEEN ENERGY AND MACRONUTRIENTS
INTAKE WITH ANTHROPOMETRIC INDICATORS IN CHILDREN. Medicina (B Aires)
2014; 45: 3–8.
10 Leroy JL, Ruel M, Habicht JP, Frongillo EA. Linear growth deficit continues to accumulate
beyond the first 1000 days in low- and middle-income Countries: Global evidence from
51 national surveys. J Nutr 2014; 144: 1460–1466.
11 de Onis M, Branca F. Childhood stunting: A global perspective. Matern Child Nutr 2016;
12: 12–26.
12 de Onis M, Garza C, Victora CG, Onyango AW, Frongillo EA, Martines J. The WHO
Multicentre Growth Reference Study: Planning, study design, and methodology. Food
Nutr Bull 2004; 25: 15–26.
13 Leroy JL, Frongillo EA, Dewan P, Black MM, Waterland RA. Can children catch up
from the consequences of undernourishment? Evidence from child linear growth,
developmental epigenetics, and brain and neurocognitive development. Adv Nutr 2020;
11: 1032–1041.

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14 Cole SZ, Lanham JS. Failure to thrive: An update. Am Fam Physician 2011; 83: 829–
834.
15 Menteri Kesehatan Republik Indonesia. PERATURAN MENTERI KESEHATAN
REPUBLIK INDONESIA NOMOR 29 TAHUN 2019 TENTANG PENANGGULANGAN
MASALAH GIZI BAGI ANAK AKIBAT PENYAKIT. 2019.
16 Wit JM. Catch-up growth : Definition, mechanism, and models. 2014.

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Fluid Management in Pediatric Shock: How Low Can We Go


a
I Nyoman Budi Hartawan
Departement of Pediatrics Udayana Universitya
Prof. Dr. I G.N.G Ngoerah General Hospital, Denpasar, Indonesiab
E-mail: [email protected]

Fluid therapy is one of the most critical elements in the management of septic shock. Fluid
resuscitation aims to restore intravascular volume, improve microcirculation, increase
cardiac output, and enhance oxygen delivery. However, excessive fluid volume or rapid
administration can lead to an increase in atrial natriuretic peptide (ANP), which causes the
breakdown of the endothelial glycocalyx, subsequently increasing endothelial permeability
(leakage syndrome), resulting in fluid loss into the extravascular space.1,2
The Surviving Sepsis Campaign recommends early resuscitation for children with septic
shock or another sepsis-related organ dysfunction. This recommendation differentiates fluid
therapy between healthcare systems with and without intensive care unit (ICU).3
In healthcare systems with the availability of ICU, it is recommended to administer fluid
boluses of up to 40-60 mL/kg (10-20 mL/kg per bolus) during the first hour, titrated with
monitoring of clinical markers of cardiac output (CO), including pulse rate, blood pressure,
capillary refill time, level of consciousness, and urine output. Fluid resuscitation should be
stopped if there is any clinical sign of fluid overload, such as pulmonary edema, hepatomegaly,
or worsening hepatomegaly.3
In healthcare systems without the availability of ICU, it is recommended not to administer
fluid boluses for children with septic shock or other sepsis-related organ dysfunction when
starting fluid therapy. It is advised to provide maintenance fluids. In healthcare systems
without ICU, if hypotension occurs, it is recommended to administer up to 40 mL/kg of
fluid bolus (10-20 mL/kg per bolus) during the first hour and titrate using clinical markers
of cardiac output (CO), with resuscitation stopped if there are signs of fluid overload. In
cases of diarrhea (gastroenteritis), maintenance fluids should be supplemented with fluids
to address ongoing loss, either orally or intravenously. Hypotension in this recommendation
is defined as systolic blood pressure less than 50 mm Hg in children ≤ 12 months, less than
60 mm Hg in children aged 1 to 5 years, and less than 70 mm Hg in children over 5 years or
according to WHO, defined as cold extremities with a prolonged capillary refill time of more
than 3 seconds and a weak and rapid pulse.5

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Fluid resuscitation must be closely monitored using clinical markers of cardiac output, serial
lactate measurements, and advanced monitoring, if available. Repeated boluses should
only be administered after re-evaluating the hemodynamic status if shock persists and there
is no sign of fluid overload.3
Hemodynamic monitoring is crucial in fluid resuscitation management. Stroke volume
variation (SVV), inferior vena cava collapsibility index, and passive leg raising are examples
of advanced hemodynamic monitoring used to assess fluid responsiveness. This assessment
is essential to prevent fluid overload.
Keywords: Fluid resuscitation; septic shock; cardiac output; fluid overload; hemodynamic
monitoring.

References:
1. Chappell D, Bruegger D, Potzel J, Jacob M, Brettner F, Vogeser M, et al. Hypervolemia
increases release of atrial natriuretic peptide and shedding of the endothelial glycocalyx.
Crit Care. 2014;18:538-46. https://doi.org/10.1186/s13054-014-0538-5
2. Kelm DJ, Perrin JT, Carti-Ceba R, Gajic O, Schenck L, Kennedy CC. Fluid overload in
patients with severe sepsis and septic shock treated with early goal-directed therapy is
associated with increased acute need for fluid-related medical interventions and hospital
death. Shock. 2015;43:68-73. https://doi.org/10.1097/SHK.0000000000000268 https://
doi: 10.1097/SHK.0000000000000268
3. Weiss SL, Peters MJ, Alhazzani W, Agus MSD, Flori HR, Inwald DP, et al. Surviving
sepsis campaign international guidelines for the management of septic shock and sepsis-
associated organ dysfunction in children. Ped Crit Care Med. 2020;21:52-106:21. https://
doi.org/10.1097/PCC.0000000000002198.--> 9
4. Maitland K, Kiguli S, Opoka RO, et al; FEAST Trial Group: Mortality after fluid bolus in
African children with severe infection. N Engl J Med 2011; 364:2483–2495
5. World Health Organization: Guideline: Updates on Paediatric Emergency Triage,
Assessment and Treatment: Care of Critically-Ill Children. Geneva, Switzerland,
World Health Organization, 2016. Available at: https://www.ncbi.nlm.nih.gov/books/
NBK350523/. Accessed August 18, 2019

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Motor Problems Related Nutritional Problems


Jufitriani Ismya
Department of Child Health, Medical Faculty of Syiah Kuala Universitya
Dr. Zainoel Abidin General Hospital Banda Aceh, Aceh, Indonesiab
E-mail: [email protected]

Undernutrition, overweight, micronutrient deficiencies, growth failure, and osteopenia are


nutritional comorbidities that affect the neurological impaired child. Motor problems related to
nutritional problems.1 Monitoring neurologically impaired children for nutritional comorbidities
as an integral part of their care. Vitamin, trace elements, and fatty acid deficiencies have
been documented in neurologically impaired children who have reduced dietary intakes.
Zink, iron, essential fatty acids, vitamins C, D, and E were reported to be deficient in 15%
to 50% of these children. The deficit of many different types of vitamins is associated
with neurologic dysfunction. The clinical presentation varies based on the type of vitamin
deficiency. The diagnosis of vitamin deficiency usually involves a combination of clinical
assessment, laboratory testing, and medical history. 1,2
Motor problem-related nutritional problems have bone-related symptoms like arthralgia, joint
swelling, musculoskeletal pain, inability to extend/straighten limbs, and difficulty/inability
to walk.3,4 Growing pain-related vitamin D deficiency, scurvy-related vitamin C deficiency,
Pediatrician should consider scurvy in all children presenting with musculoskeletal complaints,
especially in patients with risk factors for selective diet.
Growing pain is the most common form of non-specific, recurrent leg pain in childhood and
a frequent cause of pediatric outpatient visits. Mainly affects children aged 4-12 years, it is
typically non-articular, intermittent, bilateral, not associated with limited mobility, and usually
occurs in the evening or during the night. It is located in the muscle and predominantly
affects the anterior thighs, shins, calves, or back of the knees.5,6 Evan 2008 has proposed
diagnostic criteria for growing pain.7 Some studies have found an association between
vitamin D and bone mineral status with growing pain.8
Scurvy is a well-known clinical syndrome that results from vitamin C deficiency. Being rare
as compared to other nutritional deficiencies in childhood, it is rarely suspected, and this
frequently leads to a delayed diagnosis. The disease spectrum of scurvy is quite variable,
including musculoskeletal, systemic manifestations, dermatological, and dental and this
aspect can contribute to misdiagnosis. 9,10 Clinical features of scurvy even 8-12 weeks of
irregular or inadequate intake of vitamin C. In the last years, scurvy has re-emerged in the
literature, especially in children with abnormal dietary habits, mental illness, chronic renal
diseases, or neurological and developmental disorders10. Low vitamin C concentrations can

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also occur in patients overload, in healthy children without known risk factors “picky eaters”.11
Measurement of serum vitamin C is the gold standard for diagnosis., when vitamin C values
become lower than 0.2 mg/dL (200 mcg/dL) and the total body values fall below 300 mg,
the clinical manifestations of scurvy appear.10,12 Musculoskeletal manifestations such as
limping, arthralgia, myalgia, and limb or joint swellings generally follow other signs and bone
involvement, but in childhood, they may represent the first clinical manifestation requiring
medical attention, with or without cutaneous manifestations. Bone involvement in the scurvy
is typically symmetrical. Lower extremities are commonly affected, especially ankles, knees,
and hips however any joint can be involved. Leg and hip pain is the main reason for difficulty
or refusal of bearing weight and walking and in many cases is associated with edema.3,10 In
infancy, scurvy may have features of pseudo paralysis, stimulating osteomyelitis, or septic
arthritis. Laboratory investigations typically show an increase in inflammatory markers, anemia
was found in a high percentage of children with scurvy. Leukopenia and hypoalbuminemia
may also be found as markers of malnutrition. Concomitant micronutrient deficiencies other
than vitamin C deficiency may accompany scurvy, the clinicians should also check for levels
of zinc, iron, folate, vitamin B, and vitamin D.3,4
The typical radiographic finding usually appears after 3-6 months of vitamin C deficiency,
most patients in the early stage of the disease have normal radiographs or findings of diffuse
demineralization. Classic findings develop at the distal ends of the long bones and are usually
present at the knees and ankles. The most specific radiographic features include white line
Franskel, Tummerfeld zone, Pelkan spur, Wimberger ring, and Pencil thin cortex. MRI is
usually done because of the stimulating malignancy features. In treatment for scurvy there
is no standardized treatment regimen, previous studies have suggested a vitamin C dose of
100-300 mg 3 times daily for at least 1 week, followed by 100 mg daily until symptoms have
resolved. Parenteral administration is required only in patients with malabsorption. 4,10

Keywords: Motors problems, vitamin deficiency, growing pain, scurvy

References
1. Marchand V, Motil KJ, NASPHGAN Committee on Nutrition. Nutrition support for
neurologically impaired children: A clinical report of the north American society for
pediatric gastroenterology, hepatology and nutrition. J Pediatr Gastrpenterol Nutr.
2006;4:123-35.
2. Brodska HL, Klempir J, Javora J, Kohou P. The role of micronutrients in neurological
disorders. Nutrients. 2023;15:2-18.

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3. Trapani S, Rubino C, Indolfi G, lionetti P. A narrative review on pediatric Scurvy: the


last twenty years. Nutrients 2022;14:1-12.
4. Kitoh H, Sawamura K, Kaneko H, Kitamura A, Matsumaya S. Scurvy as a differential
diagnosis of diffuse musculoskeletal pain in children. Two case report. JOS Case
Report. 2022;11-4.
5. Vehapoglu A, Turel O, Turkment S, Inal BB, Askoy T, Ozgurhan G, et al. Are growing
pains related to vitamin D deficiency? Efficacy of vitamin D therapy for resolution of
symptoms. Medical Principles and Practice. 2015;24:332-8.
6. Mohanta MP. Growing: practitioners dilemma. Indian Pediatr. 2014;51:379-83
7. Evans AM. Growing pains: contemporary knowledge and recommended practice. J
FOOT ANKLE RES. 2008;1:1-5.
8. Ali MA, Haque M, Islam MI, Khan MZI. Serum vitamin D and bone mineral density in
children with growing pain in a tertiary hospital of Bangladesh. J Pediatr. 2022;12:815-
26.
9. Kaur, Sukhjot, Goraya, Singh J. Scurvy in children: down but not out. Indian J Paediatr
DE. 2021;22:1-9.
10. Agarwal A, Shaharyar A, Kumar A, Bhat AS, Misra M. Scurvy in pediatc age group- a
disease often forgotten. J.Orthop.Trauma. 2015;6:101-7.
11. Nastro A, Rosenwasser N, Daniels SP, Magnani J, Endo Y, Hampton E,et al. Scurvy
due to selective diet in a seemingly healthy 4-year- old boy. Pediatrics. 2019;144.
12. Pan T, Hennrikus EF, Henrikus WL. Modern day scurvy in pediatric orthopedics: a
forgotten illness. J. Pediatr.Orthop. 2020;41:279-84.

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Testing Strategy for Inborn Error of Metabolism in the Newborn


Klara Yuliartia
Department of Pediatrics, Universitas Indonesiaa
Cipto Mangunkusumo Hospital, Jakarta, Indonesiab
E-mail: [email protected]

Newborn Screening for phenylketonuria (PKU), an inborn error of metabolism (IEM), was the
pioneer of the universal newborn screening program. It began in the 1960s using a simple
analytic method, the Guthrie card. By the 1990s, scientific advances led to the capability to
test around 50 IEMs at once using tandem mass spectrometry (MS).
The initial aim of newborn screening was to identify infants with serious but treatable disorders
and to facilitate interventions to prevent or ameliorate the clinical consequences of the
disease. The newborn screening system consists of 5 parts: (1) newborn testing; (2) follow-
up of abnormal screening results to facilitate timely diagnostic testing and management; (3)
diagnostic testing; (4) disease management, which mostly requires multidisciplinary team;
and (5) continuous evaluation and improvement of the newborn screening system.
Among the benefits, newborn screening may detect a serious, treatable disorder before
symptoms are present, lead to treatment that can prevent serious problems including mental
retardation and death, and detect carriers of certain genetic disorders. However, it also
brings some risks: newborn screening may bring false negative or false positive results,
require repeat testing for confirmatory diagnosis, cause parental anxiety, or detect disorders
for which treatment is not effective.
The formula for special medical purpose (FSMP) for five IEMs, i.e. maple syrup urine disease
(MSUD), phenylketonuria (PKU), isovaleric acidemia (IVA), tyrosinemia, and galactosemia
have been listed in National Formularium as per December 2023, regulated by Keputusan
Menteri Kesehatan Republik Indonesia Number HK.01.07/MENKES/2197/2023. Therefore,
the requirement for universal newborn screening is that treatment should be made available
before the national screening program is met. This should prompt the government to include
those five IEMs in the newborn screening program as a public health service to reduce the
risk of a disease or its complications. Currently, 25 patients with MSUD are registered at the
Rare Disease Center of Excellence, RSCM. The majority of patients were diagnosed late
and, therefore, showed poor outcomes and died. The remainder who survived are suffering
from cerebral palsy as a complication of late diagnosis. Should IEM newborn screening
have been implemented in Indonesia, their deaths and/or complications might have been
able to be prevented.

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A wide variety of technologies can be applied to filter paper, including bacterial inhibition
assays, chromatography, enzyme-linked immunosorbent assays (ELISA), fluorescent
immunoassays (FIA), radio-immunoassays (RIA), and most recently tandem mass
spectrometry (MS/MS). The latest screening by MS/MS involving the measurement of amino
acids and acylcarnitines can detect more than 40 disorders of amino acid, organic acid, and
fatty acid metabolism. The laboratory must establish age-dependent cut-off values, as these
can vary greatly.
From the point of view of screening strategy, three types of screening are known: (1) Universal
screening, a public health service designed to identify individuals in a population who may
be at an increased risk of a certain disease (not diagnostic), (2) Clinical screening, identify
individual who already showed clinical manifestation of a certain disease and suspected
with IEM, and (3) Sibling screening, identify individual who has increased risk of a certain
disease (part of genetic counseling). The universal newborn screening in Indonesia may be
started in one province first as a pilot project.
In conclusion, the national newborn screening program for IEMs is an urge for Indonesia.
The laboratory for IEM should be established immediately and this needs support from the
government. It is important to remember that newborn screening covers the whole process
from sampling to the appropriate referral of an affected baby for the start of treatment, and
assessment of overall outcome.

Keywords: Inborn Error of Metabolism; Newborn Screening; MSUD; Phenylketonuria; IVA;


Tyrosinemia.

References:
1. Kaye CI and Committee on Genetics. Introduction to the Newborn Screening Fact Sheets.
Pediatrics 2006;118;1304
2. Wilcken B. Newborn Screening for Inborn Errors of Metabolism. In: Saudubray JM,
Carcia-Cazorla A, Baumgartner MR, Walter J, editor. Inborn Metabolic Disease Diagnosis
and Treatment. 6th ed. Heidelberg; Springer: 2016.
3. Wilson JMG, Jungner G. Principles and practice of screening for disease. World Health
Organization: Geneva; 1968.
4. Proposed international guidelines on ethical issues in medical genetics and genetics
services. WHO/HGN/GL/ETH/98/12000.
5. la Marca G, Carling RS, Moat SJ, Yahyaoui R, Ranieri E, Bonham JR, et al. Current
State and Innovations in Newborn Screening: Continuing to Do Good and Avoid Harm.
Int J Neonatal Screen. 2023;9:15. https://doi.org/10.3390/ijns9010015

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Empowering Parents in The Early Detection and Intervention of Children


With ASD
Meita Dhamayantia
Department of Child Health, Hasan Sadikin General Hospital, Faculty of Medicinea
Universitas Padjadjaran, Bandung, Indonesiab
E-mail: [email protected]

Autism Spectrum Disorder (ASD) is defined as a neurodevelopmental disorder characterized


by limited social interaction, verbal and non-verbal communication, and the presence of
repetitive interests and behaviors, beginning in early childhood, associated with a vital
genetic component as well as other causes.1,2 The spectrum can range from very mild
to severe; many (but not all) individuals with ASD require lifelong support of some kind.2
DSM-5 explicitly recognizes that ASD can be accompanied by other disorders, including
genetic disorders (e.g., fragile X syndrome) and psychiatric conditions (e.g., attention-deficit
hyperactivity disorder [ADHD]).1
Pediatricians should routinely screen for developmental delays at specific times, as the
Indonesian Ministry of Health and the Indonesian Paediatrics Society recommends. However,
they should also be explicitly screening for autism spectrum disorder (ASD) at the 18-month
and 24-month wellness visits. Screening methods have typically not been sufficiently
sensitive in that they have not identified most children with ASD in general populations in
whom parents have not already noticed a delay.3
Since ASD is a condition that typically appears in childhood, it is essential to determine the
awareness and attitudes of all families with children at an early age. When parents have
expressed a concern to a family member, friend, or professional, screening instruments
become more predictive for children as young as 18 months of age.4 A range of screening
instruments work well when someone—parent or professional—is concerned that a child
might have ASD, the most common of which is the Modified Checklist for Autism in Toddlers
(M-CHAT). Almost all children identified by these screening instruments have developmental
difficulties, although not all have ASD.5
The M-CHAT is a parent-report screening tool developed and validated for children between
16 and 30 months old. It is used to identify children who are at risk of developing ASD.
The tool contains 23 items that ask questions about a child's behavior. For example,
"Does your child take an interest in other children?". In addition, it contains a follow-up
interview conducted by healthcare professionals to determine if children receive a positive
result on the parent questionnaire. Strategies increase awareness of ASD in the family and

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community, promoting the belief that there is value in getting a diagnosis. The description of
the core features of ASD as being social communication deficits and repetitive and unusual
sensory-motor behaviors has not changed substantially since its original delineation. Low-
intensity interventions that coach parents on how to interact with their young children with
ASD can result in immediate effects on children's social behavior and communication.6 Early
parent-mediated treatments: Developmental Individual-Difference Relationship-Based Model
(DIR) or Floortime.2,7 Early Social Interaction (ESI).2,8 Early Start Denver Model (ESDM).2,9
Joint Attention Symbolic Play Engagement and Regulation (JASPER).2,10 Preschool Autism
Communication Trial (PACT).2,11
Early intervention encompasses therapies specifically designed to improve a child's
communication and social skills, which, in turn, can improve a child's quality of life. These
treatment options can and should begin as early as ASD is suspected. Most Parents of ASD
children are concerned about language development. A higher intensity of speech therapy
was frequently mentioned as a desired improvement. The importance of family involvement
in early special needs education, its close adaptation to the family, and the increasing
interest of early special needs educators in further training in engaging with autism spectrum
development indicate that early special needs education plays an increasingly vital role
in supporting families with a child on the autism spectrum. as soon as the need becomes
evident, whether or not a diagnosis has been confirmed.12 Quality service provision for ASD
requires integrated efforts of early identification, referral, and psychoeducational family
support. The Social ABCs is a parent-mediated early intervention program for toddlers
showing social-communication challenges that may be signs of autism spectrum disorder
(ASD) that is under the umbrella of Naturalistic Developmental Behavioral Interventions in
Canada. This program was successfully implemented in a community service.13

Conclusion
Families of ASD are reported to exhibit elevated levels of stress and anger.14–16 Additionally,
families face stigma due to their children having ASD.17–21 Parental guidance and support are
crucial in creating a nurturing environment that fosters the child's growth and development—
accessing resources for parents and building a solid support network.

Keywords: ASD; Family; Parents.

References
1. American Psychiatric Association. Desk reference to the diagnostic criteria from DSM-5.
Washington, DC: American Psychiatric Publishing; 2013.

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2. Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. The


Lancet. 2018;392(10146):508–20.
3. Mandell D, Mandy W. Should all young children be screened for autism spectrum
disorder? Autism. 2015;19(8):895–6.
4. Havdahl KA, Bishop SL, Surén P, Oyen A, Lord C, Pickles A, et al. The influence of parental
concern on the utility of autism diagnostic instruments. Autism Res. 2017;10(10):1672–
86.
5. McConachie H, Parr JR, Glod M, Hanratty J, Livingstone N, Oono IP, et al. A systematic
review of tools to measure outcomes for young children with an autism spectrum disorder.
Health Technol Assess. 2015;19(41):1–506.
6. Weitlauf AS, McPheeters ML, Peters B, Sathe N, Travis R, Aiello R, et al. Therapies
for Children With Autism Spectrum Disorder: Behavioral Interventions Update [Internet].
Rockville (MD): Agency for Healthcare Research and Quality (US); 2014.
7. Oono IP, Honey EJ, McConachie H. Parent-mediated early intervention for young children
with autism spectrum disorders (ASD). Cochrane Developmental, Psychosocial, and
Learning Problems Group. 2013.
8. Wetherby AM, Guthrie W, Woods J, Schatschneider C, Holland RD, Morgan L, et al.
Parent-Implemented Social Intervention for Toddlers With Autism: An RCT. Pediatrics.
2014;134(6):1084–93.
9. Romanczyk RG, McEachin J. Comprehensive Models of Autism Spectrum Disorder
Treatment. Cham: Springer International Publishing. 2016.
10. Schreibman L, Dawson G, Stahmer AC, Landa R, Rogers SJ, McGee GG, et al.
Naturalistic Developmental Behavioral Interventions: Empirically Validated Treatments
for Autism Spectrum Disorder. J Autism Dev Disord. 2015;45(8):2411–28.
11. Green J, Charman T, McConachie H, Aldred C, Slonims V, Howlin P, et al. Parent-
mediated communication-focused treatment in children with autism (PACT): a randomized
controlled trial. The Lancet. 2010;375(9732):2152–60.
12. Eckert A, Lütolf M. Originalarbeit: Autismus-Spektrum-Störungen im frühen Kindesalter.
Situationsanalyse und Handlungsempfehlungen für die Heilpädagogische Früherziehung
in der Schweiz. Frühförd Interdiszip. 2016;36(1):25.
13. Drmic I, Brian J, Roncadin C, Shaver C, Pase M, Rugajs N, et al. Community
implementation of a brief parent-mediated intervention for toddlers with probable or
confirmed autism spectrum disorder: feasibility, acceptability, and drivers of success.
Front Pediatr. 2024;11:1295294.
14. Al-Farsi O, Al-Farsi Y, Al-Sharbati M, Al-Adawi S. Stress, anxiety, and depression among
parents of children with an autism spectrum disorder in Oman: a case-control study.
Neuropsychiatr Dis Treat. 2016;12:1943–51.

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15. Bitsika V, Sharpley CF. Stress, Anxiety and Depression Among Parents of Children With
Autism Spectrum Disorder. Aust J Guid Couns. 2004;14(2):151–61.
16. Schieve LA, Blumberg SJ, Rice C, Visser SN, Boyle C. The Relationship Between Autism
and Parenting Stress. Pediatrics. 2007;119:114–21.
17. Hoogsteen L, Woodgate RL. Centering Autism Within the Family: A Qualitative Approach
to Autism and the Family. J Pediatr Nurs. 2013;28(2):135–40.
18. Kinnear SH, Link BG, Ballan MS, Fischbach RL. Understanding the Experience of Stigma
for Parents of Children with Autism Spectrum Disorder and the Role Stigma Plays in
Families’ Lives. J Autism Dev Disord. 2016;46(3):942–53.
19. Liao X, Lei X, Li Y. Stigma among parents of children with autism: A literature review.
Asian J Psychiatry. 2019;45:88–94.
20. Papadopoulos N, Sciberras E, Hiscock H, Williams K, McGillivray J, Mihalopoulos C,
et al. Sleeping Sound Autism Spectrum Disorder (ASD): a randomized controlled trial
of a brief behavioral sleep intervention in primary school‐aged autistic children. J Child
Psychol Psychiatry. 2022;63(11):1423–33.
21. Veroni E, Veroni E. The Social Stigma and the Challenges of Raising a Child with Autism
Spectrum Disorders (ASD) in Greece. Exch Interdiscip Res J. 2019;6(2):1–29.

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The Expanding Role of Telemedicine in the Management of Chronic Kidney Disease


(CKD) and Dialysis Care for Indonesian Children
Mohammad Sjaifullah Noera
Department of Child Health, Regional General Hospital Dr. Soetomoa
Universitas Airlangga, Surabaya, Indonesiab
E-mail: [email protected]

Chronic Kidney Disease (CKD) is a clinical condition characterized by a progressive and


irreversible decline in kidney function. This means that there is a continuous worsening of
kidney function that cannot return to normal. CKD has five stages, starting from asymptomatic
early-stage kidney function decline and ending in the terminal stage, which requires dialysis
and kidney transplantation. CKD is a serious health problem for children. This is not only
because of the increasing morbidity and mortality that leads to socioeconomic problems but
also because early detection is difficult, resulting in delayed treatment. Another serious issue
is that the quality of life of children with CKD is much lower compared to healthy children,
as well as the anxiety their parents feel due to the uncertainty of their child’s prognosis and
financial problems.
The goal of CKD therapy is not to cure or restore normal kidney function but to slow the
progression of kidney function decline to prevent reaching the next stage. Therefore, patients
are required to undergo regular monitoring and check-ups. Often, due to the distance to
healthcare centers, many patients are unable to receive regular treatment because of
financial constraints, time, limited transportation options, and the difficulty of mobilization
due to emerging illnesses.
The development of information and communication technology greatly assists in providing
remote healthcare services. Regular consultations can be conducted through telemedicine
with pediatric nephrology consultants. Telemedicine services can be carried out through
video calls or chat applications. Research on telemedicine for dialysis patients shows positive
results, such as ease for doctors and patients in health monitoring, reduced accommodation
costs, and decreased non-compliance in treatment or health consultations. It also minimizes
emergency room visits due to irregular consultations and improves the quality of life for
children undergoing dialysis.
Abroad, telemedicine services have been implemented with satisfactory results for both
patients and doctors. The COVID-19 pandemic has provided tangible evidence of the success
of telemedicine services. In Indonesia, telemedicine services have also been implemented.
The government and private sector have given serious attention to the implementation of
telemedicine. It is hoped that with the use of low-orbit satellites, internet services will be able
to reach various remote areas in Indonesia.
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Important considerations should include improving digital literacy for patients and healthcare
workers, the capability of virtual platforms, the security of medical information, and
government regulations to support and ensure that telemedicine services for children with
CKD and dialysis can reach remote areas throughout Indonesia.

Keywords: CKD, children, dialysis, telemedicine

References
1. Rees L, Bockenhauer D, Webb NJA, Punaro MG. Chronic Kidney Disease. In: Rees L,
Bockenhauer D, Webb NJA, Punaro MG, editors. Paediatric Nephrology. 3rd ed. Oxford:
Oxford University Press; 2019 p 451-518.
2. Pardede SO, Chunnaedy S. Penyakit Ginjal Kronik pada anak. Sari Pediatri. 2009;
11:199-206.
3. Kameswara N, Erma M, Anang M, Margo P. Digital transformation of health quality
services in the healthcare industry during disruption and society 5.0 era. Frontiers in
Public Health. 2022; 10:1-3.
4. Dhingra D, Dabas A. Global strategy on digital health. Indian Pediatr. 2020; 57:356-8.
5. Seviera AP. Hambatan telemedicine pada masa pandemi COVID-19 di Indonesia:
Literature Review. Syntax Literate: J Ilmiah Indonesia. 2024; 9:3443-455.
6. Murima WH, Prayogi ARY, Rahvy AP, Djunaedi N. Telemedicine use in health facility
during COVID-19 pandemic: Literature Review. Indonesian J Health Administration.
2022; 10:251-60.
7. Trnka P, White MM, Renton WD, McTaggart SJ, Burke JR, Smith C. A retrospective
review of telehealth services for children referred to a paediatric nephrologist. BMC
Nephrology. 2015;16:125-31.
8. Galagali PM, Ghosh S, Bhargav H. The role of telemedicine in child and adolescent
healthcare in India. Current Pediatrics Report. 2021; 9.
9. Saputro AR, Gusnadi AM, Zanah Z, Simatupang JW. Tantangan konektivitas dan
aksesibilitas dalam pengembangan pelayanan Kesehatan berbasis telemedicine di
Indonesia: sebuah tinjauan. JIE Scientific J Researchand Application of Industrial
System. 2021; 6.
10. Clark SL, Begin B, DeSouza HG, Malett K, Hanna MG. Telehealth survey of providers and
caregivers of children on peritoneal dialysis during the COVID-19 pandemic. Pediatric
Nephrology. 2023; 38:203-10.

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11. Swanson MB, Weidemann DK, Harshman LA. The impact of rural status on pediatric
chronic kidney disease. Pediatric Nephrology. 2024; 39:435-46.
12. Hewitt I, Tognoni G, Sereni F, Montini G. Provision of pediatric nephrology services in
low-middle-income countries. Pediatric Nephrology. 2024; 39:1675-7.
13. Yazicioglu B, Bakkaloglu SA, ESPN. Impact of coronavirus disease-2019 on pediatric
nephrology practice and education: an ESPN survey. Pediatric Nephrology. 2022;
37:1867-75.
14. Starr MC, Altemose K, Parsley J, Cater DT, Hains DS. Safety and timeliness of
telemedicine initiation of continuous kidney replacement therapy. Pediatric Nephrology.
2024; 39:325-9.

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Emergency In Children with Pneumonia:


Community-Acquired Pneumonia, How to Treat in Hospital Setting
Muchammad Fahrul Udin
Department of Paediatry University of Brawijaya, Malang, Indonesia
E-mail: [email protected]

Among the various types of pneumonia, Community-Acquired Pneumonia (CAP) is a major


concern in pediatrics (1). Pneumonia is the leading cause of death in children under 5
years of age worldwide. The estimated global number of deaths due to pneumonia is 0.76
million, while the mortality rate was 5.5 cases per 1,000 live births in 2015 (2). The etiologic
organisms that cause pneumonia vary widely according to the age of the patient (3).
The diagnosis of pneumonia is based on respiratory symptoms, physical examination, and/
or chest radiographic findings. Typical signs and symptoms of CAP in children include fever,
cough, decreased appetite, and hypoxemia (4). Physical examination may reveal several
pathological physical signs, especially rapid breathing (tachypnea) and difficulty breathing
(dyspnea) (5).
Chest imaging is most useful when the diagnosis is uncertain or when findings from history
and physical examination are inconsistent (Figure 1) (1). Laboratory tests performed in
children with pneumonia include routine blood tests, Arterial Blood Gas Analysis (ABG),
C-Reactive Protein (CRP), serologic tests, and microbiologic tests (5).

Figure 1. (A and B) PA and lateral chest radiographs show right middle lobe consolidation
consistent with pneumonia (6).

The Pediatric Assessment Triangle (PAT) is a rapid evaluation tool that establishes a child's
clinical status and disease category to guide initial treatment priorities (7). Indications for
hospitalization for community-acquired pneumonia patients based on clinical conditions

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include oxygen saturation, respiratory rate, presence or absence of respiratory distress,


and the family's inability to care for the child at home (Figure 2) (8). As with the emergency
department (ED) management pathway, initial attention should be focused on ensuring
adequate airway, oxygenation, ventilation, and perfusion (9).

Figure 2. CAP Diagnosis Flow and Determination of Inpatient Management (10)

It is important to maintain airway patency and administer aerosol inhalation therapy to


children with severe pneumonia (9). Pediatric patients with community-acquired pneumonia
who have oxygen saturation <92% while breathing room air should be given oxygen therapy
with a nasal cannula, head box, or mask to maintain oxygen saturation >92%. Assess vital
organ perfusion and identify signs of cardiovascular compromise due to pneumonia leading
to sepsis or septic shock (8)
In selecting empirical antibiotics, it is necessary to pay attention to the history of hospital
treatment in the last 3 months and the history of receiving parenteral antibiotics in the last
3 months (11). Children aged 2–59 months with severe pneumonia should be treated with
parenteral ampicillin (or penicillin) and gentamicin as first-line treatment. Ampicillin 50 mg/kg,
or benzylpenicillin 50,000 units per kg IM/IV every 6 hours for at least five days. Gentamicin
7.5 mg/kg IM/IV once daily for at least five days. Ceftriaxone should be used as second-line
treatment in children with severe pneumonia who have failed first-line treatment (12).

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Supportive management is also given such as oxygen therapy, infusion for rehydration and
correction of calories and electrolytes, and administration of symptomatic drugs including
antipyretics and mucolytics. If there is an indication, mechanical ventilation can be given to
the patient. Antibiotic administration is evaluated clinically in the first 48-72 hours. If clinical
improvement is obtained, therapy can be continued. However, antibiotics must be changed
if they worsen according to culture results or empirical guidelines (11).
After improvement with intravenous antibiotics in hospitalized patients, therapy is immediately
switched to oral on condition if hemodynamics are stable, clinical symptoms improve, can
take oral medication and gastrointestinal function is good. Children with severe pneumonia
can be discharged if: symptoms and signs of pneumonia disappear, oral intake is adequate,
antibiotic administration can be continued at home (orally), the family understands and
agrees to the administration of therapy and control plans, home conditions are suitable for
continued care at home (8).

Keywords: Community-acquired pneumonia; Paediatric pneumonia; Emergency; Hospital


Setting.

References:
1. Stuckey-Schrock K, Hayes BL, George CM. Community-Acquired Pneumonia in Children
[Internet]. Vol. 86. 2012. Available from: www.aafp.org/afp.
2. Liu L, Oza S, Hogan D, Chu Y, Perin J, Zhu J, et al. Global, regional, and national causes
of under-5 mortality in 2000–15: an updated systematic analysis with implications for the
Sustainable Development Goals. The Lancet. 2016 Dec 17;388(10063):3027–35.
3. Scotta MC, Marostica PJC, Stein RT. Pneumonia in Children. Kendig’s Disorders of the
Respiratory Tract in Children. 2019 Jan 1;427-438.e4.
4. Robertson G, Richards T, Renaud A, Holmes M. The Management of Community-
Acquired Pneumonia in Hospitalized Children. Vol. 18.
5. Suci LN. Pendekatan Diagnosis dan Tata Laksana Pneumonia pada Anak. Ked N Med
|. 2020;3(1).
6. Popovsky EY, Florin TA. Community-Acquired Pneumonia in Childhood. In: Encyclopedia
of Respiratory Medicine, Second Edition. Elsevier; 2021. p. 119–31.
7. Horeczko T, Enriquez B, McGrath NE, Gausche-Hill M, Lewis RJ. The Pediatric
Assessment Triangle: Accuracy of Its Application by Nurses in the Triage of Children. J
Emerg Nurs. 2013 Mar;39(2):182–9.
8. Pudjiadi AH, Hegar B, Handryastuti S, Idris NS, Gandaputra EP, Harmoniati ED.
Pedoman Pelayanan Medis Ikatan Dokter Anak Indonesia. 2009.

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9. Li W, An X, Fu M, Li C. Emergency treatment and nursing of children with severe


pneumonia complicated by heart failure and respiratory failure: 10 case reports. Exp
Ther Med. 2016 Oct 1;12(4):2145–9.
10. Smith DK, Kuckel DP, Recidoro AM. Community-Acquired Pneumonia in Children Rapid
Evidence Review Dustin K. Smith.
11. Menteri Kesehatan Republik Indonesia. Pedoman Nasional Pelayanan Kedokteran Tata
Laksana Pneumonia Pada Dewasa. 2023.
12. WHO. Revised WHO classification and treatment of childhood pneumonia at health
facilities. 2014.

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Coagulation Disorders in Neonates


Olga Rasiyanti Siregar
Department of Pediatrics, Faculty of Medicine, Universitas Sumatera Utara, Medan,
Indonesia
E-mail: [email protected]

The hemostatic system in neonates is unique from that seen in older children and adults. The
platelet counts of neonates are within similar values to that in adults. However, the function is
deprived. Meanwhile, the coagulation system is quantitatively distinct in neonates.1 Majority
of the coagulation proteins show decreased levels, except for fibrinogen, factor V, factor VIII,
and von Willebrand factor (vWF). The concentrations of vitamin-K-dependent coagulation
factors (II, VII, IX, X) and contact factors (XI, XII, prekallikreine, and high molecular weight
kininogen) are approximately 50% lower in neonates compared to adults.2 The lower levels
of coagulant protein are physiologically balanced by the lower levels of anticoagulant
proteins including antithrombin III, heparin cofactor II, protein C, and protein S.3 The distinct
procoagulant-anticoagulant factors during the newborn period is generally accepted as
putting neonates at higher risk for coagulation disorders. The coagulation disorders can be
hereditary or acquired.4 The clinical manifestations involved hemorrhagic and thrombotic
disorders in the neonates.5,6,7 Despite the relative frequency of coagulation disorders in
neonates, studies specific to this age group are relatively scarce. This review aimed to
provide an overview of neonatal hemostatic profiles and a comprehensive understanding of
coagulation disorders in neonates. Our review was based on a thorough literature search
of the Medical Subject Headings (MeSH) terms, including hemostasis or plasma or blood
coagulation disorders or coagulopathy and neonate or newborn in PubMed and Google
Scholar databases during the last 10 years. As a result, the summary of the neonatal
hemostatic system is described in Table 2. Hereditary factor deficiencies include hemophilias,
congenital protein C/S deficiency, Von Willebrand disease, rare bleeding disorders, and
congenital thrombocytopenias.4,6,11,13,14 Acquired coagulation disorders involved vitamin K
deficiency bleeding, disseminated intravascular coagulation, alloimmune thrombocytopenia,
and venous thromboembolism.7,12,13,14

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Table 1. Neonates versus adults hemostasis8,9,10


Hemostasis Neonates vs adults Approximate age of adult value
Primary hemostasis
Platelet count Same
Platelet function Lower 2-4 weeks
VWF Higher 3 months
Coagulation factors
FII, FVII, FIX, FX Lower 16 years
FV Lower 16 years
FVIII Higher 1 month
FXI Lower 1 year
FXII Lower 16 years
Fibrinogen level Same
Fibrinogen function Lower 5 years
Anticoagulation factors
Antithrombin Lower 3 months
Protein C Lower 16 years
Protein S Lower 1 month

Fibrinolysis
Plasminogen count and function Lower 6 months
tPA Higher 5 days
α2 antiplasmin Lower 5 days

Clot formation rate Higher NA

Keywords: Coagulation disorders; Coagulopathy; Neonates.

References:
1. Davenport P, Sola-Visner M. Hemostatic Challenges in Neonates. Front Pediatr 2021;
9:627715
2. Will A. Neonatal hemostasis and the management of neonatal thrombosis. Br J
Haematol 2015;169(3):324-32.
3. Saxonhouse MA. Neonatal Bleeding and Thrombotic Disorders. In: Avery's Diseases
of the Newborn (Tenth Edition). Elsevier eBooks; 2018, p 1121-1138.e4.

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4. Moiseiwitsch N, Brown AC. Neonatal coagulopathies: A review of established and


emerging treatments. Experimental Biology and Medicine 2021;246:1447–57.
5. Katsaras GN, Gialamprinou D, Papacharalampous E, et al. Neonatal bleeding disorders.
A practical diagnostic approach. DOAJ 2022.
6. Davila J. Coagulation Disorders in the Newborn. Neoreviews 2018;19:e11–21.
7. Makatsariya A, Bitsadze V, Khizroeva J, et al. Neonatal thrombosis. Journal of Maternal-
Fetal and Neonatal Medicine 2020;35:1169–77.
8. Revel-Vilk S. The conundrum of neonatal coagulopathy. Hematology 2012;2012:450–
4.
9. Haidl H, Zöhrer E, Pohl S, et al. New insights into neonatal coagulation: normal clot
formation despite lower intra-clot thrombin levels. Pediatr Res 2019;86:719–724.
10. Toulon P. Developmental hemostasis: laboratory and clinical implications. International
Journal of Laboratory Hematology 2016;38:66–77.
11. Jaffray J, et al. The bleeding newborn: A review of presentation, diagnosis, and
management. Seminars in Fetal & Neonatal Medicine 2015.
12. Barg A, Nowak-Göttl U, Kenet G. Hemostasis in the Very Young. Seminars in
Thrombosis and Hemostasis 2018.
13. Costa STB, Palaré MJ, Graça AM. Coagulation Reference Values and Indications for
the Use of Plasma Derivatives in Neonates: A Narrative Review. DOAJ 2022.
14. Hanmod S, Jesudas R, Kulkarni R, Chitlur M. Neonatal Hemostatic Disorders: Issues
and Challenges. Seminars in Thrombosis and Hemostasis 2016;42:741–51.
15. Hanmod S, Jesudas R, Kulkarni R, Chitlur M. Neonatal Hemostatic Disorders: Issues
and Challenges. Seminars in Thrombosis and Hemostasis 2016;42:741–51.
16. Nowak-Göttl U, Limperger V, Bauer A, Kowalski D, Kenet G. Bleeding issues in
neonates and infants – update 2015. Thrombosis Research 2015;135:S41–3. https://
doi.org/10.1016/s0049-3848(15)50440-4.
17. Eberl, W. (2020). Diagnostic Challenges in Newborns and Infants with Coagulation
Disorders. Hämostaseologie, 40(01), 084–087. doi:10.1055/s-0040-1701475

Table 2. Summary of article review


Type of article Year Title Study by
Review article 2012 The conundrum of neonatal coagulopathy Revel-Vilk S, 2012

Review article 2014 Interpretation of clotting tests in the neonate Pal S, et al., 2014
Neonatal haemostasis and the management
Review article 2015 Will A, 2015
of neonatal thrombosis

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The bleeding newborn: A review of


Article in press 2015 presentation, diagnosis, and management, Jaffray J, et al., 2015
Seminars in Fetal & Neonatal Medicine

Bleeding issues in neonates and infants – Nowak-Göttl U, et al.,


Review article 2015
update 2015 2015
Neonatal Hemostatic Disorders: Issues and Hanmod SS, et al.,
Review article 2016
Challenges 2016
Developmental hemostasis: laboratory and
Review article 2016 Toulon P, 2016
clinical implications.
Review article 2018 Hemostasis in the Very Young Barg A, et al., 2018
Saxonhouse MA,
Book 2018 Neonatal Bleeding and Thrombotic Disorders
2018
Review article 2018 Coagulation Disorders in the Newborn. Davila J, 2018
New insights into neonatal coagulation:
Research article 2019 normal clot formation despite lower intra-clot Haidl H, et al., 2019
thrombin levels

Diagnostic Challenges in Newborns and


Review article 2020 Eberl W, 2020 []
Infants with Coagulation Disorders

Davenport P and
Review article 2021 Hemostatic Challenges in Neonates Sola-Visner M, 2021
[1]

Neonatal coagulopathies: A review of Moiseiwitsch N, et


Review article 2021
established and emerging treatments al., 2021 [4]
Neonatal bleeding disorders. A practical Katsaras GN, et al.,
Review article 2022
diagnostic approach 2022 [ ]
Costa STB, et al.,
Coagulation Reference Values and
2022 [ ]
Review article 2022 Indications for the Use of Plasma Derivatives
in Neonates: A Narrative Review

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Tips and Pitfalls in The Screening, Diagnosis, and Management of


Autism Spectrum Disorder
Pandu Caesaria Lestari
Harapan Kita National Women and Children Health Care, Jakarta, Indonesia
Email: [email protected]

Autism spectrum disorder is a neurodevelopmental condition characterized by impairment


of verbal communication, social interaction, and a restricted repertoire of interests, activities,
and behavior. Early diagnosis is crucial for timely intervention. The correct timing and choices
of intervention for children with ASD are the key elements in the improvement in language,
cognitive, and social-emotional maturity of a child with ASD.1,2 Although one may have to
admit, that there are many challenges and pitfalls surrounding the diagnosis journey of
autism. General pediatrician holds the most important aspect in screening and referring
children with ASD risk.
Pitfalls in screening the ASD children
Additional screenings specifically for autism should be done at 18 and 24 months of age.2
However, the screening sometime is not done, until the parents speak about their concerns.
Another pitfall in screening for autism risk is not using the correct tools. Until recently, the
Modified Checklist for Autism in Toddlers, Revised with Follow-Up (M-CHAT R/F) was the
chosen tool. This revised tool reduces the false positive rate and detects more ASD cases
than the original M-CHAT.3,4
Sometimes it may seem natural for a pediatrician to reassure the parent, give the development
a chance, and wait before referring the patient. Still, one of the pitfalls after screening is failure
to refer for further diagnosis. Centre for Disease Control and Prevention has an algorithm for
follow-up pathways that can be used for healthcare providers (Figure 1).
However, since M-CHAT R/F is only eligible for 18-30 months of children, the healthcare
provider needs another tool to screen younger patients. To detect early signs of ASD in 10-14
months, the Early Screening of Autistic Traits Questionnaire (ESAT) is used.5 This tool has
14 yes-no questions for the parents and consists of domains that show typical problems in
autism. Combining these two screening tools was found to be more effective than individual
instruments alone in identifying children referred to clinical services at 18 months.2,6
One way to preserve time ergo increase parental compliance to fill the tools is using
technology. Some apps are easily accessed by the parents in the waiting room.7
Pitfalls in Diagnosis

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The most noticeable challenge surrounding the diagnosis of autism in clinical practice is the
delay of the diagnosis. Some practitioners tend to give milder diagnoses, than breaking the
bad news the parents have a child with ASD. On the other hand, overdiagnosis of children
with ASD by not comply the DSM-V criteria also happened in clinical practice.
One should not diagnose a child who has typical hand movements such as flapping for
example without any impairment in verbal communication, and social interaction. Another
example is a child with a social communication disorder who may have problems with
social interaction and communication skills but shows no restricted and repertoire interests,
activities, and behavior.
Another problem in the evaluation of a child with ASD is the timing of the examination
doesn’t describe the actual behavior. Video documentation of the child while playing alone,
interacting with friends and/or siblings, and their responses should be asked of the parents
before the referral. The use of this method has been proven to help the diagnosis of the
patients.8

Figure 1. Pediatric Developmental Screening Flowchart.3

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Pitfalls in Intervention
There are no particular therapies that will be considered gold standards for ASD since the
management of ASD consists of several simultaneous or consecutive therapies.
Since the parental concerns are usually the child’s lack of communication skills, more ASD
children have speech therapy despite managing their basic problem first. Sensory processing
disorder and restricted or repetitive behavior are a problem that may lead to failure to
achieve communication or social interaction skills if it’s not treated correctly. Sensory-based
interventions such as sensory integration occupational therapy (SI-OT) are the most highly
recommended as an initial therapy.9 Another recommended therapy is behavior therapy with
the applied behavior analysis method. This method’s goal is to improve social skills by using
intervention based on principles of learning theory. Social abilities like completing tasks,
communicating, and learning new skills. These goals wouldn’t be achieved by the child that
only given SI-OT or speech therapy alone.10
The timing of the therapy and the decision to add or stop any therapy should be done following
re-assessment after periodic time. A team consists of pediatric neurology or developmental
pediatric, and sometimes a child psychologist is advisable for managing the child. No child
should be put on therapy without proper re-evaluation or re-assessment.

Keyword: pitfalls; autism; screening; diagnosis; management

References
1. Predictors of outcomes in autism early intervention: why don't we know more? Vivanti G,
Prior M, Williams K, Dissanayake C. Front Pediatr.2014;2:58.
2. Okoye C, Obialo-Ibeawuchi CM, Obajeun OA, et al. Early Diagnosis of Autism Spectrum
Disorder: A Review and Analysis of the Risks and Benefits. Cureus. 2023;15:e43226.
3. Centers for Disease Control and Prevention. Screening and diagnosis of autism spectrum
disorder for healthcare providers. Available at: https://www.cdc.gov/ncbddd/autism/hcp-
screening.html. Accessed August 3, 2024.
4. Ramkumar Aishworiya, Van Kim Ma, Susan Stewart, Randi Hagerman, Heidi M. Feldman;
Meta-analysis of the Modified Checklist for Autism in Toddlers, Revised/Follow-up for
screening. Pediatr. 2023;151: e2022059393
5. Dietz C, Swinkels S, van Daalen E, van Engeland H, Buitelaar JK. Screening for autistic
spectrum disorder in children aged 14- 15 months. II: population screening with the Early
Screening of Autistic Traits Questionnaire (ESAT). Design and general findings. J Autism
Dev Disord. 2006;36:713-22.

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6. Beuker KT, Schjølberg S, Lie KK, Swinkels S, Rommelse NN, Buitelaar JK. ESAT and
M-CHAT as screening instruments for autism spectrum disorders at 18 months in the
general population: issues of overlap and association with clinical referrals. Eur Child
Adolesc Psychiatry. 2014;23:1081-91
7. Tim tentang anak. Rekomendasi aplikasi parenting terbaik 2024:solusi modern untuk
mendukung peran orangtua. Available at:www.tentanganak.com. Accessed August
3,2024.
8. Sutantio J, Pusponegoro HD. Validity of telemedicine for diagnosing autism spectrum
disorder: protocol-guided video recording evaluation. Telemed J E Health. 2021;27:427-
31.
9. Schoen SA, Lane SJ, Mailloux Z, May-Benson T, Parham LD, Smith Roley S. A systematic
review of ayres sensory integration intervention for children with autism. Autism Res.
2019;12:6-19.
10. Makrygianni MK, Gena A, Katoudi S, Galanis P. The effectiveness of applied behavior
analytic interventions for children with Autism Spectrum Disorder: A meta-analytic study.
Research in Autism Spec Dis. 2018;51:18-31

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How to Manage Fluid and Electrolyte in Pediatric Kidney Diseases

Retno Palupi-Barotoa, Kristia Hermawana


a
Division of Nephrology, Department of Child Health, Faculty of Medicine, Public Health
and Nursing Universitas Gadjah Mada/Dr Sardjito Hospital, Yogyakarta
E-mail: [email protected]

Fluid and electrolyte management is essential in the care of pediatric patients with kidney
problems. In healthy individuals, the kidneys remove waste products and excess fluids as
well as maintain appropriate levels of essential minerals such as calcium, phosphorus,
sodium, and potassium. However, in children with kidney diseases, these regulatory
functions are compromised, leading to significant disruptions in homeostasis. This abstract
aims to provide an updated overview of the principles and challenges in managing fluid and
electrolyte disturbances in pediatric patients, focusing on both acute and chronic kidney
diseases.
Fluid management strategies are influenced by the need to maintain optimal hydration
while avoiding fluid overload. In critically ill children, fluid resuscitation must be balanced
with the risk of precipitating fluid overload.1 Assessing fluid status in children with kidney
failure using traditional modalities, such as clinical examination (e.g skin turgor, edema, and
jugular venous pressure), daily weight measurements, and laboratory markers like serum
electrolytes and blood urea nitrogen (BUN), often presents significant limitations. These
methods can be imprecise, subject to inter-observer variability, and may not detect subtle
changes in fluid balance, especially in pediatric patients where clinical signs may be less
pronounced or difficult to assess. Moreover, laboratory markers can be influenced by various
factors unrelated to fluid status, such as nutritional status or the presence of concurrent
illnesses. Given these challenges, there is a growing need for more advanced, objective,
and reliable tools such as ultrasonography and bioimpedance analysis (BIA).2,3 Point of
care ultrasonography can be used to assess intravascular volume status and fluid excess
in third spaces while BIA provides a non-invasive, bedside method to accurately measure
body fluid compartments, offering detailed insights into extracellular and intracellular water
content. Implementing BIA as a routine bedside examination could enhance the precision
of fluid management in children with kidney failure, leading to better clinical outcomes and
more tailored treatment strategies.
Tailored fluid management in children with chronic kidney disease (CKD) significantly impacts
morbidity and mortality.1 Precise control of fluid balance is crucial in preventing complications
such as hypertension, heart failure, and pulmonary edema, which are common in this patient

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population. Proper fluid management helps to maintain optimal blood pressure, reducing
the strain on the cardiovascular system and lowering the risk of long-term organ damage.
Studies have shown that children with CKD who receive individualized fluid management
experience fewer hospitalizations and improved overall survival rates. Fluid control also
mitigates the need for aggressive diuretic therapy, which can have adverse effects, and
reduces the frequency and dosage of antihypertensive medications required to manage
blood pressure. However, when necessary, the use of antihypertensive drugs remains
essential in controlling blood pressure and protecting against the progression of kidney
damage. Therefore, a combined approach of tailored fluid management and appropriate use
of antihypertensive therapy is critical in improving the quality of life and long-term outcomes
for children with CKD.
Electrolyte imbalances are a significant risk for children with acute kidney injury (AKI) and
chronic kidney disease (CKD) due to the kidneys’ diminished ability to regulate essential
ions such as potassium, sodium, calcium, and phosphate. In AKI, the rapid decline in kidney
function can lead to severe and life-threatening imbalances, such as hyperkalemia, which
increases the risk of cardiac arrhythmias and sudden death. In CKD, chronic disturbances
in electrolyte levels contribute to long-term complications, characterized by disturbances in
mineral metabolism, bone turnover, and vascular calcification. As kidney function declines,
the ability to excrete phosphate diminishes, leading to hyperphosphatemia, which stimulates
the release of fibroblast growth factor 23 (FGF23) and suppresses the production of active
vitamin D (calcitriol). This results in decreased intestinal calcium absorption and secondary
hyperparathyroidism. Elevated parathyroid hormone (PTH) levels lead to increased bone
resorption and alterations in bone architecture, causing skeletal deformities, growth
retardation, and an increased risk of fractures. The mineral imbalances also contribute to
the calcification of soft tissues, including blood vessels, which significantly elevates the
risk of cardiovascular disease—the leading cause of death in children with CKD. Effective
management of electrolyte levels is therefore crucial in reducing the risk of fatal outcomes.
The management approach of electrolyte imbalances should be individualized, taking into
account the underlying etiology, the child’s growth and development stage, and the potential
impacts on long-term outcomes.4 Regular monitoring and early intervention with dietary
modifications, medications, and dialysis when necessary, are essential strategies to prevent
the severe consequences of electrolyte imbalances and improve survival rates in children
with AKI and CKD.

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References:
1. Selewski DT, Barhight MF, Bjornstad EC, et al. Fluid assessment, fluid balance, and fluid
overload in sick children: a report from the Pediatric Acute Disease Quality Initiative (ADQI)
conference. Pediatr Nephrol 2024; 39: 955-979. 2023/11/07. DOI: 10.1007/s00467-023-
06156-w.
2. Yuan W, Yu M, Zhang Z, et al. The value of bioimpedance analysis in the assessment of
hydration and nutritional status in children on chronic peritoneal dialysis. Ren Fail 2024;
46: 2301531. 2024/01/08. DOI: 10.1080/0886022X.2023.2301531.
3. Gorga SM, Selewski DT, Goldstein SL, et al. An update on the role of fluid overload in
the prediction of outcome in acute kidney injury. Pediatr Nephrol 2024; 39: 2033-2048.
2023/10/20. DOI: 10.1007/s00467-023-06161-z.
4. Kidney Disease: Improving Global Outcomes CKD Working Group. KDIGO 2024 Clinical
Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney
Int 2024; 105: S117-S314. 2024/03/16. DOI: 10.1016/j.kint.2023.10.018.

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Quality of Life in Adolescents with Tuberculosis and the Challenges


Rini Sekartini, Ciho Olfriani
Department of Child Health, Faculty of Medicine Universitas Indonesia
E-mail: [email protected]

Tuberculosis is still a health problem in developing countries, including Indonesia. It is


estimated that there are 850,000 adolescents suffer from tuberculosis every year. Although
effective anti-tuberculosis drugs are widely available and easy to access, the infectivity of
TBC, the chronic progression of the disease, long-term treatment for at least six months,
and the side effects of the therapy have significantly affected a patient’s quality of life.1
A study showed that patients with chronic illnesses considered that social health is as
important as physical health.2 Several studies have also confirmed that TB patients tend to
have a poorer quality of life than the general population.3,4
WHO has also recommended that quality of life must be considered as a need for every
person to achieve well-being and self-realization. In recent years, quality of life has become
an important criterion that needs to be considered in evaluating the efficiency of disease
management.3,5
WHO defines the quality of life as an individual's perception of the individual's position in
life in the context of the culture and value system in which they live, and in relation to the
individual's goals, expectations, standards, and interests. Quality of life refers to a person's
subjective assessment of the satisfaction and meaning of their life.3,6
Quality of life can impact compliance with TB treatment, which in turn can lead to poor
therapeutic outcomes, which can increase TB morbidity and mortality.6 Quality of life includes
several aspects of well-being, which are physical, psychological, economic, spiritual, and
social.2

Adolescent Characteristics and Tuberculosis


Adolescence is a critical period in biological development and social roles. Health is essential
for adolescents to achieve a successful transition from childhood to adulthood. Adolescents
require special attention in TBC management. When compared to children, teenagers have
higher mobility and a wider social circle, so the possibility of being exposed to TBC is greater.
Adolescents who suffer from TBC also have the potential to transmit TBC to other people
in various locations, such as home, dormitory, school, tutoring, and other social activities.2-6

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Quality of Life for Adolescents with Tuberculosis


Until now, there are still quite few studies evaluating the quality of life of adolescents suffering
from TB. In studying the quality of life of children and adolescents, the Pediatric Quality of
Life Inventory (PedsQL) questionnaire can be used. Each question is accompanied by five
various answer choices, which are "no", "hardly ever", "sometimes", "often", and "almost
always", which must be chosen according to the closest situation.7

Quality of Life for Adolescents with TBC in Daily Aspects


On the physic functional, teenagers often experience difficulty walking or running long
distances, pain in various parts of the body, and lack of energy. On the emotional function
scale, some tend to behave aggressively, which is caused by high knowledge about TB
disease and emotional reactions.
Adolescents with TB also feel inequality with healthy peers, due to the development of
stigma in adolescent consciousness. In terms of school functioning, teenagers more often
miss school because they feel unwell and have difficulty receiving or memorizing learning
material.6,7
Quality of Life of TB Adolescents with Other Diseases
There is no significant difference in quality of life between adolescents who experience
primary tuberculosis and secondary form of tuberculosis. However, patients with pulmonary
TB find it more difficult to carry out physical activities, such as running or walking long
distances, and they report fatigue and difficulty carrying out daily activities. This proves that
the inflammatory process in the respiratory organs is more extensive.6,7
TBC patients with secondary forms also usually require restrictions on social activities and
lots of rest, resulting in limited communication and even depression.7
The Impact of Tuberculosis on Adolescent Mental Health
TBC not only impacts the health of adolescents during the period of illness but also causes
long-term sequelae in physical and mental health. Co-infection with HIV and/or drug
resistance to M. tuberculosis strains can exacerbate these impacts. Five of twenty-three
(22%) adolescents with TB disease in Toronto, Canada, showed symptoms of depression
during TB treatment and were subsequently referred for psychiatric care. In a study in
Smolensk, Russia, 61% of adolescents undergoing TB treatment experienced anxiety,
based on the Taylor Manifest Anxiety Scale, compared with 35% of healthy adolescents
without TB disease (p<0.05).8

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Challenges of TB Management in Adolescents


Family support is the main factor in treatment compliance in adolescents with TB. Various
causes of lack of family support, such as poverty, lack of family understanding about TB, family
conflict, family neglect, or moving domicile greatly influence the success of TB treatment in
adolescents. Adolescents are also very sensitive to stigma and this is the main reason for
dropping out of TB treatment. Teenagers also tend to be afraid of people around them, such
as friends or neighbors, finding out about their illness. Many of them are reluctant or delay
taking medication when they are away from home. Health facility-based TB services, such
as community health centers, can also be a barrier to compliance, because teenagers fear
that their neighbors will see them receiving TB treatment.9,10

Reference
1. Moscibrodzki P, Enane LA, Hoddinott G, Brooks MB, Byron V, Furin J, Seddon
JA, Meyersohn L, Chiang SS. The Impact of Tuberculosis on the Well-Being of
Adolescents and Young Adults. Pathogens. 2021; 10(12):1591. https://doi.org/10.3390/
pathogens10121591
2. Hansel, N.N., Wu, A.W., Chang, B. et al. Quality of life in tuberculosis: Patient and
provider perspectives. Qual Life Res 13, 639–652 (2004). https://doi.org/10.1023/
B:QURE.0000021317.12945.f0
3. Brown J, Cappoci S, Smith C, Morris S, Abubakar I, Lipman M. Health status and quality
of life in tuberculosis. International Journal of Infectious Diseases. 2015;32:68-75. DOI:
10.1016/j.ijid.2014.12.045
4. Gao XF, Rao Y. Quality of life of a migrant population with tuberculosis in West China. Int.
J. Tuberc. Lung Dis. 2015;19(2):223–230.
5. Varni JW, Sherman SA, Burwinkle TM. The PedsQL™ Family impact model: Preliminary
reliability and validity. Health and Quality of Life Outcomes. 2004;2:55
6. Chen X, Xu J, Chen Y, Wu R, Ji H, Pan Y, Duan Y, Sun M, Du L, Gao M, Wang J, Zhou L.
The relationship among social support, experienced stigma, psychological distress, and
quality of life among tuberculosis patients in China. Sci Rep. 2021 Dec 20;11(1):24236.
doi: 10.1038/s41598-021-03811-w. PMID: 34931006; PMCID: PMC8688519.
7. Dinara A. Psychology of Health: Biopsychosocial Approach. Pg 25
8. Avdeeva, T.; Otvagin, I.; Myakisheva, T.; Rashkevich, E. Tuberculosis in Adolescents and
Young Patients in High Prevalence Region. Eur. J. Microbiol. Immunol. 2012, 2, 297–301.

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9. Enane, L.A.; Eby, J.; Arscott-Mills, T.; Argabright, S.; Caiphus, C.; Kgwaadira, B.; Steenhoff,
A.P.; Lowenthal, E.D. TB and TB-HIV Care for Adolescents and Young Adults. Int. J.
Tuberc. Lung Dis. 2020, 24, 240–249.
10. Laycock, K.M.; Eby, J.; Arscott-Mills, T.; Argabright, S.; Caiphus, C.; Kgwaadira, B.;
Lowenthal, E.D.; Steenhoff, A.P.; Enane, L.A. Towards Quality Adolescent-Friendly
Services in TB Care. Int. J. Tuberc. Lung Dis. 2021, 25, 579–583

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Cardiorespiratory Failure in Patients Hospitalized with Pneumonia


Ririe Fachrina Malisie
Faculty of Medicine Universitas Sumatera Utara
E-mail: [email protected]

Pneumonia is causing significant incidence in developing countries around the world. The
incidence is 61 million cases in the South East Asia region and 156 million cases worldwide
with an estimated 0.9–1.2 million deaths (15%) per year in children younger than 5 years.
Pneumonia is one of the leading causes of morbidity and mortality in children under five
years of age. In Indonesia in 2021, the toddler mortality rate caused by Pneumonia was
16%, it was twice fold high as above 5 years of age. Mortality cases in children might
have resulted from complications such as persistent pneumonia, acute respiratory distress
syndrome (ARDS), sepsis, parapneumonic effusion, and pericardial effusion.
Pneumonia is usually claimed as a disease confined to the lungs, but now growing evidence
suggests that pneumonia has a negative impact on multiple organ systems, including the
cardiovascular system. In adults, the high rates of cardiac events were associated with
chronic underlying diseases such as coronary artery disease, renal failure, and hypertension.
Data from studies in children with severe community-acquired pneumonia (CAP) who
developed respiratory failure and cardiac involvement have elucidated that the effects of
acute respiratory infections on the cardiovascular system were mostly derived from patients
with pneumococcal CAP. Respiratory failure in CAP is associated with cardiac involvement
in 62% of patients, even among healthy children without any cardiac risks. The majority
of the complications including myocardial injury, pericardial effusion, valvular regurgitation,
ST/T changes, and arrhythmia, were transient or mild. Significant hemodynamic changes
and increased mortality risks were observed in the patients who developed cardiac heart
failure.
We should examine to identify characteristics of cardiorespiratory failure by early recognition
and prompt therapeutic strategy implementation. Pneumonia patients may develop cardiac
arrest outside of the ICU, without apparent shock or respiratory failure. The effects are
possibly associated with infection, systemic inflammatory response, and cardiopulmonary
interaction. The heart and lung interplay occurs due to their anatomic location: they both
occupy the same thoracic cavity, connected via blood vessels. Because of this housing of
the heart within the thorax, the heart can be described as a “pressure chamber within a
pressure chamber”. Pressure changes within the thoracic cavity during the respiratory cycle
affect the pressure systems to the heart and from the heart to the extra-thoracic spaces but
do not alter the intrathoracic vascular relationships.

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Pericardial effusion, valvular regurgitation, ST/T changes, and non-fatal arrhythmia were
rather common, but these conditions were mild and without severe hemodynamic effects.
Myocardial injury was the most common finding but was typically asymptomatic, except
for the patients who developed cardiorespiratory failure before. Pericardial effusion and
valvular regurgitation were possibly associated with an inflammation of the pericardium and
valvular tissue. The evidence of pericardial effusion by computed tomography scan and
echocardiography is approximately 50% of parapneumonic effusion patients. This finding
indicates the relationship between pulmonary and pericardial infectious processes. The
causative organism spreads to the pericardium via several routes that include pulmonary
foci, the pleura, lymphatic channels of the hemithorax, and bacteria. Pneumonia affects
the entire organism and involves many organ systems. Replication of pathogens such
as Streptococcus pneumoniae or influenza virus inside the alveolar space causes tissue
damage by the release of virulence factors and leads to activation of the innate immune
system.
The Incidence of myocardial injury was suffered in approximately 60% of pneumonia
patients. Non-ischemic myocardial injury which is reflected by increases in serum troponin
levels was observed in critically ill patients without acute coronary syndrome. These
findings were possibly due to myocarditis, systemic inflammatory responses, and changes
in circulatory volume. Viral-induced myocarditis results from various mechanisms, either
direct infection of cardiac myocytes or emerging immune response. Although the virus is
the most common causative organism of pneumonia and myocarditis at this age, bacteria
also can cause both conditions. Apart from direct infection of cardiac myocytes in bacterial
infection, inflammatory cytokines, such as TNF-a and Interleukin-6, were produced, causing
myocardial inflammation. Most complications not only arise within the short-term period after
infection (30 days) with about 90% occurring within the first week, but also events that
occur later (several months up to years) are likely associated with previous lung infection.
Even children who survive the acute episode of pneumonia remain at risk for morbidity
and mortality in the post-infection period. The underlying causes for these long-term
effects remain elusive. The epidemiological studies suggest associations between acute
respiratory tract infections and increased risk for subsequent cardiovascular failure within
days and weeks to years after pneumonia. Although the majority of cardiac involvement
was mild and recovered spontaneously following pneumonia treatment, there were effects
on hemodynamic compromise and multiorgan dysfunction. Risks of infection, such as
ventilator-associated pneumonia, ARDS and sepsis, and prolonged ventilatory support were
increased. All complications have an impact on prolonged hospitalization with increasing
mortality.

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Keywords: Cardiorespiratory failure; hospitalized patient; pneumonia

References:
1. Nimdet K, Techakehakij W. Cardiac involvement in children with community-acquired
pneumonia and respiratory failure. Asian Biomed (Res Rec News) 2020;14(3):119-24.
DOI 10.1515/abm-2020-0018.
2. Brack MC, Lienau J, Kuebler WM, Witzenrath M. Cardiovascular sequelae of pneumonia.
Curr Opin Pulm Med 2019;25:257-62. DOI:10.1097/ MCP.000000000000584.
3. Hadisuwarno W, Setyoningrum RA, Umiastuti P. Host factor related to pneumonia in
children under 5 years of age. Paediatr Indones. 2015;55:248-51.
4. Kementrian Kesehatan Republik Indonesia 2022. Profil Kesehatan Indonesia tahun
2021.
5. Verhoeff K, Mitchell JR. Cardiopulmonary physiology: why the heart and lungs are
inextricably linked. Adv Physiol Educ 2017;41:348-53. DOI:10.1152/advan.00190.2016.
6. Desai A, Aliberti S, Amati F, Stainer A, Voza A. Cardiovascular complication in
Community-Acquired Pneumonia. Microorganism 2022;10:2177. https://doi.
org/10.3390/microorgnisms10112177.
7. Alvarado AC, Pinsky MR. Cardiopulmonary interaction in left heart failure. Front.
Physiol.2023;14:1-6 DOI10.3389/fphys.2023.1237741.

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Pitfalls of Crystalloid Leading to Pediatric Acute Kidney Injury


Saptadi Yuliartoa
Department of Pediatrics Faculty of Medicine, Universitas Brawijayaa
Saiful Anwar Hospital, Malangb
E-mail: [email protected]

Introduction
Acute kidney injury (AKI) is a common complication in critically ill children, with a high
prevalence across various clinical conditions such as diabetic ketoacidosis (DKA), sepsis,
asthma, and severe dehydration due to diarrhea.1–3 The administration of crystalloid solutions
is a standard resuscitative approach; however, their impact on renal outcomes remains
contentious. While some studies suggest that crystalloids, particularly high-chloride solutions
like 0.9% saline, might exacerbate renal impairment through hyperchloremia,2,4,5 others have
not demonstrated significant differences in outcomes compared to balanced solutions.4,6
This has sparked debates about the appropriateness of using crystalloid solutions in different
clinical settings and whether balanced crystalloids offer superior renal protection.2,7

Mechanism of AKI Due to Hyperchloremia


Hyperchloremia, often induced by the use of high-chloride crystalloids such as 0.9% saline,
has been implicated in AKI development through several mechanisms. Elevated serum
chloride levels can lead to renal vasoconstriction, reduced glomerular filtration rate (GFR),
and increased systemic inflammation.1,6 These factors collectively contribute to impaired renal
perfusion and potential progression to AKI.5,7 The chloride-induced renal vasoconstriction is
thought to occur via activation of the tubuloglomerular feedback mechanism and the renin-
angiotensin-aldosterone system.7

Comparative Studies on Crystalloid and Balanced Solutions


Research has explored the impact of balanced solutions versus saline on AKI incidence,
the need for renal replacement therapy (RRT), hyperchloremia, length of hospital and PICU
stay, and mortality across various patient populations. For instance, in pediatric sepsis, a
meta-analysis found that balanced crystalloids were associated with a reduced incidence of
AKI compared to isotonic saline (odds ratio [OR] 0.74).3 However, the same study showed
no significant difference in RRT requirement between the two groups. Similarly, balanced
solutions resulted in lower hyperchloremia rates

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In the context of DKA, another study compared 0.9% saline with plasma-Lyte-A, revealing
no significant difference in AKI incidence between the groups.8 This suggests that while
balanced solutions might offer theoretical benefits in reducing hyperchloremia, practical
renal outcomes do not significantly differ. In critically ill children, a systematic review
found no significant difference in AKI incidence between balanced and unbalanced fluids,
though balanced solutions were associated with improved biochemical markers like serum
bicarbonate and blood pH.4,5

Controversy in Research Findings


The discrepancies in findings among studies investigating crystalloid versus balanced
solutions reflect ongoing controversy. Some research indicates that high-chloride solutions
increase the risk of AKI, 3,6,7,9 while other studies report no substantial differences in renal
outcomes.1,2,4,5,8,10–13 The variability in results could be attributed to differences in study
design, patient populations, fluid volumes administered, and baseline renal function of the
subjects.

Recommendations for Use of Crystalloids and Balanced Solutions


The choice between crystalloids and balanced solutions in pediatric care, especially among
critically ill patients, remains a subject of intense research and debate. Current evidence
suggests that balanced solutions, such as Lactated Ringer’s and Plasma-Lyte, may offer
advantages over 0.9% saline due to their lower chloride content and closer approximation
to physiological electrolyte compositions. In the context of pediatric sepsis, several studies
have reported that balanced crystalloids are associated with a reduced incidence of AKI
and hyperchloremia, although the need for renal replacement therapy (RRT) and overall
mortality do not significantly differ between balanced and unbalanced solutions.
For patients with diabetic ketoacidosis (DKA), balanced solutions appear to manage electrolyte
imbalances more effectively than 0.9% saline, potentially reducing hyperchloremic metabolic
acidosis without significantly altering the incidence of AKI.14 Similarly, in pediatric asthma, the
use of balanced crystalloids has been linked to improved chloride and bicarbonate profiles,
although the effects on AKI incidence and other clinical outcomes remain inconclusive.13
In children with severe dehydration from diarrhea, balanced solutions are recommended
due to their favorable impact on acid-base balance and reduced risk of hyperchloremia.10
The use of balanced solutions is also advocated for critically ill children due to their potential

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renal protective effects and reduced incidence of AKI, although further research is needed
to substantiate these benefits.

Conclusion
The ongoing debate regarding the optimal fluid choice for resuscitation in critically ill
children reflects the complex interplay between fluid composition, renal outcomes, and
overall patient health. While balanced solutions demonstrate promising benefits in reducing
hyperchloremia and potentially lowering AKI rates, the evidence does not conclusively show
improved survival outcomes or reduced need for RRT compared to traditional crystalloids
like 0.9% saline. Future studies should aim to further elucidate the mechanisms by which
fluid composition affects renal function and other clinical outcomes, particularly in diverse
pediatric populations with varying underlying conditions. Until such evidence is available,
clinicians should consider individual patient needs, underlying health conditions, and
potential risks associated with each fluid type when making decisions about fluid therapy in
critically ill children.

References
1. Honore PM, Mugisha A, Kugener L, et al. The causal link between hyperchloremia and
acute kidney injury is yet to be conclusively established: We are not sure. Crit Care
2020;24(1):1–2.
2. Lehr AR, Rached-D’astous S, Barrowman N, et al. Balanced Versus Unbalanced Fluid
in Critically Ill Children: Systematic Review and Meta-Analysis∗. Pediatric Critical Care
Medicine 2022;23(3):181–91.
3. Mhanna A, Beran A, Srour O, et al. Balanced crystalloids versus isotonic saline in
pediatric sepsis: a comprehensive systematic review and meta-analysis. Baylor
University Medical Center Proceedings 2024;37(2):295–302.
4. Wang P, Huang Y, Li J, et al. Balanced crystalloid solutions versus normal saline in intensive
care units: a systematic review and meta-analysis. Int Urol Nephrol 2023;55(11):2829–
44.
5. Raman S, Gibbons KS, Mattke A, et al. Effect of Saline vs Gluconate/Acetate-Buffered
Solution vs Lactate-Buffered Solution on Serum Chloride Among Children in the
Pediatric Intensive Care Unit: The SPLYT-P Randomized Clinical Trial. JAMA Pediatr
2023;177(2):122–31.
6. Santi M, Lava SAG, Camozzi P, et al. The great fluid debate: Saline or so-called
“balanced” salt solutions? Ital J Pediatr [Internet] 2015;41(1):1–5. Available from: http://
dx.doi.org/10.1186/s13052-015-0154-2

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7. Zhang Z, Xu X, Fan H, Li D, Deng H. Higher serum chloride concentrations are associated


with acute kidney injury in unselected critically ill patients. BMC Nephrol 2013;14(1).
8. Williams V, Jayashree M, Nallasamy K, Dayal D, Rawat A. 0.9% saline versus Plasma-
Lyte as initial fluid in children with diabetic ketoacidosis (SPinK trial): A double-blind
randomized controlled trial. Crit Care 2020;24(1):1–10.
9. Hayes W. Ab-normal saline in abnormal kidney function: risks and alternatives. Pediatric
Nephrology 2019;34(7):1191–9.
10. Florez ID, Sierra J, Pérez-Gaxiola G. Balanced crystalloid solutions versus 0.9% saline
for treating acute diarrhea and severe dehydration in children. Cochrane Database of
Systematic Reviews 2023;2023(5).
11. Weiss SL, Keele L, Balamuth F, et al. Crystalloid Fluid Choice and Clinical Outcomes
in Pediatric Sepsis: A Matched Retrospective Cohort Study. Journal of Pediatrics
2017;182:304–10.
12. Martín A, Mendoza B, Chico-Fernández MA, Jm E-L, Mn P. Buffered solutions versus
0.9% saline for resuscitation in critically ill adults and children (Review). Cochrane
Database of Systematic Reviews [Internet] 2019; Available from: www.cochranelibrary.
com
13. Scioscia A, Horvat C, Moritz ML, Fuhrman D. Balanced Crystalloids versus Normal
Saline in Children with Critical Asthma. Children 2022;9(10):3–9.
14. Baalaaji M, Jayashree M, Nallasamy K, Singh S, Bansal A. Predictors of outcome of AKI
in children with diabetic ketoacidosis. Indian Pediatr [Internet] 2018;55:311–4. Available
from: https://www.indianpediatrics.net/apr2018/311.pdf

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Pediatric Inflammatory Bowel Disease


Satrio Wibowoa, Muzal Kadimb
Department of Paediatrics, Faculty of Medicine, Universitas Brawijaya, Indonesiaa
Department of Paediatrics, Faculty of Medicine, Universitas Indonesia, Indonesiab
E-mail: [email protected]

Incidence and Prevalence


The incidence and prevalence of Inflammatory Bowel Disease (IBD) among children have
been rising globally. Approximately 20-25% of all IBD cases are diagnosed before the age of
18 years. In North America and Europe, the prevalence of pediatric IBD ranges from 20 to
200 per 100,000 children. In Asia, particularly, the incidence is growing fast. Recent studies
from East Asia, report an increasing incidence of pediatric IBD.1,2,3
Personalized In IBD Pediatrics
Personalized medicine in pediatric IBD means that healthcare providers should consider
many unique aspects of a patient's clinical presentation. A pediatrician should examine
the specific symptoms, medical history, and other relevant clinical data in each patient.
This could involve tailoring diagnostic tests, monitoring specific symptoms more closely, or
choosing treatment options that are better suited to the patient's unique clinical profile.
Personalized in terms of trigger, cause, or influencing factors
The exact cause of IBD in children remains unclear, but it is believed that IBD is a result
of a complex interplay of genetic, environmental, and immune-related factors. Every single
patient might have a different underlying cause or have the most prominent influencing
factors. A strong family history of IBD is a significant risk factor. Children with parents or
siblings with IBD are at an increased risk of developing the disease themselves. Several
genetic mutations and polymorphisms have been linked to IBD, including those in the
NOD2, IL23R, and ATG16L1 genes. Defects in the mucosal barrier may allow bacteria and
other antigens to enter the gut wall, provoking an immune response. High processed foods
consumption, refined sugars, and unhealthy fats, and low in fibers, fruits, and vegetables,
are thought to alter the gut microbiome and promote inflammation. Early and frequent use of
antibiotics during childhood can disrupt the gut microbiome, leading to dysbiosis, which may
trigger inflammation. Exposure to air pollution, secondhand smoke, and other environmental
toxins may cause oxidative stress and inflammation in the gut. Reduced bacterial diversity
and an imbalance between protective and harmful bacteria may play a critical role in gut
inflammation. Stress and social problems also can influence the gut-brain axis, potentially
leading to immune system dysregulation.1,4,5

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Personalized in Diagnostic Procedures


Diagnostic procedures involve a combination of clinical evaluation, laboratory tests, imaging
studies, and endoscopic procedures. Early and accurate diagnosis is crucial for initiating
appropriate treatment and managing the disease to minimize its impact on growth and
development. A thorough medical history is the first step in diagnosing IBD. Symptoms
such as chronic diarrhea, abdominal pain, weight loss, and growth failure are common in
children with IBD. A family history of IBD or other autoimmune diseases can also raise
suspicion. The physical exam may reveal signs of malnutrition, anemia, and growth delay.
Abdominal tenderness, perianal disease, and extraintestinal manifestations like skin rashes
or joint pain may also be noted. Anemia and elevated white blood cell count in Complete
Blood Count and elevated levels of C-reactive protein can indicate inflammation. Anti-
Saccharomyces cerevisiae antibodies (ASCA) and perinuclear anti-neutrophil cytoplasmic
antibodies (pANCA) are used for the determined type of IBD. Fecal Calprotectin can
measure intestinal inflammation. Stool cultures are performed to check for pathogens such
as bacteria, parasites, and viruses. Magnetic Resonance Enterography (MRE) or Computed
Tomography (CT) Scan is effective in identifying complications like abscesses, strictures,
fistulas, and inflammation. Upper endoscopy and colonoscopy allow direct visualization of
gastrointestinal and colon mucosa and biopsies for histological examination can be taken to
confirm the diagnosis. Sometimes genetic testing or biomarker analysis is needed to identify
specific markers that predict disease behaviour or response to certain treatments.6,7,8
Personalized Treatment Plans
Treatment is designed specifically based on the child's specific disease type, severity,
location of inflammation, and response to previous therapies. This could involve selecting
medications that are more likely to be effective based on the child's unique genetic,
environmental, and microbiome factors. Managing Inflammatory Bowel Disease (IBD) in
children involves a combination of medical therapy, nutritional support, and sometimes
surgery. The goal is to control inflammation, achieve and maintain remission, promote
normal growth and development, and improve the child's quality of life. Treatment strategies
are tailored to the specific type of IBD the severity of the disease, and the child's response
to therapy. Aminosalicylates (5-ASA), Steroids, Azathioprine, and 6-mercaptopurine (6-
MP), can be used to reduce inflammation. Biological therapy such as Anti-TNF Agents
(Infliximab, adalimumab), anti-integrin, (Vedolizumab), and Janus Kinase (JAK) Inhibitors
(Tofacitinib) is used when first or second-line treatments are ineffective. The algorithm from
Joint ECCO and ESPGHAN Evidence-Based Consensus Guidelines can be used as a guide
in clinical practice. Stem Cell Therapy and Microbiome Modulation are being investigated
as potential therapies for IBD. Micronutrient like Vitamin D also seems to play an important

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role in mucosal repair. Surgery is generally reserved for complications such as strictures,
fistulas, abscesses, or when medical therapy fails.6-10
Personalized Nutritional and Lifestyle Adjustments
Dietary plans, supplements, or other lifestyle interventions may be customized based on
the child's individual needs. Exclusive Enteral Nutrition (EEN) is an exclusive intake of
a liquid formula diet and is highly effective in inducing remission in children with Crohn's
Disease. EEN helps reduce inflammation, promotes mucosal healing, and supports growth
and nutritional status. Some specific diets, like the Crohn's Disease Exclusion Diet (CDED),
may help in maintaining remission and reducing symptoms Supplementation with vitamins
and minerals, particularly iron, calcium, vitamin D, and B12, is crucial due to malabsorption
and increased needs.6,7
Personalized psychosocial and educational support
Personalized care might also involve addressing the emotional and psychological needs of
the child and family, recognizing that the impact of IBD varies among individuals. Managing
IBD in children requires addressing the psychological impact of the disease. Anxiety,
depression, and social challenges are common, and psychological support is essential.6,7
Personalized in Monitoring and Follow-Up
Children with IBD require regular follow-up to monitor growth, nutritional status, disease
activity, and potential side effects of medication. Monitoring bone density is important,
especially in children on long-term corticosteroids or those with malnutrition. Immunization
status should be reviewed, and live vaccines should be avoided in immunosuppressed
children.6,7

Keywords: Inflammatory bowel disease; child; diagnosis; therapy

References:
1. Benchimol El, Fortinsky KJ, Gozdyra P, et al. Epidemiology of pediatric inflammatory
bowel disease: a systematic review of international trends. Inflammatory Bowel
Diseases. 2011:17(1):423-439.
2. Ashton JJ, Cullen M. Afzal NA, et al. Trends in incidence, prevalence, and demographic
characteristics of pediatric inflammatory bowel disease in England: results from a large
population-based cohort, 1994-2013. Journal of Crohn's and Colitis. 2018; 12(6):708-
716.

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3. Ng SC, Shi HY, Hamidi N, et al. Worldwide incidence and prevalence of inflammatory
bowel disease in the 21st century: a systematic review of population-based studies.
The Lancet. 2018;390(10114):2769-2778.
4. Kelsen J. Baldassano R. Pediatric inflammatory bowel disease: A review. JAMA
Pediatrics. 2014:168(11):1083-1090.
5. Sila S, Jelić M. Trivić I, et al. Gut microbiota, dysbiosis, and ulcerative colitis. Frontiers
in Pharmacology. 2019;10:1076.
6. Ruemmele FM, Veres G, Kolho KL, et al. Consensus guidelines of ECCO/ESPGHAN
on the medical management of pediatric Crohn's disease. Journal of Crohn's and
Colitis. 2014:8(10):1179-1207.
7. Turner D. Levine A, Escher JC, et al. Management of Pediatric Ulcerative Colitis: Joint
ECCO and ESPGHAN Evidence-based Consensus Guidelines. Journal of Pediatric
Gastroenterology and Nutrition. 2018:67(2):257-281.
8. Henderson P, Anderson NH, Wilson DC. The diagnostic accuracy of fecal calprotectin
during the investigation of suspected pediatric inflammatory bowel disease: a
systematic review and meta-analysis. The American Journal of Gastroenterology.
2014;109(5):637-645.
9. Hyams JS, Lerer T, Griffiths A, et al. Long-term outcome of maintenance infliximab
therapy in children with Crohn's disease. Inflammatory Bowel Diseases. 2009;15(6):816-
822.
10. Wibowo S, Pramadani A, Soebandijah K, Poeranto S, Kusworini. Vitamin D3 Induce
Stem Cell Activation Via Lgr5-Bmi1 Expression and Improving Mouse Colitis Histology
Index. Narra J. 2023; 3(3):1-9

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Management of Adrenal Insufficiency in Children


Siska Mayasari Lubis
Department of Pediatrics, Faculty of Medicine, Universitas Sumatera Utara, Medan,
Indonesia
E-mail: [email protected]

Background: Adrenal insufficiency (AI) encompasses a range of disorders marked by


insufficient production of adrenal hormones due to various underlying causes. Primary
adrenal insufficiency (PAI) is a condition resulting from impaired steroid synthesis, adrenal
destruction, or abnormal gland development affecting the adrenal cortex. Acquired primary
adrenal insufficiency is termed Addison disease. Central adrenal insufficiency (CAI) is
caused by an impaired production or release of adrenocorticotropic hormone (ACTH). It
can originate either from a pituitary disease (secondary adrenal insufficiency) or from an
impaired release of corticotropin-releasing hormone (CRH) from the hypothalamus (tertiary
adrenal insufficiency). An underlying genetic cause should be investigated in every case of
AI presenting in the neonatal period or first few months of life, each necessitating distinct
management strategies to prevent complications and optimize growth and development.
This review aims to provide an extensive overview of the management of AI in children.
Methods: A thorough literature review was performed, encompassing studies, international
guidelines, cohort analyses, and expert consensus documents. The aim was to formulate
a comprehensive strategy for diagnosing, treating, and managing AI in children. Focusing
on included evidence-based diagnostic approaches, therapeutic interventions, emergency
management protocols, and long-term monitoring strategies.
Results: Diagnostic evaluation of a patient at risk of or with suspected AI includes three
diagnostic processes: 1) confirmation of the presence of AI (syndromic diagnosis); 2)
identification of the level of the hypothalamic-pituitary-adrenal (HPA) axis where the
responsible defect is located (diagnosis of location); and 3) identification of the cause
(etiological diagnosis). The management of AI requires a multidisciplinary approach to
optimize outcomes and ensure quality of life. The clinical presentation of AI is often non-
specific, making early diagnosis challenging. Common symptoms include growth faltering,
lethargy, poor feeding, abdominal pain, vomiting, and weight loss. In primary adrenal
insufficiency (PAI), both glucocorticoid and mineralocorticoid deficiencies contribute to the
clinical picture. Symptoms due to glucocorticoid deficiency include weakness, anorexia,
weight loss, and severe hypoglycemia, while mineralocorticoid deficiency can cause
hyponatremia, hyperkalemia, acidosis, tachycardia, hypotension, and salt craving. In
younger infants, AI may present insidiously with prolonged cholestatic jaundice, failure

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to thrive, recurrent hypoglycemia, micropenis, and bilateral cryptorchidism, particularly in


cases of congenital AI or secondary AI associated with multiple pituitary defects. Once CAI
is diagnosed, other pituitary hormones should be assessed and an MRI of the pituitary
region should be performed to exclude neoplastic or infiltrative processes. Primary adrenal
insufficiency (PAI) should be suspected in case of low serum cortisol with elevated ACTH
levels, elevated ACTH levels are a consequence of the lack of glucocorticoid-negative
feedback. An adrenal crisis involves symptoms such as weakness, fatigue, tachycardia,
hypotension, dizziness, nausea, vomiting, abdominal pain, diaphoresis, and seizures related
to profound hypoglycemia. If unrecognized and untreated, an adrenal crisis can progress to
coma and death. Children with symptoms like diarrhea and vomiting are at heightened risk of
adrenal crisis. Early recognition of symptoms and diagnosis using dynamic testing modalities
like the ACTH stimulation test and insulin tolerance test using diagnostic algorithms holds a
significant key to AI management.

Figure 1. Diagnosis algorithm for AI

Optimal glucocorticoid replacement therapy, tailored to individual needs and growth


trajectories, is essential for maintaining physiological cortisol levels and preventing long-term
complications. Emergency management protocols, including the availability of intravenous/
intramuscular hydrocortisone (based on Table 1) and caregiver education, are crucial

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components in preventing adrenal crises and ensuring timely intervention. By integrating


these aspects, healthcare providers can better understand the multifaceted nature of AI in
children, ensuring that diagnosis and treatment strategies are comprehensive and tailored to
individual patient needs. This approach not only aims to stabilize immediate health concerns
but also to enhance long-term outcomes and quality of life for pediatric patients with AI.

Table 1. Emergency management of adrenal crisis in children


Hydrocortisone dose
Or weight-based hydrocortisone dose and frequency
(age-based)
Less than 1 year: 25mg Children >28 days corrected gestational age:
1-5 years: 50 mg 50 mg/m2 or 2 mg/kg (max 100mg) intravenous bolus initially
6 years and over 100mg then bolus dose 6 hourly
Given intramuscularly or
intravenously Neonates <28 days corrected gestational age:
4 mg/kg intravenous bolus initially then bolus dose 6 hourly
Can consider giving 4 hourly hydrocortisone if needed
Blood glucose testing and fluid administration
Blood glucose < 3 mmol/L Shock or moderate to severe Maintenance fluids type and
dehydration amount
2 ml/kg of 10% glucose as Give 10ml/kg of 0.9% 0.9% sodium chloride or 5%
Intravenous bolus. sodium chloride as a bolus. glucose is usually an appropriate
Recheck blood glucose after Repeat if necessary. starting point:
15 min and repeat bolus if Check electrolytes 100 mL/kg/day for first 10 kg, 50
necessary. immediately at presentation mL/kg/day for second 10 Kg, 20
to inform fluid usage. mL/kg/day >20 Kg
Stabilization phase
Stable and improving 1 mg/kg (max 50 mg) intravenously 6 hourly.
Neonates: 2 mg/kg intravenously 6 hourly, can consider giving 4
hourly if needed.

Stable and tolerating drinks/ Oral sick day hydrocortisone 30mg/m2/day in four equally
diets divided doses.
Restart fludrocortisone if indicated.

Conclusion: This review highlights the imperative need for standardized guidelines

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and protocols in the management of pediatric AI to ensure timely diagnosis, appropriate


treatment, and proactive emergency response. Implementing uniform diagnostic criteria and
treatment algorithms across healthcare settings is crucial to improving care and quality of
life for children with AI. Future research should focus on refining diagnostic tools, optimizing
therapeutic regimens, and developing innovative treatment strategies to further enhance
patient outcomes.

Keywords: Adrenal Insufficiency; Adrenocorticotropic Hormone; Glucocorticoids

References:
1. Nisticò D, Bossini B, Benvenuto S, Pellegrin MC, Tornese G. Pediatric adrenal
insufficiency: challenges and solutions. Ther Clin Risk Manag. 2022;11:47-60
2. Miller BS, Spencer SP, Geffner ME, Gourgari E, Lahoti A, Kamboj MK, et al.
Emergency management of adrenal insufficiency in children: Advocating for treatment
options in outpatient and field settings. J Investig Med. 2020;68:16-25.
3. Mushtaq T, Ali SR, Boulos N, Boyle R, Cheetham T, Davies JH, et al. Emergency and
perioperative management of adrenal insufficiency in children and young people:
British Society for Paediatric Endocrinology and Diabetes consensus guidance. Arch
Dis Child. 2023;108:871-8.
4. Bizzarri C, Capalbo D, Wasniewska MG, Baronio F, Grandone A, Cappa M. Adrenal
crisis in infants and young children with adrenal insufficiency: Management and
prevention. Front Endocrinol. 2023;14:1133376.
5. Yanase T, Tajima T, Katabami T, Iwasaki Y, Tanahashi Y, Sugawara A, et al. Diagnosis
and treatment of adrenal insufficiency including adrenal crisis: A Japan Endocrine
Society Clinical Practice Guideline. Endocr J. 2016;63:765-84.
6. Bowden SA, Henry R. Pediatric adrenal insufficiency: Diagnosis, management, and
new therapies. Int J Pediatr. 2018;2018:1-8.
7. Auron M, Raissouni N. Adrenal insufficiency. Pediatr Rev. 2015;36:92-103.
8. Husebye ES, Pearce SH, Krone NP, Kämpe O. Adrenal insufficiency. The Lancet.
2021;397:613-29.
9. Eyal O, Levin Y, Oren A, Zung A, Rachmiel M, Landau Z, et al. Adrenal crises in
children with adrenal insufficiency: epidemiology and risk factors. Eur J Pediatr .
2019;178:731-8.
10. Buonocore F, McGlacken-Byrne SM, Del Valle I, Achermann JC. Current insights into
adrenal insufficiency in the newborn and young infant. Front Pediatr. 2020;8:619041.

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Blood Product Transfusion in Sepsis: When It is Not Too Late?


Susanto Nugrohoa
Hematology-Oncology Division, Department of Child Health, University of Brawijayaa
Dr. Saiful Anwar General Hospital, Malang, Indonesiab
E-mail: [email protected]

Pediatric sepsis is associated with high mortality and morbidity and requires a high level
of awareness for early diagnosis and timely treatment.1 The definition of pediatric sepsis
remains a challenge. Based on the National Guidelines for the Diagnosis and Management
of Sepsis in Children by the Indonesian Pediatric Association (2016), sepsis is defined as life-
threatening organ dysfunction caused by a dysregulated host response to infection. Organ
dysfunction was assessed based on Pediatric Logistic Organ Dysfunction-2 (PELOD-2)
score ≥11 (at hospital type A), or ≥7 (at hospital type B or C).2
Sepsis can affect hematologic and coagulation systems. The mechanism of sepsis-induced
anemia is complex, including reduced production of erythropoietin, impaired bone marrow
response to erythropoietin, and decreased red blood cell (RBC) survival. Correction of
anemia through RBC transfusion seems vital, provided that no harm.1,3 Thrombocytopenia
is a common finding during sepsis and is a marker of poor prognosis. The mechanism
remains unclear but is probably caused by decreased platelet production, increased platelet
destruction and sequestration, and increased platelet activation and consumption in thrombi
generation.1,4
Coagulopathy in sepsis is a dynamic condition that starts from coagulation disorder, can
advance to sepsis-induced coagulopathy (SIC), and finally to disseminated intravascular
coagulation (DIC). The early diagnosis of SIC and monitoring of coagulation status during
sepsis is crucial for the timely management and selection of the most suitable treatment,
including blood transfusion. Based on the SIC scoring system by the International Society
on Thrombosis and Haemostasis (2017), the SIC is diagnosed when the total SIC score is
≥4.4,5
According to the 2018 Transfusion and Anemia Expertise Initiative (TAXI) Guidelines, it is
suggested not to transfuse red blood cells (RBC) at hemoglobin (Hb) ≥7 g/dl in septic children
with stable hemodynamics. In septic children with unstable hemodynamics, RBC transfusion
can be considered at Hb ≥7 g/dl based on clinical judgment. If there is no hemorrhagic
shock or life-threatening bleeding, RBC transfusion can be given at Hb <5 g/dl and can be
considered at Hb 5-7 g/dl based on clinical judgment. Clinical judgment should be based
on evidence of inadequate cardiorespiratory support or reduced systemic oxygen delivery.
A reasonable Hb target after transfusion is 7-9.5 g/dl. However, if hemorrhagic shock or life-

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threatening bleeding is present, it is recommended to transfuse RBC, plasma, and platelets


in a ratio of 2:1:1 or 1:1:1 until the bleeding is no longer life-threatening.3,6
The 2016 Surviving Sepsis Campaign (SSC) Guidelines suggest against prophylactic
platelet transfusion based solely on platelet counts in children with sepsis or septic shock and
thrombocytopenia without active bleeding. Prophylactic platelet transfusion is recommended
when the platelet count is <10,000/ml in the absence of active bleeding. If thrombocytopenia
is accompanied by a risk of bleeding, the recommended transfusion threshold is platelet
count <20,000/ml. However, if there is significant active bleeding or planned surgery or an
invasive procedure, transfusion can be given at a platelet count <50,000/ml.5,7
Based on the evidence, it is important to reduce the inappropriate use of plasma transfusion
in sepsis-induced coagulopathy and avoid unnecessary adverse reactions. There is no
evidence about the benefit of prophylactic plasma transfusion in patients with SIC in the
absence of active bleeding. Plasma transfusion in children with sepsis is suggested if there
are prolonged PT, APTT, and/or INR accompanied by active bleeding or planned surgery or
invasive procedures.5,7

Keywords: Sepsis; Anemia; Thrombocytopenia; Coagulopathy; Blood Transfusion.

References
1. Miranda M, Nadel S. Pediatric Sepsis: a Summary of Current Definitions and
Management Recommendations. Current Pediatrics Reports 2023;11:29–39.
2. Hadinegoro SR, Chairulfatah A, Latief A, Pudjiadi AH, Malisie RF, Alam A, editors. Ikatan
Dokter Anak Indonesia. Pedoman Nasional Pelayanan Kedokteran Ikatan Dokter Anak
Indonesia Diagnosis dan Tata Laksana Sepsis Pada Anak. Jakarta: Badan Penerbit
IDAI; 2016.
3. Elshinawy M, Kamal M, Nazir H, Khater D, Hassan R, Elkinany H, et al. Sepsis-
related anemia in a pediatric intensive care unit: transfusion-associated outcomes.
Transfusions 2020;60(S1):S4–S9.
4. Gonzalez DA, Kumar R, Asif S, Bali A, Dang AK. Sepsis and Thrombocytopenia: A
Nowadays Problem. Cureus 2022;14(5):25421-7.
5. Czempik PF, Wiórek A. Management Strategies in Septic Coagulopathy: A Review of
the Current Literature. Healthcare 2023;11(2):227-39.
6. Valentine SL, Bembea MM, Muszynski JA, Cholette JM, Doctor A, Spinella PC, et al.
Consensus Recommendations for RBC Transfusion Practice in Critically Ill Children
From the Pediatric Critical Care Transfusion and Anemia Expertise Initiative. Pediatric
Critical Care Medicine 2018;19(9):884-98.

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7. Weiss SL, Peters MJ, Alhazzani W, Agus MS, Flori HR, Inwald DP, et al. Surviving
Sepsis Campaign International Guidelines for the Management of Septic Shock and
Sepsis-Associated Organ Dysfunction in Children. Pediatric Critical Care Medicine
2020;21(2):52-106.

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Cognitive Function in Children with Autism


Tjhin Wigunaa
Child and Adolescent Psychiatry Division, Department of Psychiatry Faculty of Medicine
University of Indonesiaa
dr. Cipto Mangunkusmo General Hospital, Jakarta, Indonesiab
E-mail: [email protected]; [email protected]

Autism spectrum disorder is categorized as a neurodevelopmental disorder in the Diagnostic


and Statistical Manual for Mental Disorder 5 (DSM 5). Children with ASD show persistent
deficits in social communication and social interaction across contexts, such as deficits in
social-emotional reciprocity, deficits in nonverbal communicative behaviours used for social
interaction, and deficits in developing, maintaining, and understanding relationships. They
also perform restricted, repetitive patterns of behaviour, interests, or activities, such as
stereotyped or repetitive speech, motor movement, or use of objects, the insistence on
sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal
behaviour, highly restricted, fixated interests that are abnormal in intensity or focus, and
hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of the
environment. The symptoms usually present in the early developmental period but may not
become fully manifest until social demands exceed limited capacities or may be masked by
learned strategies in later life. The symptoms should cause clinically significant impairment
in current functioning (APA, 2013).
The median male-to-female ratio was 4.2. The median percentage of autism cases with
co-occurring intellectual disability was 33.0%, and the ratio changes depending on the level
of IQ (more females with lower IQ, more identified males with higher IQ, some females at
risk for being identified later. The prevalence of ASD increased over time, Maenner et al.
(2023) estimated that one in 23 boys and one in 88 girls has ASD. However, prevalence
differs by state and by community. Much of the increase in prevalence over time is due
to expanded diagnostic criteria and improved detection. Historically, 70%-85% of autism
cases were associated with intellectual disability, but this is no longer the case. The greatest
increase in the number of new cases of ASD is accounted for by individuals with average or
above-average IQ. Fourteen percent of population-based studies reported 30% to 85.3% of
children with ASD had IQ in the average range. It is now estimated that 75%-90% of children
with ASD acquire some functional language compared to an earlier estimate that was 50%.
Even if they have optimal functional language development, they may still experience social
cognition and cognitive inflexibility; and this condition makes it difficult to deal with daily

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situations (Han et al., 2022; Zeidan et al., 2022). Hence, cognitive dysfunction is the most
challenging issue among children with ASD.
Cognitive functions refer to memory, learning, perception, and processing, including language
and behaviour. Several factors related to cognitive functions such as neural processing (pre-
and post-synaptic), hormones, blood gases, glucose levels, oxidative stress, and immune
systems (Critchley and Garfinkel, 2018). Thus, it may include the cellular and genetic levels.
In children with ASD, cognitive impairment has several types and severity. It is assumed
to be associated with neuroinflammation, dysfunctional processes on oxidative stress,
and gut-brain axis in children with ASD (Han et al., 2022). However, nowadays there are
no specific biomarkers that have been used for early detection, diagnostic, or therapeutic
purposes because of the heterogeneity of ASD manifestation and the lack of research on
these issues (Al-Mazidi SH, 2023). Meanwhile, cognitive dysfunction in children with ASD
may also be associated with sensory perception problems, especially visual processing,
tactile modalities, or hypersensitive to sounds or bright lights (O'Riordan and Passetti, 2006).
Cognitive dysfunction related to children with ASD is mostly in the areas of executive and
social cognition function. Several studies revealed a decline in cortical and cerebellar white
matter in late childhood and adolescence period compared to neurotypical children and it was
related to the above conditions. Other studies mentioned the reduced Theory of Mind (ToM)
account in children with ASD (Baron-Cohen, 1991) that related to executive dysfunction
and clinical core symptoms of ASD, i.e. interaction and social-reciprocal communication.
Cognitive function supports the optimal development of ToM by enabling children to express
their understanding of mental states that arise from an improvement in executive function
(Carlson et al., 2002). Thus, children with ASD who show executive dysfunction and further
reduced ToM might have an inability to understand the conceptual frameworks that are
required to solve problems and cognitive skills that are important to access and express
understanding (Carlson et al., 2004). Hence, children with ASD may perceive objects, social
situations, or mental constructs less as a whole and instead focus more specifically on
details of the holistic structure (Hemmers J et al., 2022).

Keywords: Social interaction; Child and adolescent; Z generation, mental health.

References:
1. Al-Mazidi SH. The Physiology of Cognition in Autism Spectrum Disorder: Current and
Future Challenges. Cureus, 2023;15(10), e46581
2. American Psyhcitaric Association. Diagnostic and Statistical Manual for Mental Disorder
5th Ed. Arlington, VA, American Psychiatric Association, 2013.
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3. Baron-Cohen S. The Development of a Theory of Mind in Autism: deviance and Delay?.


Psychiatr Clin North Am. (1991) 14:33–51.
4. Carlson SM, Moses LJ, Breton C. How specific is the relation between executive function
and theory of mind? Contributions of inhibitory control and working memory. Infant Child
Dev 2002;11:73–92.
5. Carlson SM, Moses LJ, Claxton LJ. Individual differences in executive functioning and
theory of mind: an investigation of inhibitory control and planning ability. J Exp Child
Psychol 2004; 87:299–319.
6. Critchley HD, Garfinkel SN. The influence of physiological signals on cognition. Curr
Opin Behav Sci. 2018;19:13–18
7. Han YM, Chan MM, Shea CK, Lai OL, Krishnamurthy K, Cheung MC, Chan AS.
Neurophysiological and behavioral effects of multisession prefrontal tDCS and concurrent
cognitive remediation training in patients with autism spectrum disorder (ASD): a double-
blind, randomized controlled fNIRS study. Brain Stimul 2022;15:414–425.
8. Hemmers J, Baethge C, Vogeley K, Falter-Wagner CM. Are Executive Dysfunctions
Relevant for the Autism-Specific Cognitive Profile? Frontiers in psychiatry 2022;13,
886588
9. Maenner MJ, Warren Z, Williams AR, et al. Prevalence and characteristics of autism
spectrum disorder among children aged 8 years – Autism and developmental disabilities
network, 11 sites, United States, 2020. MMWR Surveill Summ 2023;72:1-14
10. O'Riordan M, Passetti F. Discrimination in autism within different sensory modalities. J
Autism Dev Disord 2006;36:665–675.

11. Ziedan J, Fombonne E, Scorah J, et al. Global prevalence of autism: A systematic


review. Autism Network 2022; 15:778-790

Acknowledgments: The author would like to give thanks to all parents and children with
autism who have struggled and finally reached the optimal developmental level.

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Concerning Social Interaction Problems in the “Z” Generation


Tjhin Wigunaa
Child and Adolescent Psychiatry Division, Department of Psychiatry Faculty of Medicine
University of Indonesiaa
dr. Cipto Mangunkusmo General Hospital, Jakarta, Indonesiab
E-mail: [email protected]; [email protected]

Social interaction is part of the interpersonal skills that develop since the beginning of
human life, and it changes from infancy through adolescence. There are three essential
elements in interpersonal skills development, i.e. (1) the child’s ability to maintain a secure
attachment, dyadic relationship, and empathy with other kids or adults; (2) the child’s ability
to communicate both verbally or nonverbally towards his/her minds and feeling; (3) the
cognitive development such as the decline of egocentrism during adolescence period so
that they can learn from others opinions, to understand rules, norms, and values. Moreover,
cognitive development also improves the ability to understand the ideal relationships and
generate multiple solutions when they experience problems. Finally, cognitive development
ensures the competence to do a self-reflection and introspect about oneself and others; and
(4) the availability of parental identification and role modeling that can shape a child’s social
functioning and skills (Newman, 2008)
Generation Z (Gen Z) is the post-millennial generation, they are also known as centennials.
They were born between 1995 – 2010 and represent 32% of the world population these
days (LEV, 2021). It is a period of extending the use of the internet in daily life that is
not only for work or school but also for shopping, chatting, gaming, and watching TV.
Thus, this generation is mostly equipped with smartphones or tablets since the beginning
of their life and become proficient in technologies and social media compared to the
previous generation. Consequently, they may neglect their interpersonal relationships to
a greater extent, but they are the ones who give more comments to social judgment on
the Internet. They can easily get everything they want; thus, they develop as an ‘instant
generation’ who think that they can have anything immediately, a fact fostered by the digital
world in which they are immersed, and their lifestyle is also influenced by what they see
through the digital age (Jayatissa, 2023). On the other hand, Gen Z develops as a self-
driven individual who values flexibility and non-hierarchical leadership and has a pragmatic
attitude about the work they do. Moreover, Gen Z experienced several collective societal
traumas during their critical developmental periods including riots, monetary crises, natural
disasters, and corruption issues. Hence, it may affect their behaviour, values, attitude, and
way of social interaction with others or with their previous generation (Dolot, 2018).

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Based on the above explanation, Gen Z is assumed to have a challenge in face-to-face social
interaction because they are more favorable to using social media and digital communication.
The amount of time spends on digital media results in less in-person social interaction
(Ajmain, et al., 2020). Hence, Gen Z experiences more problems in social interaction, and
becomes more difficult to make friends because they may have difficulties maintaining a
secure attachment because of more mistrust experiences, dyadic relationships, and direct
communication, which may increase loneliness. In addition, during the global COVID-19
pandemic, the growing screen time has affected Gen Zer's mental well-being putting them
more at risk of having depression, anxiety, and poor self-esteem. It is said that 41% of
Gen Z had mental health issues compared to millennials and adults aged 45 and over
(Blake, 2024). Meanwhile, societal trauma may affect Gen Zer to cope in different styles and
some of them may confuse and isolate themselves because of ambiguous role modeling
and feeling differently. Thus, it may influence their social life such as lack of social skills,
problems in social interaction, and leads to more confrontation respectively (Twenge, 2017).
For future directions, mental health professionals need to understand the characteristics of
Gen Z and perceive them in positive ways without negatively judging them. Secondly, support
and teach them the basic principles of social interaction skills such as, how to effectively listen
to others, the art of reading social cues and situations, starting and maintaining friendships
by developing empathetic skills, and the beautiful sides of face-to-face interactions. Parents
who are originally from Gen X (born in 1960 – 1980) should give respect to their children
who are Gen Zer and be an appropriate social role model to be admired.

Keywords: Social interaction; Child and adolescent; Z generation, mental health.

References:
1. Ajmain TA, Fik WARWI, Alias MI, Mohamad AM. Impacts and effective communication
on Generation Z in industrial revolution 4.0 era. Journal of English & Applied Linguistics
2020;1(2):82-87.
2. Blake S. Gen Z has a loneliness problem. Available at https://www.newsweek.com/
generation-genz-loneliness-problem-mental-health-1877013. Accessed on August 03,
2024
3. Dolot A. The characteristic of Generation Z. “e-mentor” 2018;2(74): 44–50
4. Jayatissa D. Generation Z – A new lifeline: A systematic literature review. Sri Lanka
Journal of Social Sciences and Humanities 2023;3(2):179-186
5. LEV TA. Generation Z: Characteristics and Challenge to entering the world of work.
Cross-Cultural Management Journal 2021;1; 107-115

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6. Newman BM. The Development of Social interaction from infancy through adolescence.
Small Group Behavior 1976;7(1):19-32.
7. Twenge, JM. IGen: why today's super-connected kids are growing up less rebellious,
more tolerant, less happy-- and completely unprepared for adulthood (and what this
means for the rest of us). First Atria books hardcover edition. New York, NY: Atria Books;
2017.

Acknowledgments: The author would like to give thanks to all parents and clients who
have already inspired and given input in this short opinion.

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Management of Cough-Related Allergy


Wistiania
Faculty of Medicine, Central of Health Reference Hospital Dr. Kariadia
Universitas Diponegoro, Semarang, Indonesiab
E-mail: [email protected]

The objectives of this paper are:


1. To understand the pathogenesis of cough related to allergies.
2. To identify the clinical manifestations of allergy-related cough.
3. To implement appropriate management for allergy-related cough.

INTRODUCTION
In daily clinical practice, cough is a common complaint expressed by parents, often
associated with accompanying symptoms such as fever, vomiting during coughing episodes,
and a decline in the patient’s quality of life, especially in cases of recurrent cough. A patient-
based prospective cohort study conducted in a hospital setting indicated that cough is
primarily caused by acute respiratory infections, with a recurrence frequency of 5 to 8 times
per year and an illness duration of 7 to 9 days per episode. More than 90% of these cases
resolve by the third week of illness. In some instances, more frequent episodes suggest an
underlying, more severe condition, such as cystic fibrosis or primary ciliary dyskinesia. A
study by Jurca M. et al. found that cough accompanied by flu symptoms has a prevalence
of 69% to 70%. Meanwhile, cough without flu symptoms is generally triggered by physical
activity, exposure to house dust, plant pollen, or pet dander from animals like dogs or
cats. Allergy-related cough is commonly observed in allergic rhinitis and asthma. Studies
show that the prevalence of allergic rhinitis in school-aged children reaches 23%, which
is similar to the global prevalence of 10% to 30%. From the perspective of cough onset,
allergic rhinitis and asthma can present acutely, resembling conditions such as pertussis,
pneumonia, and aspiration syndrome. This paper aims to identify coughs related to allergic
diseases, recognizing that different types of coughs have distinct pathomechanisms. A
thorough understanding of these mechanisms will facilitate appropriate management.

PATHOMECHANISM OF ALLERGY-INDUCED COUGH


Cough is a defense mechanism of the human body aimed at expelling foreign materials
from the respiratory tract. It begins with the stimulation of the cough reflex arc, which

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involves cough receptors located in the respiratory tract. The stimuli may be mechanical or
chemical. Once the receptor is stimulated, efferent impulses travel to the cough center via
the phrenic nerve, vagus nerve, and spinal motor neurons, targeting the diaphragm, larynx,
trachea, bronchi, expiratory muscles, and pelvic sphincter. This results in the expulsion of
foreign materials, ensuring the lungs remain free of such substances and function properly.
In allergy-induced cough, the immune system overreacts to foreign substances, leading to
the release of a chemical called histamine. The foreign substance in this context is known
as an allergen. When histamine binds to its receptors, particularly in the upper respiratory
tract, it triggers symptoms such as a runny nose, coughing, sneezing, and swelling of the
nasal mucosa. Cough related to allergies can result from stimulation of the cough receptors
in the larynx due to postnasal drip, which is commonly observed in allergic rhinitis, acute
nasopharyngitis, and sinusitis, conditions collectively known as Upper Airway Cough
Syndrome (UACS). This syndrome may cause symptoms such as rhinorrhea, a sensation
of dripping or itching at the back of the throat, or, in some cases, no symptoms at all. The
diagnosis of postnasal drip is often confirmed by identifying "cobblestoning" patterns on
the nasopharyngeal mucosa. Additionally, histamine binding to mucosal receptors in the
respiratory tract triggers inflammation, leading to tissue leakage that manifests as nasal and
sinus congestion, along with a runny nose.

COUGH AS A SYMPTOM OF ALLERGIC DISEASES


Cough is a nonspecific clinical symptom that can accompany various diseases, making
it essential to identify any associated or underlying conditions. Allergy-induced cough is
characterized by accompanying symptoms such as a runny nose, sneezing, and nasal
congestion. It can present acutely (lasting less than 3 weeks, as seen in acute rhinitis) or
chronically (lasting 8 weeks or more, as seen in asthma). Allergy-related cough is typically
dry or non-productive.

ALLERGIC RHINITIS
Itching in the throat often triggers the cough. This is accompanied by symptoms of allergic
rhinitis, such as a runny nose and sneezing. Recurrent episodes can impair the patient’s
quality of life, causing fatigue, headaches, and ear discomfort. Sleep disturbances may also
occur, with patients waking at night due to coughing or nasal congestion. This cough persists
chronically until allergen exposure is managed. Additional symptoms may include watery
eyes, sneezing (especially in the morning), nasal discharge, upper airway obstruction, and

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tenderness over the sinus area upon palpation. Allergic rhinitis involves inflammation of
the nasal mucosa due to environmental allergens, which increase mucus production in the
nasal mucosa and lead to postnasal drip. Physical examination may reveal signs such as
allergic shiners (dark circles under the eyes) and mouth breathing due to nasal obstruction.

ASTHMA
Asthma occurs due to an excessive immune response to environmental triggers, leading
to clinical inflammation, airway obstruction, and bronchial hyperreactivity characterized by
airway constriction. Coughing in asthma results from increased mucus production, which
narrows the airways and contributes to respiratory obstruction.

Table 1. Comparison of Allergy-Induced Cough with Infection-Induced Cough


Allergy-Induced Cough Infection-Induced Cough

Type of Cough Dry cough (no mucus) Productive cough (with mucus)

Cause Allergen Virus

Duration Weeks or more Several days to weeks

Fever Negative Positive


Positive (if postnasal drip is
Throat Pain Positive
present)
Congestion, Sneezing,
Positive Positive
Runny Nose
Urticaria (Hives) Positive Negative

Cough-related to asthma commonly manifested as dyspnoe accompanied by wheezing


suggesting narrowing of lower respiratory tract. Factors associated with asthma are family
history of atopy or asthma, the onset of asthma or worsening symptoms on allergen exposure
such as house dust mite, mold, or animal danders. Other clue of cough-related to asthma
are seasonal or manifestation of the disease after an upper respiratory tract infection

MANAGEMENT OF ALLERGY-INDUCED COUGH


The primary principle of allergy-induce cough is by managing the underlying allergy,
accompanied by addressing symptoms that disrupt the patient’s daily activities. For allergic
rhinitis, allergen identification can be conducted through a skin prick test or serum examination

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for specific IgE against particular allergens. These tests are primarily performed on patients
unresponsive to empirical treatments. Preventing clinical recurrence of allergic rhinitis
involves avoiding identified allergens. In clinical practice, allergic rhinitis is classified based
on the frequency and duration of episodes and their impact on daily physical activities. For
moderate persistent allergic rhinitis, the treatment of choice includes topical corticosteroids.
Antihistamines can be added if symptoms like sneezing, itching, or rhinorrhea are present.
Therapy should be evaluated within 2 to 4 weeks. If no clinical improvement is observed,
a reassessment of the diagnosis, comorbidities, or adherence to therapy is necessary. The
general pharmacological management of allergic rhinitis includes antihistamines, intranasal
steroids, or immunotherapy. Intranasal steroids are intended to reduce nasal inflammation
and improve the nasal mucosa; they are the primary choice for allergic rhinitis cases. In
individual with asthma shows airway obstructive may need spirometry to reveal the obstructive
symptoms; as part of the allergic response, bronchodilators may be administered in addition
to antihistamines and steroids to enhance or widen the airways, improving respiratory
function. As for clinical support of airway hypersensitivity, bronchus provocation may be
performed. Meanwhile imaging may be performed if complications such as rhinosinusitis are
suspected. The main treatment of allergic rhinitis include restoring the normal function of
upper airways along with improvent of quality of life through education, control measures of
allergen avoidance, medicamentosa or in specific case of allergen-specific immunotherapy.
In term of environmental allergen control including the identification of allergen, and allergen
avoidance. Exposure to environmental allergen such as airborne pollens remain the most
challenging measures, implying that the patient must stay indoors or in close environment;
suggestion the usage of filters or humidifier eventhough not supported by research study.

REFERENCE
1. Jurca M, Ramette A, Dogaru CM, Goutaki M, Spycher BD, Latzin P, et al. Prevalence
of cough throughout childhood:A cohort study.https://doi.org/10.1371/journal.pone.
0177485
2. Lucanska M, Hajtman A, Calkovsky V, Kunc P, Pecova R. Upper Airway Cough Syndrome
in Pathogenesis of Chronic Cough. https://doi.org/10.33549/physiolres. 934400
3. Davis JA, Gudi K. Approach to the Patient with cough. https://doi.org/10.1016/
j.mcna.2020.08.013
4. Soegiarto G, Abdullah MS, Damayanti LA, Suseno A, Effendi C. The prevalence of
allergic diseases in school children of metropolitan city in Indonesia shows a similar
pattern to that of developed countries. https://doi.org/10.5415/apallergy.2019.9.e17

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5. Sienra-Monge JLL, Del-Rio-Chivardi JM, Navarrete-Rodriguez EM. Chronic cough and


acute wheezing. Dalam: Rezaei N, editor. Pediatric Allergy, https://doi.org/10.1007/978-
3-030-18282-3_38
6. Tome M, Lourenco O. Avoidance Measures for Patients with Allergic Rhinitis: A
Scoping Review. https://doi.org/10.3390/children10020300

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Disorders of Gut-Brain-Interaction: Understanding Food as


Triggers and Therapeutic Agents
Mexitalia Setiawati EMa
Department of Pediatrics and Child Health Faculty of Medicine Universitas Diponegoroa
Kariadi Hospital Semarang, Indonesiab
Email: [email protected]

The irritable bowel syndrome (IBS), previously known as functional gastrointestinal disorders
(FGID), is a chronic and frequently attenuating disorder of gut-brain interaction (DGBI).1 The
criteria of IBS were based on Rome IV Diagnostic Criteria i.e (1) Recurrent abdominal pain,
on average, at least 1 day per week in the last 3 months and associated with two or more of
the following (a) related to defecation, (b) associated with a change in frequency of stool, (c)
associated with a change in the form (appearance) of stool; and (2) Criteria fulfilled for the
last 3 months with symptom onset at least 6 months prior to diagnosis.1
In current years, many studies assess that the ingestion of food would trigger symptoms
of DGBIs. Dietary interventions and functional GI disorders have increased noticeably.
Several pathophysiological mechanisms have been suggested to explain the impact of food
on the onset of GI symptoms. One of these includes a change of GI mechanoreceptors,
chemoreceptors, and thermoreceptors liable for nutrient sensing.2,3
The role of thermosensitivity is most probably limited. While cold meals may empty more
slowly from the stomach, however, the gastric sensing of the existence of food is mostly by
mechanosensitive and volumetric sensing, whereas chemosensing of nutrient composition
ensues in the small bowel. The other explanation of nutrient chemosensing is the role of
specialized receptors that can detect all the main groups of nutrients in the upper small
bowel. The occurrence of glucose, fatty acids, and amino acids is observed through large
numbers of specific receptors or transporters.2
Food volume could be a trigger of sensing. During the process of digestion of food, a dilatation
process will occur in the proximal stomach. This will produce a reservoir that functions as a
storage of digested food without increasing the intragastric pressure. Increasing the volume
of food in the stomach will cause stretching of the mechanoreceptors in the stomach wall,
triggering a sensation of fullness and ultimately causing cessation of eating.4 The role of
chemosensing could be started from the visceral sensation of chemosensitive modalities
such as nutrient sensing, acid sensitivity, or tastant sensing. Capsaicin, the natural compound
of chili pepper, is an agonist at the transient receptor potential vanilloid type 1 (TRPV1)
channel which changes thermal and chemical stimuli into painful sensations or discomfort.4
Another possible mechanism presenting a possible defect in nutrient processing is

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demonstrated through fructose or lactose intolerance and lactase-isomaltase polymorphism


in patients with DGBI. Food-triggered symptoms might also develop from the hypersensitivity
to the distension of the bowel lumen, deteriorated by ingestion of low-absorbable high-
osmolarity aliments (e.g. FODMAPs). Deviate microbiota is an etiologic factor because it
may increase the FODMAP fermentation leading to lumen distension and, the production of
neuroactive mediators which increase visceral hypersensitivity. 3,4

FIGURE 1 Proposed pathogenetic mechanisms leading to gastrointestinal symptoms, including


bloating, after FODMAP ingestion in predisposed individuals. LPS, lipopolysaccharide; 5HT,
5-hydroxytryptamine; GI, gastrointestinal.3

A high FODMAP diet will cause dysbiosis and alteration of the gut metabolome and
microbiome. It increased hydrogen production, gram-negative bacteria overgrowth, and
consequently the luminal lipopolysaccharide, which can activate mast cells. Further, tryptase,
histamine, and prostaglandin E2 released by mast cells can increase intestinal permeability
and cause visceral sensitivity.3,5 Several bacterial mediators have been involved, including
histamine, proteases, tryptamine, 5-HT, and lipopolysaccharide. Specifically, tryptophan
intake will modulate microbial composition through its metabolism by commensal microbes
and produce several neuroactive mediators including 5-HT, tryptamine, and indols. Studies
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about the actions of fecal supernatants from IBS patients that were compared to healthy
controls revealed that IBS fecal supernatants signaling from the lumen to nerve terminals in
the intestinal wall cause visceral hypersensitivity. This outcome was blocked by histamine
antagonists in some patients and protease inhibitors in others.5
Fructose or lactose intolerance and lactase-isomaltase polymorphism in patients with
“Disorders of Gut-Brain Interaction” (DGBI) in some studies might have a role in a faulty
processing of nutrients. Food-triggered symptoms might also arise from the hypersensitivity
to the distension of the bowel lumen, deteriorated by ingestion of low-absorbable high-
osmolarity aliments (e.g., FODMAPs).2
Symptomatic therapy of IBS includes a change in eating patterns, with an emphasis on
prebiotics, probiotics, gluten, and fermentable oligo-, di-, monosaccharides, and polyols
(FODMAPs).5 Small molecules like fructose, mannitol, sorbitol, and lactulose use a direct
osmotic power, which increases intraluminal water.3 FODMAPs are badly absorbable
carbohydrates that utilize an osmotic load on the gut and are quickly fermented by colonic
bacteria, resulting in gas production causing abdominal distention, bloating, and pain.5 Study
reveals that a diet high in sucrose, polyols, and fermentable carbohydrates significantly
amplified total waste wet weight from ileostomy.3,5

Table 1. FODMAP DIET


Fructans: wheat, rye, garlic, artichokes, inulin and
F Fermentable
oligosaccharides (fiber)
O Oligosaccharides Galatians: beans, lentils, and chickpeas

D Disaccharides Lactose: milk, yogurt, ice cream, pudding and custard


Fructose (in excess of glucose): honey, agave,
M Monosaccharides
watermelon, apples, asparagus and sugar snap peas
A And Sorbitol/Mannitol: sugar-free gum, blackberries, apples,
pears, peaches, cauliflower, mushrooms and snow peas
P Polyols

A low-FODMAP food must contain less than 0.3 g per serve (g/serve) or less than 0.2 g/
serve of oligosaccharides (for core grain products, legumes, nuts, and seeds or vegetables,
fruits, and all other products, respectively); less than 0.4 g/serve of total polyols; less than
0.4 g/serve of excess fructose; and less than 1 g/serve of lactose.3
Table 2. List of foods with low fermentable oligosaccharides, disaccharides, monosaccharides,

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and polyols (FODMAP) content. 6


Nutrients Low FODMAP Content

Cereals Gluten-free products, rice, corn pasta, tortilla chips, quinoa, oats, polenta,
sourdough, noodles
Milk Lactose-free products, rice milk, soy milk, sorbets
products
Cheese Hard cheeses, Cheddar, Parmesan, mozzarella, Swiss, firm tofu, tempeh,
Brie, Camembert
Fruits Bananas, cantaloupe, carambola, durian, honeydew melon, kiwi, orange,
passion fruit, pawpaw, all berries (raspberries, blueberries, cranberries,
strawberries) except blackberries, tangelo, grapes, grapefruit, all nuts
(except cashew and pistachios, and less than ten), almonds (less than 10),
macadamia, olives, pumpkin seeds, flax and chia seeds, coconut, lemon,
limes, papaya, rhubarb
Vegetables Bamboo shoot, bok choy, capsicum, celery, chives, choko, choy sum, corn,
eggplant, green bean, bean sprouts, lettuce, parsnip, pumpkin, silverbeet,
tomato, potatoes, spring onion (green part only), garlic-infused oil, bell
peppers, Swiss chard, carrots, spinach, zucchini, beetroot (no more than
four slices), broccoli (no more than 1/2 cup)
Legumes Canned pumpkin, canned chickpeas, canned lentils
Sweeteners Honeydew, golden syrup, maple syrup, glucose, sucrose (table sugar),
aspartame, stevia, molasses, and any sweeteners not containing fructose
and not ending in ‘‘-ol’’
References Khan et al., 2015 54; Barrett, 2017 55; Varney et al., 2017 56; Monash
University Low FODMAP Diet App., 2016 57; Canadian Digestive Health
Foundation, 2019 58; Magge and Lembo, 2012 5

Note: FODMAP composition is affected by food processing techniques. Processes that


involve heating and water can reduce the content of water-soluble FODMAPs (such as
fructans and GOS) leaching into the surrounding liquid (canned legumes are lower in
FODMAP, and GOS than boiled legumes). Servings should also be considered because
an excessive intake may increase the content of the FODMAP diet (i.e., almonds and other
nuts, if less than ten pieces, are low in FODMAP; large bananas have increased FODMAP).
Gluten-free products are low-FODMAP except if they contain honey or fructose, or polyol
sweeteners.
A cross-over design compared the effect of low vs. moderate FODMAP diets on the
gastrointestinal symptoms and clinical response of the subjects with IBS revealed that the
severity of gastrointestinal symptoms, stool consistency, and frequency changed after low

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FODMAP diet intervention. The reduction of gastrointestinal symptoms did not occur in
subjects who received a moderate FODMAP diet.7 Meanwhile a large French population
cohort study showed that the daily intake of FODMAP diet was 19.4 ± 9.5 g/day. However,
the IBS subjects had lower intakes in FODMAPs than non-IBS ones (<9 g/day). It was
concluded that the higher severity of IBS subjects was associated with lower intakes.8 A
better food analysis and labeling of foods is needed to improve the knowledge regarding
possible “dangerous foods” of FODMAP as well as to the new methods to teach the LFDs
on its different phases and predictors of individual response.9 A single-group intervention of
30 children ages 7 to 12 years old with functional gastrointestinal disorders, revealed that
higher baseline quality of life was associated with better obedience to the LFD. However,
there was no evidence that obedience was associated with baseline emotional/behavioral
anxieties or greater symptom burden (eg, more frequent abdominal pain).10
A meta-analytic research comparing low FODMAP diet with traditional diet as well as to
high FODMAP diets showed that in the RCTs, the patients taking a low-FODMAP diet felt
a reduction of pain and bloating significantly compared with those receiving a traditional
diet. The reduction of abdominal pain and bloating also occurred in patients receiving a
low-FODMAP diet compared with those receiving a high-FODMAP diet. In cohort studies,
pain and bloating were significantly reduced after treatment compared with the baseline
diet.11 Meanwhile a systematic review to clarify the efficiency of the FODMAP diet on the
patients with Crohn’s disease showed that there was significant evidence that the LFD has
a promising impact on gastrointestinal symptoms in Crohn’s disease.12

Conclusion.
Food is habitually considered to be a causing factor in irritable bowel syndrome (IBS)
symptoms. A low FODMAP diet (LFD) is increasingly recommended for IBS treatment
because of its ability to reduce symptoms, especially abdominal pain and bloating. However,
it remains to be confirmed whether a low-FODMAP diet is superior to conventional IBS diets,
especially in the long term.

Keywords: gut-brain interaction, irritable bowel disease, FODMAPs, diet

References :
1. Barbara G, Cremon C, Bellini M, Corsetti M, Di Nardo G, Falangone F, et al. Italian
guidelines for the 1. management of irritable bowel syndrome. Joint Consensus from the

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Italian Societies of: Gastroenterology and Endoscopy (SIGE), Neurogastroenterology


and Motility (SINGEM), Hospital Gastroenterologists and Endoscopists (AIGO), Digestive
Endoscopy (SIED), General Medicine (SIMG), Gastroenterology, Hepatology and
Pediatric Nutrition (SIGENP) and Pediatrics (SIP). Dig. Liver Dis. 2023; 55: 187–207,
Digestive and Liver Disease 55 (2023) 187–207. https://doi.org/10.1016/j.dld.2022.11.015
2. Van den Houte K, Bercik P, Simren M, Tack J, Vanner S. Mechanisms underlying
food-triggered symptoms in disorders of gut-brain interactions. Am J Gastroenterol
2022;117:937–946. https://doi.org/10.14309/ajg.0000000000001812
3. Pessarelli T, Sorge A, Elli L, Costantino A. The low-FODMAP diet and the gluten-free
diet in the management of functional abdominal bloating and distension. Front. Nutr Sec.
Nutritional Immunology 2022; 9 https://doi.org/10.3389/fnut.2022.1007716
4. Scarpellini E, Balsiger LM, Broeders B, Van Den Houte K, Routhiaux K, Raymenants K,
et al. Nutrition and Disorders of Gut–Brain Interaction. Nutrients 2024, 16, 176. https://
doi.org/10.3390/nu16010176
5. Nordin E, Brunius C, Landberg R, Hellström PM. Fermentable oligo-, di-, monosaccharides,
and polyols (FODMAPs), but not gluten, elicit modest symptoms of irritable bowel
syndrome: a double-blind, placebo-controlled, randomized three-way crossover trial. Am
J Clin Nutr 2022;115:344–352. doi: https://doi.org/10.1093/ajcn/nqab337
6. Pensabene L, Salvatore S, Turco R, Tarsitano F, Concolino D, Baldassarre ME, et al.
Low FODMAPs diet for functional abdominal pain disorders in children: critical review
of current knowledge. J Pediatr (Rio J). 2019;95(6):642-56. https://doi.org/10.1016/j.
jped.2019.03.004
7. Algera JP, Demir D, Tornblom H, Nybacka S, Simren M, Storsrud S. Low FODMAP diet
reduces gastrointestinal symptoms in irritable bowel syndrome and clinical response
could be predicted by symptom severity: A randomized crossover trial. Clinical Nutrition
2022;41:2792e2800. https://doi.org/10.1016/j.clnu.2022.11.001
8. Schneider E, Sabaté JM, Bouchoucha M, Hercberg S, Touvier M, Benamouzig R, er al.
Fermentable oligo-di-,and mono-saccharides and polyols (FODMAPs) consumption and
irritable bowel syndrome in the French Nutrinet-santé cohort. Nutrients 2021;13;4513.
https://doi.org/10.3390/nu13124513
9. Bellini M, Tonarelli S, Nagy AG, Pancetti A, Costa F, Ricchiuti A. Low FODMAP diet:
evidence, doubts, and hopes. Nutrients 2020, 12, 148; https://doi:10.3390/nu12010148
10. Tenenbaum RB, Czyzewski D, McMeans A, Narayana V, Chumpitazi BP. Levy RL, et
al. Factors associated with adherence to a lowfermentable carbohydrate diet in children
with functional gastrointestinal disorders J Acad Nutr Diet. 2024;124(6):757-62.. https://
doi.org/10.1016/j.jand.2023.09.001

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11. Altobelli E, Del Negro V, Angeletti PM, Latella G. Low-FODMAP diet improves irritable
bowel syndrome symptoms: a meta-analysis. Nutrients 2017;9:940. https://doi:10.3390/
nu9090940
12. Popa SL, Pop C, Dumitrascu DL Diet advice for Crohn’s disease: FODMAP and beyond.
Nutrients 2020;12:3751; https://doi:10.3390/nu12123751

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NCCP iCAYA:
The Journey of Developing the Pediatric National Cancer Control Plan:
A Better Future for Indonesian Children
Eddy Supriyadia, Nur Melani Sarib, Ariawan Subagyoc, Mururul Aisyid, Teny Tjitra Sarie,
Andi Wicaksonof. Lanny Luhukayf, Sandra D. Ratihf, Judith Spijkermang, Sanjeeva
Gunasekerah, Keifer Gonzalezi, Esther Widjajai, Andini Handayanii, Catherine G. Lami,
Gertjan J. L. Kaspersg,i
a
Dr Sardjito Hospital Yogyakarta, bHasan Sadikin Hospital, Bandung, cDr Kariadi Hospital
Semarang, dDharmais National Cancer Center Hospital, Jakarta. eCipto Mangunkusumo
Hospital, Jakarta. fMinistry of Health Jakarta. gPrincess Maxima Centrum, Utrecht,
The Netherlands. hNational Cancer Institute, Sri Lanka, iSt Jude Children Research
Hospital, Memphis, USA. jEmma Children’s Hospital, Amsterdam UMC, Vrije Universiteit
Amsterdam, The Netherlands.
E-mail: [email protected]

In 2018, the World Health Organization (WHO) launched the WHO Global Initiative for
Childhood Cancer (GICC) in collaboration with St. Jude. The aims of the Initiative are two-
fold: to increase prioritization of childhood cancer through awareness raising at global
and national levels and to expand the capacity of countries to deliver the best practice in
childhood cancer care. This pivotal moment marked a significant shift as childhood cancer,
once considered a rare disease, began to draw global attention as a public health issue.
This global advocacy success has led to the prioritization of childhood cancer not only at the
international level but also at every WHO regional level, particularly in WHO-SEARO and
ultimately at the national level in countries such as Indonesia.
Despite being a relatively small population subset, childhood cancer represents a
tremendous opportunity to demonstrate success with health investments. The economic
analysis conducted by global health economists demonstrates that investing in childhood
cancer treatment is crucial, beneficial, and cost-effective (1). Each day, over 1,000 children
are diagnosed with cancer worldwide. In high-income countries, more than 80% of these
children survive, representing remarkable progress in science, innovation, and public health.
However, for children in low- and middle-income countries (LMICs), the reality remains stark:
many face death, significant strain on their families, and a loss of potential. This disparity
can and must be addressed (2).
In Indonesia, with a population of approximately 80 million children (ages 0-18), it is estimated
that more than 10,000 children with cancer develop cancer annually. However, only around
2,000 patients are registered to receive care at health facilities that provide specialized

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pediatric oncology services, and the 3-year survival rate hovers around 20-30%. This is a
significant gap that needs to be bridged. Every child with cancer deserves better access
to care. The momentum for action has already begun. Governments have committed to
prioritizing childhood cancer through World Health Assembly Resolutions. In Indonesia, this
commitment is reflected in the development of a comprehensive Pediatric National Cancer
Control Plan (NCCP) with a clear goal: to improve the overall survival rate and quality of life
for children with cancer.
WHO has identified six common index cancers as a starting point for improving global
pediatric cancer outcomes: Acute lymphoblastic leukemia (ALL), Burkitt lymphoma, Hodgkin
lymphoma, retinoblastoma, Wilms tumor, and Low-grade glioma (3). Focusing on these six
cancers, which represent 50-60% of all childhood cancer cases, will help countries like
Indonesia see what is working and where improvements are needed. Proven therapies
already exist for these diseases, offering an opportunity to strengthen our healthcare
systems. This group will be a pathfinder for strengthening other childhood cancers overall.
To achieve this goal, strategic planning is essential. Indonesia's pediatric oncology community,
collaborating with international partners such as St. Jude Global (US) and Princess Maxima
Center (Netherlands), has actively advocated for a stronger focus on childhood cancer.
This advocacy has resulted in renewed commitments, including appointing key figures and
establishing a core team dedicated to developing the national strategic plan. A core Ministry-
led team has been designated to join a global cohort of 21 country teams across all 6 WHO
regions in the 2024 NCCP iCAYA (National Cancer Control Planning integrating Children,
Adolescents & Young Adults) training and knowledge exchange series on practical policy
challenges and solutions, helping teams apply one of the methodologies used in drafting this
plan, the WHO CureAll technical package (4) which guides countries in advancing childhood
cancer care as part of GICC. As a complementary step, we followed the tool C5 (Country
Collaboration for Childhood Cancer Control). C5 is a tool developed by SJCRH to facilitate
multi-stakeholder strategic planning to improve childhood cancer care. C5 is underpinned
by a Health Systems Plus framework (Figure 1) adapted for childhood cancer from the WHO
health systems building blocks and systems thinking. Part of the St. Jude Global Childhood
Cancer Analytics Resource and Epidemiological Surveillance System (SJCARES) Systems
tool suite, it is designed to appraise and strengthen the health system environment with
sustainable interventions across national, regional, and global contexts. Weekly intensive
meetings and support from NGOs and international collaborators identifying and mapping
data from 200+ health facilities and stakeholder groups via C5, coupled with reviewing
existing sample policies from St. Jude’s global Policies tool suite, and site visits culminating
in a national workshop have resulted in a policy document that will soon undergo national

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review. This policy will lay the foundation for a cohesive, comprehensive approach to
managing childhood cancer in Indonesia. Through a detailed country assessment using the
WHO building blocks and a thorough systems-oriented SWOT analysis, we have identified
the critical areas for improvement. These priorities are mapped within the CureAll framework,
leading to the creation of Indonesia's version of the CureAll strategy.

Figure 1. Health systems plus framework adapted for children with cancer

Strategic Framework of the Pediatric NCCP


Vision: Transforming childhood cancer care by ensuring equitable access to quality care for
all children in Indonesia.
Mission: to implement a collaborative, multi-sectoral approach for children with cancer, from
diagnosis to survivorship, aimed at improving survival rates, and quality of life and reducing
the overall burden of the disease by 2030.
Goal: By 2030, achieve at least a 50% survival rate for children with cancer in Indonesia and
improve their quality of life.
Strategic Pillars are illustrated in Figure 2 and consist of 4 pillars and 3 integrated enablers.

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1. Center of Excellence and Care Networking: Establish timely and accurate diagnosis
and treatment for children with cancer. Create 4-6 centers of excellence and a robust
care network across Indonesia and develop shared-care models, enhance workforce
competencies, and improve infrastructure.
2. Universal Health Coverage: Ensure all children in Indonesia have access to essential
health services for childhood cancer. Expand the national health insurance to cover early
and appropriate diagnosis, treatment, and palliative care.
3. Comprehensive Treatment Regimens: Develop national guidelines, protocols, and
SOPs for high-priority childhood cancers. Ensure access to quality-assured drugs and
technologies for diagnosis and treatment.
4. Evaluation and Monitoring with Information Systems: Strengthen cancer registries and
information systems for ongoing monitoring and evaluation. Build a national cancer
research network to guide policy and care improvements.
Enablers:
To ensure success, advocacy, funding, and governance are key enablers. Advocacy efforts
will focus on raising awareness across all sectors, and funding will be leveraged through
partnerships with NGOs and private sectors. Strong governance will ensure that all initiatives
align with the national childhood cancer strategy.

Figure 2. The framework of the Indonesia National Childhood Cancer Control Plan

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References
1. Soliman R, Oke J, Sidhom I, Bhakta N, Bolous NS, Tarek N, Ahmed S, Abdelrahman H,
Moussa E, Zamzam M, Fawzy M. Cost-effectiveness of childhood cancer treatment in
Egypt: lessons to promote high-value care in a resource-limited setting based on real-
world evidence. EClinicalMedicine. 2023 Jan 1;55.
2. World Health Organization. International Childhood Cancer Day 2024: reducing
the survival gap. WHO EMRO. https://www.emro.who.int/media/news/international-
childhood-cancer-day-2024-reducing-the-survival-gap.html. Published 2024. Accessed
September 2, 2024.
3. World Health Organization. Global Initiative for Childhood Cancer [Internet]. 2020
Nov [cited 2024 Sep 4]. Available from: https://www.who.int/docs/default-source/a-
future-for-children/booklet-global-initiative-for-childhood-cancer-2-november-2020.
pdf?sfvrsn=3ec028f2_1
4. Lam CG, Vasquez L, Loggetto P, Fuentes-Alabi S, Gonzalez Ruiz A, Benitez Majano S,
Jarquin-Pardo M, Maza M, Spencer J, Metzger ML, Luciani S. Partnering to implement the
Global Initiative for Childhood Cancer in the Americas: prioritizing systems strengthening.
Revista Panamericana de Salud Pública. 2023 Mar 27;47:e41.

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Indonesian Neonatal Registry:


What Can We Learn from it to Improve Neonatal Outcome
Rinawati Rohsiswatmo, Angelica Diana Vita, and Mika Windani
Department of Perinatology, Cpto Mangunkusumo General Hospital, Universitas
Indonesia, Jakarta, Indonesia
E-mail: [email protected]

Reducing the neonatal mortality rate is a crucial national and global objective, integral to
achieving the Sustainable Development Goals (SDGs) by 2030.1 Indonesia's efforts are
already aligned with these targets, demonstrating a commitment to reaching the goal of
significantly lowering neonatal mortality. However, to achieve the broader vision of "Indonesia
Emas" by 2045, it is essential to also consider both short-term and long-term follow-up,
particularly concerning preterm infants who contribute the highest to mortality and morbidity
rates.2
Utilizing the national registry, a short-term goal is set to strengthen national health
governance. One of the key efforts is to enhance the reporting and review of maternal
and neonatal deaths through continuous data collection, analysis, and interpretation via
the Maternal and Perinatal Death Surveillance and Response (MPDSR) system to reduce
maternal and neonatal mortality rates. Aligning with the longer-term target, Indonesia is set
to improve its quality and competitiveness in human resources. The national registry also
enables Indonesia to assess its current status and plan future actions effectively. It facilitates
the evaluation of progress achieved, determines whether efforts have been successful, and
identifies the factors contributing to success or failure.3
The Maternal Perinatal Death Notification (MPDN) application plays a vital role in this
process by facilitating the reporting of neonatal deaths via the Internet.4 Benchmarking with
international registries, such as Australia’s Australian and New Zealand Neonatal Network
(ANZNN), reveals several key aims for enhancing Indonesia's neonatal data collection.
Current data collected by MPDN in Indonesia is more limited. It includes basic information
such as birth weight and gestational age; APGAR scores at 1 and 5 minutes; presence of
congenital abnormalities; causes of death; and complications such as asphyxia, infections,
and respiratory distress. MPDN also records the timing of death, distinguishing between early
neonatal death within the first 7 days and late neonatal death within 28 days. However, it
lacks the depth of data available in ANZNN, particularly in areas such as head circumference,
length, detailed tracking of complications, and long-term follow-up outcomes.5
Reflecting on the Indonesia Neonatal Registry, Indonesia has begun implementing newborn
screening in accordance with the WHO-SEARO recommendation in 2022, which emphasizes

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the importance of universal newborn screening for three key conditions: eye abnormalities,
hearing impairment, and neonatal hyperbilirubinemia. If not detected early and managed
adequately, these conditions can have serious implications on a child’s overall development,
including delayed motor and language skills, and impaired emotional, social, and cognitive
development, with potentially lifelong consequences. This screening initiative is intended to
support long-term health outcomes for Indonesia's newborn population.6
Consistency in national data collection is also essential for reliable and comparable results
across different regions. The MPDN serves as a foundational tool in this endeavor, supporting
data collection, analysis, and the development of recommendations aimed at reducing
neonatal mortality and improving overall neonatal care. Through continued improvements
and benchmarking against international standards, Indonesia can enhance its neonatal
health strategies and contribute to better outcomes for future generations.

Keywords: neonatal mortality rate; SDGs; MPDN; registry

References:
1. UNICEF. Child survival and the SDGs 2024. https://data.unicef.org/topic/child-survival/
child-survival-sdgs/.
2. PPN/Bappenas K. INDONESIA EMAS 2045 2024. https://indonesia2045.go.id/.
3. Dinas Kesehatan Provinsi Sumatra Selatan. Pemantauan Pelaksanaan AMPSR,
dan Orientasi Sistem Informasi Matneo, MPDN, dan E-Kohort 2022. https://dinkes.
sumselprov.go.id/2022/10/pemantauan-pelaksanaan-ampsr-dan-orientasi-sistem-
informasi-matneo-mpdn-dan-e-kohort/.
4. Dinas Kesehatan Kota Salatiga. Pertemuan Sosialisasi MPDN 2024. https://dinkes.
salatiga.go.id/pertemuan-sosialisasi-mpdn/.
5. Chow SSW, Creighton P, Holberton JR, Chambers GM, Lui K. REPORT OF THE
AUSTRALIAN AND NEW ZEALAND NEONATAL NETWORK. 2021.
6. World Health Organization. Universal newborn screening implementation guidance.
2024.

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Indonesian Preterm Baby Screening


Rinawati Rohsiswatmo, Angelica Diana Vita, and Mika Windani
Department of Perinatology, Cipto Mangunkusumo General Hospital, Universitas
Indonesia, Jakarta, Indonesia
E-mail: [email protected]

Indonesia experiences a high incidence of preterm births, with approximately 600,000


preterm births annually, placing a significant burden on the country’s healthcare system.1
Preterm birth is a critical focus within the Sustainable Development Goals (SDGs), which
aims to "ensure healthy lives and promote well-being for all at all ages." Based on Maternal
Perinatal Death Notification (MPDN) data from 2023, the primary causes of neonatal deaths
are low birth weight (LBW) and prematurity.2 Furthermore, to fulfill the broader vision of
"Indonesia Emas" by 2045, it is vital to consider both short-term and long-term follow-up,
especially for preterm infants, who account for the highest rates of mortality and morbidity.
Therefore, early detection and comprehensive care strategies are crucial for improving
outcomes for preterm infants.3
The Barker hypothesis, or Fetal Origins of Adult Disease (FOAD), further underscores the
importance of early neonatal screening, particularly for preterm infants, due to the long-term
implications of fetal health on adult disease outcomes.4 Early detection and intervention
during the neonatal period, particularly for preterm infants, can mitigate risks of chronic
diseases in adulthood. By age 2, the human brain reaches 83% of its development and 95%
by age 6, highlighting the critical importance of early and continuous monitoring during this
period.5 While all infants benefit from standard newborn screening, preterm infants require
additional follow-up to address the higher risks of developmental delays and complications.6
Preterm birth is associated with over 75% of all perinatal mortality and also poses a
threefold risk for stunting.9,10 The follow-up care for preterm infants must not only address
immediate concerns of mortality but also short-term outcomes such as respiratory distress
syndrome (RDS), symptomatic patent ductus arteriosus (PDA), necrotizing enterocolitis
(NEC), retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH), periventricular
leukomalacia (PVL), and bronchopulmonary dysplasia (BPD).11 In addition to short-term
complications, prematurity can affect long-term outcomes, including neurodevelopmental
delays, intelligence quotient (IQ), and organ function. Thus, follow-up care is crucial for both
preterm and non-preterm infants to ensure the advancement of the nation’s health and well-
being.12
In accordance with global guidelines, including the 2017 Recommendations for Preventive
Pediatric Health Care from the American Academy of Pediatrics (AAP), consistent and

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comprehensive pediatric health supervision should be maintained, with care extending


until 21 years of age.7 Moreover, follow-up screenings for preterm infants—based on
recommendations from PAHO, WHO, Texas Health and Human Services, and Texas
HHCP—should include head ultrasound, hearing assessments, retinopathy of prematurity
(ROP) screening, and anemia screening. Currently, newborn screening is not yet fully
standardized across Indonesia, thus far includes hearing assessments, ROP screening,
congenital hypothyroidism screening, and congenital heart disease (CHD) screening.13
The urgent need for a standardized and comprehensive newborn screening program in
Indonesia is crucial for improving neonatal outcomes and achieving national and global
health goals.

Keywords: preterm birth, neonatal screening, FOAD, MPDN

References:
1. Rohsiswatmo R, Hikmahrachim HG, Sjahrulla MAR, Marsubrin PMT, Kaban RK, Roeslani
RD, et al. The Cohort of Indonesian Preterm Infants for Long-term Outcomes (CIPTO)
study: a protocol. BMC Pediatr. 2023;23:1–7.
2. KEMKES RI. MPDN 2023. mpdn.kemkes.go.id.
3. PPN/Bappenas K. INDONESIA EMAS 2045 2024. https://indonesia2045.go.id/.
4. Malhotra N, Malhotra J, Bora NM, Bora R, Malhotra K. Fetal origin of adult disease.
Donald Sch J Ultrasound Obstet Gynecol. 2014;8:164–77.
5. Kim JC, Wang L, Shen D, Lin W. Biomechanical Analysis of Normal Brain Development
during the First Year of Life Using Finite Strain Theory. Sci Rep. 2016;6:1–13.
6. Dion-Berboso AG, Cabic AG, Carluen-Nario I, Valeza G, Alcausin MML. AB058. Newborn
screening in preterm babies at the Newborn Screening Center-National Institutes of
Health, Manila: impact, implications, and outcomes on its first year of implementation.
Ann Transl Med. 2015;3:5839.
7. Principles O. 2017 Recommendations for Preventive Pediatric Health Care. Pediatrics.
2017;139.
8. World Health Organization. Standards for improving the quality of care for small and sick
newborns in health facilities. 2020.
9. Sefidkar R, Zayeri F, Kazemi E, Salehi M, Dehnad A, Hafizi M. A trend study of preterm
infant mortality rate in developed and developing countries over 1990 to 2017. Iran J
Public Health. 2021;50:369–75.
10. Sania A, Spiegelman D, Rich-Edwards J, Hertzmark E, Mwiru RS, Kisenge R, et al. The
contribution of preterm birth and intrauterine growth restriction to childhood undernutrition
in Tanzania. Matern Child Nutr. 2015;11:618–30.

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11. Deniz Aatalay, Ozgul Salihoglu, Emrah Can, Aysegul Beskarde SH. Short-Term Outcomes
of Very Low Birth Weight Infants Born at a Tertiary Care. Iran J Pediatr. 2013;23:205–11.
12. Allotey J, Zamora J, Cheong-See F, Kalidindi M, Arroyo-Manzano D, Asztalos E, et al.
Cognitive, motor, behavioural and academic performances of children born preterm: a
meta-analysis and systematic review involving 64 061 children. BJOG An Int J Obstet
Gynaecol. 2018;125:16–25.
13. Dahliana JK. “Skrining” pada bayi baru lahir, yang perlu diketahui oleh Orangtua. 2017.

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When to Suspect Immunodeficiency in Mycobacterium Infection


Rizqi Amaliaa
Allergy Immunology Division, Child Health Department, dr. Cipto Mangunkusumo Hospitala
Child Health Department, Faculty of Medicine, Universitas Indonesiab
E-mail: [email protected]

Introduction
Until now, tuberculosis (TB) is still a global health burden. Around 10.6 million people in the
world suffer from TB, with almost half (46%) in Southeast Asia. About one-tenth or 1 million of
the world's population with TB are children aged <15 years. Indonesia is the second largest
TB contributing country in the world after China with 9.7% of cases occurring in children.
In addition to the health burden caused by Mycobacterium tuberculosis, infections caused
by non-tuberculous mycobacterium (NTM), especially Mycobacterium avium complex and
Mycobacterium chelonae-abscessus complex have also increased.
Immunodeficiency, both primary and secondary, will result in individual susceptibility to
infections including mycobacterial infections. Unlike healthy individuals, mycobacterial
infections in individuals with immunodeficiency are more likely caused by low pathogenicity
mycobacterium. In individuals with immunodeficiency, clinical manifestations due to
mycobacterial infections are usually more severe, recurrent, or have high morbidity and
mortality.

Immune Response to Mycobacterium


Mycobacteria are aerobic bacteria from the Actinomycetota phylum. To date, there are
approximately two hundred species of mycobacteria. Only a small number of mycobacteria
species are true pathogens, while 95% of other mycobacteria are environmental bacteria
that are saprophytic or under certain conditions can turn into opportunistic pathogens.
According to their growth rate, mycobacteria can be divided into slow growers and rapid
growers. Pathogenic mycobacteria are generally included in the slow-grower group, while
saprophytic or opportunistic germs generally belong to the rapid-grower group.
Mycobacterium tuberculosis complex, Mycobacterium leprae, Mycobacterium marinum,
and ulcerans are true pathogens that belong to the slow-grower group. The species
included in the Mycobacterium tuberculosis complex are Mycobacterium tuberculosis,
Mycobacterium africanum, Mycobacterium orygis, Mycobacterium bovis, Mycobacterium
microti, Mycobacterium canettii, Mycobacterium caprae, and Mycobacterium pinnipedii.
These mycobacteria share genetic similarities and can cause tuberculosis in humans and

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mammals. Mycobacterium avium complex is one of the MNTs that belongs to the slow-
growing group, while Mycobacterium chelonae-abscessus complex is an MNT that belongs
to the rapid-growing group.
The immune response to mycobacteria involves an interaction between the innate and
adaptive immune systems. The dynamic interaction between the two will determine the
outcome of infection in an individual. An adequate response will result in the elimination
or suppression of mycobacteria, while an inadequate response will result in mycobacterial
replication leading to inflammation and tissue damage.
Macrophages are innate immune cells that first encounter Mycobacterium tuberculosis.
Alveolar macrophages will phagocyte inhaled Mycobacterium tuberculosis. Various
antimicrobial mechanisms such as phagolysosomes, autophagy, oxygen radicals, and
inducing metabolism towards inflammatory conditions are used by macrophages to
eliminate Mycobacterium tuberculosis. In certain conditions that do not allow elimination,
alveolar macrophages become a niche that supports the replication and persistence of
Mycobacterium tuberculosis during the latent phase.
The interaction between innate and adaptive immunity against Mycobacterium tuberculosis
is linked by dendritic cells. The dendritic cells function as antigen-presenting cells. It also
produces a costimulatory that modulates the T helper differentiation process. However,
the specific role of dendritic cells in immunity against Mycobacterium tuberculosis is still
controversial. Current evidence cannot determine whether dendritic cells enhance cellular
immunity against Mycobacterium tuberculosis.
T helper lymphocytes are adaptive immune cells that play a significant role in immunity
against Mycobacterium tuberculosis. TH1 lymphocytes communicate with macrophages
through the IL-12/23 – IFNγ pathway. Macrophages or other phagocytic cells that phagocytose
mycobacteria will activate pattern recognition receptors (PRRs) in the cytoplasm and induce
the production and secretion of IL-12 and IL-23. These cytokines will then bind to their
receptors on the membrane of TH1 lymphocytes and NK cells. The binding of IL-12 and IL-
23 to their receptors will induce the production of IFNγ using various transcription factors.
Conversely, IFNγ produced by TH1 lymphocytes will bind to its receptors on the membrane of
macrophages and dendritic cells. The interaction of IFNγ with its receptor and the interaction
of CD40L with CD40 provide signals to macrophages to increase their intracellular killing
ability.
Along with the interaction of the innate and adaptive immune systems, a complex mechanism
is formed that aims to prevent the spread of mycobacteria in the form of granulomas.
Granulomas occur in many individuals infected with Mycobacterium tuberculosis. T helper

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lymphocytes and TNF play a significant role in granuloma formation and protection against
the host.

Immunodeficiency and Susceptibility to Mycobacterium


Immunodeficiency is a condition caused by the failure of the immune system to function due
to a defect or absence of one of the components of immunity. Primary immunodeficiency or
inborn error of immunity (IEI) is a group of diseases caused by a single genetic mutation in
the germline (monogenic germline mutation). The mutation causes loss of expression, loss-
of-function (LOF), or gain-of-function (GOF) of the protein encoded by the gene. Individuals
with IEI will experience a phenotype in the form of susceptibility to infection, allergies,
autoimmune, autoinflammatory, or malignancy. In 2022, there were 435 genetic defects
identified to have an association with IEI.
Most IEI with mycobacterial susceptibility has defects in T lymphocytes, the number and
function of phagocytes, especially macrophages, or the IL-12/23 – IFNγ pathway. Genetic
defects in the first two groups have susceptibility to infection that is not limited only to
mycobacteria. Meanwhile, defects in one component of the IL-12/23 – IFNγ pathway or what
is known as Mendelian susceptibility of mycobacterial disease (MSMD) have susceptibility
to mycobacterial infection and several other pathogens that are more limited.
Severe combined immunodeficiency (SCID) is an IEI characterized by the absence of T
lymphocytes. Infants with SCID who are accidentally vaccinated with BCG can experience
an adverse effect ranging from lymphadenitis to disseminated BCG. In a cohort study of
349 infants with SCID who received the BCG vaccine, 51% experienced adverse effects.
Other mycobacterial infections such as NTMs and TB are less common. Often, most SCID
patients have already experienced mortality due to other infections before being exposed to
mycobacteria other than Mycobacterium bovis from BCG.
Chronic granulomatous disease (CGD) is an IEI that has a defect of respiratory burst in
phagocyte cells. Individuals with CGD will experience susceptibility to pathogens whose
main elimination mechanism is through this process, one of which is Mycobacterium. Like
SCID, individuals with CGD can experience adverse effects of the BCG vaccine. In addition
to Mycobacterium bovis, individuals with CGD are also susceptible to TB with manifestations
of recurrent pulmonary TB or pulmonary TB with extensive lesion images.
Mendelian susceptibility of mycobacterial disease (MSMD) is a type of IEI with defects in
components of the IL-12/23 – IFNγ pathway. There are currently nineteen genes whose
defects cause the phenotype of MSMD. The majority will result in reduced production or

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response to IFNγ. The penetrance of genetic defects in MSMD is inversely proportional to the
severity of the phenotype. MSMD groups with more severe IFNγ deficiency are susceptible
even to weakly virulent mycobacteria, while MSMD groups with milder IFNγ deficiency have
more selective susceptibility.

Figure 1. Schematic illustration of IL-12/23 – IFNγ pathway

In addition to primary immunodeficiencies, various other conditions that cause secondary


immunodeficiencies can cause susceptibility to mycobacteria. The most common secondary
immunodeficiency associated with mycobacteria is HIV infection. Individuals with HIV
infection, especially those who are already AIDS, can experience susceptibility to TB, NTMs,
and BCG, often with severe (extrapulmonary) or recurrent clinical manifestations.
The use of immunosuppressants such as systemic steroids, biological agents, and
chemotherapy can reduce the number or function of various components of the immune
system that play a role in eliminating mycobacterial infections. The decrease in number
and function can then cause its vulnerability. It is important to screen for mycobacterial
infections, especially TB, before starting treatment. Evaluation of TB infection can be
repeated immediately if symptoms are found during treatment.

Table 1. Characteristics of mycobacterial infections in secondary immunodeficiencies and


primary immunodeficiencies/ inborn error of immunity

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NTMs BCG TB Other Pathophysiology


infection
Secondary immunodeficiencies

HIV infection + + + Yes T helper cell defect

Immunosuppressive Immune cell function


+ ? + Yes
treatment impairment

Primary immunodeficiencies/ inborn error of immunity

Severe combined
- + + Yes T cell defect
immunodeficiency
Quantitative defect of
GATA2 deficiency + - + Yes monocytes, DC, and
PAP
Chronic granulomatous Respiratory burst defect
+/- + + Yes
disease in all phagocytic cells
Impaired CD40-
Ectodermal dysplasia -
+ + + Yes dependent IL-12
immunodeficiency
production
Impaired CD40-
CD40L deficiency + + + Yes dependent IL-12
production
STAT1 deficiency
+ + - Yes Impaired IFNγ response
(autosomal recessive)

IRF8 deficiency Absence of monocytes


- + - Yes
(autosomal recessive) and DC

TYK2 deficiency
- + + Yes Impaired IFNγ response
(autosomal recessive)

Mendelian susceptibility to mycobacterial disease

IFN-γ receptor
+ + + No Impaired IFNγ response
deficiency

STAT1 deficiency
+ + + No Impaired IFNγ response
(autosomal dominant)

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gp91phox deficiency Respiratory burst defect


- + + No
(X-linked recessive) in macrophages

IRF8 deficiency Absence of


- + - No
(autosomal dominant) CD11C+ CD1c+ DC
Impaired CD40-
NEMO deficiency
+ + + No dependent IL-12
(X-linked recessive)
production
IL-12 and IL-12
+ + + Yes Impaired IFNγ response
receptor deficiency

ISG15 deficiency
- + - Yes Impaired IFNγ response
(autosomal recessive)

Conclusion
Despite being very ubiquitous, mycobacterium could be one of the hallmark infections in
immunodeficiency. Immunodeficiency should be considered severe, persistent, recurrent, or
caused by low pathogenicity mycobacterium infection including Mycobacterium bovis.

Keywords
Mycobacterium; Tuberculosis; Primary Immunodeficiencies; Inborn Error of Immunity.

Reference
1. World Health Organization. Global TB report 2023. WHO: Geneve;2024.
2. de Martino M, Lodi L, Galli L, Chiappini E. Immune Response to Mycobacterium
tuberculosis: A Narrative Review. Front Pediatr. 2019;7:350. doi: 10.3389/
fped.2019.00350.
3. Boisson-Dupuis S, Bustamante J, El-Baghdadi J, Camcioglu Y, Parvaneh N, El
Azbaoui S, et al. Inherited and acquired immunodeficiencies underlying tuberculosis in
childhood. Immunol Rev. 2015;264:103-20. doi: 10.1111/imr.12272.
4. Boisson-Dupuis S, Bustamante J. Mycobacterial diseases in patients with inborn errors
of immunity. Curr Opin Immunol. 2021;72:262-71. doi: 10.1016/j.coi.2021.07.001.
5. Errami, A, El Baghdadi J, Ailal F, Behnsain I, OazahrouK, Abel L, et al. Mendelian
susceptibility to mycobacterial disease: an overview. Egypt J Med Hum Genet.
2023;24:7. doi: 10.1186/s43042-022-00358-x.

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Cough: Do We Need Antibiotic?


Suryadi N. N. Taturaa
Tropic and Pediatric Infection Division, Department of Child Health, University of Sam
Ratulangia
R. D Kandou General Hospital, Manado, Indonesiab
E-mail: [email protected]

Cough is the most common complaint of pediatric respiratory diseases leading parents to
bring their children for hospital visits worldwide. It is a protective reflex, under both voluntary
and involuntary control to expulse irritants located on upper or lower respiratory airways.1
It has three phases 1) deep inspiration, 2) glottis closure with diaphragm relaxation and
expiratory muscle contraction, and 3) glottis opening. Beneficial for mucociliary clearance,
but somehow it is frustrating and irritating for both children and parents.1,2
Normally, a healthy child coughs between 10 to 11 times a day, and in postinfectious
conditions could last more than 8 weeks. An abnormal cough associated with an underlying
disease is classified by duration (acute or chronic), timing (day or night), type (wet or dry),
age of the child, and specific etiology.2
According to cough duration, cough is divided into acute (< 3 weeks), subacute (3-8 weeks), and
chronic (>8 weeks).4 But recent guidelines recommend children cough more than 4 weeks as
chronic cough.5 History of fever, parent’s report of choking or children activity before onset, atopic
history, refractory episode, specific symptoms (weight loss, wheezing, post nasal drip, barking
cough), comorbidities (HIV, malnutrition, congenital heart disease) and further supporting
examination (x-ray, chest CT, spirometry, Mantoux, XpertMTB/RIF assay, or bronchoscopy)
according to each clinical approach also needed to differentiate the diagnosis.4,6,7

Figure 1. Cough classification according to duration6

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Acute cough in upper respiratory infections (URTIs) experienced several times a year in
children, is self-limiting and only needs supportive treatment.2 In a study to compare the
effectiveness of antibiotic use with supportive treatment for acute cough revealed that it
could be unnecessary and showed only little benefit in acute cough.3 It spontaneously
resolves within 2-3 weeks without any treatment and antibiotics use are not effective nor
recommended.8 Antibiotic use could be considered in prolonged acute cough that is clinically
appropriate for pertussis infection or bacterial rhinosinusitis.9
Pertussis children above or less than 1 year respectively are recommended to be treated
with macrolide for 3 and 6 weeks.9 In conditions when macrolide resistance is considered,
cefoperazone-sulbactam, meropenem, ampicillin, ceftriaxone, ceftazidime, and trimethoprim-
sulfamethoxazole could be the alternative.10 A metanalysis of acute uncomplicated bacterial
sinusitis revealed a high clinical improvement after antibiotic treatment, moreover in children
with fever and purulent nasal discharge.11 Amoxicillin, amoxicillin-clavulanate, levofloxacin,
cefuroxime, ampicillin-sulbactam, and ceftriaxone are effective for children with bacterial
rhinosinusitis.12
Further investigation to rule out cardiac or gastro-oesophageal reflux in children with chronic
cough is recommended. Targeted antibiotic using amoxicillin-clavulanate for 2 weeks in wet
or productive chronic cough unrelated to an underlying disease or specific symptoms (cough
with feeding or clubbing finger) is recommended (Grade 1A).8
A resolution of cough after antibiotic for more than 2 weeks, presence of airway neutrophilia
with a positive culture of the respiratory pathogen (H. influenzae, S. pneumoniae, and M.
catarrhalis), and normal chest x-ray support the diagnosis of protracted bacterial bronchitis
(PBB). 8,13,14 Amoxicillin-clavulanate is the drug of choice for PBB in children, 2- or 4-week
duration of antibiotic had no significant difference, however, a longer duration of treatment
significantly prolonged the next episode and improved quality of life.14,15
The common cause of cough in children is acute URTIs, therefore early antibiotic use for
cough in children should be considered carefully to prevent inappropriate antibiotic use. A
message of warning signs (tachypnea, progressive cough, and persistent fever) for parents
is recommended.1 Even though the use of honey as an alternative to antibiotics revealed
low-quality evidence, however, it decreased the frequency of cough and improved sleep
quality. It would be better than no treatment for cough, but the risk of botulism should be
cautioned for parents.16

Keywords: Cough; Antibiotic

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References:
1. Kasi AS, Kamerman-Kretzmer RJ. Cough. Pediatr Rev. 2019;40:157-167.
2. Goldsobel AB, Chipps BE. Cough in the pediatric population. J Pediatr. 2010;156:352-8.
3. Zanasi A, Lanata L, Saibene F, Fontana G, Dicpinigaitis PV, Venier V, et al. Prospective
study of the efficacy of antibiotics versus antitussive drugs for the management of URTI-
related acute cough in children. Multidiscip Respir Med. 2016;11:29.
4. Shields MD, Bush A, Everard ML, et al. Recommendations for the assessment and
management of cough in children. Thorax. 2008;63:iii1-iii15.
5. Chang AB, Oppenheimer JJ, Irwin RS; CHEST Expert Cough Panel. Managing Chronic
Cough as a Symptom in Children and Management Algorithms: CHEST Guideline and
Expert Panel Report. Chest. 2020;158:303-329.
6. Marseglia GL, Manti S, Chiappini E, Brambilla I, Caffarelli C, Calvani M, et al. Acute
cough in children and adolescents: A systematic review and a practical algorithm by
the Italian Society of Pediatric Allergy and Immunology. Allergol Immunopathol (Madr).
2021;49:155-169.
7. Fouda, E.M., Shaaban, H.H., Elattar, M.M., Mostafa, A.S., Hamed, D.H., Saleh, A.S.M., et
al. Chronic cough in children: an evidence-based clinical practice guideline adapted for
the use in Egypt using ‘Adapted ADAPTE’. Egypt Pediatric Association Gaz.2024;72:18.
8. Vogelberg C, Cuevas Schacht F, Watling CP, Upstone L, Seifert G. Therapeutic principles
and unmet needs in the treatment of cough in pediatric patients: review and expert survey.
BMC Pediatr. 2023;23:34.
9. Shields MD, Thavagnanam S. The difficult coughing child: prolonged acute cough in
children. Cough. 2013;9:11.
10. Mi YM, Hua CZ, Fang C, Liu JJ, Xie YP, Lin LN, et al. Effect of Macrolides and β-lactams
on Clearance of Bordetella pertussis in the Nasopharynx in Children With Whooping
Cough. Pediatr Infect Dis J. 2021;40:87-90.
11. Shannon J. Conway, Grace D. Mueller, Nader Shaikh. Antibiotics for Acute Sinusitis in
Children: A Meta-Analysis. Pediatrics. 2024;153:e2023064244.
12. Leung AK, Hon KL, Chu WC. Acute bacterial sinusitis in children: an updated review.
Drugs Context. 2020;9:2020-9-3.
13. Gallucci M, Pedretti M, Giannetti A, di Palmo E, Bertelli L, Pession A, et al. When the
Cough Does Not Improve: A Review on Protracted Bacterial Bronchitis in Children. Front
Pediatr. 2020;8:433.
14. Wiltingh H, Marchant JM, Goyal V. Cough in Protracted Bacterial Bronchitis and
Bronchiectasis. J Clin Med. 2024;13:3305.
15. Ruffles TJC, Goyal V, Marchant JM, Masters IB, Yerkovich S, Buntain H, et al. Duration
of amoxicillin-clavulanate for protracted bacterial bronchitis in children (DACS): a multi-
centre, double blind, randomised controlled trial. Lancet Respir Med. 2021;9:1121-1129.

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Early Recognition in Neonate with Critical Congenital Heart Disease:


Clinical Point of View
Tunjung Wibowo
Department of Child Health, Faculty of Medicine, Public Health and Nursing, Universitas
Gadjah Madaa
Sardjito General Hospital, Yogyakarta, Indonesiab
email: [email protected]

Approximately 25% of congenital heart disease is critical congenital heart disease (CCHD)
which requires surgery or catheter-based intervention in the first year of life. Some of the
conditions included in CCHD are ductal dependency and cyanotic lesions and forms of
CHD that may not require surgery during the neonatal period but still require intervention in
the first year of life, such as large ventricular septal defect or atrioventricular canal defect.
Delay in diagnosis and timely referral to a tertiary center increases the risk of morbidity and
mortality. Most CCHDs are symptomatic, however, some of them (4-31%) can be undetected
until discharged from the hospital (1).
Diagnosing the illness will be aided by knowledge of its risk factors. Several conditions have
been proven to increase the risk of CHD. The risk of CHD (excluding isolated patent ductus
arteriosus [PDA]) is two to threefold higher in preterm (gestational age <37 weeks) compared
with term infants. Having parents or siblings with non-syndromic isolated CHD increases
the risk of CHD by three- to fourfold higher than that of the general population. CHD is
also commonly found in patients with genetic syndromes. Several maternal conditions such
as diabetes mellitus, hypertension, obesity, phenylketonuria, thyroid disorders, systemic
connective tissue disorders, and epilepsy have been proven to increase the risk of CHD.
Assisted reproductive technology has been linked to increased risk of CHD. Some congenital
infections may increase the risk of CHD (1,2).
Not all CCHDs have clinical manifestations of cyanosis early in life. The two most frequent
CCHDs with cyanosis as a clinical symptom are Tetralogy of Fallot (TOF) and D-transposition
of the great arteries (D-TGA), both having an incidence of between 0.2 and 0.5 per 1000
infants. Whereas Coarctation of the aorta (COA) is the most prevalent noncyanotic CCHD
(0.2 to 0.6 per 1000 births)(1).
The timing of clinical presentation varies with the underlying lesion and its dependence upon
a PDA. In low- and middle-income countries, approximately 50% of patients have a late
diagnosis. Implementation of pulse oximetry screening has been shown to reduce the delay
in diagnosis by approximately 7 to 10%. The screening study of 39,821 newborns in Sweden
found that neonates in regions without routine pulse oximetry screening were more likely to

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be discharged with undiagnosed duct-dependent CCHD (3). The most commonly reported
delayed diagnoses are COA, interrupted aortic arch, aortic stenosis, hypoplastic left heart
syndrome, transposition of the great arteries, pulmonary valve stenosis, and TOF (1,4).
Early presentation of CCHD can be a serious and life-threatening manifestation including
Shock, Cyanosis, Tachypnea, and other signs of pulmonary edema. The following are
several CCHDs whose clinical manifestation is shock: Hypoplastic left heart syndrome,
Critical aortic valve stenosis, Critical coarctation of the aorta, and Interrupted aortic arch
(1). Ductal-dependent CHD lesions that are associated with right-to-left shunting across
the PDA are characterized by differential cyanosis, in which the upper body is pink, and
the lower body is cyanotic. The sensitivity, Specificity, and Positive Predictive Value pulse
oximetry for early detection of CCHD were 30.8, 99.9, and 80%, respectively (4).
Late presentation of CCHD including feeding difficulties (lethargy and tiring with early
stopping of feeding), respiratory distress and tachypnea, central cyanosis or persistent
pallor, unexplained irritability, excessive sweating that is increased with feeding and may
occur during sleep, poor weight gain, decreased activity, or excessive sleeping(1).

Keywords: Critical congenital heart disease, cyanotic, symptom, sign

Reference
1. Altman CA. Evaluation of suspected critical congenital heart disease (CHD) in the
newborn. UpToDate [Internet]. 2024; Available from: www.uptodate.com
2. Øyen N, Poulsen G, Boyd HA, Wohlfahrt J, Jensen PKA, Melbye M. Recurrence of
congenital heart defects in families. Circulation. 2009;120(4):295–301.
3. Granelli ADW, Wennergren M, Sandberg K, Mellander M, Bejlum C, Inganäs L, et al.
Impact of pulse oximetry screening on the detection of duct dependent congenital
heart disease: A Swedish prospective screening study in 39 821 newborns. BMJ.
2009;338(7687):145–8.
4. Knapp A, Kemper A, Prosser L PJ. Evidence review: critical congenital cyanotic heart
disease. Crit Congenit Hear Dis Final Draft. 2010;2010:1–41.

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Artificial Intelligence and Big Data in Nutrition and Metabolic Disease


Care: Ethical, Privacy, Security, and Bias Issues
Titis Prawitasaria
Department of Child Health, Faculty of Medicine, Universitas Indonesiaa
Dr Cipto Mangukusumo Hospital, Jakarta, Indonesiab
E-mail: [email protected]

1. Introduction
Artificial Intelligence (AI) in healthcare is rapidly growing and can potentially transform how
clinical nutrition and metabolic disease are approached. It is crucial in supporting healthcare
professionals, empowering them to make well-informed decisions regarding their patients'
nutritional needs and disease prevention and management.1,2 However, integrating AI in
nutrition and metabolic disease raises ethical and regulatory issues, including data privacy
and bias concerns.1-3

2. Terminology
Artificial intelligence (AI) is a technology that enables computers and machines to simulate
human learning, comprehension, problem-solving, decision-making, creativity, and autonomy.
To comprehend generative AI entirely, it is essential to understand the technologies on
which generative AI tools are built: machine learning (ML) and deep learning (DL). Machine
learning is an AI system that enables machines to learn from historical data. It applies
computer algorithms to capture behaviour and patterns in systems and processes based
on the input and output data. Inspired by the human brain's structure, DL involves artificial
neural networks with multiple hidden layers to process complex data (Figure 1).1,2,4,5

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Figure 1. Development of Artificial Intelligence1,5

3. Applications of AI in Nutrition and Metabolic Disease


a. Nutritional assessment and administration1,2
Artificial intelligence devices have been developed that could assist nutritional
assessments with unprecedented accuracy. These have been designed to use acoustic
variables, the motion of the jaw, and visual images of chewing and eating. Using these
techniques, DL can help to provide a dietetic assessment. The deep learning could
also enable patients undergoing enteral or parenteral support to undergo regular
assessment. Alongside standard anthropometry, AI is adopted to facilitate identifying
and measuring the appropriate radiological image efficiently. With DL software,
assessing muscle mass in hospitalized patients becomes more accurate. Another
advantage of using AI is that it can resume differential diagnosis for genetic disorders

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and metabolic diseases.


b. Prescribing1,2
Nutritional support prescribing, including enteral and parenteral methods, involves
different formulas and varies widely in their ingredients, with more choices for
parenteral support, including custom-made bags, multi-chamber bags (MCB), and a
combination of them. Machine learning could analyze databases quickly and accurately
to determine the most suitable enteral or parenteral nutrition plan based on a patient's
needs, considering other factors like nutritional status and laboratory tests.
c. Monitoring1,2,6
Patients receiving nutritional support, including those at home, require close monitoring,
including assessments of their physical well-being, biochemical parameters, quality
of life, and nutritional status. AI could coordinate and collate these parameters to
highlight abnormal results to responsible clinicians or prompt patients to attend
relevant appointments. Deep learning could be applied to guide a patient according
to the results of these monitoring investigations or to coordinate appropriate follow-up
appointments in the outpatient setting. Some AI innovations support assessing and
monitoring hydration, early sepsis, and detection of catheter-related bloodstream in
home parenteral support. A recent study developed a self-management application
that helps Maple syrup urine disease (MSUD) patients manage their diet in a way that
is easier, more accurate, and more intelligent than it was with paper records.
Chatbots could play a role in any healthcare service by providing artificial support to
a patient's home, from scheduling to arranging deliveries, filling a repeat prescription,
or promoting healthy eating and lifestyle modifications. Generative AI capabilities will
offer even more enhanced functionality with their understanding of everyday language
and complex queries.
d. Predicting outcomes1,2,7-9
Artificial intelligence algorithms can forecast interactions between drugs and
biological targets. They can use machine learning techniques that consider genetics,
metabolomics, gut microbiome, lifestyle, and environment to offer more precise and
efficient nutritional recommendations tailored to an individual's profile alongside their
lifestyle or environment. AI algorithms can pinpoint factors contributing to developing
specific health conditions and deliver personalized recommendations to mitigate the
risk.

4. Ethical, Privacy, Security, and Bias Issues in AI


The recent document from the Professional Practice Committee of the European Federation
of the Associations of Dietitians (EFAD) on AI ethics highlights the potential "dehumanization"

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of care alongside AI's possible benefits.2,10 Patient-centered communication methods prove


challenging to implement via technology.2 There is also a risk of overestimating promising
tech solutions, leading to further issues.2,3
Considering the privacy of personal data is crucial, thus it needs stringent security and
confidentiality.2,3 Controlling access to an individual's data is vital, and such data must not
be used for discriminatory practices in insurance or employment.2,3 The use of genetic data
introduces further complexities as the underlying mechanisms of predictive algorithms
are often unclear.2,3,9 Ensuring the safety of personal data and protecting human rights
is essential alongside AI implementation. Unauthorized access and misuse of electronic
medical records are additional concerns, with such breaches potentially leading to privacy
violations.2,3 The dynamic nature of health information technology could also leave AI
systems is being "vulnerable".2

Keywords: Artificial Intelligence; Big Data; Nutrition; Metabolic Disease; Privacy;

References
1. Bond A, Mc Cay K, Lal S. Artificial intelligence & clinical nutrition: What the future might
have in store. Clinical Nutrition ESPEN. 2023;57:542-9.
2. Detopoulou P, Voulgaridou G, Moschos P, Levidi D, Anastasiou T, Dedes V, Diplari
EM, Fourfouri N, Giaginis C, Panoutsopoulos GI, Papadopoulou SK. Review Artificial
intelligence, nutrition, and ethical issues: A mini-review. CNOS. 2023;50:46-56.
3. Siau K, Wang W. Artificial Intelligence (AI) Ethics: Ethics of AI and Ethical AI. J Database
Manag. 2020;31(2);74-87.
4. Pettit RW, Fullem R, Cheng C, Amos CI. Artificial intelligence, machine learning, and
deep learning for clinical outcome prediction. Emerg Top Life Sci. 2021;5:729e45.
5. IBM. Design for AI. Available at: https://www.ibm.com. Accessed September 3, 2024.
6. Banjar, H.R. A Smart Monitoring System for Self-Nutrition Management in Pediatric
Patients with Inherited Metabolic Disorders: Maple Syrup Urine Disease (MSUD).
Healthcare. 2023;11:178-95.
7. Warburton JB, Ashton J, Dhar A, Tham T, Allen PB, Hoque S, Lovat LB, Sebastian
S. Review Artificial intelligence and inflammatory bowel disease: practicalities and
future prospects. Frontline Gastroenterology 2022;13:325–31.
8. Qasrawi, R, Sgahir, S, Nemer M, Halaikah M, Badrasawi M, Amro M, Polo SV; AbuAl-
Halawa D, Mujahed D, Nasreddine L, et al. Machine Learning Approach for Predicting
the Impact of Food Insecurity on Nutrient Consumption and Malnutrition in Children
Aged 6 Months to 5 Years. Children. 2024:11;810-26.

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9. Kirk D, Catal C, Tekinerdogan B. Precision nutrition: A systematic literature review.


Comput Biol Med. 2021;133:104365.
10. European Federation of the Associations of Dietitians. EFAD 2022 supplementary
document to the current international Code of Ethics. 2022.

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The Use of Digital Technology in the Diagnosis and Management of


Neurological Disorders in Indonesian Children
Irawan Mangunatmadjaa,b, Setyo Handryastutia,b, Achmad Raflia,b, Amanda Soebadia,b, Dara
Ninggar Santosoa,b, Ivan Riyanto Widjajaa,b, Jennie Dianita Sutantiob, Pandu Caesaria
Lestaria,b, Arifiantoa,b, Hardiono D. Pusponegoroa,b
a
Neurology Working Group of The Indonesian Pediatric Society
b
Faculty of Medicine Universitas Indonesia – Dr. Cipto Mangunkusumo General Hospital,
Jakarta
E-mail: [email protected]

Neurological disorders present a growing global health concern, impacting individuals


across all ages, and poses a particularly significant burden on children. This burden is
acutely felt in limited-resource countries like Indonesia, where access to specialized and
sub-specialized healthcare, diagnostic tools, and treatment options are often limited.
However, the rise of digital technologies offers a promising avenue to bridge these gaps
and improve the lives of children with neurological disorders. This paper examines the
potential of digital technologies to transform the diagnosis and management of neurological
disorders in children within the context of limited-resource countries, focusing specifically
on Indonesia. By exploring the opportunities and challenges presented by telemedicine,
mobile health applications, and artificial intelligence, this paper aims to highlight how The
Neurology Working Group of the Indonesian Pediatric Society (IPS) invented the technology
that can contribute to a more equitable and effective healthcare system for children with
neurological disorders in Indonesia.
The importance of digital technology in facilitating the detection and management
of diseases has significantly increased since the COVID-19 pandemic. During the global
lockdown, numerous healthcare facilities implemented Telemedicine to facilitate medical
consultations between patients and healthcare professionals, which has been particularly
advantageous, not only in diagnosing newly diagnosed diseases and their treatments, but
also in ensuring the continuity of chronic illness monitoring and their respective specialized
medication prescriptions. Our working group has used this strategy since the onset of the
pandemic, benefiting our patients, particularly those with chronic disorders (e.g., epilepsy,
cerebral palsy, etc.) and patients in peripheral or remote regions of Indonesia.
The challenges in diagnosing and managing neurologic disorders stem not only
from the inherent complexities of these conditions, but also from the scarcity of pediatric
neurology consultants and their uneven distribution throughout Indonesia, particularly in
remote regions. Furthermore, Indonesia's geographic archipelago impedes the diagnosis

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and care strategies for our patients. To address this issue, we have established The Pediatric
Neurologic Assistance (Pendampingan Neurologi Anak Indonesia) WhatsApp Group for
general practitioners and pediatricians throughout Indonesia.1 If they encounter challenges
in diagnosing or treating neurologic patients in their areas, they are encouraged to report their
cases in the group chat, where the cases will be discussed and they will receive guidance
on the patient management. Subsequent to the initial treatment, we recommend them to the
nearest pediatric neurologist for additional clinical guidance, if feasible. Biweekly, we host
webinars or discussion sessions for the physicians enrolled in this group.
Alongside the online monitoring system for our patients, we have established a registry
for epilepsy patients that may be completed via an online form. Parents or caregivers of
children with epilepsy were invited to our Epilepsy Support Group (Ruang Peduli Epilepsi
Anak Indonesia), where they can share their experiences, provide mutual support, and
exchange information. We also developed a monitoring diary provided to them.2 In addition,
our epilepsy monitoring diary has been developed into a mobile application, i.e., Epilepsy
Free, which is available for free download in Android and iOS by caregivers.3 Parents or
caregivers were invited into a WhatsApp group, wherein board-certified pediatric neurologists
could be consulted with essential adjustments to antiepileptic drug dosages, should they be
unable to attend healthcare facilities.
Teleconsultations were performed through video calls and WhatsApp. The WhatsApp
application has significantly facilitated our numerous disease-specific teleconsultations and
monitoring efforts. We also established a WhatsApp group for our drug-resistant epilepsy
patients advised for a ketogenic diet, in order to follow their progress and dietary excursions.
Furthermore, we have created a guidebook that functions as both a food diary4 and a recipe
book5 featuring keto-friendly Indonesian meals for parents and caregivers. The copyrights
for these books have been patented and registered.
In the field of neurodevelopment, an alarming trend has emerged in recent years,
with a significant increase in children experiencing speech delays. While the causes
are multifaceted, current investigations indicate the possible influence of the COVID-19
pandemic. This pandemic forced unprecedented social isolation and disrupted early
intervention services during a critical window for language development in young children.
Among the various causes, autism spectrum disorder (ASD) stands out as a prevalent
cause. With regard to this issue, we have developed an online questionnaire, namely
the Kuesioner Keterlambatan Bicara Anakku, which utilizes an scoring system to assist
parents and general pediatricians in conducting online screenings for children's speech
development.6,7 A telemedicine system utilizing protocol-guided video recording assessment

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was also developed, enabling online assessment of speech delay for diagnosing autism
spectrum disorder, based on videos recorded by parents or caregivers.8,9 In addition, for
the children with an established diagnosis of ASD, an online behavioral verbal therapy
training module has been developed for these children and their caregivers. This module
consisted of serial pre-recorded videos, enabling parents and caregivers to conduct distance
learning through our pre-recorded videos and perform the behavioral and verbal therapy at
home.10,11 Furthermore, we consistently utilize social media platforms, including Instagram,
to disseminate pediatric neurology-related health education content through posts from
the official accounts of IPS, Ruang Peduli Epilepsi Anak Indonesia, and several pediatric
neurologists' personal accounts. The contents have been meticulously checked and curated
to guarantee the reliability of information provided to patients and their caregivers.
The integration of digital technology has ushered us in a new era for diagnosing
and managing neurological disorders in children. From sophisticated imaging techniques
that offer unprecedented views into the developing brain to telehealth platforms that bridge
geographical barriers and interactive applications that facilitate personalized therapy, digital
tools are transforming pediatric neurology. As technology continues to advance, we will
anticipate even more innovative applications that will empower clinicians, enhance early
detection, and ultimately improve the lives of children with neurological disorders.

References
1. Ruang Pendampingan Dokter Anak atau Dokter Umum di Daerah Terpencil dalam
bidang Neurologi. Hak Kekayaan Intelektual Kementrian Hukum dan Hak Asasi
Manusia (No. EC002022511378), 2022.
2. Buku Pendampingan Pasien Anak dengan Epilepsi. Hak Kekayaan Intelektual
Kementrian Hukum dan Hak Asasi Manusia (No. EC00202177052), 2021.
3. Aplikasi Epilepsy Free Journey. Hak Kekayaan Intelektual Kementrian Hukum dan
Hak Asasi Manusia (No. EC00202245786), 2022.
4. Buku Panduan Diet Ketogenik (Modified Atkins Diet) untuk Epilepsi Resisten Obat
pada Anak. Hak Kekayaan Intelektual Kementrian Hukum dan Hak Asasi Manusia
(No. EC00202229429), 2022.
5. Buku Kumpulan Menu Diet Ketogenik (Modifiet Atkins Diet) untuk Anak dengan
Epilepsi Intraktabel. Hak Kekayaan Intelektual Kementrian Hukum dan Hak Asasi
Manusia (No. EC00202322994), 2023.

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27 – 28 September 2024 PRE-KONIKA XIX Workshops SOLO


27 – 28 September 2024 KONIKA XIX Organization Meetings SEMARANG
29 September – 01 October 2024 KONIKA XIX Scientific Congress & Exhibition SEMARANG
HARRIS & SWISS-BELINN SARIPETOJO HOTEL-SOLO I PADMA HOTEL-SEMARANG

6. Widjaja IR, Pusponegoro HD, Kaswandani N, Handryastuti S, Gunardi H, Sjakti HA,


Solek P. Anakku Speech-Delay Questionnaire (ASDQ) diagnostic study for autism
spectrum disorder in children age 18 months to 3 years with speech delay [tesis].
[Jakarta, Indonesia]: Universitas Indonesia; 2020.
7. Buku Petunjuk Kuesioner Keterlambatan Bicara Anakku (Anakku Speech Delay
Questionnaire – ASDQ). Hak Kekayaan Intelektual Kementrian Hukum dan Hak
Asasi Manusia (No. EC00202179719), 2021.
8. Sutantio JD, Pusponegoro HD, Sekartini, R. Validity of telemedicine for diagnosing
autism spectrum disorder: protocol-guided video recording evaluation. Telemed J E
Health. 2021;4:427-31.
9. Protokol Rekaman Video Diagnosis Autisme. Hak Kekayaan Intelektual Kementrian
Hukum dan Hak Asasi Manusia (No. EC00202009803), 2020.
10. Lestari PC, Pusponegoro HD, Kaswandani N, Gunardi H, Prayitno A, Soebadi A.
Effectiveness of Teleheatlh Verbal Behavior Therapy in the form of mand and tact
training by parents for children with autism spectrum disorder. [tesis]. [Jakarta,
Indonesia]: Universitas Indonesia; 2023.
11. Video Pelatihan Terapi Perilaku Mand and Tact pada Anak dengan Gangguan
Spektrum Autisme. Hak Kekayaan Intelektual Kementrian Hukum dan Hak Asasi
Manusia (No. EC00202383668), 2023.

166 PROCEEDING BOOK KONIKA XIX

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