Study Guide Tayang Blok Emergency 2017

Study Guide Emergency Medicine September 2017
INTRODUCTION
Emergency Medicine has long been established especially in Australasia, Canada, Ireland,
the United Kingdom and the United States, in Asiaothe emergency medicine officially
inauguration of Asian Society of Emergency Medicine in Singapore on the 24th of October
1998 at the first Asian Conference on Emergency Medicine which as Prof.DR.dr. Eddy
Rahardjo,SpAnKIC and dr. Tri Wahyu Murni sat as member of Board Director.
It is thus sometimes seen to be synonymous with emergency medical careand within the
province and expertise of almost all medical practitioners. However, theEmergency Medicine
incorporates the resuscitation and management of allundifferentiated urgent and emergency
cases until discharge or transfer to the care ofanother physician. Emergency Medicine is an
inter-disciplinary specialty, one which isinterdependent with all other clinical disciplines. It
thus complements and does not seekto compete with other medical specialties.
Basic science concepts to help in the understanding of the phatophysiology and treatment of
disease.The medical curriculum has become increasingly vertically integrated, with a much
greater use of clinical examples and cases to help in the understanding of the relevance of the
underlying basic science, The Emergency Medicine block has been written to take account
of this trend, and to integrate core aspects of basic science, pathophysiology and treatment
into a single, easy to use revision aid.
In accordance the lectures that have been full integrated for studens in 6Th semester,
period of 2012, one of there is The Emergency Medicine Block.
There are many topics will be discuss as below:
Seizure and mental status changes, acute Psychiatric episode, Acute respiratory distress
syndrome and failure, Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding)
,Shock, Cardiac critical care (Cardiac arrest and CPR), Emergency toxicology and poisoning,
Pregnancy induce Hypertension, Shoulder dystocia, Urologic concern in critical care,
Phlegmon, Acute Blistering and Expoliative skin, Trauma which potentially disabling and
Life threatening condition and Basic Clinical Skill
Beside those topics, also describes the learning outcome, learning objective, learning task,
self assessment and references. The learning process will be carried out for 4 weeks (20
days).
Due to this theme has been prepared for the second time, so many locking mill is available
on it. Perhaps it will better in the future
Thank you.
Planner
Medical Education Unit Faculty of Medicine Udayana University 1

CURRICULUM CONTENTS
Mastery of basic knowledge with its clinical and practical implication.
Establish tentative diagnosis, provide initial management and refer patient with :
Seizure and mental status changes
Acute Psychiatric episode
Acute respiratory distress syndrome and failure
Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding)
Shock (adult and pediatric patient)
Cardiac critical care (Cardiac arrest and CPR)
Emergency toxicology and poisoning
Pregnancy induce Hypertension, Shoulder dystocia
Urologic concern in critical and non critical care
Phlegmon
Brain Resusscitation
Acute Blistering and Expoliative skin
Trauma which potentially disabling and Life threatening condition
SKILLS
To implement a general strategy in the approach to patients with critical ill through
history and physical examination and special technique investigations
To manage by assessing, provide initial management and refer patient with critical ill
PERSONAL DEVELOPMENT/ATTITUDE
Awareness to :
Ethic in critical care
Basic principle of critical care
The importance of informed consent to patient and family concerning critical ill
situations
Risk of patient with critically ill and its prognosis
COMMUNITY ASPECT :
Communicability of the critical cases
Cost effectiveness
Utilization of health system facilities
Critical ill patient

PLANNERS TEAM
NO. NAME DEPARTMENT

1. Dr.dr.Tjok Gde Agung Senapathi,Sp.AnKAR Anesthesiology and
(Coordinator) Intensif Terapy
2. Dr.dr. Gd Wirya Kesuma Duarsa, SpU,MKes Urologic Surgery
3. dr. IGN Budiarsa,SpS Neurology
4. dr. Sari Wulan,SpTHT KL ENT
5. Drg. Lestari Sudirman Dentistry
6. Dr.dr. I Putu Pramana Anesthesiology and
Suarjaya,SpAn.M.Kes.KMN.KNA Intensif Terapy
7. Dr.dr. Agus Somya, SpPD. KPTI Internal Medicine
8. dr. Putu Andrika, SpPDKIC Pulmonology
9. Dr.dr.Dyah Kanyawati, SpA(K) Pediatric
10. Dr.dr. Wayan Megadana, SpOG(K) Obstetric-Gynecologic
11. dr. Endang Sriwidiyanti, SpOG Obstetric-Gynecologic
12. Dr.dr. Gede Megaputra, SpOG(K) Obstetric-Gynecologic
13. dr. Wayan Yudiana, SpU Urologic Surgery
14. Dr.dr.Tjokorda Bagus Jayalesmana,SpKJ Psychiatric
15. dr. Nyoman Suryawati, SpKK Dermatology
16. dr. Sri Laksminingsih SpR (K) Radiology
17. dr. IA Sriwijayanti,MBioMed,SpS Neurology
18. dr. IGAG Utara Hartawan,SpAn.MARS Anesthesiology and
Intensif Terapy
19. dr. Nyoman Budihartawan,M.Sc,SpA Pediatrician
20. dr. IGN. Mahaalit Aribawa,SpAn.KAR Anesthesiology and
Intensif Terapy
21. Dr.dr. Ketut Suyasa, SpB. SpOT(K)Spine Ortophedic Surgery
22. dr. IGN. Wien Aryana,SpOT Ortophedic Surgery
23. dr. Wayan Sucipta,SpTHT KL ENT
24. dr. Ida Bagus Krisna Jaya Sutawan,SpAn.M.Kes Anesthesiology and
Intensif Terapy
LECTURERS
NO. NAME DEPARTMENT PHONE

1. Dr.dr.Tjok Gde Agung Anesthesiology 081337711220
Senapathi,Sp.AnKAR (Chairman) and Intensif
Terapy
2. Dr.dr. I Ketut Suyasa, Surgery 081558724088
SpB,SpOT(K)
3. dr. IGN Budiarsa,SpS Neurology 0811399673
4. dr. Sari Wulan,SpTHT KL, dr. ENT 081237874447(SW)
Wayan Sucipta,SpTHT KL 08125318941 (WS)
5. drg. Lestari Sudirman Dentistry 08155764446
6. Dr.dr. I Putu Pramana Anesthesiology 0811394811 (PRAM) /
Suarjaya,SpAn.M.Kes.KMN.KNA and Intensif 08123836470 (KRIS)
& dr. Ida Bagus Krisna Jaya Terapy
Sutawan,SpAn.M.Kes

7. Dr.dr. Agus Somya, SpPD(KPTI) Internal 08123989353

Medicine
8. dr. Putu Andrika,SpPDKIC Pulmonology 08123875875
9. Dr.dr. Dyah Kanyawati, SpA(K) Pediatric 081285705152
10. Dr.dr. Wayan Megadana, SpOG(K) Obstetric- 08123917002
Gynecologic
11. dr. Endang Sriwidiyanti, SpOG Obstetric- 081558314827
Gynecologic
12. Dr.dr. Gede Megaputra, SpOG(K) Obstetric- 08123636172
Gynecologic
13. Dr.dr. Gd Wirya Kesuma Duarsa, Surgery 081338708195 (YUD)
SpU,MKes, dr. Wayan Yudiana, 081338333951 (GWK)
SpU
14. Dr.dr.Tjokorda Bagus Psychiatric 0816295779
Jayalesmana,SpKJ
15. dr. Nyoman Suryawati, SpKK Dermatology 0817447279
16 dr. Sri Laksminingsih SpR (K) Radiology 08164745561
17. dr. IA Sriwijayanti,MBioMed,SpS Neurology 081337667939
18. dr. IGAG Utara Anesthesiology 081138914910
Hartawan,SpAn.MARS and Intensif
Terapy
19. dr. Nyoman Pediatrician 081236333221
Budihartawan,M.Sc,SpA
20. dr. IGN. Mahaalit Anesthesiology 0811396811
Aribawa,SpAn.KAR and Intensif
Terapy
21. Dr.dr. Ketut Suyasa, SpB. Ortophedic 081558724088
SpOT(K)Spine Surgery
22. dr. IGN. Wien Aryana,SpOT Ortophedic 0811385263
Surgery
23. dr. AA Gde Yuda Asmara, SpOT Ortophedic 081337870347
(K) Surgery
24. dr. Made Agus Dwianthara Sueta, Digestive 081338648424
SpB KBD Surgery

FACILITATOR SEMESTER VII

MEDICAL EMERGENCY
Regular Class (Class A)
Venue
No Name Group Departement Phone
(3rd floor)
3rd floor:
1 dr. Komang Ayu Kartika Sari, MPH A1 Public Health 082147092348
R.3.09
Dermato- 3rd floor:
2 dr. Nyoman Suryawati, M.Kes, Sp.KK A2 0817447279
venerology R.3.10
Dr.dr I B G Fajar Manuaba, Sp.OG, 3rd floor:
3 A3 Obgyn 081558101719
MARS R.3.11
3rd floor:
4 Dr. dr. I Wayan Suranadi, Sp.An. KIC A4 Anesthesi 08123847675
R.3.12
dr. Henky, Sp.F., M.Bioethics Forensic 08123988486 3rd floor:

5 B10 R.3.13
3rd floor:
dr. Sri Laksminingsih, Sp.Rad A6 Radiology 08164745561
6 R.3.14
Dr. dr. I Gusti Ayu Sri Mahendra Dewi, Anatomy 3rd floor:
7 A7 081338736481
Sp.PA(K) Phatology R.3.15
3rd floor:
8 dr. I Putu Budhiastra, Sp.M (K) A8 Opthalmology 085238238999
R.3.16
3rd floor:
9 Dr. dr. I Made Oka Adnyana, Sp.S(K) A9 Neurology 0817347697
R.3.17
Dr. dr. I Wayan Putu Sutirta Yasa., Clinical 3rd floor:
10 A10 08123953344
M.Si Phatology R.3.19
Regular English (Class B)
Venue
No Name Group Departement Phone
(3rd floor)
3rd floor:
1 Dr. dr. I Ketut Suyasa, Sp.B. Sp.OT(K) B1 Orthopaedic 087862400166
R.3.09
dr. I Made Putra Swi Antara, Sp.JP(K), 3rd floor:
2 B2 Cardiology 08123804782
FIHA R.3.10
dr. Ni Made Renny Anggreni Rena, Internal 3rd floor:
3 B3 081803651656
Sp.PD Medicine R.3.11
Dr. dr.Elysanti Dwi Martadiani, Sp.Rad 3rd floor:
4 B4 Radiology 081805673099
(K) R.3.12
Anatomy 3rd floor:
5 dr. Herman Saputra. Sp.PA(K) B5 081338981853
Phatology R.3.13
dr. Made Agus Dwianthara Sueta, 3rd floor:
6 B6 Surgery 081338648424
Sp.B-KBD R.3.14
3rd floor:
7 Dr. dr. A.A. Mas Putrawati T., Sp.M(K) B7 Opthalmology 08123846995
R.3.15
dr. I Nyoman Gede Budiana, Sp.OG 3rd floor:
8 B8 Obgyn 08123997401
(K) R.3.16
dr. Dewa Ayu Mas Shintya Dewi, 3rd floor:
9 B9 Anasthesi 085238514999
Sp.An R.3.17
Dr. dr. Made Ratna Saraswati, Sp.PD- Internal 3rd floor:
10 B10 08123814688
KEMD-FINASIM Medicine R.3.19

TIME TABLE
EMERGENCY BLOCK 2017
Regular Class
DAY/DATE TIME LEARNING VENUE CONVEYER
ACTIVITY
1. 08.00- Highlight in Class room Dr.dr. Tjok Gde Agung
Mon, 09.00 Emergency Senapathi, Sp.AnKAR
11 Sept Medicine
2017 (Coordinator)
09.00- Individual Learning -
10.30
10.30- SGD Disc room Facilitators
12.00
12.00- Break
12.30
12.30- Student Project
14.00
14.00- Plenary Class room Dr.dr. Tjok Gde Agung
15.00 Senapathi, Sp.AnKAR
2. 08.00- Lecture 2. Class room dr. IGN Budiarsa,SpS
Tue, 09.00 Status Epilepticus
12 Sept and Other Seizure
2017 Disorders
10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room dr. IGN Budiarsa,SpS
15.00
08.00- Lecture 3. Class room dr. Ida Ayu
09.00 Coma and Sriwijayanti,MBioMed,SpS
Decrease of
Consciousness
09.00- Individual Learning
3. 10.30
Wed, 10.30- SGD Disc room Facilitators
13 Sept 12.00
2017 12.00- Break
12.30
14.00
14.00- Plenary Class room dr. Ida Ayu
15.00 Sriwijayanti,MBioMed,SpS

4. 08.00- Lecture 4. Class room Dr.dr. Tjokorda Bagus

Thu, 09.00 Acute Psychiatric Jayalesmana,SpKJ
14 Sept Episodes
2017 09.00- Individual Learning
10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room Dr.dr. Tjokorda Bagus
15.00 Jayalesmana,SpKJ
5. 08.00- Lecture 5. Class room dr Sari Wulan, SpTHT-
Fri, 09.00 Acute Respiratory KL(K) / dr Wayan
15 Sept Distress Syndrome Sucipta,SpTHT-KL ( and
2017 and Failure ENT Team), dr. Putu
Andrika, SpPDKIC, Dr. dr
Dyah Kanya wati,SpA (K),
dr. Srie Laksminingsih,
SpRad
10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room dr Sari Wulan, SpTHT-
15.00 KL(K) / dr Wayan
Sucipta,SpTHT-KL ( and
ENT Team), dr. Putu
SpRad

ACTIVITY
Mon, 09.00 Bleeding KL(K), dr. Sucipta, SpTHT
18 Sept Disorder(Epistaxis, KL ( and ENT Team)
2017 Hemorrhage In Dr.dr Wayan Megadhana,
Pregnancy) and SpOG(K) (and OBGYN
Airway Team)
Obstruction


10.30
12.00
12.00- Break
12.30
14.00
15.00 KL(K), dr. Sucipta, SpTHT
KL ( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
7. 08.00- Lecture 7. Class room dr. IGAG. Utara Hartawan,
Tue, 09.00 Shock SpAn MARS
19 Sept dr.Nyoman
2017 Budihartawan,MSc,SpA
10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room dr. IGAG. Utara Hartawan,
15.00 SpAn MARS
dr.Nyoman
Budihartawan,MSc,SpA
8. 08.00- Lecture 8. Class room dr. IGN. Mahaalit Aribawa,
Wed, 09.00 Cardiac Arrest and SpAn KAR
20 Sept +
2017 Cardiopulmonary
Resuscitaton
10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room dr. IGN. Mahaalit Aribawa,
15.00 SpAn KAR
9 08.00- Lecture 9. Class room Dr.dr. Agus Somya, SpPD
Fri, 09.00 Emergency KPTI
22 Sept Toxicology and
2017 Poisoning


10.30
12.00
12.00- Break
12.30
14.00
14.00- Plenary Class room Dr.dr. Agus Somya, SpPD
15.00 KPTI

ACTIVITY
10. 08.00-09.00 Lecture 10 Class room Dr.dr. I Gede Mega

Mon, Hypertension In Putra, SpOG(K)
25 Sept Pregnancy
2017 09.00-10.30 Individual Learning -
10.30-12.00 SGD Disc room Facilitators
12.00-12.30 Break
12.30-14.00 Student Project
14.00-15.00 Plenary Class room Dr.dr. I Gede Mega
Putra, SpOG(K)
11 08.00-09.00 Lecture 11. Class room dr. Endang
Tue, Shoulder Dystocia Sriwidiyanti,SpOG
26 Sept
12.00-12.30 Break
14.00-15.00 Plenary Class room dr. Endang
Sriwidiyanti,SpOG
12. 08.00-09.00 Lecture 12. dr. Nyoman Suryawati
Wed, Acute Blistering and Sp.KK
27 Sept Exfoliative Skin
10.30-12.00 SGD Fasilitator
12.00-12.30 Break
14.00-15.00 Plenary dr. Nyoman Suryawati
Sp.KK

13. 08.00-09.00 Lecture 13. Dr.dr. Ketut Suyasa,

Thu, Trauma Which SpB SpOT(K) Spine
28 Sept Potentially Disabling dr. IGN Wien Aryana,
2017 and life Threatening SpOT
Conditions
09.00-10.30 Individual Learning -

10.30-12.00 SGD Disc room Fasilitators
12.00-12.30 Break
14.00-15.00 Plenary Dr.dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien Aryana,
SpOT

ACTIVITY
14 08.00-09.00 Lecture 14. Class room drg. Lestari Sudirman
Mon, Phlegmon Dr.dr. I Pt Pramana
2 Oct Brain Resuscitation Suarjaya, SpAn.MKes,
2017 KMN KNA/dr. IB
Krisna Jaya Sutawan,
SpAn MKes
09.00-10.30 Individual Learning - -
12.00-12.30 Break
14.00-15.00 Plenary Class room drg. Lestari Sudirman
Dr.dr. I Pt Pramana
Suarjaya, SpAn.MKes,
KMN KNA/dr. IB
Krisna Jaya Sutawan,
SpAn MKes
15 08.00-09.00 Lecture 15. Class room Dr.dr. Gede Wirya
Tue, Urologic Concern in Kusuma Duarsa,
3 Oct Critical Care for M.Kes, SpU(K)
2017 NonTrauma Case
09.00-10.30 Individual Learning -

12.00-12.30 Break

14.00-15.00 Plenary Class room Dr.dr. Gede Wirya

Kusuma Duarsa,
M.Kes, SpU(K)
08.00-09.00 Lecture 16. Class room

16 Urologic Concern in dr. Wayan Yudiana,
Wed, Critical Care for SpU
4 Oct Trauma Case
2017 09.00-10.30 Individual Learning - -
12.00-12.30 Break
14.00-15.00 Plenary Class room dr. Wayan Yudiana,
SpU
1 08.00-selesai Basic clinical skill Clinical skill Dr.dr. Ketut Suyasa,

Thu, (1/2) lab SpB. SpOT(K)Spine
5 Oct Basic Trauma Care dr. IGN. Wien
2017 (English Class jam Aryana, SpOT
08.00-11.30 WITA; dr. AA Gde Yuda
Regular class jam : Asmara, SpOT (K)
12.30-15.00 WITA) dr. Made Agus
Dwianthara Sueta,
SpB KBD
2 08.00-selesai Basic clinical skill SMF Dr.dr.Tjok Gde

Fri, (1/2) Anestesiologi Agung
6 Oct CPR dan Terapi Senapathi,Sp.AnKA
2017 (Regular Class jam Intensif R
08.00-11.30 WITA; Dr.dr. I Putu
English Class jam Pramana
12.30-15.00) Suarjaya,SpAn.M.K
es.KMN.KNA
dr. IGN. Mahaalit
Aribawa,SpAn.KA
R
dr. Ida Bagus
Krisna Jaya
Sutawan,SpAn.M.K
es dr. IGAG Utara
Hartawan,SpAn.M
ARS
dr. IGAG Utara
Hartawan,SpAn.
MARS
3 08.00-Finish
Mon, Student Project
9 Oct
2017

4
Tue, Prepare For
10 Oct Examination
2017
Thu,
12 Oct EXAMINATION
2017
NB
Tanggal 20 September 2017 kuliah dr. IGN. Mahaalit Aribawa, SpAn KAR pindah
ke tanggal 26 September 2017
Tanggal 22 September 2017 kuliah Dr.dr. Agus Somya, SpPD KPTI pindah ke
tanggal 20 September 2017
Tanggal 26 September 2017 kuliah dr. Endang Sriwidiyanti,SpOG pindah ke
English Class
ACTIVITY
1. 09.00- Highlight in Class room Dr.dr. Tjok Gde Agung
Mon, 10.00 Emergency Senapathi, Sp.AnKAR
11 Sept Medicine
2017 (Coordinator)
10.00- Student Project -
11.30
11.30- Break
12.00
13.30
13.30- SGD
15.00
15.00- Plenary Class room Dr.dr. Tjok Gde Agung
16.00 Senapathi, Sp.AnKAR
2. 09.00- Lecture 2. Class room dr. IGN Budiarsa,SpS
Tue, 10.00 Status Epilepticus
12 Sept and Other Seizure
2017 Disorders
11.30
11.30- Break Disc room Facilitators
12.00
13.30
13.30- SGD
15.00

15.00- Plenary Class room dr. IGN Budiarsa,SpS

16.00
09.00- Lecture 3. Class room dr. Ida Ayu
10.00 Coma and Sriwijayanti,MBioMed,SpS
Decrease of
Consciousness
3. 11.30
Wed, 11.30- Break Disc room Facilitators
13 Sept 12.00
2017 12.00- Individual Learning
13.30
13.30- SGD
15.00
15.00- Plenary Class room dr. Ida Ayu
16.00 Sriwijayanti,MBioMed,SpS
4. 09.00- Lecture 4. Class room Dr.dr. Tjokorda Bagus
Thu, 10.00 Acute Psychiatric Jayalesmana,SpKJ
14 Sept Episodes
2016 10.00- Student Project
11.30
12.00
13.30
13.30- SGD
15.00
15.00- Plenary Class room Dr.dr. Tjokorda Bagus
16.00 Jayalesmana,SpKJ
Fri, 10.00 Acute Respiratory KL(K) / dr Wayan
15 Sept Distress Syndrome Sucipta,SpTHT-KL ( and
2017 and Failure ENT Team), dr. Putu
SpRad
11.30
12.00
13.30
13.30- SGD
15.00


16.00 KL(K) / dr Wayan
Sucipta,SpTHT-KL ( and
ENT Team), dr. Putu
SpRad

ACTIVITY
6. 09.00- Lecture 6. Class room dr Sari Wulan, SpTHT KL,
Mon, 10.00 Bleeding dr. Sucipta, SpTHT KL
18 Sept Disorder(Epistaxis, ( and ENT Team)
2017 Hemorrhage In Dr.dr Wayan Megadhana,
Pregnancy) and SpOG(K) (and OBGYN
Airway Team)
Obstruction
11.30
12.00
13.30
13.30- SGD
15.00
15.00- Plenary Class room dr Sari Wulan, SpTHT KL,
16.00 dr. Sucipta, SpTHT KL
( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
7. 09.00- Lecture 7. Class room dr. IGAG. Utara Hartawan,
Tue, 10.00 Shock SpAn MARS,
19 Sept dr.Nyoman
2017 Budihartawan,MSc,SpA
11.30
12.00
13.30
13.30- SGD
15.00

15.00- Plenary Class room dr. IGAG. Utara Hartawan,

16.00 SpAn MARS,
dr.Nyoman
Budihartawan,MSc,SpA
8. 09.00- Lecture 8. Class room dr. IGN. Mahaalit Aribawa,
Wed, 10.00 Cardiac Arrest and SpAn KAR
20 Sept +
2017 Cardiopulmonary
Resuscitaton
11.30
12.00
13.30
13.30- SGD
15.00
15.00- Plenary Class room dr. IGN. Mahaalit Aribawa,
16.00 SpAn KAR
9 09.00- Lecture 9. Class room Dr.dr. Agus Somya, SpPD
Fri, 10.00 Emergency KPTI
22 Sept Toxicology and
2017 Poisoning
11.30
12.00
13.30
13.30- SGD
15.00
15.00- Plenary Class room Dr.dr. Agus Somya, SpPD
16.00 KPTI

ACTIVITY
10. 09.00-10.00 Lecture 10. Class room Dr.dr. Gede Megaputra,
Mon, Pregnancy Induce SpOG(K)
25 Sept Hypertension
2017 10.00-11.30 Student Project -
11.30-12.00 Break Disc room Facilitators
12.00-13.30 Individual Learning
13.30-15.00 SGD
15.00-16.00 Plenary Class room Dr.dr. Gede Megaputra,
SpOG(K)

11. 09.00-10.00 Lecture 11. Class room dr. Endang

Tue, Shoulder Dystocia Sriwidiyanti,SpOG
26 Sept
13.30-15.00 SGD
15.00-16.00 Plenary Class room dr. Endang
Sriwidiyanti,SpOG
12. 09.00-10.00 Lecture 12. dr. Nyoman Suryawati
Wed, Acute Blistering and Sp.KK
27 Sept Exfoliative Skin
11.30-12.00 Break Fasilitator
13.30-15.00 SGD
15.00-16.00 Plenary dr. Nyoman Suryawati
Sp.KK
13. 09.00-10.00 Lecture 13. Dr.dr. Ketut Suyasa,
Thu, Trauma Which SpB SpOT(K) Spine
28 Sept Potentially Disabling dr. IGN Wien Aryana,
2017 and life Threatening SpOT
Conditions
10.00-11.30 Student Project -

11.30-12.00 Break Disc room Fasilitators
13.30-15.00 SGD
15.00-16.00 Plenary Dr.dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien Aryana,
SpOT

ACTIVITY
14 09.00-10.00 Lecture 14. Class room drg. Lestari Sudirman
Mon, Phlegmon/ Dr.dr. I Pt Pramana
2 Oct Brain Resuscitation Suarjaya, SpAn
2017 MKes.KMN.KNA/dr.
IB Krisna Jaya
Sutawan, SpAn MKes
10.00-11.30 Student Project - -
13.30-15.00 SGD

15.00-16.00 Plenary Class room drg. Lestari Sudirman

Dr.dr. I Pt Pramana
Suarjaya, SpAn
MKes.KMN.KNA/dr.
IB Krisna Jaya
Sutawan, SpAn MKes
15 09.00-10.00 Lecture 15. Class room Dr.dr. Gede Wirya
Tue, Urologic Concern in Kusuma Duarsa,
3 Oct Critical Care for M.Kes, SpU(K)
2017 NonTrauma Case
10.00-11.30 Student Project -

13.30-15.00 SGD
15.00-16.00 Plenary Class room Dr.dr. Gede Wirya
Kusuma Duarsa,
M.Kes, SpU(K)
09.00-10.00 Lecture 16. Class room

16 Urologic Concern in dr. Wayan Yudiana,
Wed, Critical Care for SpU
4 Oct Trauma Case
2017 10.00-11.30 Student Project - -
13.30-15.00 SGD
15.00-16.00 Plenary Class room dr. Wayan Yudiana,
SpU
1 08.00-selesai Basic clinical skill Clinical skill Dr.dr. Ketut Suyasa,

Thu, (1/2) lab SpB. SpOT(K)Spine
5 Oct Basic Trauma Care dr. IGN. Wien
2017 (English Class jam Aryana, SpOT
08.00-11.30 WITA; dr. AA Gde Yuda
Regular class jam : Asmara, SpOT (K)
12.30-15.00 WITA) dr. Made Agus
Dwianthara Sueta,
SpB KBD
2 08.00-selesai Basic clinical skill SMF Dr.dr.Tjok Gde
Fri, (1/2) Anestesiologi Agung
6 Oct CPR dan Terapi Senapathi,Sp.AnKA
2017 (Regular Class jam Intensif R
08.00-11.30 WITA; Dr.dr. I Putu
English Class jam Pramana
12.30-15.00) Suarjaya,SpAn.M.K
es.KMN.KNA
dr. IGN. Mahaalit
Aribawa,SpAn.KA

R
dr. Ida Bagus
Krisna Jaya
Sutawan,SpAn.M.K
es dr. IGAG Utara
Hartawan,SpAn.M
ARS
dr. IGAG Utara
Hartawan,SpAn.M
ARS
3 08.00-Finish Team
Mon,
9 Oct Student Project
2017
4
Tue, Prepare For
10 Oct Examination
2017
Thu,
12 Oct EXAMINATION
2017
NB
Tanggal 20 September 2017 kuliah dr. IGN. Mahaalit Aribawa, SpAn KAR pindah
ke tanggal 26 September 2017
Tanggal 22 September 2017 kuliah Dr.dr. Agus Somya, SpPD KPTI pindah ke
Tanggal 26 September 2017 kuliah dr. Endang Sriwidiyanti,SpOG pindah ke

ASSESSMENT METHOD
Assessment will be carried out onthe day written according to class calendar. There will be
100 questions consisting mostly of Multiple Choice Questions (MCQ) and some other types
of questions. The minimal passing score for the assessment is 70.Other than the examinations
score, your performance and attitude during group discussions will be consider in the
calculation of your average final score.Final score will be sum up of student performance in
small group discussion (5% of total score) and score in final assessment (95% of total score).
Clinical skill will be assessed in form of Objective structured clinical examination (OSCE) at
the end of semester as part of Basic Clinical Skill Blocks examination.
STUDENT PROJECT
Students have to write a paperwork with topic given by the lecturer. The topic will be
chosen randomly on the first day. Each small group discussion must work on one paperwork
with different tittle. The paperwork will be written based on the direction of respective
lecturer. The paperwork is assigned as student project and will be presented in class. The
paper and the presentation will be evaluated by respective facilitator and lecturer.
Format of the paper :
1. Cover Title (TNR 16)

Name Green coloured cover
Student Registration Number
Faculty of Medicine, Udayana University 2017
2. Introduction
3. Journal critism/literature review
4. Conclusion
5. References
Example :
Journal
Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA
Protection from Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79-
84.

Textbook
Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 4th
ed. Pennysylvania: WB Saunders Co. Pp 1636-1642.
Note.
Minimum 10 pages; line spacing 1.5; Times new roman 12
LEARNING PROGRAMS
Abstracts of Lectures
Lecture 1 : HIGHLIGHT EMERGENCY

DISASTER PREPAREDNESS
Tjokorda Gde Agung Senapathi
Disasters have claimed millions of lives and cost billions of dollars world-wide in the past
few decades. Examples of large-scale disasters include the terrorist attacks of September 11,
2001; the 2004 Pacific Ocean tsunami; the 2010 earthquake in Haiti; the 2011 earthquake
and tsunami in Japan; and Superstorm Sandy of 2012. Emergency physicians frequently have
extensive responsibilities for community and hospital-level disaster preparedness and
response.
DISASTER DEFINITION
The World Health Organization defines a disaster as a sudden ecologic phenomenon

of sufficient magnitude to require external assistance. A disaster is an event that overwhelms
the resources of the region or location in which it occurs. Furthermore, a hospital disaster
may similarly be defined as an event that overwhelms the resources of the receiving hospital.
A hospital disaster may be of any size and is not limited to mass casualty incidents. A single
patient who ingested an organic phosphorous pesticide may overwhelm the resources of a
hospital if that hospital is not prepared to decontaminate external to the ED. A single patient
with suspected small-pox or a single influential patient (e.g., world leader or a celebrity) may
use so many ED resources that it affects the care of other patients.
Whether an event is a disaster further depends on the time of day, nature of the
injuries, type of event, and the amount of preparation time before the arrival of patients. The
ED surge capacity (ability of the ED to care for more patients than is typical) may be
severely limited by hospital overcrowding.
When it appears that the normal procedures of an ED may be interrupted by an event,

there must be policies and procedures in place to activate a disaster response, direct the
mobilization of personnel and equipment, and permit the rapid triage, assessment,
stabilization, and definitive care of victims.
TYPES OF DISASTERS
Disasters are subdivided into several categories (Table 1). External disasters occur at
locations that are physically separate from the hospital (e.g., transportation accident,
industrial accident). An internal disaster is an event that occurs within the confines of the

hospital (e.g., bomb scare, laboratory accident involving radiologic agents, power failure).
Disasters can be both internal and external (e.g., earthquake with mass casualties as well as
damage to the internal hospital).
Table 1 Types of Disarter
Disaster
Definition Examples
Type
Earthquakes,tsunamis,tornadoes,
Natural Disastercausedbyanaturally
hurricanes/typhoons,volcanic
disaster occurringevent
eruption,pandemicinfluenza
Vehiclecrashes(e.g.,car,plane,bus),
Manmade Nonnaturaleventsthatarenot masscasualtyevents,explosions,
disaster purposefullyproduced fires,industrialaccident/chemical
release
Terrorist Eventsthatarepurposefully EventsofSeptember11,2001,aswell

related producedinanefforttocause asintentionalchemical,biological,
disaster terror radiologic,ortoxinreleases
Hazardousmaterialsspillinhospital
Internal Aneventthatoccurswithinthe
laboratory,fireorexplosionwithin
disaster hospital
hospital,powerfailure
External Aneventthatoccursexternalto Transportationaccident,industrial

disaster thehospital accident
Acute Disasterthatoccursinanarrow Explosion,industrialrelease,

disaster andwelldefinedtimeframe earthquake
Disasterwithnowelldefined
Pandemicinfectiousdisease,
Nonacute startpointorcontinuous
incrementalreleaseofabiologicalor
disaster productionofcasualtiesovera
toxin(e.g.,anthraxsentthroughmail)
broadtimeframe
DISASTER CHARACTERISTICS
Regardless of the cause, most disasters have common characteristics that are

important for disaster preparedness and planning. In an acute disaster, or a disaster with an
identifiable time of onset that produces casualties (e.g., explosion, chemical release, fire,
earthquake), the event is followed by a large number of minimally injured patients presenting
to the nearest hospitals, usually without prehospital triage or evaluation. This is typically
followed by prehospital transport of the most affected patients to the same hospitals. Initial
patients can be expected within minutes, and peak volumes can be expected at 2 to 3 hours
after the event. The vast majority (~80%) of patients are not transported by prehospital
agencies, but instead self-transport by car, van, police vehicle, cabs, foot, or any means
available to the nearest ED. Even in acute events, ED volumes tend to remain elevated for
days to weeks after events. In nonacute events, such as a pandemic of an infectious disease,
ED volumes have a slower onset of surge, but ED and hospital volumes remain elevated for
extended periods.
Based on previous events, common factors that may hinder ED response are listed in
Table 2. A large amount of federal funding has been supplied to address these issues, but they
likely remain as the major common limitations to effective ED disaster response.
Table2Factors That May Hinder ED Response to Disasters
PoorcommunicationbetweenEDanddisasterscene
Poorcommunicationwithinthehospital(e.g.,EDtoemergencyoperationscenter,emer
gencyoperationscentertopatientcareareas)
Inability to control volunteer healthcare personnel who are unfamiliar with the ED
functionandtheirrolesindisasterresponse
InabilitytoengageandcontrolconvergenceofmediatotheED
Inabilitytoengage,control,anddirectvisitorswhoaresearchingforlovedonesInability
tocontrollargenumbersofpatients(i.e.,crowdcontrol)
Difficultymaintaininghighstaffingneedsforextendedperiods
DISASTER PREPAREDNESS AND PLANNING
Planning for any type of disaster consists of common elements. A hospital disaster
planning group is responsible for generating the hospitals emergency operations plan.
Include a diverse membership of hospital employees and decision makers. The group should
meet on a regular basis to assess hazards, develop and update short- and long-term disaster
plans, plan exercises and training, and redesign the disaster plan based on evaluations of
exercises and real events.
The general components of the disaster plan include hazard vulnerability analysis,
compliance with agency requirements, hospitalcommunity coordination, integration with
national response assets, and training and disaster drills. Develop specific plans (for
radiation, explosions, mass casualties, decontamination) based on an assessment of the
potential disasters in the area as well as study of the events that would cause the most
disruption to the ED and hospital.
Lecture 2 : SEIZURE AND MENTAL CHANGES DISORDER
STATUS EPILEPTICUS

IGN Budiarsa
Status epilepticus is defined as a continuous or intermittent seizure activity for more than 5
minutes without regaining consciousness. It means the seizure can take the form of
prolonged seizure or repetitive attack without recovery in between. The etiology of status
epilepticus approximately 30% of all cases is caused by withdrawal of anticonvulsant,
cerebrovascular diseases and alcohol withdrawal.
There are various types of status epilepticus and a classification :
(Table below)
Status epilepticus confined to early childhood
1. Neonatal status epilepticus
2. Status epilepticus in specific neonatal epilepsy syndrome
3. Infantil spasms
Status epilepticus confined to later childhood

1. Febrile status epilepticus
2. Status in childhood partial epilepsy syndrome
3. Status epilepticus in myoclonic static epilepsy
4. Electrical status epilepticus during slow wave sleep
5. Landau Kleffer syndrome
Status epilepticus occurring in childhood and adult life

1. Tonic clonic status epilepticus
2. Absence status epilepticus
3. Epilepsia partialis continua
4. Status epilepticus in coma
5. Specific form of status epilepticus in mental retardation
6. Syndrome of myoclonic status epilepticus
7. Simple partial status epilepticus
8. Complex partial status epilepticus
In clinical practice status epilepticus classified :

A. Convulsive status epilepticus
B. Non convulsive status epilepticus
Principle of management of status epilepticus

1. Lifesaving (ABC)
2. Stop seizures immediately
3. Manage in ICU
Lecture 3 : COMA AND DECREASE OF CONCIOUSNESS
IA Sriwijayanti
AIM:
Describe condition of coma and altered states of consciousness, know the current definition
of coma and altered states of consciousness, etiology, mechanism based of altered states of

consciousness, clinical presentation, diagnostic work-up including history, clinical

examination and early management of altered states of consciousness.
LEARNING OUTCOMES:
1. Know current definition of coma and altered states of consciousness
2. Understand and be able explain etiology and mechanism based of coma and altered
states of consciousness
3. Be able to explain a comprehensive history, clinical examination and assessment of
comatose patients and altered states of consciousness.
4. Understand early management of altered states of consciousness
ABSTRACT
Impaired consciousness is among the most difficult and dramatic of clinical
problems. The ancient Greeks knew that normal consciousness depends on an intact brain,
and that impaired consciousness signifies brain failure. The brain tolerates only limited
physical or metabolic injury, so that impaired consciousness is often a sign of impending
irreparable damage to the brain.
Consciousness can be defined by two components: arousal and awareness. Disorders
of Consciousness (DOC) are characterized by disrupted relationship between these two
components. Coma is described by the absence of arousal and, hence of awareness whereas
the vegetative state is defined by recovery of arousal in the absence of any sign of awareness.
In the minimally consciousness state, patient show preserved arousal level and exhibit
discernible but fluctuating signs of awareness.
At the bedside, arousal (also called vigilance or alertness) is observed by looking at
the presence of eye opening. At neuroanatomical level, the level of arousal is mainly
supported by the brainstem and thalami. Awareness, the second component of consciousness,
refers to consciousness perception which include cognition, experience from the past and
present and intentions. At neuroanatomical level, awareness is underpinned by the cerebral
cortex, and mainly through a wide frontoparietal network. Awareness can be further divided
into awareness of the environment and awareness of self. Awareness of the environment can
be defined as the conscious perception of ones environment through the sensory modalities,
whereas awareness of self is a mental process that does not require the mediation of the
senses and is not related to external stimuli for its presence.
Altered states of consciousness may have an organic or functional cause. This
condition represents a spectrum of disease presentations from profoundly depressed arousal
requiring emergent intubation to severe agitation and confusion requiring restraint and
sedation. Initial stabilizing measures are often needed before complete history and physical
examination can be performed (Lee, 2014).
All unconscious patients should have neurological examinations to help determine
the site and nature of the lesion, to monitor progress, and to determine prognosis.
Neurological examination is most useful in the well-oxygenated, normotensive,
normoglycemic patient with no sedation, since hypoxia, hypotension, hypoglycemia and
sedating drugs profoundly affect the signs elicited. Therefore, immediate therapeutic
intervention is a must to correct aberrations of hypoxia, hypercarbia and hypoglycemia.
Medications recently taken that cause unconsciousness or delirium must be identified
quickly followed by rapid clinical assessment to detect the form of coma either with or
without lateralizing signs, with or without signs of meningeal irritation, the pattern of
breathing, the size and reactivity of pupils and ocular movements, the motor response, the
airway clearance, the pattern of breathing and circulation integrity, etc.

Coma may result from a variety of conditions including intoxication, metabolic

abnormalities, central nervous system diseases, acute neurologic injuries such as stroke,
hypoxia or traumatic injuries including head trauma caused by falls or vehicle collisions.
Looking for the pathogenesis of coma, two important neurological components must
function perfectly that maintain consciousness. The first is the gray matter covering the outer
layer of the brain and the other is a structure located in the brainstem called the reticular
activating system (RAS or ARAS), a more primitive structure that is in close connection with
the reticular formation (RF), a critical anatomical structure needed for maintenance of
arousal. It is necessary to investigate the integrity of the bilateral cerebral cortices and the
reticular activating system (RAS), as a rule. Unilateral hemispheric lesions do not produce
stupor and coma unless they are of a mass sufficient to compress either the contralateral
hemisphere or the brain stem (Bateman 2001). Metabolic disorders impair consciousness by
diffuse effects on both the reticular formation and the cerebral cortex. Coma is rarely a
permanent state although less than 10% of patients survive coma without significant
disability (Bateman 2001); for ICU patients with persistent coma, the outcome is grim.
Maneuvers to be established with an unconscious patient include cardiopulmonary
resuscitation, laboratory investigations, a radiological examination to recognize brain edema,
as well as any skull, cervical, spinal, chest, and multiple traumas. Intracranial pressure and
neurophysiological monitoring are important new areas for investigation in the unconscious
patient.
Lecture 4 : ACUTE PSYCHIATRIC EPISODE
Tjokorda Bagus Jayalesmana
Objective:
1. To describe etio-pathogenesis and pathophysiology of acute psychiatric episodes
2. To implement a general strategy in the approach to patients with acute psychiatric
episodes through history and special technique investigations
3. To manage by assessing, provide initial management and refer patient with acute
psychiatric episodes
4. To describe prognosis patient with acute psychiatric episodes
Emergency occur in psychiatric just as we do in every field of medicine. However,

psychiatric emergencies are often particularly disturbing because we do not just involve the
bodys reactions to an acute disease state, as must as actions directed against the self or
others. These emergencies, such as suicidal acts, homicidal delusions, or a serve in ability to
care for oneself, are more likely than medical ones to be sensationalized when they are
particularly dramatic or bizarre. Frequently identified medical causes of abnormal behavior
include hypoglycemia, hypoxia, seizures, head trauma, and thyroid abnormalities. Patients
should also be assessed for the presence of delirium or dementia, as both have potentially
treatable causes.
Psychosis is difficult term to define and is frequently misused, not only in the
newspaper, movies, and on television, but unfortunately among mental health professionals
as well. Stigma and fear surround the concept of psychosis and the average citizens worries
about long-standing myths of mental illness, including psychotic killers, psychotic rage, and
equivalence of psychotic with the pejorative term crazy. Aggressive and hostile symptoms
can overlap with positive symptoms but specifically emphasize problems in impulse control

History and physical examination, including a neurologic and mental status

examination, may be sufficient to determine whether the patient has an acute psychiatric
illness. However, any abnormality noted from the history and physical exam warrants further
evaluation and treatment looking for a medical etiology. Once medical issues have been
addressed, patients with presentation of psychosis, depression, anxiety, suicidal, or homicidal
ideation need an appropriate psychiatric evaluation and disposition. Clinical judgment is
often necessary to determine the need for admission in patients with chronic suicidal or
homicidal ideation, and patients with other psychiatric illnesses and the potential inability to
care for oneself.

LECTURE 5 : ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE
Putu Andrika
ARDS is an emergency in the lung area due to disturbance in alveolocapiler

membrane permeability by a number of thing causing liquid accumulation/build up inside
alveoli or bronchus oedema. While ARF is a kind of ARDS complication which is a
distability of lung to do respiration function causing accumulation of CO 2 and decrease in O2
inside the artery. Incident of ARDS is high. In the USA, 150.000 cases were found per year
and 50% of them died due to breathing failure.
Diagnosed based on : complaint, sudden breathing difficulties, coughing, tiredness
and decrease in consciousness and usually preceded by basic illness and triggering factors.
On the thorax photo it was found infiltrate diffuse in the two lungs region, while in ARF
depend on basic illness. The important thing is examination of blood gas analyses where
there is a decrease on PaO2 until below 50 and PaO2 above 50 or refer to as rule of fifty.
Principle of procedure is to give the Oxygen, CO2 removal either with or without
ventilator, liquid restriction, clearing of breathing pathway, overcoming obstruction using
bronchodilator, etc.
Learning Objective
Students are able to describe pathogenesis, to set diagnoses, propose examination, give
medication and evaluate ARDS and ARF patients.

ACUTE UPPER AIRWAY OBSTRUCTION
Wayan Sucipta,
Abstract
Acute upper airway obstruction is a life-threatening emergency that requires
immediate intervention. Airway obstruction can be the result of a variety of disorders,
including trauma, neoplasm, infection, inflammatory process, neurologic dysfunction,
presence of a foreign body, hemorrhage, and anatomic condition. Affected sites can include
the oral cavity, oropharynx, hypopharynx, larynx, and trachea. Presentation of the symptom:
dyspnea, stridor, chest retractions, tachypnea and tachycardia, hoarseness. Physical
examination: mirror or fiberoptic laryngoscopy should be performed. The chest should be
examined visually and by auscultation. Vital sign should be determined. Pulse oximetry is
also useful for measures arterial oxygen saturation. Laboratory: Arterial blood gases should
be obtained. Imaging studies: chest or soft tissue neck radiographs, sometime need CT
Scan. Management: Acute upper airway obstruction can cause respiratory distress. The
dicision to use a particular approach depends upon numerous factors, including the degree,
cause, location, and evolution of the obstruction. See the figure:

NEONATAL RESUSCITATION and ELECTROLITE IMBALANCE
Diah Kanyawati
Abstract
Ninety percent of asphyxia insults occur in the antepartum or intrapartum periods a a result
of placental insufficiency. After delivery, the babys ineffective respiratory effort and
decrease cardiac output. Hypoxic tissues begin anaerobic metabolism, producing metabolic
acids that are initially buffered by bicarbonate.
The incidence of perinatal asphyxia usually related to gestational age and birth weight. The
basic goal of resuscitation are : to expend the lungs and maintain adequate ventilation and
oxygenation, to maintain adequate cardiac output and tissue perfusion. Neonatal resuscitation
equipment and emergency medications should be immediately available.
RADIOLOGY
Srie Laksminingsih
Learning Objective
At the end of meeting, the student will be able to :
1. Describe the radiology imaging of thorax photo for IRDS (Idiopathic Respiratory
Distress Syndrome) case, Bronchopneumonia, CHD, Pericardial Effusion, Lung
Edema, Pneumothorax, Pleural Effusion, Vena Cava Superior Syndrome.
2. Describe the imaging of abdominal plain photo in : Illeus Obstruction, Paralytic
Illeus, Stone in the Urinary Bladder, Peritonitis, NEC, Cholelithiasis & Acute
Cholecystitis.
Lecture 6 : BLEEDING DISORDER
HEMORRHAGE IN PREGNANCY : ANTEPARTUM AND POST PARTUM
Wayan Megadhana
ANTEPARTUM HEMMORRHAGE
COMPETENCE
Manage pregnancy with Placenta previa and abruption placenta
Placenta Previa
Definition
A condition where the placenta intrudes the lower uterine segment, which resulted in it
covering the internal uterine os partialy or completely during the 20th week of pregnancy or
further.
Classification
Classification:
Placenta previa: the placenta covers the internal oral ostium partially or completely.

Low placenta: placenta implanted in the lower uterine segment where the placental tip does
not reach the edges of the internal uterine os and there is peripheral spacing of more than 2
cm around the internal uterine os. Formerly called marginal placenta previa.
Epidemiology
Incidence of Placenta previa is 1 in 300 - 400 deliveries.
Etiology is still unknown, incidence increases with age, multiparity, parity, history of
cesarean section, smoking.
Pathophysiology
The low-lying placenta is present in 28% of pregnancies <24 weeks, as the lower uterine
segment is not established. In accordance with the enlargement of the upper segment of the
uterus and the formation of the lower uterine segment, the placenta will move its position
upward (placental migration). Thus, ultrasound should be repeated at 32-34 weeks of
pregnancy.
Risk of maternal and fetal: postnatal bleeding, anesthesia and surgical complications, air
embolism, postpartum sepsis, placenta accreta, recurrence 4-8%, prematurity, IUGR,
congenital malformation, malpresentation, fetal anemia.
Initial bleeding is mild, recurrent bleeding is more severe and can lead to shock, early
bleeding in general occurs at 33 weeks. At bleeding in <32 weeks, beware for infection of the
urine tract, vaginitis and cervicitis
Diagnosis
Bright red vaginal haemorrhage without any pain in the second or third trimester of
pregnancy, with peak incidence in 34 weeks of pregnancy.
Speculum examination, palpation of fornices and internal examination on the operating
table (double set up)
Sterile internal examination should not be done.
Ultrasound, a quick and standard examination to determine the location of the placenta.
MRI
Management
Abdominal termination in case of massive vaginal bleeding or life threatening condition
especially for mother and fetus
If the fetus is preterm and there is no persistent active bleeding, conservative management
with close observation in the obstetric room.
Tocolytic therapy is administered up to 48 hours after admission.
For pregnancies approaching full term without bleeding, make schedule for cesarean
section.
Elective SC at 37th weeks of pregnancy, vertical incision is recommended.
Special attention to placenta previa in post SC wound scarring for possible placenta
accreta / increta / percreta (incidence increases 30%)
Solusio Placenta (placenta abruption)
Definition
Detachment of placenta partially or completely from its normal implant site on the uterine
wall after 20th weeks of gestation and prior to delivery.
Epidemiology

Incidence increases in accordance to advanced maternal age, multiparity, history of

maternal shock, poor nutrition, hypertension, chorioamnionitis, sudden decompression after
ruptured membranes in overdistended uterus such as twin and polyhydramnios, abdominal
trauma, external cephalic versus circular placenta, folic acid deficiency, Compression of the
inferior vena cava and lupus anticoagulant. In smoker and cocaine users, decidual necrosis
on the edge of the placenta.
5-17% recurrence after 1 episode in previous pregnancy and 25% after 2 previous episodes
of pregnancy.
Pathophysiology
The primary etiology is still unknown.
The risk of hypovolemic shock, acute renal failure, DIC, postnatal bleeding and
fetomaternal haemorrhage.
Predisposing factors
- Demographic factors
- Hypertension and preeclampsia
- Premature rupture of membranes
- Smoking
- Cocaine
- SLE
- Thrombophilia
- Mioma uteri
- A previous placenta abruption
Diagnosis
Placental abruption has a rapid onset with abdominal pain, vaginal bleeding and tenderness.
Clinical symptoms are often followed by increased contraction and persistent hypertonia.
Clinical symptoms: fetal tachycardia / IUFD, Virchow's triad of focal or common uterine
pain, increased tone, and vaginal bleeding (85%), 15% in concealed type. Ultrasound: helps
in concealed types which is retroplacental sonolucent areas, placental site to differentiate
with placenta previa.
Management
Management of placental abruption depends on clinical conditions, gestational age and
amount of bleeding.
Perform blood / fluid resuscitation as needed
If the fetus dies or not mature enough to live outside the uterus, vaginal delivery may be
considered.
Cesarean section, respond time is important for perinatal outcome.
POSTPARTUM HEMMORRHAGE
COMPETENCE
1. Management of postpartum hemorrhage
Definition and classification

Postpartum hemorrhage (PPS) is generally defined as blood loss from the genital tract of >
500 ml after vaginal delivery or > 1000 ml after delivery by cesarean section. This limitation
has become difficult, given the estimated loss of blood is usually not as much as it actually
is, sometimes only half from the truth. The blood mixes with amnionic fluid or with urine.
Blood is also absorbed by sponges, towels, and cloths, in buckets and on the floor. Therefore,
an estimated loss of blood that exceeds "average" or 500 mL should be an obstetric concern
for the possibility of excessive bleeding.
Postpartum hemorrhage may be minor (500-1000 ml) or major (> 1000 ml). Major bleeding
can be divided into moderate (1000-2000 ml) or heavy (> 2000 ml). Postpartum hemorrhage
may be caused by four factors: weakness of uterine tone to stop bleeding from placental
insertion (tone), rupture of the perineum, vagina, to uterine lining (trauma), placental remains
or blood clots that block adequate uterine contractions (tissue), and clotting factor disorders
(thrombin).
Postpartum hemorrhage is divided into 2, namely:

1. Primary postpartum haemorrhage: postpartum haemorrhage occurring within the first 24
hours of labor.
2. Secondary postpartum haemorrhage: postpartum haemorrhage occurring after the first 24
hours of labor
Predisposing factors
- Placental abnormalities
Placenta previa
Placental Solution
Placenta adhesiva
Ectopic pregnancy
Hydatidiform mole
- Trauma of the birth canal

Episiotomy
Obstetric surgery
Sectio cesarea
Hysterectomy
uterine rupture
- Obstetric factors
Obesity
Previous post-natal bleeding
Sepsis syndrome
preeclampsia
- Atonia uteri
Overdistention
Labor induction
Abnormal labor
- Concomitant coagulopathy
Placental Solution
IUFD
Massive transfusion

Etiology
1. Primary postpartum hemorrhage is often caused by placental retention, laceration of birth
canal, rest placenta, uterine atony, uterine inversion, uterine rupture, clotting disorders.
2. Secondary postpartum bleeding is often caused by rest placenta, from a former cesarean
section, infection / endometritis.
General prevention and treatment

Although efforts have been made to prevent postpartum bleeding, eventually some women
still require therapy for excessive bleeding. Multiple interventions (medical, mechanical,
invasive surgery, and non-surgical) that require different techniques and skills may be needed
to control the bleeding. Effective postpartum bleeding therapy often requires simultaneous
multidisciplinary interventions. Health workers should start resuscitation efforts as soon as
possible, establish the cause of the bleeding, seek other departments healthcare workers,
such as obstetrics, anesthesia and radiology. Avoiding delays in diagnosis and therapy will
have a significant impact on sequelae and prognosis (life expectancy).
If postpartum hemorrhage occurs, the first cause of bleeding should be determined first, then
the management is performed simultaneously, including the repair of uterine tone, evacuation
of residual tissue, and open wound suture accompanied by preparation of clotting factor
correction. The following stages of PSS management can be abbreviated as
HAEMOSTASIS.
Bleeding is usually caused by tone, tissue, trauma or thrombin. If uterine atony develops,
repair the uterine tone. If the cause of bleeding comes from the tissue, do evacuate the
remaining tissue of the placenta. Conduct an open wound suture in case of trauma and
clotting factor correction if there is interference with the thrombin.
Management is done with the principle of "HAEMOSTASIS", namely:

- Ask for HELP
Immediately request help or be referred to the hospital if the birth is midwife / public health.
The presence of obstetricians, midwives, anesthesiologists, and hematologists is very
important.
- Assess (vital parameters, blood loss) and Resuscitate
It is important to immediately assess the amount of blood that comes out as accurately as
possible and determine the degree of hemodynamic change. The value of the level of
consciousness, pulse, blood pressure, and when facility permits, oxygen saturation should be
monitored.
When installing an intravenous line with a 14G-16G albocath, immediate blood samples
should be taken to check for hemoglobin, clotting profiles, electrolytes, blood type
determination, and crossmatch
- Establish Etiology, Ensure Availability of Blood, Ecbolics (Oxytocin, Ergometrin or
Syntometrine bolus IV / IM)
While resuscitation is ongoing, attempts are made to determine the etiology. Evaluate uterine
contractions, look for free fluid in the abdomen, if there is a risk of trauma (former cesarean
section, difficult artificial delivery) or when the patient's condition is worse than the amount
of blood coming out.
When placental retention occurs after vaginal delivery, uterine tamponade may be conducted
while waiting for surgery / laparotomy
- Massage the uterus
Massive bleeding that occurs after the birth of placenta should be treated promptly with
uterine massage and uterotonic drug delivery. If the uterus remains soft, internal bimanual

compression should be performed using the fist inside to suppress the anterior fornix so that
it is pushed upward and the outer palm presses on the back of the fundus so that the uterus is
compressed.
- Oxytocin infusion / prostaglandins - IV / per rectal / IM / intramyometrial
40 units of Oxytocin in 500 cc of normal saline can be administered with the speed of 125 cc
/ hour. Avoid excess fluid because it can cause pulmonary edema to cerebral edema which
can eventually cause seizures due to hyponatremia.
Administration of ergometrine as a second line of oxytocin may be given intramuscularly or
intravenously. Initial dose is 0.2 mg (slowly), additional dose of 0.2 mg can be given after 15
minutes if still needed. The dosage may be repeated every 2-4 hours if necessary.
- Shift to theater - exclude retained products and trauma / bimanual
If massive bleeding persists, immediately evacuate the patient to the operating room. Ensure
examination to exclude any residual placenta or amniotic membrane. If there is suspicion of
remaining tissue, do the curettage action immediately. Bimanual compression can be done as
long as the mother is taken to the operating room
- Tamponade balloon / uterine packing (conservative, non-surgical)
If bleeding persists, consider the possibility of coagulopathy accompanying refractory atony.
Uterine tamponade may help reduce bleeding. This action can also allow for freezing factor
correction. Tamponade test can be done by using Tube Sengstaken which has a positive
predictive value of 87% to assess the success of management Postpartum hemmorrhage.
- Apply compression sutures - B-Lynch / modified (conservative surgery)
In making decisions, consideration between sustaining life and the desire to maintain fertility
should always be made. Before attempting any conservative surgical procedure, the patient
should be reassessed based on the estimation of the amount of blood coming out, ongoing
bleeding, hemodynamic state, and parity.
- Systematic pelvic devascularization - uterine / ovarian / quadruple / internal iliac

Ligation a. Uterine and ligation a. Hypogastrics
- Interventional radiologist, if appropriate, uterine artery embolization
- Subtotal / total abdominal hysterectomy
.
EPISTAXIS
SARI WULAN
ENT TEAM
Objective
Able :
1. To explained anatomi, histologi and phisiology of the nose
2. To explained etiology that cause epistaksis
3. To explained patophisiology & the simtomp of epistaksis
4. To explained and choose the adding examination ( lab, x-ray, nasoendoscopi)
5. To make diagnosis base on phisical diagnostic
6. To explained the therapy of epistaksis
7. To do work-up to epistaksis
Abstract

Epistaksis is one of emergency case in ENT field, that can be fatal if not threaten well. The
bleeding comes from the nose n mouth, because epistaksis caused by an alteration of normal
hemostasis whitin the nose. Hemostasis is compromised by mucosal abnormalities, vessel
pathology or disorders of coagulation. Etiology of epistaxis may be local or systemic. The
local epistaxis commonly causes by mild trauma, climate changing, infection. The systemic
can be caused by systemic ds, ex. hypertension, malignancy, dengue fever, hemophilia.
Epistaksis mostly can stopped spontaneously, only 1-2% patient must be refered to hospital.
Management of epistaxis is stop the bleeding, avoid complication treatment of initial
disorders.
Gambar 1. Vaskularisasi septum nasi

Tabel 1. Etiologi epistaksis
Penyebab lokal Penyebab sistemik

Sering Jarang Sering Jarang
Trauma wajah Mukosa kering Hereditary Hemorrhagic Tuberkulosis
Mengorek hidung Inhalasi kimiawi Telangiectasia (HHT) Mononukleosi
Benda asing Barotrauma Leukemia s
Perforasi septum Sinusitis Trombositopenia Demam
Deviasi atau spina septum Rinitis Anti platelet (aspirin, scarlet
Polip hidung Lesi metastatik clopidogrel) Demam
Tumor sinonasal Angiofibroma juvenil Polisitemia vera reumatik
Tumor nasofaring Iritasi lingkungan Anemia aplastik Sifilis
Hemangioma hidung Hemofilia Penyakit
Obat antikoagulan hepar
(heparin, warfarin) Uremia
Defisiensi vitamin K ISPA
Penyakit Von Willebrand
Penanganan :
Penekanan pada cuping hidung selama 15 menit, disertai kompres es di bagisn
pangkal hidung. Bila perdarahan berlanjut, dapat dipasang tampon anterior. Persiapan alat
meliputi lampu kepala, speculum hidung, pinset, alat penghisap (suction) hidung, alat kauter
dan tampon hidung (kassa pita)
Gambar 2. Pemasangan tampon pita pada epistaksis


ALGORITME EPISTAKSIS
EPISTAKSIS
-Anamnesis riwayat penyakit, tentang perdarahan,

riwayat trauma, penggunaan obat2an, kebiasaan
merokok/ alkohol Syok hipovolemik, penderita
-Pemeriksaan klinis/ Laboratorium tua, risiko perdarahan profus Resusitasi cairan
Identifikasi lokasi perdarahan (rinoskopi anterior, nasoendoskopi rigid/ fleksible):

-Anterior
-Posterior
-Lokasi perdarahan tidak jelas
-Evaluasi dan terapi kausa

Tindakan lokal menghentikan perdarahan: untuk mencegah kekambuhan
-kauter (kimiawi/ elektrik) Berhasil -Edukasi &self care penderita
-tampon hidung ( anterior & posterior) untuk mencegah kekambuhan
Tidak ada
perdarahan lagi
Tidak berhasil
Berhasil
Angkat tampon
Tampon hidung ulang 48-72 jam
Perdarahan tidak berhenti Perdarahan

berulang
Identifikasi kausa
Gangguan faal
perdarahan
Intervensi pembedahan:
-Septum koreksi
-Ligasi arteri karotis eksterna
-Ligasi arteri maksillarisinterna
-Ligasi arteri sfenopalatina
-Ligasi arteri etmoidalis
Embolisasi arteri maksilaris & cabangnya
Radiasi (kasus-kasus malignansi) Berhasil
Kasus HHT (Laser, fibrin glue, nasal obliterasi)
Konsultas-rawat bersama Hematologis-onkologis:

Koreksi gangguan koagulopati:
-FFP - vit K
-cryprecipitate -trombosit
Penatalaksanaan dengan fibrin glue

LECTURE 7 : SHOCK IN ADULT
IGAG Utara Hartawan
OBJECTIVE
1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patient's approach to shock through symptoms,
physical examination and special technique examination.
3. Able to perform assessment, differential diagnosis, provide early treatment and refer
patients with shock
4. Knowing the patient's prognosis with shock
INTRODUCTION
Shock is a clinical expression of circulatory failure that results in inadequate cellular
oxygen utilization. Shock is a common condition that often occurs in critical conditions,
which occurs in more than one-third of patients treated in intensive care. The diagnosis of
shock can be established based on clinical, haemodynamic and biochemical criteria, which
can generally appear in 3 forms. The first is arterial hypotension, but the magnitude of
hypotension can vary widely, especially in patients with chronic hypertension. Typically, in
adults, the systolic arterial pressure is less than 90 mmHg or an average arterial pressure less
than 70 mmHg, with tachycardia. Secondly, there is a clinical sign of tissue hypoperfusion,
seen through the three "Windows" of the body: skin (cold and moist skin, with
vasoconstriction and cyanosis), kidney (urine output <0.5 ml per kilogram body weight per
hour), and neurologic (changed mental state, which usually includes obtundation,
disorientation, and confusion). Third, accompanied by conditions of hyperlactatemia, which
indicate abnormal cellular oxygen metabolism (> 1.5 mmol per liter). Shocks are classified
as: hypovolemic, cardiogenic, obstructive and distributive.
PATHOPHYSIOLOGY
Shock may originate from four conditions of pathophysiological mechanisms:
hypovolemia (from internal or external fluid loss), cardiogenic factors (eg, acute myocardial
infarction, end-stage cardiomyopathy, advanced heart valve disease, myocarditis, or cardiac
arrhythmias), obstructive (eg embolism Lung, cardiac tamponade, or tension pneumothorax),
and distributive factors (such as severe sepsis or anaphylaxis with the release of
inflammatory mediators). The first three mechanisms are characterized by low cardiac output
and, therefore, inadequate oxygen transport. In distributive shocks, the major deficits are
located on the peripheral, accompanied by decreased systemic vascular resistance and
oxygen extraction disorders. Usually, in such cases cardiac output increases, although it may
be low due to associated myocardial depression. Patients with acute circulatory failure often
have this combination. For example, patients with distributive shock from severe
pancreatitis, anaphylaxis, or sepsis also experience hypovolemia and cardiogenic shock in
the form of myocardial depression.
The three main factors that determine the delivery of oxygen to the tissues are
cardiac output, defined as the stroke volume of heart rate; oxygen saturation bound to Hgb
/ O2 X100 capacity and the amount of dissolved oxygen in the blood, defined as O2
content (ml/dl blood) = ( Hgb x 1.39 X% sat O2 + (0.003 x PaO2).
Any or all of these factors may be disrupted resulting in a decrease in the release of
oxygen to tissue levels in the vital organs. The result of a disturbance in these vital organs is

called shock. Shock begins with a simple state, to the very severe state of the imbalance
between the supply and the need for oxygen.
Hypovolaemia leads to increased activity of baroreceptor of the aortic arch and
carotid. There is also an increase in baroreceptor activity in the right atrium. The activity of
the sympathetic nervous system increases and results in stimulation of the heart and
peripheral vasoconstriction. The pituitary gland releases ACTH and ADH, resulting in
increased cortisol levels in the blood and sodium and water retention. Increased adreno-
cortical activity was soon followed by epinephrine and norepinephrine release. Increased
plasma renin-angiotensin-aldosterone results in greater water and sodium retention and
peripheral vasoconstriction occurs more severely. As the hypovolemia weighs up, the
compensation mechanism becomes lost and the organ functional disorder becomes more
severe.
In addition, the vasoactive hormone is released during shock syndrome, such as
prostaglandin, histamine, bradykinin, serotonin, -endorphin, MDF (myocardial depressant
factor) and cachectin. All of these substances will affect the perfusion of internal organs and
may increase the permeability of blood vessels and myocardium and platelet function.
SYMPTOMPS
Hypotension and vasoconstriction appear in hemorrhagic shock, hypovolemic shock
and cardiogenic shock due to decreased perfusion and abnormalities of vital organs. Where
there is a change of the regional vascular resistance thereby reducing the perfusion pressure,
thus perfusion to the vital organs can be maintained. In general, the skin becomes cold, moist
and wrinkled. Superficial veins will collapse. Brain circulation is also disrupted as well as
skin and other organs, which can lead to classic symptoms of confusion and disorientation.
Cerebral perfusion pressure is the difference between mean arterial pressure and intracranial
pressure or right atrial pressure, which is higher (CPP = MAP - ICP). Brain auto regulation is
still good at mean arterial pressure between 50 mmHg and 150 mmHg with a rightward shift
in chronic hypertension. In hypotension that accompanies shock occurs mental status
changes ranging from agitation, anxiety accompanied by feelings of hovering, then going
into a coma. This occurs due to the decrease of cerebral perfusion below the critical value.
Of course the patient's response will be clear and appropriate after resuscitation action to
improve the hemodynamic state in shock.
Table 1. Early symptoms on shock
Organ System Clinical signs / symptoms Cause
CNS Decrease of conciousness Decrease in CPP
CVS Tachycardia The Adrenergic Stimulus
Dysrhythmias Ischemic Coronary
Hypotension Decreased contractility,
MDF ischaemia, or RVF,
also decreased SVR or
preload
Murmurs Valvular dysfunction
JVP increase / decrease Decrease in volume /
preload or RV failure
Respiration Takipneu Pulmonary edema,

respiratory muscle failure,

sepsis, acidosis, hypoxemia
Renal Oliguria Decreased perfusion,
constriction of afferent
arterioles
Skin Cold, pale, sweat Vasoconstriction,
sympathetic stimulation
Other Lactic acidosis Anaerobic metabolism
Fever Infection of hepatic
dysfunction
CNS=central nervous system; CVS=cardiovascular system; CPP=cerebral perfusion

pressure; MDF=myocardial depressant factor; RVF=right ventricular failure;
SVR=systemic vascular resistance.
The state of shock will affect the heart. Coronary perfusion pressure (pressure
difference between diastolic pressure and left ventricular diastolic end pressure) will
decrease due to hypotension and shock. Tachycardia or bradycardia reflex will also decrease
diastolic filling of the coronary arteries. A decrease in mean arterial pressure is an important
sign due to decreased systolic blood pressure; Peripheral vascular pressure increases and
cardiac output decreases.
In septic shock where cardiac output increases and systemic vascular resistance
decreases, heat, seizures and blood cell count are often elevated in this state. The pulse
becomes fast and not palpable. Increased left ventricular diastolic end pressure may result in
pulmonary edema and respiratory failure that may occur along with hypoxemia. If diastolic
pressure decreases, coupled with increased LVEDP (left ventricle end-diastolic pressure)
indicates coronary hypo perfusion and myocardial ischemia. Diastolic blood pressure is
directly related to arterial vasoconstriction, whereas pulse (systolic-diastolic) is associated
with large stroke volume and number of aortic branches and aortic stiffness. Systolic blood
pressure reflects all combinations of these factors. In cardiogenic shock that may be due to
chronic heart failure (CHF), shortness, tachypnea, pulmonary edema with a decrease in PaO2
and the sound gallop or the third heart sounds (S3 gallop).
The renal auto regulation system is also maintained, but with decreased perfusion due
to hypotension, decreased glomerular filtration, which is clinically known as oliguria (<25-
30 ml / hr / 70 kg). In this situation there will be redistribution of cortical renal blood flow to
the medulla and urine becomes more concentrated. Sodium urine decreased <10 mEq / L.
The presence of oliguria is one sign of shock, and urine repair is an important key in
successful resuscitation in shock patients. Sometimes a lot of urine production occurs in
renal failure and is confusing at the start of the diagnosis, especially in kidneys with normal
or increased urine production.
Integumentary systems are also affected by decreased perfusion and vasoconstriction
reflected from cold skin, changing from pale to grayish to cyanosis. The activity of the
sympathetic nervous system results in increased production of sweat (a cholinergic
sympathetic response).
Metabolic acidosis almost always accompanies shock with the accumulation of lactic
acid into hypoxemia. Anaerobic metabolism as a complication due to decreased liver
function that can produce lactic acid.

Thus, shock indicates a perfusion disorder characterized by decreased cardiac output

or distribution disturbance. It may also be the inability of the tissue to utilize a substrate,
thereby resembling a state of hypo perfusion. Blood flow to various organs is seen from the
relationship between perfusion pressure and blood vessel resistance in these organs. In
shock, this relationship is influenced by many factors.
PRIORITY AND TARGET THERAPY

In general, there are four phases in shock treatment. Target therapy and monitoring
need to be adapted to each phase. In the first phase (salvage), the goal of therapy is to
achieve minimum blood pressure and adequate cardiac output for minimal survival. Close
monitoring is required; in many cases, invasive monitoring can also be used in arterial and
central venous catheters. Lifesaving procedures (e.g., surgery for trauma, pericardial
drainage, revascularization for acute myocardial infarction, and antibiotics for sepsis) are
needed to treat the underlying cause. In the second phase (optimization), the goal is to
increase the availability of cellular oxygen, as well as interventions that target hemodynamic
status. Adequate hemodynamic resuscitation reduces inflammation, impaired mitochondrial
function, and caspase activation. Measurement of SvO2 and lactate can help guide therapy.
Cardiac monitoring should be considered. In the third phase (stabilization), the goal is to
prevent permanent organ dysfunction, even after hemodynamic stability has been achieved.
The supply of oxygen to the tissues is no longer a major problem, and the organ of support
becomes more relevant. Finally, in the fourth phase (de-escalation), the goal is to wean
patients from vasoactive agents and achieve spontaneous polyuria conditions or provoke
fluid elimination through the use of diuretics or ultrafiltration to achieve a negative fluid
balance. However, specific treatment of course depends on the type of shock and
pathophysiology causes the shock.
Shock Hipovolemik/Hemoragik
In hypovolemic shock indicates the occurrence of bleeding. It is important to know
the percentage of blood volume lost as a basis in providing appropriate therapy. In general,
physical examination alone is not enough, but by following the scheme this can be helped.
As an assumption that the perceived normal blood volume is 7.5 ml / kgbb, the hypovolemic
shock is divided into four groups based on the estimated number of bleeds:
I. 10-15% blood loss from Estimate Blood Volume (EBV) causes mild
tachycardia and shock has not occurred.
II. Blood loss of 15-25% of EBV (1000-1250ml / 70kg) arises moderate shock,
with tachycardia, systolic pressure and pulse pressure drop, slightly increased
diastolic pressure, slow capillary refill. Urine production is still within normal
limits.
III. Blood loss 25-35% EBV (1250-1750 ml / 70kg) causes severe shock, with
prominent symptoms: the skin is cold, wrinkled, and pale. Blood pressure
decreased between 30-40% (systolic pressure and pulse pressure) and an
increase in diastolic pressure of about 15-20%. Vasoconstriction stands out and
oliguria develops. Prominent CNS disorder is confusion, which is severe until
stupor occurs. Tachypnea results from secondary metabolic acidosis to
hypoxemia, tissue hypo perfusion and anaerobic metabolism. The pulse rate is
greater than or equal to 120x / min.

IV. Blood loss of 35-45% of EBV (1750-2250 ml / 70 kg) causes very severe
shock, usually a preterminal condition. Unmeasured blood pressure, peripheral
pulses are not palpable and carotid pulse is also may not palpable.
Hemorrhagic shock is accompanied by hemodilution and widespread plasma volume
expansion at any given time and therefore, the hematocrit does not change for 3 to 4
hours in acute bleeding.
SHOCK CARDIOGENIC
Cardiogenic shock (CGS) is a shock characterized by many factors that interfere with the
normal functioning of the heart, or (in particular) adverse factors to preload, afterload,
contractility, heart rate or heart rhythm. For example right or left ventricular myocardial
infarction, and in situations where cardiac pump failure, or ventricular filling or impaired
cardiac discharge.
The above changes occur in hypovolemic / hemorrhagic shock and also in cardiogenic
shock. In cardiogenic shock caused by myocardial infarction, there is a decrease in mean
arterial pressure, cardiac output, stroke work index, left ventricular diastolic end pressure
and volume and venous oxygen content. Heart rate, central venous pressure and
increased arterial and venous oxygen content, and peripheral vascular resistance also
increase as a result of compensation. The basic problem is the failure of the heart to
pump blood to peripheral tissue, whatever the cause. Therapy in all types of shock, aimed
at the underlying cause while conducting circulatory resuscitation efforts. What is more
important is to save myocardial ischemia and limit the size of infarction through
improvement of hemodynamic abnormalities and dysrhythmias. Myocardial
revascularization, balloon angioplasty and thrombolytic therapy are all part of the
treatment plan.
SEPTIC SHOCK
Incident and Etiology
One of the most common forms of distributive shock is septic shock. The complication of
this shock is about 40% of cases by bacteremia gram negative, with a mortality rate of
around 40-90%. Septic shock may be caused by bacteria, both gram-negative and gram-
positive (gram - endotoxin and gram + endotoxin); For example, staphylococci, S.
pneumonia, N.meningitidis, H.gonorrhea or Clostridia, sepsis; Fungi, rickettsia or
viruses. Lipopolysaccharides from endotoxin released from gram-negative cell wall
bacteria may be a major part of this syndrome. Septic shock is caused by sequester or
misdistribution of normal or high cardiac output in different parts of the body. Tumor
necrosis factor (cachectin) is known to be a very important mediator of clinical and
humoral manifestations in shock caused by endotoxins (A- and -O lipid chains) or by all
gram-negative bacteria. Vasoactive mediators such as histamine, complement activation,
quinine activation (especially precancerrein), prostaglandins and possibly other
substances that give rise to vasodilation without compensation to maintain cardiac
output. Leucocyte aggregation may cause capillary blockage with inadequate blood flow
results in capillaries. Micro vascular thrombosis is determined by the amount of platelets
and clotting factors and manifestations of stimuli of fibrinolysis systems such as DIC and
resulting bleeding. DIC is caused by sepsis associated with a decrease of factor XII, but
endotoxin is triggered by intrinsic and extrinsic blood clotting systems.
One theory says that hemorrhagic shock can develop into septic shock as a result of
increased permeability of mucous membranes that facilitate enteric bacteria entering the
bloodstream. In this model, severe cellular damage increases the permeability of cell
membranes and extracellular fluid displacement into cells associated with impaired cell

barrier function and disrupts the entry of gram negative or gram-positive bacteria into the
bloodstream. This cellular damage can be overcome if resuscitation is successful,
secondary phase bacteremia can be delayed. Survival may be improved if pre shock
therapy is anticipated with broad-spectrum antibiotics. Both gram-positive and gram-
negative bacteria appear to cause both cardiovascular abnormalities.
Clinical Manifestations
The cardiovascular system is affected by septic shock, at both the myocardial and
peripheral levels. Misdistribution of blood flow followed by myocardial depression, with
normal or increased bulk followed by decreased systemic vascular resistance (SVR).
Heart rate increased, meanwhile mean arterial pressure, stroke volume, stroke work,
oxygen consumption and arterial venous oxygen content all decreased. As already
explained, cardiac output may have been normal or increased. Patients with this
condition require large amounts of fluids due to peripheral vasodilation. The decrease of
Left Ventricular Ejection Fraction (LVEF) and Right Ventricular Ejection Fraction
(RVEF) especially biventricular dilatation occurs 2-4 days after onset of hypotension.
Patients who can be rescued from a septic shock their hemodynamic value will return to
their original state of 7-10 days from the onset of septic shock. It has been argued that
what can be saved in septic shock is more likely than cannot be saved with decreased
LVEF and left ventricular dilatation, where left ventricular dilatation gives the impression
of a compensatory effort through the Frank-Starling mechanism. The irreversible to
normal heartbeat, cardiac output or systemic vascular resistance (SVR), whereas
improvement can occur within 24 hours. Mortality can generally be seen from
hypotension that is irreversible due to depression of systemic vascular resistance (SVR)
and cardiac depression so that normal values cannot be maintained within normal limits
or above normal until the patient dies. So at first hyper dynamic state with high and
normal cardiac output with low cardiac filling pressure and decreased systemic vascular
resistance. The oxygen saturation of the mixed-vein may be normal or low. In high
cardiac output, where abnormal systolic function (decreased stroke volume and
decreased ejection of left ventricular fraction) and ventricular compliance. The
relationship between pulmonary capillary pressure (PCWP) and left ventricular diastolic
end (LVEDV) volume is not normal. At the next stage, there is a decrease in dynamic
state and the picture resembles a cardiogenic shock. Regarding respiration, where
respiratory frequency increases, hyperpnoea, tachypnea and respiratory alkalosis. The
antigen-antibody complex activates the complement system. Septicemia is often followed
by ARDS as a complication. Patients with manifest dyspnea, hypoxemia, bilateral diffuse
pulmonary infiltrate, reduction of lung compliance and have usually unchanged
pulmonary capillary pressure from the baseline (especially if lung function before shock
is normal).
Therapy
The primary goal of treating patients with septic shock is eradication / removal of causal
factors, such as infection, the harmful effects of bacterial toxins or endogenous toxins
from the host and attempts to improve the cardiovascular system and other systems.
Many ongoing research experiments to study drugs to counteract the effects of toxins on
septic shock. For the practical use of anesthesia, most of these are clinically unimportant
and are mentioned only for the completeness of the data. Currently, monoclonal
antibodies as part of gram-negative bacteria, naloxone, prostaglandin inhibitors, lipid X,
tumor necrosis factor antibodies (TNF), genetically engineered protease inhibitors and
other recombinants or synthetic protease inhibitors. Cardiovascular support for septic
shock patients consists of fluids and vasopressors required.

Fluid is required for optimization of preload and cardiac output above normal values so
that MAP returns to the baseline if possible or at least initially 60 mmHg. Pulmonary
capillary pressure (PCWP) is optimally 12-15 mmHg and should be monitored by
invasive techniques with pulmonary artery catheter. The selected fluid type did not seem
to provide much benefit with respect to the expected results, although experimental
experiments in experimental animals with septic shock resulted in a significant
improvement in cardiac output, Lung Water Extravascular Extension (PVR) and Venous
Admixture (VR) vascular cavity when given Dextran 70 compared to Ringer's Lactate.
Fluid resuscitation has shown effective results for increasing oxygen delivery (DO2) and
oxygen consumption (VO2) in septic shock.
The arrangement of ventricular function following Frank-Starling law and the category
of patients corresponding to the functional can assist in decision-making of inotropic
drugs, diuretics and vasopressors for patient resuscitation. Optimal oxygen transport
through correction of anemia and also followed by improvement in serum albumin levels
of at least 2 g / 100 ml is important as adjunctive therapy. If only with volume correction
alone the hypotension is not corrected, while maintaining the pulmonary capillary
pressure (PCWP) greater than or equal to 15mmHG, the vasopressor may be added
cautiously, starting with low dopamine doses (1-3g / kg / min) and norepinephrine If
large doses of dopamine are ineffective to increase mean arterial pressure (MAP) or side
effects (tachycardia, dysrhythmias). If norepinephrine is also ineffective, it should be
substituted with epinephrine or dobutamine or when low cardiac output is required to use
beta-mimetic adrenergic agonism.
OBSTRUCTIVE SHOCK
Obstructive shock is a form of shock associated with physical obstruction of
the great vessels or the heart itself. Pulmonary embolism and cardiac tamponade are
considered forms of obstructive shock. Obstructive shock has much in common
with cardiogenic shock, and the two are frequently grouped together. It was described as
involving obstruction to flow in the cardiovascular circuit and characterized by
impairment of diastolic filling or excessive afterload. The consequent obstruction of blood
flow into or out of the heart causes a decrease in cardiac output, and hence inadequate
oxygen delivery, which is manifest by the classic signs and symptoms of the shock state.
Obstructive shock is rare in pediatrics, though the most common causes generally include
tension pneumothorax, cardiac tamponade, and pulmonary embolism. Also included in
this category physiologically, and more specific to pediatrics, are congenital heart lesions
characterized by left ventricular outflow tract obstruction, including critical aortic
stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart
syndrome. Herein, we will briefly review the major causes of obstructive shock found in
children.
Tension Pneumothorax
A pneumothorax is defined as the accumulation of air in the pleural space, a cavity
that is normally filled with a small amount of pleural fluid. It can be spontaneous (more
common in adolescent males) or secondary to underlying lung pathology, such as trauma
(both penetrating and blunt trauma), asthma, cystic fibrosis, and pneumonia. Also
included in this subcategory are iatrogenic causes such as barotrauma during positive
pressure ventilation or during placement of central venous catheters in the chest vessels.
The incidence of secondary pneumothorax in pediatric patients is not well described,
however, in critically ill children requiring mechanical ventilation it is reported to be 4-
15%. Notably, the incidence of secondary pneumothorax in mechanically ventilated
pediatric patients has declined markedly since the introduction of protective lung

strategies. Pneumothoraces can be well tolerated in some patients, though signs and
symptoms of obstructive shock can develop if the pneumothorax is under tension. In this
scenario, the air
in the pleural space continues to collect under a one-way or ball valve effect, such that air
enters during inhalation, but cannot exit during exhalation. Eventually, enough air
accumulates such that the intrathoracic pressure of the affected hemi-thorax equilibrates
with atmospheric pressure, leading to complete lung collapse or atelectasis. Air under
tension also causes a shifting of the mediastinum, compression and total collapse of the
lung and great vessels, thereby compromising both cardiovascular and respiratory
function. Studies in animal models have shown that the early clinical features of a tension
pneumothorax include hypoxemia, tachycardia, and respiratory distress due to
compression and collapse of lung segments. As mechanical compromise of venous
structures develops, there is a drastic and profound reduction in venous return to the heart
as well, clinically manifested by symptoms of shock and poor perfusion. Thus, overt
hypotension may be a late sign. Complete occlusive mechanical compression is suggested
by equalization of the Mean Intrathoracic Pressure (MIP) and Central Venous Pressure
(CVP), which is a very late event and results in cardiovascular collapse. Treatment of a
tension pneumothorax requires emergent needle decompression, usually performed by
placing a sterile needle in the second intercostal space along the midclavicular line.
Definitive treatment requires thoracostomy tube placement.
Cardiac Tamponade
The pericardial sac around the heart is relatively noncompliant, and the accumulation
of even small amounts of fluid can be sufficient to produce cardiac tamponade
physiology. While acute pericardial fluid changes are usually symptomatic, the chronic
accumulation of fluid may occur with little to no hemodynamic derangements, as the
pericardium slowly stretches to accommodate the excess volume over time. Pericardial
effusions can develop as a result of any type of pericardial inflammation (i.e.,
pericarditis), causing a range of physiologic perturbations along the spectrum of minor
flu-like symptoms (i.e., manifestations of the pericarditis itself) to a life-threatening state
characterized by cardiac tamponade and obstructive shock. Historically, the most common
cause of
pericardial effusions was infectious pericarditis, though a recent review suggests that
idiopathic and neoplastic causes are much more frequent due to the success of childhood
vaccinations. Other common causes include postpericardiotomy syndrome (following
cardiac surgery for congenital heart disease) and trauma, most often causing
hemopericardium. Effusions may also develop as a result of a central line that erodes
through the thin wall of the right atrium, a phenomenon that appears primarily limited to
neonates and young infants. The pathophysiology of cardiac tamponade is welldescribed.
Briefly, increased intrapericardial pressure limits venous return to the heart and causes
right ventricular compression. There is a progressive decline in right ventricular end-
diastolic volume as diastolic filling lessens, worsening cardiac output. In severe
tamponade, venous
return during inspiration into the compressed right ventricle bows the interventricular
septum into the left ventricle, further diminishing systemic cardiac output. As pericardial
pressure increases and surpasses ventricular end-diastolic pressure, the ventricular
volumes grow smaller and smaller and cardiac output worsens. Tamponade is a clinical
diagnosis and classically, patients with critical cardiac tamponade present with Becks
triad of symptoms including hypotension, quiet (muffled) heart sounds, and raised

jugular venous pressure. Patients may present with dyspnea, compensatory tachycardia,
and poor perfusion. On auscultation, a friction rub and distant heart sounds may be
present. Pulsus
paradoxus, defined as a decline in systolic blood pressure greater than or equal to 10 mm
Hg during inspiration, results from the inspiratory reduction in pleural pressure that
produces a fall in left ventricular output and arterial systolic pressure. An
electrocardiogram may show electrical alternans due to the heart swinging within the
large effusion. Formal evaluation with an urgent echocardiogram should be performed in
those patients with symptoms suspicious for cardiac tamponade. However, emergent
management should not wait for echocardiography and is frequently based upon the
recognition of tamponade physiology in the appropriate clinical context.
Pericardiocentesis is the lifesaving procedure of choice for children with cardiac
tamponade and can safely be done with bedside echocardiographic guidance. Medical
stabilization with fluid resuscitation and inotropic support is temporary at best and
somewhat controversial as fluid
resuscitation may worsen tamponade physiology, especially in children who are either
normovolemic or hypervolemic. In the latter scenario, fluid administration will increase
intracardiac pressures further, hence increasing intrapericardial pressures and worsening
tamponade.
Pulmonary Embolism
Pulmonary embolism (PE) is uncommonly diagnosed in children, making its true
incidence difficult to determine. However, the incidence of PE does appear to be on the
rise, though this may be due to a heightened index of clinical suspicion and better
recognition by pediatric providers. Alternatively, it may be due to the fact that more
children are
surviving from previously fatal conditions that place them at an increased risk for
developing PE, such as congenital heart disease and malignancy. In addition, more
children are requiring central venous catheterization for vascular access, a major risk
factor for venous thromboembolism (VTE), which can lead to a PE. PE is frequently fatal
and difficult to diagnose. In a recent literature review comparing pediatric PE with adult
PE, pediatric cases were more often diagnosed at autopsy and were associated with a
higher mortality rate than adults. The clinical presentation often is confusing, perhaps
compounded by the fact that very few pediatricians have much experience with this
disorder. Results of screening
tests, such as oxygen saturation, electrocardiography, and chest radiography, may be
normal. Thus, a high index of clinical suspicion is necessary. Evaluation should be
performed with spiral computed tomography (CT) venography, which is now widely
considered the study of choice due to its >90% sensitivity and specificity in adults.
Ventilation/ Perfusion (V/Q) scans are also available but are more difficult to obtain and
to interpret in pediatrics. As a cause of cardiogenic shock, a massive PE has a
profound impact upon gas exchange and hemodynamics. Obstruction to flow through the
pulmonary artery results in increased dead space ventilation where affected lung
segments are ventilated but not perfused, observed clinically as a substantial decrease in
the end-tidal CO2 (ETCO2) that no longer reflects arterial PCO2. A widened alveolar-
arterialgradient (A-a) is present as well. The mechanism for hypoxemia likely involves
several mechanisms. In some pediatric patients, an intracardiac right-to-left shunt through
a patent foramen ovale may be present and as right atrial pressure increases and
eventually exceeds the left atrial pressure, deoxygenated blood can shunt directly into the
systemic circulation. In addition, V/Q mismatching is compounded by the accompanying

fall in cardiac output that results from massive PE, leading to mixed venous
desaturation. PE increases the right ventricular (RV) afterload, resulting in an increase in
the RV end-diastolic volume (EDV). The increase in RVEDV adversely affects
left ventricular hemodynamics through ventricular interdependence. Specifically, the
interventricular septum bows into the left ventricle (LV) and impairs diastolic filling,
resulting in decreased LV preload and subsequently diminished cardiac output and
hypotension. These physiologic phenomenon are manifested by respiratory
distress, hypoxia, and decreased cardiac output with signs of shock.
Treatment of an acute pulmonary embolus in children should begin with initiation of
a heparin infusion with or without fibrinolytic agents such as tPA, depending on the
child and the extent of the clot. In the resolution period, the child will then warrant at least
3-6 months of anticoagulation with low molecular weight heparin (LMWH) or warfarin.
MONITORING SHOCK
Hemodynamic Monitoring
Patients with shock are a critical condition and require invasive hemodynamic
monitoring especially in cases where vasoactive drugs are used for resuscitation or are
used to support the cardiovascular system. Generally, it is classified into routine and
exceptional or non-routine monitoring. Regular monitoring are used in patients with
critical condition who receive / get state of the art care in the intensive care room.
Extraordinary or non-routine monitoring are used in patients who need to be monitored
continuously in the ICU, for example in the extravascular lung water.
Meanwhile, blood pressure changes must be correctly measured in shock because
blood flow is determined by the relationship between cardiac output and systemic
vascular resistance, but in shock, blood pressure should be measured by continuous
monitoring with beat to beat arterial pressure. To be able to see the rapid changes can be
installed sphygmomanometer or Doppler placed on the artery line. In addition,
monitoring of all patients includes: heart rate and rhythm, breath frequency, body
temperature, right and left heart pressure, ECG and hematocrit. In the installation of
arterial catheters that settle arterial blood samples can be taken in a peiodic manner to
determine the state of electrolytes and the properties of blood clotting and arterial lactate
levels. The catheter insertion into the pulmonary artery may be excellent for assessing
pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and other
parameters including vascular resistance. Pulmonary artery catheters have the ability to
assess venous blood saturation, particularly in patients with cardiogenic shock. Central
venous pressure monitoring is sometimes used to determine or determine the amount of
blood lost, given that a 500-800ml blood loss for 70kg weight will lower central venous
pressure by about 7cmH2O.
Patients with shock who also get general anesthesia, decreased arterial blood pressure
may be faster than patients who are not publicly anesthetized because the compensation
of tone sympathetic nervous system is removed by anesthesia and in this patient, invasive
blood pressure monitoring by continuously beat to beat, will be very helpful. Korotkoff
sounds decreased or inaudible in severe shock which received general anesthesia and
subsequently assisted with an invasive monitor.
Assessment of electrolytes and hematocrit from arterial blood samples can provide
important information during resuscitation and shock management. Assessment of blood
volume and circulatory function can be better assessed in patients who have serial
laboratory results. Blood loss of about 3-4 times in acute bleeding can lead to significant
changes in hematocrit. The decrease in capillary hydrostatic pressure with bleeding is
characterized by increased intravenous interstitial fluid absorption. As a result,

intravascular fluids multiply and hematocrit decreases as a result of fewer percentage of

red blood cells in intravascular fluid. It should still be assessed during shock therapy and
monitoring of fixed hemodynamic variables, and there is no evidence to suggest that
simple correction by assessment of common parameters can result in greater outcomes or
lower morbidity.
Of the hemodynamic variables, two things that need attention in the assessment of
shock sufferers are: oxygen delivery and oxygen consumption.
Oxygen delivery (DO2) is the result of arterial oxygen content and cardiac index.
DO2 = CaO2 x CI x 10, where CaO2 = 1.39 x Hgb x% saturation + (PaO2 x 0.003) and
CI = cardiac output / body surface area. The normal value for DO2 is 520-720ml / min /
m2.
Oxygen consumption (VO2) is the result of arterial oxygen content minus venous
oxygen content and cardiac index times 10 (VO2 = CaO2 - CVO2 x CI x 10). The
normal value for VO2 is 100-180ml / min / m2. VO2 describes the sum of all oxidative
metabolic outcomes and thus is a measure of total body metabolism.
Of the hemodynamic variables that need attention include the counting of shunt
fraction Q2 / Qt and A-aDO2 or the oxygen difference between alveolar and arterial. The
direct flow of the pulmonary artery catheter is a therapeutic change in shock sufferers
with modification of Starling's law. In general, it is used given that the mean pulmonary
artery pressure of about 5-10mmHg is greater than the pulmonary capillary wedge
pressure (PCWP), and the pulmonary arterial diastolic pressure is approximately 0-
3mmHg greater than PCWP. PCWP is almost identical with left atrial pressure or
diastolic final pressure except in cases with mitral stenosis, where the left ventricular end
diastolic pressure (LVEDP) can not be determined or estimated from pulmonary capillary
wedge pressure (PCWP). Cardiac output may also be demonstrated by using
thermodilatory techniques if there is no intracardiac shunt (left to right or right to left).
Central Vein Pressure
Interpreting Central Venous Pressure (CVP) separately on the shock has a small value
of significance. Central venous pressure response to fluids is questionable, although
important as a guide in therapy. If the central venous pressure changes little or does not
change with the increase in pulse pressure after fluid administration, subsequent fluid
administration may be indicated. If CVP increases after fluid bolus or doubt, subsequent
fluid administration may be discontinued and to achieve the desired blood pressure, need
to be pharmacologically or otherwise.
Pulmonary Arterial Diastolic Pressure (PAdP)
PAdP is usually worth about 1-2mmHg greater than pulmonary capillary pressure
(PCWP) in the absence of pulmonary hypertension. If PAdP is reduced PCWP greater
than 5mmHg, it means pulmonary hypertension. PAdP changes are used to assess the
benefits of the effects of fluid therapy on shock.
Lactate levels
Monitoring arterial lactate levels is important in shock and associated with prognosis.
In shock, lactate levels increase and the lactate-pyruvate ratio also increases. Arterial
blood lactate levels are greater than 2.5mM / L, statistically the likelihood of survival
decreases dramatically and at 4.5mM / L, the chance of survival is only about 50%.
When more than 7.0mM / L the chance to survive less than 10%.
Patients who can be rescued from shock seem to have low lactate levels compared
with those that do not and also appear to decrease lactic acid at least 10% per hour
immediately after therapy, while patients who can not be saved by therapy, lactate levels
do not decrease. The level of lactate is expressed in milligrams of milliliters or milliliters
of perliter. Apparently, lactate levels may be measured from arterial blood or from a

central vein of the pulmonary artery with the same degree of accuracy. One study showed
that there was no correlation between arterial blood lactate levels and oxygen delivery
changes in septic shock or non septic shock. However, continuous monitoring of lactate
levels is very useful to know the severity of shock.
SHOCK IN PEDIATRIC
I Nyoman Budi Hartawan
Abstracts
Shock is divided into three major categories: hypovolemic, cardiogenics, and distributive,
with a degree of overlap. Hypovolemic shock is result of inadequate circulating blood
volume owing to blood or fluid loss or of insufficent fluid intake. Cardiogenic shock occurs
when cardiac compensatory mechanisms fail and may occur in infants and young children
and in patients with preexisting myocordinal disease or injury. Distributive shock, such as
septic and anaphylactic shock, is associated with peripheral vasodilations, arterial and
capillary shunting past tissue beds with pooling of venous blood, and decreased venous
return to the heart. Shock is clinical diagnosis, but its recognition remain problematic in
children. Shock may be present long before hypotention occurs. Children will often maintain
their blood pressure until late stage of shock; therefore, the presence of systemic hypotention
is not required to make the diagnosis of shock in chldren, as it is an adult. For example septic
shock in pediatric patients has been define as tachycardia (which may be absent in the
hypothermic patient) with signs of decreased perfusion, including decreased peripheral
pulses, compared with central pulses, altered alertnes, flash capillary refill or capillary refill
> 2secs, mottled or cool extremities, and decrease urine output. Hypotention ia a sign of late
and decompensated shock in children. If present in a child with these other featur
Lecture 8 : CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION
IGN Mahaalit Aribawa
Objective :
1. To describe etio-pathogenesis and pathophysiology of cardiac arrest
2. To implement a general strategy in the approach to patients with cardiac arrest
through history, physical examination and special tehnique investigations.
3. To manage by assesing, provide initial resuscitation and refer patient with post
resuscitation cardiac arrest
4. To describe prognosis patient with post cardiac arrest
Abstract
Medical emergencies that threaten lives can occur anywhere, anytime and to anybody. It
can be because of a disease or due to road accident, drowning, poisoning and others that are
capable of causing respiratory and cardiac arrest.
Air way obstruction such as hypoventilation, respiratory arrest, shock, even cardiac
arrest, causes death quickly if fast and appropriate help is not given. Death of patients due to
the causes mentioned above can be avoided if resuscitation is done immediately on the spot.
Permanent brain damage can occur if blood circulation has stopped for more than a few
minutes (now it has been agreed more than 4-6 minutes) or after a trauma with severe

hypoxia or loss of lots of blood which are not corrected. If resuscitation is given immediately
and correctly brain death can be avoided and the patient recovers completely.
General strategy to obtain the diagnosis of acute respiratory failure and cardiac arrest, is
done by a subjective approach or anamnesis and objective approach with physical
examinations and few other diagnostic criteria to find the primary signs and symptoms of
respiratory and cardiac arrest. The diagnosis of respiratory and cardiac arrest should be done
immediately and accurately. Delay in diagnosis will cause delay in resuscitation and this will
cause death to even the patients with higher living chances.
Resuscitation can be done anywhere, anytime, with or without equipment by trained
whether public or health personnel. CPR (cardiopulmonary resuscitation) is an effort of
medical emergency to cure respiratory function and circulation which has failed drastically
on a patient that has the chances of living.
For an immediate failure, the lung and heart are in good shape, compared to those due to
chronic diseases, that cure is possible. Besides that, how are we to know a patients condition
that still has a chance of living? To know the prognosis, a senior doctor/consultant with
knowledge, experience and mature considerations is needed.
Lecture 9 :EMERGENCY TOXICOLOGY AND POISONING
Agus Somya
LEARNING OBJECTIVE
5. To describe general approach of acute intoxication/poisoning
6. To describe general management of acute intoxication/poisoning
7. To describe management of methanol intoxication
8. To describe management of opiate intoxication
9. To descripe management of organophospate intoxication
10. To describe management of caustic intoxication
ABSTRACT
General approach and management of acute intoxication/poisoning

Acutely poisoned patients are commonly encountered in Emergency Centres. Acute
intoxication/poisoning (accidental or intentional) requires accurate assessment and prompt
therapy. Early identification of the involved toxin/s is crucial and the majority will be
identified by a thorough history and physical examination. An ABC-approach should be
followed ensuring a protected airway, adequate ventilation and hemodynamic stability.
Supportive and symptomatic care remains the cornerstone of treatment. A stepwise approach
may be followed to decrease the bioavailability of toxins. Indications, contra-indications,
risks and dosage regimens are describe for decontamination procedures including both
termination of topical exposures and decreasing exposure to ingested toxins. Furthermore,
procedures to increase the elimination of toxins and a short section covering specific toxins
and their antidotes are also included
Organophosphat poisoning
Organophosphorus pesticide self-poisoning is a major clinical and public-health
problem across much of rural Asia. Of the estimated 500000 deaths from self-harm in the
region each year, about 60% are due to pesticide poisoning.

Organophosphorus pesticides inhibit esterase enzymes, especially

acetylcholinesterase in synapses and on red-cell membranes, and butyrylcholinesterase in
plasma. Although acute butyrylcholinesterase inhibition does not seem to cause clinical
features, acetylcholinesterase inhibition results in accumulation of acetylcholine and
overstimulation of acetylcholine receptors in synapses of the autonomic nervous system,
CNS, and neuromuscular junctions. The subsequent autonomic, CNS, and neuromuscular
features of organophosphorus poisoning are well known
Clinical features of organophosphorus pesticide poisoning including:
- overstimulation of muscarinic acetylcholine receptors in the parasympathetic system
Bronchospasm, Bronchorrhoea, Miosis, Lachrymation, Urination, Diarrhoea,
Hypotension, Bradycardia, Vomiting, Salivation.
- overstimulation of nicotinic acetylcholine receptors in the sympathetic system:
Tachycardia, Mydriasis, Hypertension, Sweating.
- overstimulation of nicotinic and muscarinic acetylcholine receptors in the CNS:
Confusion, Agitation, Coma, Respiratory failure.
- overstimulation of nicotinic acetylcholine receptors at the neuromuscular junction:
Muscle weakness, Paralysis and Fasciculations
Treatment includes resuscitation of patients and giving oxygen, a muscarinic

antagonist (usually atropine), fluids, and an acetylcholinesterase reactivator (an oxime that
reactivates acetylcholinesterase by removal of the phosphate group). Respiratory support is
given as necessary. Gastric decontamination should be considered only after the patient has
been fully resuscitated and stabilised. Patients must be carefully observed after stabilisation
for changes in atropine needs, worsening respiratory function because of intermediate
syndrome, and recurrent cholinergic features occuring with fat-soluble organophosphorus.
Caustic agent intoxication

Caustic ingestions may cause widespread injury to the lips, oral cavity, pharynx, and
the upper airway. The effect that these agents have on the esophagus accounts for most of the
serious injuries and long-term complications. The nature of the injury caused by caustic
ingestion is determined by a number of factors including the identity of the agent, the amount
consumed, the concentration, and the length of time the agent is in contact with a given
tissue. Caustic materials cause tissue injury by chemical reaction. These materials are
generally acidic or alkali. Usually, acids with pH less than 3 or bases with pH greater than 11
are of the greatest concern for caustic injury.
The esophagus is the site of most long-term sequelae from caustic ingestion. Injury to
the esophagus is rapid, as described above, for both acids and alkalis, but this acute tissue
disintegration and deep tissue penetration may continue for hours. Injury progresses within
the first week after ingestion, with inflammation and vascular thrombosis. A developing ulcer
with fibrin crust will be seen in a few days. Granulation tissue develops between 2 to 4 days
and is revealed under shed necrotic tissue by days 15 to 20.
After caustic ingestion, patients may present with a combination of many symptoms
or none at all depending on the nature of the agent, the specifics of the ingestion (quantity,
intent, timing), and what tissues were affected.
Induction of emesis should be avoided to prevent further injury as the agent is
vomited. Neutralization of the caustic material should be avoided because of the potential for
causing an exothermic injury, which may worsen an existing injury.
Opioid intoxication

Opioid analgesic overdose is a preventable and potentially lethal condition that

results from prescribing practices, inadequate understanding on the patient's part of the risks
of medication misuse, errors in drug administration, and pharmaceutical abuse. Three
features are key to an understanding of opioid analgesic toxicity. First, opioid analgesic
overdose can have life-threatening toxic effects in multiple organ systems. Second, normal
pharmacokinetic properties are often disrupted during an overdose and can prolong
intoxication dramatically.3 Third, the duration of action varies among opioid formulations,
and failure to recognize such variations can lead to inappropriate treatment decisions,
sometimes with lethal results
Opioids increase activity at one or more G-proteincoupled transmembrane
molecules, known as the mu, delta, and kappa opioid receptors.
The presence of hypopnea or apnea, miosis, and stupor should lead the clinician to
consider the diagnosis of opioid analgesic overdose, which may be inferred from the patient's
vital signs, history, and physical examination. In patients with severe respiratory depression,
restoration of ventilation and oxygenation takes precedence over obtaining the history of the
present illness or performing a physical examination or diagnostic testing
Naloxone, the antidote for opioid overdose, is a competitive mu opioidreceptor
antagonist that reverses all signs of opioid intoxication.
Metanol Intoxication
Methanol (methyl alcohol, CH3OH) is the simplest type of alcohol, very light,
volatile, colorless, flammable, distinctive smell a little sweeter than etanol.3 methanol is used
for industrial products, and also as a mixture with ethanol to drink Traditional hard.
Industrial products that use methanol is a liquid car cleaner, solvent paints, cleansers,
perfumes, car fuel and other industrial products.
Methanol poisoning is a major disruption to the central nervous system, the optic
nerve and basal ganglia. The formic acid acts cause toxicity to the eye by inhibiting
cytochrome oxidase in the optic nerve, interrupting the flow axoplasma. While substances
that contribute to the occurrence of metabolic acidosis and decreased plasma bicarbonate is
formaldehyde, formic acid and lactic acid.
Toxic doses of methanol ranges between 15-500 cc of methanol solution containing
40% to 60-600 cc of methanol. Methanol poisoning begins with mild drunk and sleepy.
Followed by a latent phase (40 minutes - 72 hours) which is the period without symptoms,
due to the slow production of formaldehyde and formic acid. This phase was followed by the
appearance of metabolic acidosis, anion gap and impaired of vision. Visual disturbances such
as blurred to decrease visual acuity. In the later phase of seizures, coma and death. Slower
onset of methanol poisoning if the patient is also taking ethanol simultaneously.
On laboratory examination found an increase in serum osmolality, anion gap, serum
lactic acid and metabolic acidosis. Definitive diagnosis and monitoring of treatment response
based on the examination of serum methanol levels.
Specific Management of acute methanol poisoning include:
- Inhibitors of alcohol dehydrogenase
- Treatment with Co-factor: folinic acid 50 mg IV or folic acid 50 mg IV every 6
hours.
- Sodium Bicarbonate
- Hemodialis: Hemodialis is the fastest way of issuing metabolic toxic acid and methan

Lecture 10 :
PREGNANCY INDUCED HYPERTENSION
Gede Megaputra
OBGYN Team
Objective :
1. Define pregnancy induced hypertension
2. Review appropriate fetal/maternal assessment
3. Discuss appropriate anti hypertension and anti seizure therapy
4. Recognize when and how to transport patient with pregnancy induced hypertension
Hypertensive disorders in pregnancies are the leading causes of maternal death in emerging
countries. All caregivers must be able to promptly recognized the signs, symptoms and
laboratory findings of gestational hypertension with or without proteinuria and with other
adverse manifestation. Caregivers must appreciate fully the seriousness of gestational
hypertension, its potential for multi organ involment and the risk for perinatal and maternal
morbidity and mortality. The appropriate management of gestational hypertension may vary
based on the availability of resources. In this lecture student will discuss such as : the
classification and definition of hypertensive disorders in pregnancy; management and
treatment of gestational hypertension.
Severe gestational hypertension is an obstetrical emergency, which requires prompt

recognition, stabilization of mother and fetus and multi disciplinary approach to
management and treatment
Lecture 11 :
SHOULDER DYSTOCIA
Endang Sriwidiyanti
OBGYN Team
Objective
1. Define shoulder dystocia
2. Review appropriate fetal/maternal assessment
3. Discuss the risk factors of shoulder dystocia
4. Discuss the complications of shoulder dystocia
5. Discuss appropriate management of shoulder dystocia
Shoulder dystocia is one of emergency problems during delivery. Following the

delivery of the head, there is impaction of the anterior shoulder on the symphysis pubis in the
AP diameter, in such a way that the remainder of the body cannot be delivered in the usual
manner. More than 50% of cases shoulder dystocia occur in the absence of any identified risk

factor. The student will discuss the assessment of shoulder dystocia, the complication for
fetus and mother, identification of risk factor, and management
10.1. DEFINITION
After the birth of the head, external rotation will take place which causes axis of the
head to be on the normal axis to the spine. Generally shoulder will be on the oblique axis
under the pubic ramus. Pushing of the mother will cause the anterior shoulder become under
the pubis. If the shoulder fails to hold a rotation of adjusting to the axis of tilted pelvis and
remain in the anteroposterior position, the baby will most collision front shoulder to the
symphysis. 1,2
Shoulder dystocia is mainly caused by deformities of the pelvis, the failure of the
shoulder to "folded" into the pelvis (eg on macrosomia) caused by active phase and short
second stage of labor in multiparas so the descence of the head is too quickly, causing the
shoulder does not fold through the birth canal or head has through the middle pelvis after a
prolong of the second stage of labor before the shoulder successfully folded into the pelvis. 3
The main mechanism behind the occurrence of shoulder dystocia is the retention of
the anterior shoulder behind the pubic symphysis, while the posterior shoulder is usually
located in the maternal pelvis (Figure 10.1.). In rare situations, both shoulders are retained
above the pelvic brim. 4
Figure 10.1. The main mechanism behind the occurrence of shoulder dystocia
retention of the anterior fetal shoulder above the pubic symphysis
10.2. INCIDENCE
An overall incidence between 5.8-7 in 1000 of vaginal deliveries is reported in the
largest observational studies 4, while others studies find incidence of 1-2 in 1000 birth and 16
in 1000 birth of baby weight more than 4000 gram.3

10.3. RISK FACTORS 4
The main risk factors for shoulder dystocia are listed in Table 10.1. Previous
shoulder dystocia stands out as a major risk factor for recurrence, and it is reported to be 10
times higher than in the general population, for an overall incidence of 125%. The
anatomical characteristics of the maternal pelvis that predispose to shoulder dystocia and
may cause it to be recurrent in nature are poorly understood. When additional risk factors are
present, such as maternal diabetes or suspected fetal macrosomia or when previous fetal
injury occurred in association with shoulder dystocia, serious consideration should be given
to elective caesarean delivery, and this option should be discussed with the mother. 4
Another major risk factor is fetal macrosomia, and when coexistent with poorly
controlled maternal diabetes, an additional 24-fold risk is present, posed by the increased
diameter of the fetal shoulders. 4
Table 10.1. Main Risk Factors for Shoulder Dystocia 4
Risk Factor
Previous shoulder dystocia

Fetal macrosomia and its associated risk factors
Pre-existing or gestational diabetes
Maternal obesity
Excessive weight gain during pregnancy
Post-term pregnancy
Slow progress of labour vaginal delivery
Prolonged first and/or second stage
Need for labour acceleration
Instrumental
The majority of cases of shoulder dystocia occur in pregnancies that have no risk
factors, and when one is present, the majority of cases do not develop this complication.
There is therefore wide agreement within the medical community that shoulder dystocia is
generally an unpredictable situation. Nevertheless, identification of risk factors is useful for
anticipating of the situation, so that an experienced team can be on hand at the time of
delivery. 4
10.4. COMPLICATIONS
Complications of shoulder dystocia are described in Table 10.2. The most frequent
complication of shoulder dystocia is brachial plexus injury, of which Erbs palsy is the
usual presentation. The latter manifests by a characteristic position of the affected arm that
hangs by the side of the body and is rotated medially. The forearm is usually extended and
pronate (Fig. 10.2). It affects about 0.15 % of all births, and in some countries, the incidence
appears to be decreasing. Older studies report brachial plexus injury to occur in 216 % of
shoulder dystocias, but recent data from centres performing regular staff training refer that
this can be reduced to about 1.3 %. Brachial plexus injury appears to be related mainly to the
traction force applied on the fetal head. Improved awareness of the fact and simulation-based
training of the force that can be safely applied to the fetal head may be responsible for the
decreasing incidence of this complication. 4

Of all brachial plexus injuries diagnosed at birth, the majority disappear after
treatment, and only 1023% remain after 12 months. In the majority of cases of residual
paralysis, some degree of recovery is achievable after surgery. 4
Shoulder dystocia is also a cause of perinatal mortality, although the incidence

appears to have decreased in the last decades. Confidential enquiries carried out in the
United Kingdom indicate that it may be responsible for about 8% of intrapartum fetal deaths.
The main cause of perinatal death is acute fetal hypoxia/acidosis. 4
There is uncertainty about how many minutes may elapse before the fetus is at risk of
injury from acute hypoxia/acidosis. The phenomenon is probably faster when there are
nuchal cords and when cord clamping takes place before the shoulders are released. 4
Figure. 10.2 Newborn with a right arm
position typical of Erbs paralysis. 4
Compression of fetal neck vessels may also play an important part in the patho-
physiological mechanism, and it may be the main cause of cerebral injury when no nuchal
cords are present. Again, umbilical blood gas values may not translate the severity of
hypoxia/acidosis occurring in the brain, and hypoxic-ischaemic encephalopathy has been
documented in cases with only moderate acidemia on cord gas analysis. In a small but well-
documented observational study, no cases of hypoxic- ischaemic encephalopathy were found
when resolution took less than 5 min, and only mild cases of hypoxic-ischaemic
encephalopathy were reported when it lasted 59 min. Serious complications of
hypoxia/acidosis were only described in one case where more than 12 min elapsed. 4
Table 10.2. Complications of Shoulder Dystocia4
Newborn Complications
Death (8%)
Asphysxia and its complications

Fracture of Clavicula, humerus

Brachial Plexus Injury (most common)
Maternal Complications
Postpartum haemorrhage (11%)
Uterine Rupture
Bladder rupture
Dehiscence of pubic symphisis
Sacro-iliac joint dislocation
Although there are no certainties as

to the time that may elapse before the fetus is at risk of injury from hypoxia/acidosis, it
seems wise not to clamp nuchal cords after the head is delivered unless there is no other
alternative and to attempt resolution preferably within 5 min. When 12 min have elapsed,
fetal prognosis is likely to be poor. Different timings must be considered when fetal
oxygenation is already compromised before the occurrence of shoulder dystocia or when
there is fetal growth restriction. 4
Rarer complications of shoulder dystocia are fractures of clavicle and humerus, the
majority of which are iatrogenic in nature, consequent to the manoeuvres used for resolution
of the situation, and they usually heal without sequelae after immobilisation. 4
The most frequent maternal complications are vaginal and perineal lacerations, and
some studies report anal sphincter lacerations to occur in about 4% of shoulder dystocia
cases. 4
Postpartum haemorrhage affects about 11% of cases and can be caused by birth
canal lacerations and more frequently by uterine atony. Rare cases of uterine rupture, bladder
rupture, dehiscence of the pubic symphysis and sacroiliac joint dislocation have also been
described. 4
10.5. DIAGNOSIS 3
Turtle sign
Prolonged second stage of labour
Fail to deliver the baby with maximal effort and proper management

Figure. 10.3 Turtle sign, with the lower structures of the fetal head depressing the
maternal perineum 4
10.6 MANAGEMENT
Requirement 3
Maternal vital condition is sufficient to work together to completing deliveries
The mother has the ability to pushing
The passage and the pelvic outlet are adequate for the baby's body accommodation
The baby is still alive or are expected to survive
Not monstrum or congenital abnormality that prevents the delivery of baby
The management mnemonic "ALARMER"
1. Principles : Do not 4 P :

Panic

Pulling (the head of the baby)

Pushing (the fundal of uterine)

Pivoting (the head of the baby with coccygeus as fulcrums
2. Ask For Help :

The mother of patient

Husband

Midwife

Physician in charge or other paramedic
3. Lift the buttock- McRoberts Maneuver

The McRoberts maneuver was described by Gonik and associates (1983) and named
for William A. McRoberts, Jr., who popularized its use at the University of Texas at
Houston. The maneuver consists of removing the legs from the stirrups and sharply
flexing them up onto the abdomen (Fig. 10.4). Gherman and associates (2000) analyzed
the McRoberts maneuver using x-ray pelvimetry. They found that the procedure caused
straightening of the sacrum relative to the lumbar vertebrae, rotation of the symphysis
pubis toward the maternal head, and a decrease in the angle of pelvic inclination.
Although this does not increase pelvic dimensions, pelvic rotation cephalad tends to free
the impacted anterior shoulder. Gonik and coworkers (1989) tested the McRoberts
position objectively with laboratory models and found that the maneuver reduced the
forces needed to free the fetal shoulder. 4

a b
Figure 10.4. a. McRobert's Maneuver, the maneuver consists of removing the legs from
the stirrups and sharply flexing the thighs up onto the abdomen. b. The McRoberts
maneuver and the assistant is also providing suprapubic pressure simultaneously (arrow).
2,4
4. Anterior Disimpaction
4.1. Suprapubic Pressure (Manuver Massanti )
Suprapubic pressure on the baby's anterior shoulder toward the chest of the
baby.
Figure 10.5. Suprapubic Pressure 2
4.2. Rubin Manouver

vaginal approach
adduction anterior shoulder by pressing the posterior shoulder towards the
chest
Consider episiotomy
Rubin (1964) recommended two maneuvers. First, the fetal shoulders are rocked
from side to side by applying force to the maternal abdomen. If this is not successful,
the pelvic hand reaches the most easily accessible fetal shoulder, which is then
pushed toward the anterior surface of the chest. This maneuver most often abducts
both shoulders, which in turn produces a smaller shoulder-to-shoulder diameter. This
permits displacement of the anterior shoulder from behind the symphysis. 4

Figure 10.6. Rubin Manouver. A. The shoulder-to-shoulder diameter is aligned

vertically. B. The more easily accessible fetal shoulder (the anterior is shown here) is
pushed toward the anterior chest wall of the fetus (arrow). Most often, this results in
abduction of both shoulders, which reduces the shoulder-to-shoulder diameter and frees
the impacted anterior shoulder 1
5. Rotate the posterior shoulder- Corkscrew/ Wood Maneuver
Woods (1943) reported that by progressively rotating the posterior shoulder 180 degrees
in a corkscrew fashion, the impacted anterior shoulder could be released. This is
frequently referred to as the Woods corkscrew maneuver. 4
Figure 10.7. Wood Maneuver. The hand is placed behind the posterior shoulder of the
fetus. The shoulder is then rotated progressively 180 degrees in a corkscrew manner so
that the impacted anterior shoulder is released 1
6. Manual removal of posterior arm / Schwartz and Dixon Maneuver

Pressure on antecubital fosa to flexi the forearm

move the forearm anteriorly.

Reach the forearm or the fingers


Deliver the posterior shoulder
Figure 10.8. Schwart and Dixon Maneuver 3
7. Episiotomy-consider

Help Wood Manouver or giving more space to deliver the posterior arm, rotate
the chest and ease reaching the posterior shoulder 3
8. Roll over / All-Fours Manoeuvre / Gaskins Manouvre

This manoeuvre consists of placing the labouring woman on her hands and knees and
applying continuous and gentle axial traction on the fetal head, to release what was
previously the posterior shoulder (Fig. 10.9). Its place in the shoulder dystocia
management protocol is currently unclear, particularly in hospital environments. It is
mostly used in community settings when only one birth attendant is present and where
an 83 % success rate has been reported. In hospital settings, it may be attempted before
the exceptional manoeuvres described below are considered. 4

Figure. 10.9 All-fours manoeuvre with axial traction being applied on the fetal head. 4
9. Last Efforts
9.1. Break The Clavicle

Deliberate fracture of the anterior clavicle by using the thumb to press it toward and
against the pubic ramus can be attempted to free the shoulder impaction. In practice,
however, deliberate fracture of a large neonate clavicle is difficult. If successful, the
fracture will heal rapidly and is usually trivial compared with brachial nerve injury,
asphyxia, or death. 1
9.2. Cephalic replacement (Zavenelli Manouver)

ZavanellisManoeuvre (Cephalic replacement followed by caesarean section was
described for the first time in 1978, and it is performed in the operating theatre under
general anaesthesia with halogenated agents. The manoeuvre starts with slow rotation of
the fetal head to an occiput-anterior position, followed by flexion of the fetal neck and
application of firm and continuous pressure for the reintroduction of the fetal head in the
maternal pelvis (Fig. 10.10). An immediate caesarean section follows. A small number of
case series are reported in the literature with varying success rates and usually low
maternal morbidity, but uterine rupture and subsequent need for hysterectomy have also
been described. When fetal prognosis is reserved, maternal morbidity becomes the main
priority, and this is probably the less traumatic alternative for her. 4

Figure. 10.10. Zavanellis manoeuvre. 4
9.3. Symphysiotomy
This technique has been described for the resolution of obstructed labour since the nineteenth
century, but its current use in high-resource countries is limited to cases of shoulder dystocia
and retention of the after-coming head. Symphysiotomy is associated with important
maternal morbidity, so it should probably be the last option when fetal prognosis is poor. The
procedure can be performed under regional, general and local anaesthesia with opiate
sedation. It should be preceded by antibiotic prophylaxis, bladder catheterisation, shaving
and disinfection of the pubic area. Before incision, two assistants hold the mothers legs 60
80 apart, after removing them from the bed stirrups. This avoids sudden leg abduction when
the symphysis is opened, which can cause urethral injury. 4

Figure. 10.11 The main steps of symphysiotomy
With a hand introduced in the vagina to push the urethra aside, a transabdominal vertical
incision is performed with a long scalpel between the lower two-thirds and the upper third of
the pubic symphysis (Fig. 10.11). Pushing the handle upwards will open the lower two-
thirds. The scalpel is then reintroduced into the incision with the blade facing upwards and
the handle pushed downwards to open the remaining upper third. It is usually possible to
separate the pubic bones by about 23 cm, and this allows the shoulders to be released. After
closing the abdominal skin, the maternal pelvis is bound with an orthopaedic strap, and
bladder catheterisation is maintained for 48 hours. 4
In the absence of complications, the patient is maintained in lateral decubitus for two days,
and assisted walking starts on the third. Among the reported complications are para-urethral
lacerations, vulval oedema and skin incision haematomas. Difficulties in mobilisation may
persist for several months in 12 % of cases. 4

10. After procedure 3

Post partum haemorrhage anticipation
Exploration of lasceration and tear
Examination of the baby
Explain to the patient
Record the procedure
Lecture 12 : DERMATO - EMERGEMENCIES
Nyoman Suryawati
Objective
To understand the basic principle of acute blistering and exfoliative skin
Able to identify a case with acute blistering and exfoliative skin
Able to manage and referral a case with acute and exfoliative skin
Abstract
Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis
StevensJohnson syndrome (SJS) and Toxic epidermal necrolysis (TEN) are acute life-
threatening mucocutaneous reactions characterized by extensive necrosis and detachment of
the epidermis, with a mortality rate reaching 30%. The pathophysiology of EN is still
unclear; however, drugs are the most important etiologic factors. Both SJS and TEN are
differs only in the final extent of body surface involved: (1) SJS, less than 10% of body
surface area (BSA); (2) SJS/TEN overlap, between 10% and 30%; (3) TEN, more than 30%
of BSA.
Nonspecific symptoms such as fever, headache, rhinitis, cough, or malaise may
precede the mucocutaneous lesions by 1 to 3 days. Pain on swallowing and burning or
stinging of the eyes progressively develop, heralding mucous membrane involvement. The
eruption is initially symmetrically distributed on the face, the upper trunk, and the proximal
part of limbs. The initial skin lesions are characterized by erythematous, dusky red, purpuric
macules, irregularly shaped, which progressively coalesce. Nikolskys sign (dislodgement of
the epidermis by lateral pressure) is positive on erythematous zones. At this stage, the lesions
evolve to flaccid blisters, which spread with pressure and break easily. The necrotic
epidermis is easily detached at pressure points or by frictional trauma. Mucous membrane
involvement (nearly always on at least two sites) is observed in approximately 90% of cases
and can precede or follow the skin eruption.
SJS and TEN are a life-threatening disease that requires optimal management: early
recognition and withdrawal of the offending drug and supportive care in an appropriate
hospital setting. The patient must be transferred to an intensive care unit or a burn center.
Prompt referral reduces risk of infection, mortality rate, and length of hospitalization.
Specific therapy including immunosuppressive and/or anti-inflammatory therapies, antibiotic
therapy only if clinical infection is suspected. Supportive care consists of fluid replacement,
early nutritional support, aseptic and careful handing to reduce the risk of infection.

Staphylococcal Scalded Skin Syndrome
Staphylococcal Scalded Skin Syndrome (SSSS) is the term used to define a potentially life-
threatening, blistering skin disease caused by exfoliative toxins (ETs) of certain strains of
Staphylococcus aureus (usually phage group 2). ETs are serine proteases that bind to the cell
adhesion molecule desmoglein 1 and cleave it, resulting in a loss of cellcell adhesion.
The onset of SSSS may either be acute with fever and rash or be preceded by a
prodrome of malaise, irritability, and cutaneous tenderness, often accompanied by purulent
rhinorrhea, conjunctivitis, or otitis media. Within 12 days the rash progresses from an
exanthematous scarlatiniform to a blistering eruption. Very superficial tissue paper-like
wrinkling of the epidermis, which is characteristic, progresses to large flaccid bullae in
flexural and periorificial surfaces. A positive Nikolsky sign can be elicited by stroking the
skin, which results in a superficial blister. One or two days later, the bullae rupture and their
roofs are sloughed, leaving behind a moist, glistening, red surface along with varnish-like
crusts. At this stage, the clinical appearance closely resembles that of extensive scalding.
Mucous membranes are usually spared by bullae and erosions. Days later, due to generalized
shedding of the epidermis, scaling and desquamation progressively occur. The skin returns to
normal in 23 weeks.
Patients with SSSS require hospitalization because, besides the appropriate systemic
antibiotic therapy, intensive general supportive measures are needed. The mainstay of
treatment is to eradicate staphylococci from the focus of infection, which in most cases
requires intravenous (IV) antistaphylococcal antibiotics. The use of suitable antibiotics,
combined with supportive skin care and management of potential fluid, and electrolyte
abnormalities due to the widespread disruption of barrier function, will usually be sufficient
to ensure rapid recovery. Major complications of SSSS are serious fluid and electrolyte
disturbances. The mortality in uncomplicated pediatric SSSS is very low (2%) and is not
usually associated with sepsis.
LECTURE 13 : TRAUMA WHICH POTENTIALLY DISABLING AND LIFE

THREATENING CONDITIONS
I Ketut Suyasa, IGN Wien Aryana
AIMS:
Establish tentative diagnosis, provide initial management and/or refer patient with:
Trauma Which Potentially Disabling and Life Threatening Condition.
LEARNING OUTCOMES:
Establish tentative diagnosis, provide initial management and/or refer patient with:
Trauma Which Potentially Disabling and Life Threatening Condition
CURRICULUM CONTENTS:
1. Trauma Which Potentially Disabling and Life Threatening Condition
2. Diagnosis, provide initial management and/or refer patient with: Trauma Which
Potentially Disabling and Life Threatening Condition

ABSTRACTS
The initial assessment and management of seriously injured patients is a challenging

task and requires a rapid and systematic approach. This systematic approach can be practised
to increase speed and accuracy of the process but good clinical judgement is also required.
Although described in sequence, some of the steps will be taken simultaneously. The aim of
good trauma care is to prevent early trauma mortality. Early trauma deaths may occur
because of failure of oxygenation of vital organs or central nervous system injury, or both.
Injuries causing this mortality occur in predictable patterns and recognition of these patterns
led to the development of advanced trauma life support (ATLS) by the American College of
Surgeons. A standardised protocol for trauma patient evaluation has been developed. The
protocol celebrated its 25th anniversary in 2005. [ Good teaching and application of this
protocol are held to be important factors in improving the survival of trauma victims
worldwide.
Initial assessment
Resuscitation and primary survey.

Secondary survey.
Definitive treatment or transfer for definitive care.
1. Resuscitation and primary survey
For speed and efficacy a logical sequence of assessment to establish treatment priorities must
be gone through sequentially although, with good teamwork, some things will be done
simultaneously (resuscitation procedures will begin simultaneously with the assessment
involved in the primary survey, ie lifesaving measures are initiated when the problem is
identified). Special account should be taken of children, pregnant women and the elderly as
their response to injury is modified..
The primary survey is according to:
A = Airway maintenance cervical spine protection
The key = Look, Listen, Feel. Ensure the airway is open obstructions, airway is clear,
Trachea is midline and Mandibular or maxillofacial fracture.
Assume a cervical spine injury with any multisystemtrauma, especially with an altered level
of consciousness or blunt injury above the clavicle.
Recognition of: Stridor, change of voice quality, obvious trauma

Major problems:
1. obstructions,
2. Laryngeal injury,
3. Posterior dislocation / fracture dislocation of the sternoclavicular joint.

Management: Establishing a patent airway/ ET intubation; closed reduction.
B = Breathing and ventilation

Potentially Disabling and Life Threatening Condition:
Recognition of: Neck vein distention, respiratory effort and quality changes,
cyanosis
Major problems:
1. Tension pneumothorax:
Clinical diagnosis
Chest pain, air hunger, respiratory distress, tachycardia, hypotension,
tracheal deviation, unilateral absence of breath sounds, neck vein
distention, cyanosis. (V.S. cardiac tamponade)
Hyperresonant percussion.
Immediate decompression: Needle decompression/ chest tube.
2. Open pneumothorax:
2/3 of the diameter of the trachea impaired effective ventilation
Sterile occlusive dressing, taped securely on 3 sides.
Chest tube (remote)
3. Flail chest:
2 ribs fractured in two or more places.
Severe disruption of normal chest wall movement.
Paradoxical movement of the chest wall.
Crepitus of ribs.
The major difficulty is underlying lung injury ( pulmonary
contusion)
Pain.
Adequate ventilation, humidified oxygen, fluid resuscitation.
The injured lung is sensitive to both underresuscitation of shock and
fluid overload.
4. Massive hemothorax:
Compromise respiratory efforts by compression, prevent adequate
ventilation.
C = Circulation with haemorrhage control

Blood loss is the main preventable cause of death after trauma. To assess blood loss rapidly
observe:
Assessment: Pulse quality, rate and regularity. BP, pulse pressure, observing
and palpating the skin for color and temperature. Neck veins.
Important notes: Neck veins may not be distented in the hypovolemic patient
with cardiac tamponade, tension pneumothorax,or traumatic diaphragmatic
injury.
Monitor with: Cardiac monitor/pulse oximeter.
Major problems:
1. Massive hemothorax:
Rapid accumulation of > 1500 mL o blood in the chest cavity.

Hypoxia
Neck veins may be flat secondary to hypovolemia
Absence of breath sounds and/or dullness to percussion on one side of the chest
Management: Restoration of blood volume and decompression of the chest
cavity.
Indication of thoracotomy: a. Immediately 1500 mLof blood evacuated. b.
200mL/hr for 2-4 hrs. c. Patients physiology status. d. Persistent blood
transfusion requirements.
2. Cardiac Tamponade
Cardiac tamponade is usually due to penetrating cardiac injuries and are a
leading cause of traumatic death.
Diagnosis : Cardiac tamponade requires prompt recognition and treatment. Signs
and symptoms range from rarely stable to Becks triad of hypotension, CVP
above 12cc of water and muffled heart sounds
Auscultation of the thorax is performed specifically to evaluate the clarity of
heart tones and breath sounds. Muffled heart tones are an indication of blood in
the pericardium. A systolic - to diastolic gradient of less then 30 mmHg,
associated with hypotension is consistent with cardiac tamponade.
Neck veins are distended. Central venous pressure is elevated.
The X-ray film may demonstrate a widening of the cardiac silhouette. The ultrasound
scan shows presence of blood in pericardial space.
Electrocardiograph is not particularly helpful.
Prompt definitive therapy is imperative. This includes antishock therapy,
pericardiocentesis (possibly under U.S. guide), emergency thoracotomy and suture of the
wound.
3. Tension Pneumothorax
Tension pneumothorax develops when air enters the pleural space but cannot exit and as
a result there is a progressively increasing intrathoracic pressure in the affected
hemithorax resulting in impaired central venous return and mediastinal shift.
Clinically, the patient experiences dyspnea, complains of chest pains, and becomes
cyanotic because of shunting in the collapse of lung and has hemodynamic instability
because decrease is venous return for endopleural hypertension.
The presence of hyper-resonance and the absence of breath sounds, together with X-ray
examination, should be useful in confirming the cause of the emergency.
A chest X-ray film indicates that the trachea and mediastinum are deviated to the side
opposite the tension pneumothorax, while on the ipsilateral side intercostal spaces are
widened and the diaphragm is pushed downward.
The emergency require immediate thoracosintesis and thoracostomy with underwater-
seal drainage.
4. Blunt Abdominal trauma

Mechanism of Injury:
Blunt Trauma:
Spleen, liver, retroperitoneal hematoma
Penetrating Trauma:

Stab: Liver, small bowel, diaphragm, colon

Gunshot: small bowel, colon, liver, abdominal vascular structures.
Assessment:
History.
PE:
Inspection
Auscultation:
1. Bowel sounds
Percussion
1. signs of peritonitis
2. Tympanic/ diffuse dullness
Palpation
1. Involuntary muscle guarding
Evaluation of penetrating wounds:
Determine the depth
Assessing pelvic stability:
Manual compression
Penile, perineal and rectal examination:
1. Presence of urethral tear.
2. Rectal exam: Blunt (sphincter tone, position of the prostate, pelvic bone
fractures), Penetration (sphincter tone, gross blood from a perforation)
Vaginal examination
Gluteal examination
Intubation:
Gastric tube:
Relieve acute gastric dilatation.
Presence of blood
Urinary catheter:
Relieve urine retention
Monitoring urine output.
Caution: The inability to void, unstable pelvic fracture,blood in the
meatus, a scrotal hematoma, perineal ecchymoses, high-riding prostate.
X-rays studies:
Special diagnostic studies in blunt trauma:
DPL
Ultrsonography
Computed tomography
Special diagnostic studies in penetrating trauma:
Lower chest wounds
Anterior abdominal
Flank/back
Indications For Celiotomy

Based on abdominal evaluation
Blunt: Positive DPL/ ultrasound
Blunt: Recurrent hypotension despite adequate resuscitation
Peritonitis
Penetrating: Hypotension
Penetrating: Bleeding from the stomach, rectum, GU tract.

Gunshot wounds: Traversing the peritoneal cavity

Evisceration
5. Pelvic Fractures:
Assessment:
The flank, scrotum and perianl area should be inspected
Blood at the urethral meatus, swelling/bruishing/laceration in the
peritoneum, vagina, rectum, or buttock open pelvic facture
Palpation of a high-riding prostate gland.
Manual manipulation of the pelvis should be performed only once.
Management Pelvic fracture:
Exsanguination with/without Blood pressure stabilizees Blood Pressure normal

open pelvic fracture with difficulty and and closed/unstable or
(BP<70mmHg) closed/unstable fracture stable fracture (BP 120
(BP 90-110mmHg) mmHg)
Initiate ABCDEs Initiate ABCDEs Initiate ABCDEs
If transfer neccessary, apply If transfer neccessary, apply

PASG PASG If transfer neccessary,
apply PASG
If open go to OR for possible supraumbilical DPL or
perineal exploration and Ultrasound to exclude Evaluate for other injuries
celiotomy ; if closed, intraperitoneal hemorrhage.
supraumbilical DPL or Apply fixation device if
Ultrasound to exclude needed for patient mobility
intraperitoneal hemorrhage. Positive Negative
After celiotomy Reduce

reduce & apply & apply
Positive Negative fixation device fixation
as appropriate device as
After operation Red uce & appropriate
reduce & apply apply
fixation device fixation device
as appropriate as appropriate
Hemodynamically
Hemodynamically Abnomal
Abnomal
Angiography
Angiography
D = Disability: neurological status

Rapid neurological assessment is made to establish:

Level of consciousness, using Glasgow Coma Scale

Pupils: size, symmetry and reaction.
Any lateralising signs.
Level of any spinal cord injury (limb movements, spontaneous respiratory effort).
E = Exposure/environmental control
Undress the patient, but prevent hypothermia.
Additional considerations to primary survey and resuscitation
ECG monitoring:
Urinary/gastric catheters:
Other monitoring:
Pulse rate,[12] blood pressure, ventilatory rate, arterial blood gases, body temperature
and urinary output.
Carbon dioxide detectors may identify dislodged endotracheal tubes.
Pulse oximetry measures oxygenation of haemoglobin colorimetrically (sensor on
finger, ear lobe, etc.).
Diagnostic procedures: X-rays most likely to guide resuscitation early on, especially in
blunt trauma, include:

CXR.

Pelvic X-ray. It has been suggested that CT scans may be used in some stable
patients.[13]

Lateral cervical spine X-ray.

FAST (= focused assessment with sonography for trauma), eFAST (= extended
focused assessment with sonography for trauma) and/or CT scanning to detect occult
bleeding.
Lecture 14 : PHLEGMON / LUDGIGS ANGINA
Putu Lestari Sudirman
Objective :
1. To describe etio-pathogenesis and pathophysiology of phlegmon

2. To implement a general strategy in the approach to patients with phlegmon, physical
examination and special technique investigations.
3. To manage by assessing and refer patient phlegmon
4. To describe prognosis patient with phlegmon

Abstract
Phlegmone / Ludwig's angina is a diffuse cellulitis is on spasia sublingual, submental and
submandibular bilateral, sometimes up about spasia pharingeal. Cellulitis starts from the
bottom up. Often bilateral, but when just about one side / unilateral called Pseudophlegmon.
Often caused by primary infection of cellulitis come from M1, M2 lower jaw, other causes
(Topazian, 2002): sialodenitis submandibular gland, compund mandibular fractures,
lacerations of the soft mucosa of the mouth, stab wounds basic secondary infection of the
mouth and oral malignancy.
Clinical symptoms of phlegmon, such as edema on both sides floor of the mouth, walked
quickly spread to the neck just a few hours, the tongue uplifted, progressive trismus, chewy
consistency - stiff as a board, swelling redness, neck loses its normal anatomy, often febrile /
increase in body temperature, pain and difficulty in swallowing, droling, sometimes up tough
talk and breathe and stridor (inspiratory rough sound, because the narrowing of the airways
in the oropharynx, subglottic or tracheal)
Phlegmone / Ludwig's angina requiring treatment as soon as possible, in the form of: referral
for hospitalization, intravenous antibiotics high doses, typically used for initial therapy in
combination with Ampisillin metronidazole, intravenous fluid replacement, drainage, as well
as the handling of the airway, such as endotracheal intubation or tracheostomi if needed.
Local symptoms include swelling of the soft tissue / spasia, pain, heat and redness in the area
of swelling, swelling caused by edema, cellular infiltration, and sometimes because of pus,
diffuse swelling, chewy consistency - hard as a board, sometimes accompanied by trismus
and sometimes floor of the mouth and tongue raised. Systemic symptoms such as high
temperature, rapid and irregular pulse, malaise, lymph nodes, increasing the number of
leukocytes, rapid breathing, face reddish, dry tongue, delirium, especially at night, dysphagia
and dyspnoea and stridor. Prognosis in case of phlegmon depending on patient age, the
condition of the patient come first to get treatment and also depending on conditions
Systemic patients.
If there are signs of systemic conditions such as malaise and high fever, presence of
dysphagia or dyspnoea, dehydration or drinking less patient, thought to decrease resistance to
infection, septicemia, and toxic infiltration into anatomic regions are dangerous and require
general anesthesia for drainage, required serious treatment and hospital care as soon as
possible. Should always be controlled airway, endotracheal intubation or tracheostomy. Four
basic principles infection treatments (Falace, 1995), namely: eliminating causa (If the
patient's general condition possible to be done This procedure, by way of cause tooth
extraction), drainage (drainage Incision can be done intra and extra oral, or can be done
simultaneously in the case - severe cases. Determining the location of the incision by
spasium involved). In the administration of antibiotics to consider whether the patients had
history of allergy to certain antibiotics, especially if given in Intravenous it is necessary to do
skin test beforehand. antibiotics are given
for 5-10 days (Milloro, 2004) Suppotive Care, such as rest and adequate nutrition,
administration analgesic and anti-inflammatory (nonsteroidal anti-inflammatory painkillers
such as diclofenac (50 mg / 8 hours) or Ibuprofen (400-600 mg / 8 hours) and if
Corticosteroids granted, it should be added pure analgesics, such as paracetamol
antiinflammatory given in (650 mg / 4-6 hours) and / or low opioids such as codeine (30mg /
6 h)), granting the application of external heat (hot compresses) or orally (mouthwash).

Traumatic Brain Injury Resuscitation

I Pt Pramana Suarjaya/ IB Krisna Jaya Sutawan
Learning Obyektif
1. To describe Traumatic Brain Injury (TBI)
2. To implement Glasgow Coma Scale to classiflying severity of TBI
3. To implement initial brain recucitation
a. Primary survey
i. Airway
ii. Breathing/Ventilation
iii. Circulation
iv. Disability
v. Exposure
b. Secondary survey
4. To describe management of elevated ICP
Abstract
Traumatic Brain Injury (TBI)

TBI is a nondegenerative, noncongenital insults to the brain from external mechanical
force, possibly leading to permanent or temporary impairment of cognitive, physical, and
psychosocial functions, with an associated diminished or altered state of consciousness. TBI
from trauma results from two distinct processes: primary injury and secondary injury.
Primary injury is the damage produced by the direct mechanical impact and the acceleration-
deceleration stress onto the skull and the brain tissue, which results in skull fractures and
intracranial lesions. The intracranial lesions are further classified into two types: diffuse
injury and focal injury.
1. Diffuse brain injury
a. Brain concussion : loss of consciousness lasting < 6 hours
b. Diffuse axonal injury : traumatic coma lasting > 6 hours
2. Focal brain injury
a. Brain contusion
b. Epidural hematoma (EDH)
c. Subdural hematoma (SDH)
d. Intracerebral hematoma (ICH)
Secondary injury develop within minutes, hours or days of the initial injury and cause
further damage to nervous tissue. The common denominators of secondary injury are
cerebral hypoxia and ischemia. Secondary injuries are caused by the following disorders:
1. Respiratory dysfunction: hypoxemia, hypercapnia
2. Cardiovascular instability: hypotension, low cardiac output (CO)
3. Elevation of ICP
4. Metabolic derangements
Glasgow Coma Scale (GCS) to classifying severity of TBI

GCS is composed of three components: eye opening (1 to 4 points), verbal response
(1 to 5 points) and motor response (1 to 6 points). The sum of these components defines the
TBI severity classification into :
1. Severe : GCS score of 3 to 8
2. Moderate : GCS score 9 to 13
3. Mild : GCS score 14 and 15

Glasgow Coma Scale for all age group

4 years to Adult Child < 4 years Infant
Eye Opening
4 Spontaneous Spontaneous Spontaneous
3 To speech To speech To speech
2 To pain To Pain To Pain
1 No respon No respon No respon
Verbal response
5 Alert and oriented Oriented, social, coos, babbles
speaks, interacts
4 Disoriented Confused speech, Irritable cry
disoriented,
consolable, aware
3 speaking but nonsensical Inappropriate cries to pain
words,inconsolable,
unaware
2 Moan or unintelligible Incomprehensible, Moans to pain
sounds agitated, restless,
unaware
1 No response No response No response
Motor response
6 Follows commands Normal, spontaneous Normal, spontaneous
movements movements
5 Localizes pain Localizes pain withdraws to touch
4 Moves or withdraws to Withdraws to pain withdraws to pain
pain
3 Decorticate flexion Decoritcate flexion Decorticate flexion
2 Decerebrate extension Decerebrate extension decerbrate extension
1 No response No response No response
Initial Brain Resuscitation
Patients who have TBI should be either treated at a designated trauma center that has
neurosurgical coverage or transferred to such a center after initial stabilization. The prompt
assessment and management of TBI begin with the treatment of associated injuries that may
cause hypoxia, hypoventilation and shock. This is best accomplished using a systematic
approach such as the Advanced Trauma Life Support (ATLS) Algorithm, which consists of
primary and secondary surveys.
1. Primary Survey
A brief history is obatained according to the AMPLE mnemonic (Allergies,
Medications, Past medical history, Last meal, Event). Examination and immediate
resuscitation are performed according to ABCDE mnemonic (Airway, Breathing,
Circulation, Disability, Exposure). Plans for initial operative or non-
operativemanagements are based on the results of the primary and the secondary
surveys.
a. Airway : in the setting of TBI, airway management is performed with
particular attention to changes in mean arterial pressure (MAP), ICP, arterial
oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2) and cervical
stability.

i. Indications for intubation include inability to protect the airway,

difficulty with oxygenation or ventilation, shock, a GCS score < 9, and
rapid neurologic deterioritation
ii. Manual inline stabilization (MILS)
iii. Rapid squence induction (RSI)
iv. Induction agent that can be used are propofol, thiopental and
etomidate.
v. Several neuromuscular blocking drugs are appropriate for TBI such as
succinylcholine, rocuronium and mivacurium.
vi. As with all intubations, airway manager should consider awake-
topical intubation if they are uncertain about their ability to establish
an airway quickly and safely.
vii. Lidocaine IV
viii. Laryngeal mask airway (LMA) devices are useful backup tools for
ventilation and intubation. Surgical airway techniques, such as
cricothyroidotomy and tracheostomy are also backup methods for
intubation.
ix. Endotracheal intubation must be confirmed by physical examinaton
plus a method for CO2 detection such as colorimetric or continous
capnography.
x. Chest x-ray are useful for verification of endotracheal tube positionas
well as identificationof associated chest pathology such as
pneumothorax, lung contusion, and pulmonary edema.
b. Breathing/ventilation
i. High-flow oxygen is provided as supplement to all patients before
intubation to prevent hypoxia and provide sufficient apneic time in
case further RSI is needed.
ii. Oxygen saturation should be maintained above level now concidered
acceptable for patients who have acute respiratory distress syndome.
iii. Positive-pressure ventilation is provided as needed to maintain
adequate ventilation and oxygenation.
iv. The PaCO2 should be kept at normocarbia
v. Sedation : The ideal sedative drug in TBI should have rapid onset and
offset, anticonvulsant properties, and favorable effects on CPP.
vi. Analgesia and blunting of stimulation associated with the endotracheal
tube can be achieved with opioids
c. Circulation: Systemic hypotension is one of the major contributor to poor
outcome after TBI. When necessary, fluid resuscitation is initiated
immediately, inotropic and vasopressor drugs are administered as required to
stabilize the blood pressure (BP) at or above 90 mmHg.
i. Life-threatening cardiogenic shock as from tension pneumothorax and
cardiac tamponade is identified and either controlled or treated
definitively.
ii. Hypovolemic shock should be resuscitated.
iii. Total osmolality is the most important factor in determining brain
edema formation.
iv. Patient who have a low hematocrit may require a tranfusion.
v. Glucose-containing solutions are avoided.
vi. Inotropes and vasopressors. If the BP and cardiac output (CO) cannot
be restored through fluid resuscitation, the administration of

intravenous inotropic and vasopressor drugs may be necessary. An

infusion of either phenylephrine or dopamine is recommended to
maintain the CPP above 60 mmHg.
d. Disability : When not absolutely contraindicated by the need for immediate
endotracheal intubation, the initial neurological assessment should be
performed before the administration of sedative or neuromuscular-blocking
drugs. Neurological status is assessed by using GCS with attention to the
signs and symptoms of increased ICP and brain herniation. In addition, the
examiner notes the pupillary response and diameter, presence of lateral
deficits, and level of spinal motor and sensory deficits. Emergency therapy for
brain herniation includes reassessment and treatment of extracranial insults
such as hypoxia and shock, head elevation to 30o, mannitol infusion, brief
hyperventilation, and surgical decompression.
e. Exposure : The patient is fully undressed and examination for any associated
injuries while precautions are taken to avoid hypothermia.
2. Secondary survey
a. The secondary survey includes a more complete history and physical
examination as well as laboratory and ancillary testing to diagnose the extent
of TBI and associated injuries.
b. Commonly requested investigation include x-ray examination of the chest and
pelvis, complete metabolic panel, complete blood count, clotting parameters,
serum osmolarity, urinalysis, ethanol blood level.
c. Unless contraindicated by need for immediate laparotomy or other procedure
to prevent death from shock, all TBI patients should have a non-contrast
computed tomographic (CT) scan of the head and cervical spine as soon as
possible.
Management of elevated ICP
The reduction of elevated ICP and the maintenance of BP are crucial in the
management of intracranial hypertension because CPP is directly related to both MAP and
ICP. ICP monitoring is recommended in patient who have CT evidence of elevated ICP
including midline shift, effaced ventricles, compressed basal cisterns, or the presence of an
intracranial space-occupying lesion.
1. Hyperventilation: when evidence of transtentorial herniation in patients who have
severe TBI exist, hyperventilation should be instituted because hyperventilation can
reduce ICP rapidly and effectively.
2. Diuretic therapy: manitol is administered to patients in whom transtentorial
herniation is suspected. The serum osmolality is monitor frequently.
3. Posture: a head-up tilt to 10o to 30o facilitates cerebral venous and CSF drainage and
lower ICP.
4. Barbiturate: are known to exert cerebral protective and ICP-lowering effects. High
dose barbiturate therapy may considered in severely head injuries patients whose
intracranial hypertension is refractory to maximal medical and surgical ICP-lowering
therapy. However the prophylactic use of barbiturate come is not indicated.
5. Decompressive craniectomy: is an surgical advanced treatment option for ICP control
in severe TBI.

Lecture 15 : UROLOGYC CONCERN IN CRITICAL CARE FOR NON TRAUMA

CASE
Gede Wirya Kusuma Duarsa
Objectives
1. To understand the basic principles of non trauma urologic emergency
2. Comprehend the definition, etiology, special investigation and basic management the acute
urinary retention, acute scrotum, penile emergencies, priapism, external genital trauma,
anuria, urosepsis, Fourniers gangrene, colic, hematurisa, etc.
Abstract
The primary care physician plays a key role in the diagnosis and initial management of
most urologic emergencies. It is critical to stratify patients into those who require urgent care
(eg, phimosis, epididymitis) and those who require emergent care (eg, Fournier's gangrene,
testis torsion, anuria, ureteral or renal colic, hematuria, acute urinary retention, priapism,
external genital trauma, urosepsis, acute scrotum, etc.), because the time to therapy may
significantly impact on outcome between these two groups. Mismanagement of these
conditions may result in significant sequelae, which are preventable in most cases.
Fortunately, most urologic emergencies are precisely diagnosed with a combination of
clinical acumen and appropriate radiologic or adjunctive studies. This article reviews the
diagnosis and management of the most common urologic emergencies, and highlights
pragmatic information of use to the general practitioner
Acute urinary retention is defined as the sudden inability to void despite a distended
bladder (urine volume in the bladder more than its capacity). It is usually preceded by a
history of progressively decreasing force of stream. The most common obstructive cause of
acute urinary retention is benign prostatic hyperplasia. Prostate cancer, urethral strictures,
bladder stones or bladder tumors may also cause obstructive urinary retention, hematuria and
clots should be suspected of harboring an underlying bladder tumor. Less common
obstructive etiologies include urethral foreign bodies, penile constricting bands, and meatal
stenosis. The most common infectious cause for acute retention is acute prostatitis. Other
infectious causes of retention include urethral herpes, periurethral abscesses, and tuberculous
cystitis. There are many pharmacologic agents that may contribute to urinary retention.
Neurogenic causes of urinary retention may be broadly categorized into upper motor neuron
lesions, lower motor neuron lesions, and peripheral nerve lesions.
The initial diagnosis of the patient who presents with acute scrotal pain may be
challenging. Although testis torsion is the least common cause of the acute scrotum, it should

be high in the differential diagnosis because testicular salvage rates correlate inversely with
time to exploration. Most patients suffer from epididymitis, torsion of a testicular appendage.
The availability of more accurate radiologic imaging studies has helped to reduce the
incidence of negative scrotal explorations, but the importance of the initial evaluation and
clinical findings still remains the most powerful tool in correctly treating the acute scrotum.
Testis torsion may occur in the neonatal period secondary to lack of fixation of the
tunica vaginalis to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion
has a low salvage rate. If the tunica vaginalis inserts in an abnormally high position on the
spermatic cord (the bell clapper deformity), the testis may freely rotate on the cord. Testis
torsion may occur in the neonatal period secondary to lack of fixation of the tunica vaginalis
to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion has a low salvage
rate. If the tunica vaginalis inserts in an abnormally high position on the spermatic cord (the
bell clapper deformity), the testis may freely rotate on the cord. This is known as
intravaginal torsion, and testis ischemia is dependent on the number of rotations of the
cord. The spermatogenic cells are the most sensitive to ischemia, whereas the testosterone-
producing Leydig's cells are more resistant. Salvage of testicular function is close to 100% if
detorsion occurs within 6 hours of pain onset, but this drops to less than 20% beyond 12
hours. Successful treatment is time dependent in this case
Epididymitis arises from pain and swelling of the epididymis. It usually arises
secondary to infection or inflammation from the urethra or bladder. If the process remains
untreated, it may involve the adjacent testis and scrotum, and eventually result in abscess
formation. Fever and leukocytosis are present in between 30% and 50% of cases. Antibiotic
treatment for epididymitis depends on patient age and probable underlying pathogen.
Neisseria gonorrhoeae and Chlamydia trachomatis account for most cases in men under 35,
and these may be treated with intramuscular ceftriaxone plus a course of doxycycline. In
men over 35, urine culture usually reveals Escherichia coli, and treatment consists of an oral
fluoroquinolone for 21 days.
Necrotizing fasciitis of the scrotum and perineum (Fournier's gangrene) is a rare but
life-threatening cause of acute scrotal pain. It is typically found in debilitated or
immunocompromised patients with significant medical comorbidities, particularly diabetes
and alcoholism. The infection usually originates from a perianal or periurethral source, and
includes multiple pathogens, including E coli, Bacteroides, and Streptococci. Patients present
with early systemic toxicity, and genital examination typically reveals erythema, tenderness,
induration, and crepitus. The perineum may appear frankly necrotic and foul smelling.
Phimosis results from stenosis of the distal aspect of the foreskin, preventing it from
being successfully retracted over the glans. It is a physiologic finding in uncircumcised
infants, and physiologic adhesions typically prevent complete retraction of the foreskin in
this age group. Forcible retraction of the foreskin should not be attempted because it may
actually tear the adhesions and create pathologic phimosis. Phimosis is rarely an emergent
condition, but it may rarely cause urinary retention if the foreskin has sealed off. In this case,
the preputial sac balloons out with each void. Temporary or emergent management of this
condition includes hemostat dilation of the stenotic foreskin. Topical steroids have been
successful in progressively reducing phimosis, but circumcision should be considered in
chronic or refractory cases.
Paraphimosis arises when the foreskin has been retracted proximal to the glans, and
cannot be returned to its normal position secondary to a tight, constricting ring of skin. With
time, the retracted prepuce becomes edematous because of impaired venous and lymphatic
drainage. Treatment of paraphimosis is urgent reduction of the foreskin.
Priapism is defined as a prolonged, painful erection that is unrelated to sexual arousal.
Although the corpora cavernosa are typically rigid and filled with stagnant blood, the glans

and corpus spongiosum remain flaccid. Stuttering priapism refers to recurrent painful
erections with intervening detumescence, whereas malignant priapism implies a locally
invasive malignant condition in the corpora, and is frequently a preterminal event.
Penile fracture (or rupture) implies disruption of the tunica albuginea surrounding the
corpora cavernosa. This injury typically occurs during vigorous intercourse, when the rigid
penis is misdirected against the partner's pubic bone, and results in buckling trauma. This
injury may also be self-inflicted by abrupt bending of the erect penis during masturbation.
The classic history involves the scenario described previously, with patients usually reporting
a popping sound as the tunica tears, followed by pain, swelling, and rapid detumescence.
Blood in urine is a common symptoms in urology. There are many causes of
Haematuria including medical bleeding and surgical bleeding. Prompt diagnosis and good
management will prevent further damage or complication.
Lecture 16 : UROLOGYC CONCERN IN CRITICAL CARE FOR TRAUMA CASE

Wayan Yudiana
Objectives
1. To understand the basic principle and pathophysiology of genitourinary injuries

2. To describes the clinical features and investigations of genitourinary trauma
3. To provide an appropriate management of genitourinary trauma
Abstract
Traumatic injuries to the genitourinary system are commonly divided into injuries to the
kidney, ureter, bladder, urethra and the external genitalia.
The kidneys are the most commonly injured genitourinary organs from external trauma.
Advances in radiographic staging, improvements in hemodynamic monitoring, and wider use
of angioembolization have improved the rates of renal preservation and decreased
unnecessary surgery.
Iatrogenic ureteral injury most commonly occurs during hysterectomy. An unrecognized or

mismanaged ureteral injury can lead to significant complications.
Most bladder injuries occur in association with blunt trauma. Eighty-five percent of these
injuries occur with pelvic fractures, with the remaining 15% occurring with penetrating
trauma and blunt mechanism not associated with a pelvic fracture.
Urethral injury is predominantly a male problem. Injuries to the posterior urethra are mostly
secondary to pelvic fractures, while injuries to the anterior urethra are caused by straddle-
type or penetrating injuries. Urethral injuries from trauma constitute only 10% of all GU
injuries.
Injuries to the external genitalia (ie, the penis and the scrotum) are usually secondary to
injuries caused by penetration, blunt trauma, sexual pleasure enhancing devices, and
mutilation (self-inflicted or otherwise).
The primary goal in the management of the genitourinary injuries is to preserve the maximal
amount of functional tissue while minimizing the complication. Complications can occur

because of missed urologic injury at the time of initial presentation, the nature and severity
of the injury itself, and/or inadequate or inappropriate initial management. Minimizing
delayed complication occurrence can be achieved by appropriately staging the injuries,
followed by the proper selection of surgery of expectant therapy.
LEARNING TASK
Lecture 1 : HIGHLIGHT EMERGENCY MEDICINE
Case 1
There is an earthquake report in village with estimately 500 people. From the report, 12
people have been found dead, 50 people have either minor or major injury, and 120 people
have not been found. You are a head of emergency department in nearby hospital.
1. Is this a disaster? If true, what kind of disaster is it from the source of disaster?
2. How do you prepare to treat the victims of this event?
3. If you make a support area, what components should be there?
4. Specify the components that must exist in triage team
Case 2
From 50 people with injuries was found,
- 12 people complaining pain, hungry, and cold. They asked for the food
- 5 people shout loudly in pain
- 10 people are not making any sound, still breath irregulerly
- 10 people are not breathing
How do u clasify these victims? After u clasify, how do u treat them?
LEARNING TASK
Lecture 2 : STATUS EPILEPTICUS AND OTHER SEIZURE DISORDERS
SELF ASSESSMENT
1. Able to explain the causes of status epileptikus
2. Able to give first aid for status epileptikus
3. Able to identify patient with refractory epilepsy
LEARNING TASK
Lecture 3 : COMA AND DECREASE OF CONSCIOUSNESS
SCENARIO
A 50 year old man was found lying in the bed by his wife in a coma. On exam, his blood
pressure was 190/100 mmHg, temperature was 37 deg.celcius, pulse was 55 and regular and
respirations rate were 10 per minute. No recent trauma was evident. Finger stick showed a
glucose of 150. He didnt open his eyes and didnt respond to voice, but supraorbital pressure

caused withdrawal to firm pinch on the left side, but not on the right side. We also found this
patient with paralysis facial nerve on the right side.
SELF ASSESSMENT
1. How is pathophysiology mechanism to develop coma in this case?
2. How is structural coma distinguished from metabolic coma?
3. What could be the differential and possible diagnosis to this case?
4. How to manage and provide initial management and when do you refer the patient?
LEARNING TASK
Lecture 4 : ACUTE PSYCHIARTIC EPISODE
1. The Presence of medical illness should be strongly considered when psychiatric

symptoms appear suddenly in a previously well-functioning person. An old patient
with psychotic symptoms appearing for the first time, an awareness or conviction that
the symptoms are foreign, and especially with concomitant symptoms of cognitive
dysfunction should be considered to have a possible organic illness.
a) A patient with delirious condition usually have personality disorders
b) Increase of temperature, pulse and respiratory rate is common in psychiatric
patient, especially paranoid schizophrenia.
c) Suicide attempted are an easily manage, because they are only seeking
attention
d) Cognitive dysfunction should be considered to have a possible organic illness.
e) A patient under the age 30 with psychotic symptoms appearing for the first
time should be considered to have an organic brain disorder.
2. The patient was a 25-year old female graduate student in physical chemistry who was
brought to the emergency room by her roommates, who found her sitting in her car
with the motor running and the garage door closed at 1.00 AM. She was crying,
looked tiredness, and difficulty in falling a sleep. What is the considerable of the
patient treatment?
SELF ASSESSMENT
1. Mampu menegakkan diagnosis Gangguan Mental Organik, membedakannya dengan

Gangguan Psikosis fungsional lainnya.
2. Mampu melakukan wawancara singkat untuk menggali data dan merencanakan
pemeriksaan penunjang yang diperlukan untuk kasus-kasus Accute Psychiatry.
3. Mampu membuat perencanaan awal untuk menangani kasus-kasus Accute Psychiatry.
4. Mengerti etio-patogenesis, pato-fisiologis dan psikodinamika terjadinya kasus-kasus
Accute Psychiatry.
5. Mampu membuat prediksi/prognosis suatu kasus AccutePsychiatry serta tahu kapan
harus merujuk pasien tersebut.
LEARNING RESOURCES
1. Kaplan & Saddocks Synopsis of Psychiatry, 10th ed
2. Kaplan & Saddocks Study Guide and Self Examination Review in Psychiatry, 7th ed.

LEARNING TASK
Lecture 5 : ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE
CASE 1 :
A patient was brought to emergency unit by their family with complaint for sudden
breathing difficulties and decrease in consciousness. Five days before the patient suffered
from high temperature until shivering together with purulent cough and breathing
difficulties. During physical examination it was found T. 100/70, N. 120/m, RR. 30 times/m
temp.39 oC. in the lung it was found ronki diffuse, wheezing. On the thorax photo it was
found homogen covering on the two lung areas and consolidation in the center right side
part. During examination of blood gas analyses it was found PaO 2, 45 mmHg while PaCO2
65 mmHg.
SELF ASSESSMENT
1. Discuss about that case assessment
2. Other recommended examination
3. What is the procedure
4. How is the pathophysiology of ARDS
5. Explain etiopathogenesis of ARF
6. Distinguish between ARF Hypoxemia and Hyperkapnea
7. Objective of ventilator installation
RESOURCES
Polly E. Parson, MD. Acute Respiratory Distress Syndrome in Michael E. Hanley, Carolyn
H. Welsh, Lange Current Diagnosis & Treatment in Pulmonary Medicine 2003, 161 166.
ACUTE UPPER AIRWAY OBSTRUCTION ENT
LEARNING TASK :
Case 2.
Male, 9 month years old complained by his parent with dyspneu, stidor and cough,
immediately after choking peanut without history of upper respiratory infection.
QUESTION
1. What you should ask to complete the anamnesis?
2. What will you find from the physical examination?
3. What kind of other examination to support the diagnosis?
4. What possibility diagnosis of this patient?

5. How to manage and provide initial management and when do tou refer the patient?
LEARNING TASK
Case:
A mother of 6 years old child complained about difficult breathing with her child after eating
grape. There is no fiver. ENT condition with normal limited.
Task:
1. What are other helpful informations you should get from his mother for complete
management of this case?
2. Considering the onset of manifestation: please describe other clues you should find
during physical examination on this child!
3. Do you need laboratory investigation?
4. What are your suggestions for the mother?
5. What are your planning for manage this case?
Self assessment:
1. What causes acute upper airway obstruction?
2. Describe the etiopathogenesis of foreign body airway obstruction.
3. Describe the risk factor of foreign body airway obstruction.
4. Describe symptom and sign of foreign body airway obstruction.
5. Describe the imaging studies of acute upper airway obstruction.
6. Describe the management of acute upper airway obstruction.
NEONATAL RESUSCITATION
LEARNING TASK :
Case 3 :
A baby born at 33 weeks gestation following a caesarean section present with respiratory
distress soon after birth with bradypnoea (RR : 18 times/minutes). Heart rate 80
times/minutes regulary. The baby is requiring oxygen, an intravenous line inserted to provide
maintenance fluids. The mother had a temperature of 380 C.
TASK :
1. What is the diagnosis?
2. What investigation should be carried out?
3. What treatment would you institute of this condition?
4. Despite your effort above the baby has a cardio respiratory arrest with the ECG
monitor, what is the immediate management?
5. what is the prognosis?
SELF ASSESSMENT :
1. To describe definition of perinatal asphyxia
2. To describe pathophysiology and etiology of asphyxia
3. To describe :
Perinatal management
Delivery room management
Postnatal management

4. To describe prognosis of perinatal asphyxia
RADIOLOGY
LEARNING TASK
1. Describe the radiology imaging of thorax which is specific for :

a. IRDS
b. Bronchopneumonia
c. Congenital Heart Disease
d. Lung Edema
e. Pneumothorax
f. Pleural Effusion
g. Vena Cava Superior Syndrome.
SELF ASSESMENT :
1. A mother who have a new born baby complaint that her babys lips is blue and
always breathing so fast.
a. What kind of congenital anomalies do you think about this case ?
b. What kind of simple radiology examination that you suggest to do ?
c. What kind of radiology imaging you can find in this case ?
2. An old man, complaint cough with sputum every morning, suddenly feel shortness
of breath and suffered from ches pain in his right chest, Patient also complaint that
he didnt got a fever.
a. What do you think about this case ?
b. What kind of radiology examination that you suggest to do ?
c. What kind of radiology imaging you can find in this case ?
LEARNING TASK
Lecture 6 : BLEEDING DISORDERS
Epistaxis
Learning task
1. Female, 22 yo, pregnant 20 week gestation, comes to fast track because of bleeding of the
nose.
a. What kind of information that we need more?
b. Describe the pathophisiology, why is this happened?
c. What kind of complication that can be occurred in this patient? How to avoid it?
2. A boy, 6 yo, company by the parents complaining about habitual bleeding

a. What question we sould asked in order to recover the caused?
b. Explained the pathophisiology in this boy!
c. How to avoid bleeding int the future?
Hemorrhage in Pregnancy
CASE 2 :

A 25 years old G3 woman presents to the maternity unit with vaginal bleeding. Fetal heart
rate is 140 per minute and her blood pressure is 110/60 and her HR is 85/minute. Fundal
height is 28 cm. she has been given nothing. What are the possible diagnosis?
CASE 3 :
You have just delivered a 37 weeks twins pregnancy pervaginam. The third stage is
complicated by postpartum hemorrhage unresponsive to uterine massage and use of
oxytocin. What would your next management steps be ?
LEARNING TASK
Lecture 7 : SHOCK IN ADULT
Essay
1. 22 year old male presents following a motorcycle crash. He complains of the inability to
move or feel his legs. His blood pressure is 80/50 mm Hg, heart rate is 100, respiratory
rate is 20. GCS is 15. Temp 37 Oxygen is 99%on 2L nasal prongs. Chest X-ray, pelvic
X-ray, FAST are normal. Extremities are normal.
a. What the diagnose

b. Describe the emergency problem of the patient
c. How the management
2. Male 56 years admitted to the ICU for 1 week initially treated patients with symptoms of
urinary tract infections. Patient suddenly loss of consciousness followed by shortness
followed decreased urine output. On Physical examination are BP 90/50 pulse 120 RR 30
temp 40
a. Diagnose for ths patient
b. Decribe the management
3. A 67 year man unconcious felt down from 5 meters of tree, there are stab wound in
posteror of head. The backbone are fuly pain and cant move legs. On Physical
examination are BP 80/50 pulse 88RR 20 temp 37. Paraparese found in lower extremitas
a. what is the diagnose
b. what the supporting examination do you need?
c. describe the management this patient
4. A 24 year woman arrives in ER with dyspneau and skin rash on her chest and
abdominal, the woman unconsious and her lip was thiked and numbness, history of
allergic was denied. On Physical examination are BP 100/90 Pulse 100x/menit RR
37x/mnt temp 37, wheezing +/+ on right and left pulmo, rhonki -/- angioodema was
found.
a. Diagnose the patient
b. The different diagnose are
c. can describe the algorithm of management
d. Describe the Hypersensitivity Reaction

5. 22-year-old man sustains a shotgun wound to the left shoulder. His blood pressure is
initially 80/40. After two liters of Ringer's lactate solution his blood pressure
increases to 122/84. His pulse rate is now 100 beats per minute and his respiratory
rate is 28 breaths per minute. His breath sounds are decreased in the left hemithorax,
a. Diagnose and the differential diagnosis
b. Describe the management
SHOCK IN PEDIATRIC
Learning Task
Case 1
A 5 years old boy with body weight 20 kg, came with chief complain cold in palms and soles
since 24 hours before admitted to the hospital. History of fever occurred 5 days before
admitted to the hospital, but 1 day before admitted, the fever being decreased. The patient
had been urinated 10 hours before admitted to the hospital.
Physical examination
Patient with decreased of consiousness, pulse 140 x/minute regular smooth pulsation,
capillary refill time > 2 seconds.
Complete blood count
WBC: 2.000/uL, Hb: 15 g/dL, HCT: 45%, Plt: 20.000/uL
Self Assesment
1. Discuss about the assessment
2. Discuss about the therapy
3. Discuss about the monitoring
LEARNING TASK
Lecture 8 : CARDIAC ARREST AND CPR
Case Scenario 1
As on duty doctor at hospital, you are received emergency call from 2nd floor hospital.
The nurse said that there is a 70 yo male patient, diagnose as stable angina, suddenly
suffered SOB after eating, getting worse shortly, but still concious. After 10 minute, the
patient became unconcious.
1. Describe briefly the immediate act of first aid that should be done to
overcome the emergency and what is the next step/therapy?
2. What happen to her?
3. Can we prevent this patient became unconcious?
Case Scenario 2
A 30 year old woman attends your clinic with asthma attack. She has a long history of
asthma, with severe attacks requiring hospitalisation. Despite continuous nebulised
salbutamol, she rapidly gets worse over about ten minutes with severe respiratory

distress, she is unable to talk and is becoming increasingly confused and unconcious.
From the monitor you already attach, the ECG shown takikardi and became bradikardia
and continue to asystole.
1. Based on immediate observation, what is the patient going through and what
actions should be done ?
2. Based on your analysis what would have caused this emergency and explain
its pathogenesis and pathophysiology.
3. Can you prevent this patient from asystole? Explain it.
4. Explain the management of asystole.
Case Scenario 3
85 year old man is delivered by car to your clinic. He was found collapsed 10 minute ago
by his family in the garden. At Physical examination, no pulse at a.jugularis, no heart
sound. A monitor is attached and the rhytm is VF.
1. What are you going to do?
2. How long we need to do CPR at this patient?
3. Explain the algorithm of Shockable cardiac arrest
Case Scenario 4
As doctor on duty at emergency room, you received a 50 years old man with history of
chest pain and suddenly unconscious in front of you. After doing fast examination, you
diagnose the patient as cardiac arrest with VT pulseless
1. Explain about the resuscitation team to perform good CPR on this patient.
2. How would you build a good resuscitation team?
3. Explain how would you doing defibrillation on this patient.
SELF ASSESSMENT
1. Explain the etiopathogenesis and pathophysiology of cardiac arrest
2. Explain the Guideline of BLS and ALS
3. Explain about shockable and non shockable cardiac arrest.
4. Explain the complication and prognosis of cardiac arrest.
LEARNING TASK
Lecture 9 : EMERGENCY TOXICOLOGY AND POISONING
Case 1
Male 25 years, came to the ER carried by his family in a state of unconsciousness. After
approximately 24 hours ago attend the party. Previous patients with mild drunk and sleepy,
then complained of blurred vision and blind
Learning task 1
1. Describe the symptoms and clinical signs in these cases?
2. What are the other anamnesis and the other physical examination that needed
3. What the laboratory examination is needed to confirm the diagnosis
4. What the differential diagnosis above case
5. What the diagnosis above case

6. How to manage the above case
Case 2
Male 20 years, student, came to the ER Sanglah, was brought by his parents in a state of
unconsciousness. On physical examination found coma, blood pressure 80/60 mm Hg, pulse
48 beats per minute, frequency of breathing 12 times per minute. The pupils: miosis.
Abdominal examination: decreased bowel sounds. At the forearm found needle track marks.
Learning task 2
Case 3
Male, 20 years old, a builder, came to the ER escorted by his friend, the pain after
accidentally ingesting drinking colored floor cleaning liquid is clear and odorless. On
physical examination lip until pharing area look red and swollen.
Learning task 3
Case 4
Male 30 years old come to the ER, in between by his girlfriend, complained of fatigue and
vomiting - vomiting after drinking Baygon (insecticide), approximately 6 hours ago. Patients
also complain of frequent urination and defecation. On physical examination found the pulse
of 48 beats per minute, miosis, lacrimation, salivation.
Learning task 4
How to manage the above case
LEARNING TASK
Lecture 10 : PREGNANCY INDUCED HYPERTENSION

CASE :
A 35 years-old G1P0 woman present for her prenatal visit at 34 weeks gestation. Her BP is
165/110. she has no history of hypertension. What steps do you perform as part of your
initial investigation?. And what is the plan for management and treatment of his case ?
LEARNING TASK
Lecture 11 : SHOULDER DYSTOCIA
LEARNING TASK
You are urgently called to the delivery room of a 26-year-old woman to help deliver the
baby. The mother is 41 weeks into her second pregnancy, having had a normal term delivery
of a 3.97 kg female infant 2 years ago. Nuchal and anomaly scans were normal and
antenatal care was unremarkable. The baby was moving normally prior to labour.
When she arrived on labour ward contracting, the symphysio-fundal height was noted to be
41 cm. At first assessment the cervix was 3 cm dilated and she was advised to continue
mobilizing. Spontaneous rupture of membranes occurred and she was examined again after
4h and the cervix was still 3 cm. A oxytocine infusion was commenced to augment labour
and an epidural sited, with cardiotocograph monitoring also commenced. After 4h, the cervix
was 7cm and then 10cm after a further 4h. The woman was encouraged to start active
pushing and 35 min later the head had crowned in a direct occipito-anterior position.
The midwife noticed that the head did not extend normally on the perineum and that the chin
appeared to be wedged against the perineum. She had attempted delivery of the shoulders
with the next two contractions but this had not been achieved.
Questions
1.What is the diagnosis?
2. What are the risk factors in this case?
3. How would you manage this scenario?
4. What kind of complications that possibly happened in this case?
SELF ASSESSMENT
6. Discuss the diagnosis of shoulder dystocia

7. Discuss the incidence of shoulder dystocia
8. Discuss the risk factors of shoulder dystocia
9. Discuss the complications of shoulder dystocia
10. Discuss appropriate management of shoulder dystocia
LEARNING TASK
Lecture 12 : ACUTE BLISTERING AND EXFOLIATIVE SKIN

Case 1
A 18 years old male come to emergency unit sanglah hospital with blistering skin rash. He
had fever, malaise and diarrhea 7 days before and get medication such us cotrimoxazole,
parasetamol, and multivitamin tablets from general practitioner. Two days later, he developed
erythematous lesions over his extremities, face and trunk. Patient with weak condition, BP
110/80 mmHg, temp 40C, RR 20x/minutes. From eye examination there is redness on
conjungtiva, from mouth and genetalia examination we find multiple erosion with
hemmoragic crust. From his extremities, face and trunk we find multiple purpuric lesion and
some part of rash with bullous and erotion that involve 35% BSA.
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What other information do you need to support the diagnosis?
3. What other examination you should do to this patient?
4. What monitoring should you do to this patient?
5. How do you manage this patient?
6. What is the complication of this condition?
SELF ASSESSMENT
1. Describe the principle clinical features of SJS, TEN.
2. Describe the pathogenesis of SJS, TEN.
3. Explain more detail the basic principle of management of SJS, TEN.
4. Describe the prognosis and complication of SJS, TEN.
Case 2
A 3 months baby come to dermatology polyclinic Sanglah hospital with skin rash all over the
body. She had a fever, cough and rhinitis 4 days before. Two days later, she developed
erythematous rash around the nose and the rash widespread all over her body with the skin
peel easyly. Her mother give her paracetamol syrup but there is no improvement. Patient
with weak condition, temp 39.5C, RR 28x/minutes. Skin effloresence from face, trunk,
back, and extremities, we find erythematous macule, some part of the lesion with multiple
vesicle and desquamation skin.
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What is the other differential diagnosis for this case?
3. What other information do you need to support the diagnosis?
4. What other examination you should do to this patient?
5. What monitoring should you do to this patient?
6. How do you manage this patient?
7. What is the complication of this condition?
SELF ASSESSMENT
1. Describe the principle clinical features of SSSS.
2. Describe the pathogenesis of SSSS.
3. Explain more detail the basic principle of management of SSSS.
4. Describe the prognosis and complication of SSSS.

LEARNING TASK
Lecture 13 : TRAUMA WHICH POTENTIALLY DISABLING AND LIFE
THREATENING CONDITIONS
SELF DIRECTING LEARNING
Basic knowledge that must be known:

1. Airway management
2. Breathing Management
3. Circulatory management
4. Disability Management
SCENARIO
Male 42 years old, came to our hospital Unconcious, On Primary survey : airway
clear, Breathing : Repiratory rate 28 x/minute, Circulatory : Blood pressure 80/60 mmhg and
Heart rate 120 x/minute. Disability Pain Response. He was motor cyclist and hit by a car. On
physical examination: shortening of his left lower leg and false movement found.
1. What are the patient problem?
2. What are the symptom and sign of Tension Pneumothorax, Massive Hematothorax
and Cardiac Tamponade?
3. How you manage the patient ?
A 33 year old woman is involved in a head-on motor vehicle crash. It took 30 minutes to
extricate her from the car. Upon arrival in the emergency department, her heart rate is 120
beats per minute, BP is 90/70 mmHg, respiratory rate is 16 breaths per minute, and her GCS
score is 15. Examination reveals bilaterally equal breath sounds, anterior chest wall
ecchymosis, and distended neck veins. Her abdomen is flat, soft, and not tender. Her pelvis is
stable. Palpable distal pulses are found in all 4 extremities.
1. What are the patient diagnosis?
2. How you manage the patient ?
Learning Task
1. Hematothorax & Massive Hemathotorax?
2. Simple Pneumothorax, Open Pneumothorax and Tension Pneumothorax?
3. Cardiac Tamponade?
Self Assessment
1. Describe about Life threathening condition in breathing ?
LEARNING OBJECTIVE
Establish tentative diagnosis, provide initial assessment in circulatory
Scenario

A 25 year old man is brought to a hospital with a general surgeon after being involved in a
motor vehicle crash. He has a GCS of 13 and complains of abdominal pain. His blood
pressure was 80 mm Hg systolic by palpation on arrival at the hospital, but increases to
110/70 mm Hg with the administration of 2 liters of intravenous fluid. His heart rate remains
120 beats per minute.His blood pressure falls to 70 mm Hg after CT Scan.
What are the patient problem?
What are the symptom and sign of abdominal trauma and pelvic trauma ?
How you manage the patient ?
Learning Task
Abdominal Trauma?
Pelvic Trauma ?
Self Assessment
Describe about Life threathening condition in circulation ?
LEARNING TASK
Lecture 14 : PHLEGMON
1. Patient female, 28 years old, with complaints of pain in the lower chin, up to the front
of the neck feel hard when touched, fever, difficulty swallowing and difficulty
breathing, the patient appears weak. Intra-oral examination is difficult because
patients with difficulty opening the mouth, tongue looks lifted and swelling of the
gums behind that cover most of the right mandibular M3. Pain in the gums behind the
perceived than 4 days ago, the patient just gargling with warm salt water when not
withstand the pain.
a. As a doctor what would you do?
b. What examinations will you do for this case?
c.What is the diagnosis?
d. What does your planning for management in this case?
2. Patient male, 38 years old, come to RSPTN with dread because of the pain that is felt
in mandibulla left with swelling to the left cheek, intra oral condition appears to exist
in the dental caries with mobillity o2 M2 residual roots on the left, buccal fold appears
elevated, palpation there is fluctuation exudate. Dental pain is felt starting from 3
days ago but have not had time to check to the dentist, just buy painkillers to reduce
the pain.
a. What you should ask to complete the anamnesis?
b. What is the diagnosis?
c. What does your planning for management in this case?
3. Patient woman, 38 years old, with complaints mandibulla swollen and hard when
touched on the lower jaw side since a few months ago, seemed teeth no complaints.
There is no pain and illness but the patient had never examined the situation to the
doctor or dentist.

a. What you should ask to complete the anamnesis?

b. What is the diagnosis?
c. What does your planning for management in this case?
Self Assassment:
1. Explain the difference between mandibulla with phlegmon abscess?

2. In addition to any abscess mandibulla differential diagnosis of phlegmon?
3. Discuss with your group the most important management of phlegmon?
BRAIN RESUSSCITATION
Case disscusion
Uncooperative, agitated 28 years old male is brought to emergency room after motorcycle
accident. The examination show that the patient is gurgling, and when he was given pain
stimulation, he was opening his eyes, speaking nonsensical and withdrawing from pain.
Blood pressure 85/45 mmHg, pulse 115 x/sec, respiratory rate 25 x/sec, and saturation
oxygen 90-92 %
1. How do you classified the patient according to severity of the TBI? What is your plan
for this patient?
2. Will you intubate the patients? Why?
3. Will you give this patients fluids resuscitation? Why? And what kind of fluid will you
choose for this patients?
4. When do you suspect this patients have an elevated ICP or brain herniation?
5. What do you know about first and second tier therapy?
LEARNING TASK
Lecture 15 : UROLOGIC CONCERN IN CRITICAL CARE FOR NON TRAUMA
CASE
Case 1 An Old man that unable to void
A 65-year-old man with multiple medical problems presented with complaints that he could
not void and had pain in the lower abdomen since yesterday. He had a mild dementia, so
much of the history was from his wife, who accompanied him to the clinic. She stated that he
had neither incontinence, fever, nausea, nor vomiting, and he had not had any recent acute
illnesses. The patient had not had any recent change in medications, doses, or frequency of
dosing of his pain medication. He had similar problems in the past, but the symptoms had
resolved after he underwent a transurethral resection of the prostate (TURP) 4 years ago. His
wife also stated that he had been complained of frequently in mictie, incontinence, small
caliber urination for last 1 month.
The patient's medical history was extensive. He had also type 2 diabetes, hypertension
anglaucoma
His medications included an extended-release morphine tablet for pain, insuline for his

diabetes, and recently discontinued ramipril and hydrochlorothiazide, which he had taken in
the past for his hypertension. On examination, he was mildly tender over the bladder, which
was palpably distended. He attempted to void for a urinalysis specimen and was unable to do
so. A Foley catheter was placed, and 350 mL of urine was collected. The urinalysis showed a
trace of protein, and laboratory results were otherwise negative; the pH was 7.3.
Question Learning Task
1. What are some possible causes of acute urinary retention?

2. What tests would be helpful in determining the cause of this patient's urinary retention?
3. What treatments would be useful in relieving the symptoms?
4. What is the definitive treatment for this case?
4. What are some complications of untreated acute urinary retention?
Self Assesment
1. What is Fournier gangrene? And how to manage this gangrene?
2. Why contrast study should not be perform in colic episode?
3. How to manage the ureteral colic?
4. What is the differential diagnosis of hematuria?
5. How to establish the rupture of penile tunica albugenia? tWhat is the complication of
penile fracture? How to prevent those complications?
6. What is the definition of anuria? Name conditions or diseases that may result in anuria?
How to manage the anuria condition?
7. Explain about urosepsis and its management.
8. What is risk factors of Priapismus? And what will you do if the patient come to your
emergency room?
LEARNING TASK
Lecture 16 : UROLOGIC CONCERN IN CRITICAL CARE FOR TRAUMA CASE
LEARNING TASK TRAUMA UROLOGI
1. Seorang laki2 50 thn datang ke UGD setelah tertembak di bagian perut kanan atas 1 jam
sebelumnya. Kencing berwarna merah. vital sign stabil.Jelaskan;a. Informasi anamnesa
dan pemeriksaan fisik yang anda perlukan?b. Pemeriksaan penunjang yang anda
sarankan?c. Manajemen kasus diatas?
2. Seorang laki2 25 thn datang ke UGD dengan keluhan keluar darah menetes dari ujung
kemaluan setelah jatuh dari tangga dalam posisi terduduk. Jelaskan ;a. Informasi
anamnesa dan pemeriksaan klinis yang anda butuhkan?b. Pemeriksaan penunjang yang
anda sarankan?c. Manajemen kasus diatas?
3. Seorang laki -laki datang ke ugd dengan nyeri perut bawah dan kencing tersendat
bercampur darah, setelah kecelakaan lalu lintas. Perut bawah terbentur stir saat
mengendarai mobil 2 jam sblm ke ugd. Pemeriksaan fisik vital sign stabil, ditemukan
jejas supra symphisis dan nyeri tekan. Di UGD dilakukan pemasangan kateter urine tapi
tidak keluar urine. pasien kesakitan mengeluh tidak bisa kencing. Jelaskan ;a. Diagnosa
yang paling mungkin?b. Pemeriksaan penunjang yang anda sarankan?b. Manajemen
kasus diatas?
4. Seorang anak laki2 12 thn mengeluh luka pada scrotum setelah terjatuh dari sepeda.

kencing tersendat dan pemeriksaan fisik tampak luka terbuka pada scrotum kiri
sepanjang 4 cm. Jelaskan;a. Informasi anamnesa dan pemeriksaan fisik yang anda
perlukan?b. pemeriksaan penunjang yang anda sarankanb. Manajemen kasus diatas?
5. Seorang wanita datang ke UGD dengan keluhan nyeri pinggang kanan dan kencing
bercampur darah setelah kecelakaan lalu lintas. Vital sign saat datang stabil, tapi 30 mnt
kemudian tekanan darah 90/60 dan nadi 102x/mnt, tidak membaik dengan pemberian
cairan kristaloid. jelaskan ;a. Informasi anamnesa dan pemeriksaan fisik yang anda
perlukan?b. Pemeriksaan penunjang yang anda sarankan?c. Manajemen kasus diatas?

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Study Guide Emergency Medicine September 2017

Medical Education Unit Faculty of Medicine Udayana University 1

Mastery of basic knowledge with its clinical and practical implication.

Medical Education Unit Faculty of Medicine Udayana University 2

NO. NAME DEPARTMENT

NO. NAME DEPARTMENT PHONE

Medical Education Unit Faculty of Medicine Udayana University 3

7. Dr.dr. Agus Somya, SpPD(KPTI) Internal 08123989353

Medical Education Unit Faculty of Medicine Udayana University 4

FACILITATOR SEMESTER VII

dr. Henky, Sp.F., M.Bioethics Forensic 08123988486 3rd floor:

Medical Education Unit Faculty of Medicine Udayana University 5

Medical Education Unit Faculty of Medicine Udayana University 6

4. 08.00- Lecture 4. Class room Dr.dr. Tjokorda Bagus

DAY/DATE TIME LEARNING VENUE CONVEYER

Medical Education Unit Faculty of Medicine Udayana University 7

09.00- Individual Learning -

Medical Education Unit Faculty of Medicine Udayana University 8

09.00- Individual Learning

DAY/DATE TIME LEARNING VENUE CONVEYER

10. 08.00-09.00 Lecture 10 Class room Dr.dr. I Gede Mega

Medical Education Unit Faculty of Medicine Udayana University 9

13. 08.00-09.00 Lecture 13. Dr.dr. Ketut Suyasa,

09.00-10.30 Individual Learning -

DAY/DATE TIME LEARNING VENUE CONVEYER

09.00-10.30 Individual Learning -

Medical Education Unit Faculty of Medicine Udayana University 10

14.00-15.00 Plenary Class room Dr.dr. Gede Wirya

08.00-09.00 Lecture 16. Class room

1 08.00-selesai Basic clinical skill Clinical skill Dr.dr. Ketut Suyasa,

2 08.00-selesai Basic clinical skill SMF Dr.dr.Tjok Gde

Medical Education Unit Faculty of Medicine Udayana University 11

Medical Education Unit Faculty of Medicine Udayana University 12

15.00- Plenary Class room dr. IGN Budiarsa,SpS

Medical Education Unit Faculty of Medicine Udayana University 13

15.00- Plenary Class room dr Sari Wulan, SpTHT-

DAY/DATE TIME LEARNING VENUE CONVEYER

Medical Education Unit Faculty of Medicine Udayana University 14

15.00- Plenary Class room dr. IGAG. Utara Hartawan,

DAY/DATE TIME LEARNING VENUE CONVEYER

Medical Education Unit Faculty of Medicine Udayana University 15

11. 09.00-10.00 Lecture 11. Class room dr. Endang

10.00-11.30 Student Project -

DAY/DATE TIME LEARNING VENUE CONVEYER

Medical Education Unit Faculty of Medicine Udayana University 16

15.00-16.00 Plenary Class room drg. Lestari Sudirman

10.00-11.30 Student Project -

09.00-10.00 Lecture 16. Class room

1 08.00-selesai Basic clinical skill Clinical skill Dr.dr. Ketut Suyasa,

Medical Education Unit Faculty of Medicine Udayana University 17

Medical Education Unit Faculty of Medicine Udayana University 18

Format of the paper :

1. Cover Title (TNR 16)

Medical Education Unit Faculty of Medicine Udayana University 19

Lecture 1 : HIGHLIGHT EMERGENCY

Tjokorda Gde Agung Senapathi

The World Health Organization defines a disaster as a sudden ecologic phenomenon

When it appears that the normal procedures of an ED may be interrupted by an event,

Medical Education Unit Faculty of Medicine Udayana University 20

Table 1 Types of Disarter

Terrorist Eventsthatarepurposefully EventsofSeptember11,2001,aswell

External Aneventthatoccursexternalto Transportationaccident,industrial

Acute Disasterthatoccursinanarrow Explosion,industrialrelease,

Medical Education Unit Faculty of Medicine Udayana University 21