study guide tayang blok emergency 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

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

PLANNERS TEAM

NO. NAME DEPARTMENT

1. Dr.dr.Tjok Gde Agung Senapathi,Sp.AnKAR (Coordinator)

Anesthesiology and 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. 6.

Drg. Lestari Sudirman Dr.dr. I Putu Pramana

Suarjaya,SpAn.M.Kes.KMN.KNA

Dentistry

Anesthesiology and 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. 17. 18. 19. 20. 21. 22. 23. 24.

dr. Sri Laksminingsih SpR (K) dr. IA Sriwijayanti,MBioMed,SpS dr. IGAG Utara Hartawan,SpAn.MARS dr. Nyoman Budihartawan,M.Sc,SpA dr. IGN. Mahaalit Aribawa,SpAn.KAR Dr.dr. Ketut Suyasa, SpB. SpOT(K)Spine dr. IGN. Wien Aryana,SpOT

dr. Wayan Sucipta,SpTHT KL

dr. Ida Bagus Krisna Jaya Sutawan,SpAn.M.Kes

Radiology Neurology Anesthesiology and Intensif Terapy Pediatrician Anesthesiology and Intensif Terapy Ortophedic Surgery Ortophedic Surgery ENT Anesthesiology and Intensif Terapy LECTURERS

NO. NAME DEPARTMENT PHONE

1. Dr.dr.Tjok Gde Agung

Senapathi,Sp.AnKAR (Chairman)

Anesthesiology and Intensif Terapy

081337711220

2. Dr.dr. I Ketut Suyasa, SpB,SpOT(K)

Surgery 081558724088

3. dr. IGN Budiarsa,SpS Neurology 0811399673

4. dr. Sari Wulan,SpTHT KL, dr. Wayan Sucipta,SpTHT KL

ENT 081237874447(SW)

08125318941 (WS)

5.

6. drg. Lestari SudirmanDr.dr. I Putu Pramana

Suarjaya,SpAn.M.Kes.KMN.KNA

Dentistry Anesthesiology and Intensif

08155764446

0811394811 (PRAM) / 08123836470 (KRIS)

& dr. Ida Bagus Krisna Jaya Sutawan,SpAn.M.Kes

Terapy

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

Medicine 08123989353

8. dr. Putu Andrika,SpPDKIC Pulmonology 08123875875

9. Dr.dr. Dyah Kanyawati, SpA(K) Pediatric 081285705152

10. Dr.dr. Wayan Megadana, SpOG(K) Obstetric-Gynecologic

08123917002

11. dr. Endang Sriwidiyanti, SpOG

Obstetric-Gynecologic 081558314827

12. Dr.dr. Gede Megaputra, SpOG(K) Obstetric-Gynecologic

08123636172

13. Dr.dr. Gd Wirya Kesuma Duarsa, SpU,MKes, dr. Wayan Yudiana, SpU

Surgery 081338708195 (YUD) 081338333951 (GWK)

14. Dr.dr.Tjokorda Bagus

Jayalesmana,SpKJ Psychiatric 0816295779

15. dr. Nyoman Suryawati, SpKK Dermatology 0817447279

16 17. 18. 19. 20. 21. 22. 23. 24.

dr. Sri Laksminingsih SpR (K) dr. IA Sriwijayanti,MBioMed,SpS dr. IGAG Utara

Hartawan,SpAn.MARS dr. Nyoman

Budihartawan,M.Sc,SpA dr. IGN. Mahaalit Aribawa,SpAn.KAR Dr.dr. Ketut Suyasa, SpB. SpOT(K)Spine

dr. IGN. Wien Aryana,SpOT dr. AA Gde Yuda Asmara, SpOT (K)

dr. Made Agus Dwianthara Sueta, SpB KBD Radiology Neurology Anesthesiology and Intensif Terapy Pediatrician Anesthesiology and Intensif Terapy Ortophedic Surgery Ortophedic Surgery Ortophedic Surgery Digestive Surgery 08164745561 081337667939 081138914910 081236333221 0811396811 081558724088 0811385263 081337870347 081338648424

FACILITATOR SEMESTER VII MEDICAL EMERGENCY

Regular Class (Class A)

No Name Group Departement Phone ₍₃Venuerd _floor)

1 dr. Komang Ayu Kartika Sari, MPH A1 Public Health 082147092348 3rd floor:_R.3.09

2 dr. Nyoman Suryawati, M.Kes, Sp.KK A2 _venerologyDermato- 0817447279 3rd floor:_R.3.10

3 Dr.dr I B G Fajar Manuaba, Sp.OG, _MARS A3 Obgyn 081558101719 3rd floor:_R.3.11

4 Dr. dr. I Wayan Suranadi, Sp.An. KIC A4 Anesthesi 08123847675 3rd floor:_R.3.12

5 dr. Henky, Sp.F., M.Bioethics B10 Forensic 08123988486 3rd floor:_R.3.13

6 dr. Sri Laksminingsih, Sp.Rad A6 Radiology 08164745561 3rd floor:R.3.14

7 Dr. dr. I Gusti Ayu Sri Mahendra Dewi, _Sp.PA(K) A7 _PhatologyAnatomy 081338736481 3rd floor:_R.3.15

8 dr. I Putu Budhiastra, Sp.M (K) A8 Opthalmology 085238238999 3rd floor:_R.3.16

9 Dr. dr. I Made Oka Adnyana, Sp.S(K) A9 Neurology 0817347697 3rd floor:_R.3.17

10 Dr. dr. I Wayan Putu Sutirta Yasa., _M.Si A10 _PhatologyClinical 08123953344 3rd floor:_R.3.19

Regular English (Class B)

No Name Group Departement Phone ₍₃Venuerd _floor)

1 Dr. dr. I Ketut Suyasa, Sp.B. Sp.OT(K) B1 Orthopaedic 087862400166 3rd floor:_R.3.09

2 dr. I Made Putra Swi Antara, Sp.JP(K),_FIHA B2 Cardiology 08123804782 3rd floor:_R.3.10

3 dr. Ni Made Renny Anggreni Rena, _Sp.PD B3 _MedicineInternal 081803651656 3rd floor:_R.3.11

4 Dr. dr.Elysanti Dwi Martadiani, Sp.Rad _(K) B4 Radiology 081805673099 3rd floor:_R.3.12

5 dr. Herman Saputra. Sp.PA(K) B5 _PhatologyAnatomy 081338981853 3rd floor:_R.3.13

6 dr. Made Agus Dwianthara Sueta, _Sp.B-KBD B6 Surgery 081338648424 3rd floor:_R.3.14

7 Dr. dr. A.A. Mas Putrawati T., Sp.M(K) B7 Opthalmology 08123846995 3rd floor:_R.3.15

8 dr. I Nyoman Gede Budiana, Sp.OG _(K) B8 Obgyn 08123997401 3rd floor:_R.3.16

10 Dr. dr. Made Ratna Saraswati, Sp.PD-_KEMD-FINASIM B10 _MedicineInternal 08123814688 3rd floor:_R.3.19

TIME TABLE

EMERGENCY BLOCK 2017 Regular Class

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER 1. Mon, 11 Sept 2017 08.00-09.00 Highlight in Emergency Medicine (Coordinator)

Class room Dr.dr. Tjok Gde Agung Senapathi, Sp.AnKAR

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. Tjok Gde Agung

Senapathi, Sp.AnKAR 2. Tue, 12 Sept 2017 08.00-09.00 Lecture 2. Status Epilepticus and Other Seizure

Disorders

Class room dr. IGN Budiarsa,SpS

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. IGN Budiarsa,SpS

3. Wed,

13 Sept

2017

08.00-09.00 Coma andLecture 3. Decrease of Consciousness

Class room dr. Ida Ayu

Sriwijayanti,MBioMed,SpS 09.00-10.30 Individual Learning 10.30-12.00

SGD Disc room Facilitators

12.00-12.30

Break

14.00-15.00

Plenary Class room dr. Ida Ayu

Sriwijayanti,MBioMed,SpS 4. Thu, 14 Sept 2017 08.00-09.00 Lecture 4. Acute Psychiatric Episodes

Class room Dr.dr. Tjokorda Bagus Jayalesmana,SpKJ 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. Tjokorda Bagus

Jayalesmana,SpKJ 5. Fri, 15 Sept 2017

08.00-09.00 Acute RespiratoryLecture 5. Distress Syndrome

and Failure

Class room dr Sari Wulan, SpTHT-KL(K) / dr Wayan

Sucipta,SpTHT-KL ( and ENT Team), dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya wati,SpA (K), dr. Srie Laksminingsih, SpRad 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 Sari Wulan, SpTHT-_{KL(K) / dr Wayan}

Sucipta,SpTHT-KL ( and ENT Team), dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya wati,SpA (K), dr. Srie Laksminingsih, SpRad

DAY/DATE TIME LEARNING

ACTIVITY

6. Mon, 18 Sept 2017 08.00-09.00 Lecture 6. Bleeding Disorder(Epistaxis, Hemorrhage In Pregnancy) and Airway Obstruction

Class room dr Sari Wulan, SpTHT- KL(K), dr. Sucipta, SpTHT KL ( and ENT Team) Dr.dr Wayan Megadhana, SpOG(K) (and OBGYN Team)

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 Sari Wulan,

SpTHT-KL(K), dr. Sucipta, SpTHT KL ( and ENT Team) Dr.dr Wayan Megadhana, SpOG(K) (and OBGYN Team) 7. Tue, 19 Sept 2017

08.00-09.00 Lecture 7.Shock Class room dr. IGAG. Utara Hartawan, SpAn MARS dr.Nyoman

Budihartawan,MSc,SpA

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. IGAG. Utara Hartawan,

SpAn MARS dr.Nyoman Budihartawan,MSc,SpA 8. Wed, 20 Sept 2017 08.00-09.00 Lecture 8. Cardiac Arrest and

+

Cardiopulmonary Resuscitaton

Class room dr. IGN. Mahaalit Aribawa, SpAn KAR

09.00-10.30 Individual Learning

- 10.30-12.00

SGD Disc room Facilitators

12.00-12.30

12.30-14.00

Student Project

14.00-15.00

Plenary Class room dr. IGN. Mahaalit Aribawa,

SpAn KAR 9 Fri, 22 Sept 2017 08.00-09.00 Lecture 9. Emergency Toxicology and Poisoning

Class room Dr.dr. Agus Somya, SpPD KPTI

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. Agus Somya, SpPD

KPTI

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER 10. Mon, 25 Sept 2017

08.00-09.00 Lecture 10

Hypertension In Pregnancy

Class room Dr.dr. I Gede Mega Putra, SpOG(K)

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

Tue,

26 Sept

2017

08.00-09.00 Lecture 11.

Shoulder Dystocia

Class room dr. Endang

Sriwidiyanti,SpOG

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. Endang

Sriwidiyanti,SpOG 12.

Wed,

27 Sept

2017

08.00-09.00 Lecture 12.

Acute Blistering and Exfoliative Skin

dr. Nyoman Suryawati Sp.KK

09.00-10.30 Individual Learning

-10.30-12.00 SGD Fasilitator

12.30-14.00 Student Project

14.00-15.00 Plenary dr. Nyoman Suryawati

Sp.KK 13.

Thu,

28 Sept

2017

08.00-09.00 Lecture 13.

Trauma Which Potentially Disabling

and life Threatening Conditions

Dr.dr. Ketut Suyasa, SpB SpOT(K) Spine dr. IGN Wien Aryana, SpOT

09.00-10.30 Individual Learning

-10.30-12.00 SGD Disc room Fasilitators

12.00-12.30 Break

12.30-14.00 Student Project

14.00-15.00 Plenary Dr.dr. Ketut Suyasa,

SpB SpOT(K) Spine dr. IGN Wien Aryana, SpOT

DAY/DATE TIME LEARNING

ACTIVITY

VENUE CONVEYER

14 Mon,

2 Oct

2017

08.00-09.00 Lecture 14.

Phlegmon Brain Resuscitation

Class room drg. Lestari Sudirman Dr.dr. I Pt Pramana Suarjaya, SpAn.MKes, KMN KNA/dr. IB Krisna Jaya Sutawan, SpAn MKes

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 drg. Lestari Sudirman

Dr.dr. I Pt Pramana Suarjaya, SpAn.MKes, KMN KNA/dr. IB Krisna Jaya Sutawan, SpAn MKes

15 Tue,

3 Oct

2017

08.00-09.00 Lecture 15.

Urologic Concern in Critical Care for NonTrauma Case

Class room Dr.dr. Gede Wirya Kusuma Duarsa, M.Kes, SpU(K)

09.00-10.30 Individual Learning

12.00-12.30 Break

12.30-14.00 Student Project

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

Kusuma Duarsa, M.Kes, SpU(K) 16 Wed, 4 Oct 2017

08.00-09.00 Lecture 16.

Urologic Concern in Critical Care for

Trauma Case

Class room

dr. Wayan Yudiana, SpU

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. Wayan Yudiana,

SpU 1

Thu, 5 Oct 2017

08.00-selesai Basic clinical skill (1/2)

Basic Trauma Care (English Class jam 08.00-11.30 WITA; Regular class jam : 12.30-15.00 WITA)

Clinical skill

lab  Dr.dr. Ketut Suyasa,SpB. SpOT(K)Spine  dr. IGN. Wien

Aryana, SpOT  dr. AA Gde Yuda

Asmara, SpOT (K)  dr. Made Agus

Dwianthara Sueta, SpB KBD 2 Fri, 6 Oct 2017

08.00-selesai Basic clinical skill (1/2)

CPR

(Regular Class jam 08.00-11.30 WITA;

English Class jam 12.30-15.00)

SMF

Anestesiologi dan Terapi Intensif

 Dr.dr.Tjok Gde Agung

Senapathi,Sp.AnKA R

 Dr.dr. I Putu Pramana

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

Mon, 9 Oct 2017 Student Project 4 Tue, 10 Oct 2017 Prepare For Examination Thu, 12 Oct 2017 EXAMINATION 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 tanggal 22 September 2017

English Class

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER 1. Mon, 11 Sept 2017 09.00-10.00 Highlight in Emergency Medicine (Coordinator)

Class room Dr.dr. Tjok Gde Agung Senapathi, Sp.AnKAR

10.00-11.30 Student Project

- 11.30-12.00 Break 12.00-13.30 Individual Learning 13.30-15.00 SGD 15.00-16.00

Plenary Class room Dr.dr. Tjok Gde Agung

Senapathi, Sp.AnKAR 2. Tue, 12 Sept 2017

09.00-10.00 Status EpilepticusLecture 2. and Other Seizure

Disorders

Class room dr. IGN Budiarsa,SpS

10.00-11.30

Student Project

- 11.30-12.00

12.00-13.30 Individual Learning 13.30-15.00 SGD 15.00-16.00

Plenary Class room dr. IGN Budiarsa,SpS

3. Wed, 13 Sept 2017 09.00-10.00 Lecture 3. Coma and Decrease of Consciousness

Class room dr. Ida Ayu

Sriwijayanti,MBioMed,SpS 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. Ida Ayu

Sriwijayanti,MBioMed,SpS 4. Thu, 14 Sept 2016

09.00-10.00 Acute PsychiatricLecture 4. Episodes

Class room Dr.dr. Tjokorda Bagus Jayalesmana,SpKJ

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. Tjokorda Bagus

Jayalesmana,SpKJ 5. Fri, 15 Sept 2017 09.00-10.00 Lecture 5. Acute Respiratory Distress Syndrome and Failure

Class room dr Sari Wulan, SpTHT-KL(K) / dr Wayan

Sucipta,SpTHT-KL ( and ENT Team), dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya wati,SpA (K), dr. Srie Laksminingsih, SpRad

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 Sari Wulan,}

SpTHT-KL(K) / dr Wayan

Sucipta,SpTHT-KL ( and ENT Team), dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya wati,SpA (K), dr. Srie Laksminingsih, SpRad

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER 6. Mon, 18 Sept 2017

09.00-10.00 Lecture 6.Bleeding Disorder(Epistaxis,

Hemorrhage In Pregnancy) and

Airway Obstruction

Class room dr Sari Wulan, SpTHT KL, dr. Sucipta, SpTHT KL ( and ENT Team)

Dr.dr Wayan Megadhana, SpOG(K) (and OBGYN Team)

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 Sari Wulan, SpTHT KL,dr. Sucipta, SpTHT KL ( and ENT Team)

Dr.dr Wayan Megadhana, SpOG(K) (and OBGYN Team) 7. Tue, 19 Sept 2017

09.00-10.00 Lecture 7.Shock Class room dr. IGAG. Utara Hartawan,SpAn MARS, dr.Nyoman

Budihartawan,MSc,SpA

10.00-11.30

Student Project

- 11.30-12.00

Break Disc room Facilitators

12.00-13.30 Individual Learning

15.00-16.00

Plenary Class room dr. IGAG. Utara Hartawan,

SpAn MARS, dr.Nyoman Budihartawan,MSc,SpA 8. Wed, 20 Sept 2017 09.00-10.00 Lecture 8. Cardiac Arrest and

+

Cardiopulmonary Resuscitaton

Class room dr. IGN. Mahaalit Aribawa, SpAn KAR

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. IGN. Mahaalit Aribawa,

SpAn KAR 9 Fri, 22 Sept 2017 09.00-10.00 Lecture 9. Emergency Toxicology and Poisoning

Class room Dr.dr. Agus Somya, SpPD KPTI 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. Agus Somya, SpPD KPTI

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER 10. Mon, 25 Sept 2017

09.00-10.00 Lecture 10.

Pregnancy Induce Hypertension

Class room Dr.dr. Gede Megaputra, SpOG(K)

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,

11. Tue,

26 Sept

2016

09.00-10.00 Lecture 11.

Shoulder Dystocia

Class room dr. Endang

Sriwidiyanti,SpOG

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. Endang

Sriwidiyanti,SpOG 12.

Wed,

27 Sept

2016

09.00-10.00 Lecture 12.

Acute Blistering and Exfoliative Skin

dr. Nyoman Suryawati Sp.KK

10.00-11.30 Student Project

-11.30-12.00 Break Fasilitator

12.00-13.30 Individual Learning 13.30-15.00 SGD

15.00-16.00 Plenary dr. Nyoman Suryawati

Sp.KK 13.

Thu,

28 Sept

2017

09.00-10.00 Lecture 13.

Trauma Which Potentially Disabling

and life Threatening Conditions

Dr.dr. Ketut Suyasa, SpB SpOT(K) Spine dr. IGN Wien Aryana, SpOT

10.00-11.30 Student Project

-11.30-12.00 Break Disc room Fasilitators

12.00-13.30 Individual Learning 13.30-15.00 SGD

15.00-16.00 Plenary Dr.dr. Ketut Suyasa,

SpB SpOT(K) Spine dr. IGN Wien Aryana, SpOT

DAY/DATE TIME LEARNING

ACTIVITY VENUE CONVEYER

14 Mon,

2 Oct

2017

09.00-10.00 Lecture 14.

Phlegmon/ Brain Resuscitation

Class room drg. Lestari Sudirman Dr.dr. I Pt Pramana Suarjaya, SpAn MKes.KMN.KNA/dr. IB Krisna Jaya Sutawan, SpAn MKes

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 drg. Lestari Sudirman Dr.dr. I Pt Pramana Suarjaya, SpAn MKes.KMN.KNA/dr. IB Krisna Jaya Sutawan, SpAn MKes 15

Tue,

3 Oct

2017

09.00-10.00 Lecture 15.

Urologic Concern in Critical Care for NonTrauma Case

Class room Dr.dr. Gede Wirya Kusuma Duarsa, M.Kes, SpU(K)

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 Wirya

Kusuma Duarsa, M.Kes, SpU(K) 16 Wed, 4 Oct 2017

09.00-10.00 Lecture 16.

Urologic Concern in Critical Care for

Trauma Case

Class room

dr. Wayan Yudiana, SpU

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. Wayan Yudiana,

SpU 1

Thu, 5 Oct 2017

08.00-selesai Basic clinical skill (1/2)

Basic Trauma Care (English Class jam 08.00-11.30 WITA; Regular class jam : 12.30-15.00 WITA)

Clinical skill

lab  Dr.dr. Ketut Suyasa,_{SpB. SpOT(K)Spine}

 dr. IGN. Wien Aryana, SpOT  dr. AA Gde Yuda

Asmara, SpOT (K)  dr. Made Agus

Dwianthara Sueta, SpB KBD 2 Fri, 6 Oct 2017

08.00-selesai Basic clinical skill (1/2)

CPR

(Regular Class jam 08.00-11.30 WITA;

English Class jam 12.30-15.00)

SMF

Anestesiologi dan Terapi Intensif

 Dr.dr.Tjok Gde Agung

Senapathi,Sp.AnKA R

 Dr.dr. I Putu Pramana

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 Mon, 9 Oct 2017

08.00-Finish

Student Project

Team

4 Tue, 10 Oct

2017

Prepare For Examination

Thu, 12 Oct

2017

EXAMINATION

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 tanggal 22 September 2017

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 Block’s 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 :

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.

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 

Type  Definition  Examples 

Natural 

disaster  Disaster caused by a naturally occurring event 

Earthquakes, tsunamis, tornadoes,  hurricanes/typhoons, volcanic  eruption, pandemic influenza 

Man­made 

disaster  Nonnatural events that are not purposefully produced 

Vehicle crashes (e.g., car, plane, bus),  mass casualty events, explosions,  fires, industrial accident/chemical  release 

Terrorist­ related  disaster 

Events that are purposefully  produced in an effort to cause  terror 

Events of September 11, 2001, as well as intentional chemical, biological,  radiologic, or toxin releases 

Internal 

disaster  An event that occurs within the hospital 

Hazardous materials spill in hospital  laboratory, fire or explosion within  hospital, power failure 

External 

disaster  An event that occurs external to the hospital  Transportation accident, industrial accident  Acute 

disaster  Disaster that occurs in a narrow and well­defined time frame  Explosion, industrial release, earthquake 

Nonacute  disaster 

Disaster with no well­ defined  start point or continuous  production of casualties over a  broad time frame 

Pandemic infectious disease, 

incremental release of a biological or  toxin (e.g., anthrax sent through mail) 

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.

Table 2 Factors That May Hinder ED Response to Disasters

Poor communication between ED and disaster scene 

Poor communication within the hospital (e.g., ED to emergency operations center, emer­ gency operations center to patient care areas)

Inability   to   control   volunteer   healthcare   personnel   who   are   unfamiliar   with   the   ED function and their roles in disaster response 

Inability to engage and control convergence of media to the ED

Inability to engage, control, and direct visitors who are searching for loved ones Inability to control large numbers of patients (i.e., crowd control)

Difficulty maintaining high staffing needs for extended periods

DISASTER PREPAREDNESS AND PLANNING

Planning for any type of disaster consists of common elements. A hospital disaster planning group is responsible for generating the hospital’s 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, hospital–community 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 one’s 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 body’s 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 CO2 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 baby’s 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:

• 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.

• 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

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

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

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 Mengorek hidung Benda asing Perforasi septum

Deviasi atau spina septum Polip hidung

Tumor sinonasal Tumor nasofaring Hemangioma hidung

Mukosa kering Inhalasi kimiawi Barotrauma Sinusitis Rinitis

Lesi metastatik Angiofibroma juvenil Iritasi lingkungan

Hereditary Hemorrhagic Telangiectasia (HHT) Leukemia

Trombositopenia Anti platelet (aspirin,

clopidogrel) Polisitemia vera Anemia aplastik Hemofilia

Obat antikoagulan (heparin, warfarin) Defisiensi vitamin K Penyakit Von Willebrand

Tuberkulosis Mononukleosi s

Demam

scarlet

Demam reumatik Sifilis Penyakit hepar Uremia ISPA

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)

ALGORITME EPISTAKSIS

EPISTAKSIS

-Anamnesis riwayat penyakit, tentang perdarahan, riwayat trauma, penggunaan obat2an, kebiasaan merokok/ alkohol

-Pemeriksaan klinis/ Laboratorium

Identifikasi lokasi perdarahan (rinoskopi anterior, nasoendoskopi rigid/ fleksible): -Anterior

-Posterior

-Lokasi perdarahan tidak jelas

Tindakan lokal menghentikan perdarahan: -kauter (kimiawi/ elektrik)

-tampon hidung ( anterior & posterior) Berhasil

-Evaluasi dan terapi kausa untuk mencegah kekambuhan -Edukasi &self care penderita untuk mencegah kekambuhan

Tidak berhasil

Tampon hidung ulang

Berhasil

Tidak ada perdarahan lagi

Angkat tampon 48-72 jam

Perdarahan tidak berhenti Perdarahan berulang

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)

Kasus HHT (Laser, fibrin glue, nasal obliterasi) Berhasil

Konsultas-rawat bersama Hematologis-onkologis: Koreksi gangguan koagulopati:

-FFP - vit K -cryprecipitate -trombosit Penatalaksanaan dengan fibrin glue

Syok hipovolemik, penderita

tua, risiko perdarahan profus Resusitasi cairan

Identifikasi kausa

Gangguan faal perdarahan

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, β-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

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 40°C, 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 39.5°C, 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 o_{2 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?