Study Guide Medical Emergency semester VII tayang 1 September 2016

EMERGENCY MEDICINE

INTRODUCTION

Emergency Medicine has long been established especially in Australasia, Canada, Ireland, the United Kingdom and the United States, in Asia othe 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 care and within the province and expertise of almost all medical practitioners. However, the Emergency Medicine incorporates the resuscitation and management of all undifferentiated urgent and emergency cases until discharge or transfer to the care of another physician. Emergency Medicine is an inter-disciplinary specialty, one which is interdependent with all other clinical disciplines. It thus complements and does not seek to 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 6 Th _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

 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

 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

NO. NAME DEPARTMENT

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

Anesthesiology and Intensive Terapy

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

3. dr. IGN Budiarsa,SpS Neurology

4. dr.Sari Wulan,SpTHT-KL(K), dr.Wayan Sucipta, SpTHT-KL

ENT

5. drg. Putu Lestari Sudirman,M.Biomed Dentistry

6. dr. I Ketut Agus Somia, SpPD(KPTI) Internal Medicine

7. dr. Putu Andrika, SpPDKIC Internist

8. Dr.dr. Dyah Kanyawati, SpA(K) Pediatric

9. Dr.dr. Wayan Megadhana, SpOG(K) Obstetric-Gynecologic

10. dr. Endang Sriwidiyanti, SpOG Obstetric-Gynecologic

11. dr.I Gede Mega Putra, SpOG(K) Obstetric-Gynecologic

12. dr. Gede Wirya Kesuma Duarsa, SpU,MKes; dr.

Kadek Budi Santosa, SpU Surgery

13. Dr.dr.Cokorda Bagus Jayalesmana,SpKJ Psychiatric

14. dr. Nyoman Suryawati, SpKK Dermatology

15 16. 17. 18.

dr. Srie Laksminingsih SpR(K)

dr.IGAG Utara Hartawan,SpAn.MARS dr. IGN Mahaalit Aribawa,SpAnKAR dr. IA Sriwijayanti,M.Biomed,SpS

Radiology

Anesthesiology and Intensive Terapy Anesthesiology and Intensive Terapy Neurology

LECTURERS

NO. NAME DEPARTMENT PHONE

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

Anesthesiology and Intensive Terapy

081337711220 2. Dr. dr. I Ketut Suyasa, SpB,

SpOT(K)Spine

Surgery 081558724088

3. dr. IGN Budiarsa,SpS Neurology 0811399673

4. dr.SariWulan,SpTHT-KL(K), dr.Wayan Sucipta,SpTHT-KL

ENT 081237874447(SW

)

08125318941 (WS) 5. drg. Putu Lestari Sudirman,

M.Biomed

Dentistry 081239885740

6. dr. I Ketut Agus Somia, SpPD(KPTI)

Internal Medicine 089617587075

7. dr. Putu Andrika,SpPDKIC Internist 08123989192

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

19. Dr.dr. Wayan Megadana, SpOG(K) Obstetric-Gynecologic 08123917002

10. dr. Endang Sriwidiyanti, SpOG Obstetric-Gynecologic 081236745839

11. dr. I Gede Mega Putra, SpOG(K) Obstetric-Gynecologic 08123636172

12. dr.Gede Wirya Kesuma Duarsa, SpU,MKes; dr. Kadek Budi Santosa, SpU

Surgery (Urology) 08155753377

(GWK);

081339977799 (BS)

13. Dr. dr. Cokorda Bagus Jayalesmana, SpKJ

Psychiatric 0816295779

14. dr. Nyoman Suryawati, SpKK Dermatology 0817447279

15 16. 17. 18.

dr. Srie Laksminingsih SpR (K) dr. IGAG Utara Hartawan, SpAn. MARS

dr.IGN Mahaalit Aribawa, SpAn KAR

dr. IA Sriwijayanti,MBioMed,SpS

Radiology

Anesthesiology and Intensive Terapy Anesthesiology and Intensive Terapy Neurology

08164745561 08123868126 0811396811 081337667939

FACILITATORS

Regular Class (Class A)

No Name Group Departement Phone ₍₂Venuend _floor)

1

dr. A.A.Ayu Dwi Adelia Yasmin, M.Biomed, Sp.JP.FIHA

A1

Cardiology 087861402169 2nd floor:

R.2.09 2 dr. I G N Sri Wiryawan,

M.Repro A2

Histology 082341768888 2nd floor:

R.2.10

3 Ni Putu Wardani, Sp.An, _M.Biomed A3 DME 08113992784 2nd floor:_R.2.11

4 dr. Yukhi Kurniawan, Sp.And A4 Andrology 08123473593 2nd floor:_R.2.12

5 dr. Putu Yuliandari, S.Ked A5 Microbiology 089685415625 2nd floor:

R.2.13

6 dr. Yuliana, M.Biomed A6 Anatomy 085792652363 2nd floor:

R.2.14

7 dr. Ida Bagus Putrawan, _Sp.PD A7 Interna 081236194672 2nd floor:_R.2.15

8 Dr.dr. Ni Putu Sriwidyani , _Sp.PA A8 _AnatomyClinical 081337115012 2nd floor:_R.2.16 9 dr. Ni Luh Putu Ariastuti,

MPH A9

Public Health 0818560008 2nd floor:

R.2.20 10 dr. I Made Suka Adnyana, _Sp.BP-RE A10 Surgery 081236288975 2nd floor:_R.2.23 11 dr. I Dewa Ayu Inten Dwi _{Primayanti, M.Biomed} A11 Fisiology 081337761299 3nd floor:_R.3.20 12 dr. I Made Agus Kresna

Sucandra, Sp.An A12

Anasthesi 081805470888 3nd floor:

R.3.23

English Class (Class B)

No Name Group Departement Phone ₍₂Venue nd _floor)

1 Dr.dr. Tjok G A Senapathi, _{Sp.An. KAR} B1 Anasthesi 081337711220 2nd floor:_R.2.09 2 dr. Agung Nova Mahendra,

M.Sc B2

Pharmacology 087861030195 2nd floor:

3 Dr.dr. Ni Nyoman Sri

Budayanti, Sp.MK (K) B3

Microbiology 08553711398 2nd floor:

R.2.11 4 Dr.rer.Nat. dr. Ni Nyoman Ayu_{Dewi, M.Si} B4 Biochemistry 081337141506 2nd floor:_R.2.12

5 I Ketut Mariadi, Sp.PD B5 Interna 08123853700 2nd floor:

R.2.13

6 Dr.dr. Ni Made Linawati, M.Si B6 Histology 081337222567 2nd floor:

R.2.14 7 dr. I Wayan Aryabiantara, _{Sp.An. KIC} B7 Anasthesi 08123822009 2nd floor:_R.2.15 8 dr. Made Agus Dwianthara _{Sueta, Sp.B-KBD} B8 Surgery 081338648424 2nd floor:_R.2.16

9 Dr.dr. Susy Purnawati, M.KK B9 Fisiology 08123989891 2nd floor:

R.2.20

10 dr. Putu Aryani, MPH B10 Public Health 082237285856 2nd floor:

R.2.23

11 dr. I Made Oka Negara, FIAS B11 Andrology 085935054964 3nd floor:_R.3.20

12 dr. I G A Sri Darmayani,

Sp.OG B12

DME 081338644411 3nd floor:

TIME TABLE

Regular Class (Class A)

DAY/DATE TIME LEARNING ACTIVITY VENUE CONVEYER 1. Thu, 1 Sept 2016 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. Fri, 2 Sept 2016 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. Mon, 5 Sept 2016 08.00-09.00 Lecture 3. Coma and 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 12.30-14.00 Student Project 14.00-15.00

Plenary Class room dr. Ida Ayu

Sriwijayanti,MBioMed,SpS 4. Fri, 9 Sept 08.00-09.00 Lecture 4. Acute Psychiatric Episodes

Class room Dr.dr. Tjokorda Bagus Jayalesmana,SpKJ

2016 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. Tue, 13 Sept 2016 08.00-09.00 Lecture 5. Acute Respiratory Distress Syndrome and Failure

Class room dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya Wati,SpA (K), dr. Sucipta, SpTHT KL dr. Srie Laksminingsih, SpR 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 ENT,

Pulmo, Pediatric, Radiology 6. Wed, 14 Sept 2016 08.00-09.00 Lecture 6. Bleeding Disorder(Epistaxis

, Hemorrhage In Pregnancy)

Class room dr Sari Wulan, SpTHT- KL(K),( 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), ( and ENT Team) Dr.dr Wayan Megadhana, SpOG(K) (and OBGYN Team) 7. Thu, 15 Sept 2016 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

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. Mon, 19 Sept 2016 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 Break 12.30-14.00 Student Project 14.00-15.00

Plenary Class room dr. IGN. Mahaalit Aribawa,

SpAn KAR 9 Tue, 20 Sept 2016 08.00-09.00 Lecture 9. Emergency Toxicology and Poisoning

Class room dr. IKetut Agus Somia, 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. I Ketut Agus Somia,

SpPD KPTI 10. Wed, 21 Sept 2016 08.00-09.00 Lecture 10 Hypertension In Pregnancy

Class room 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. I Gede Mega Putra,

SpOG(K) 11. Thu, 22 Sept 2016 08.00-09.00 Lecture 11. Shoulder Dystocia

Class room dr. Endang

Sriwidiyanti,SpOG

-10.30 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. Fri, 23 Sept 2016 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

12.00-12.30 Break 12.30-14.00 Student Project 14.00-15.00

Plenary dr. Nyoman Suryawati

Sp.KK 13. Tue, 26 Sept 2015 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 14 Mon, 27 Sept 2016 08.00-09.00 Lecture 14. Phlegmon

Class room drg. Putu Lestari Sudirman

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. Putu Lestari

15 Tue, 28 Sept 2016 08.00-09.00 Lecture 15. Urologic Concern in Critical Care for

NonTrauma Case

Class room dr. Gede Wirya Kusuma

Duarsa, M.Kes, SpU(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. Gede Wirya Kusuma

Duarsa, M.Kes, SpU(K)

16 Wed, 29 Sept

2016

08.00-09.00 Urologic ConcernLecture 16. in Critical Care for

Trauma Case

Class room

dr. Budi Santosa, 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. Budi Santosa, SpU

1 Thu, 30 Sept 2016 08.00-selesai Student Project Presentation and Examination Theater Room FK UNUD Team 2 Fri, 3 Oct 2016 08.00-selesai Student Project Presentation and Examination Theater Room FK UNUD Team 3 Mon, 4 Oct 2016

08.00-Finish Basic clinical skill(1) CPR (English Class and Regular)

Clinical skill

lab Team

4 Tue, 5 Oct 2016 08.00- Finish

Basic clinical skill (2)

Basic Trauma Care (English Class and

Regular) Clinical skill lab Team Thu, 6 Oct 2016 Prepare For Examination

Fri, 7 Oct

2016

EXAMINATION

English Class (Class B) DAY/DAT

E

TIME LEARNING ACTIVITY

VENUE CONVEYER

1. Thu, 1 Sept

2016

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.

Fri, 2 Sept

2016

09.00-10.00 Lecture 2.

Status Epilepticus and

Other Seizure Disorders

Class room dr. IGN Budiarsa,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. IGN Budiarsa,SpS

3. Mon, 5 Sept

2016

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.

Fri, 9 Sept

2016

09.00-10.00 Lecture 4.

Acute Psychiatric 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

5. Tue, 13 Sept

2016

09.00-10.00 Lecture 5.

Acute Respiratory Distress Syndrome and

Failure

Class room dr. Putu Andrika, SpPDKIC, Dr. dr Dyah Kanya

Wati,SpA (K), dr. Sucipta, SpTHT KL

dr. Srie Laksminingsih, SpR

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 ENT

Pulmo, Pediatric, Radiology 6. Wed, 14 Sept 2016

09.00-10.00 Lecture 6.

Bleeding Disorder(Epistaxi s, Hemorrhage In

Pregnancy)

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

7. Thu, 15 Sept

2016

09.00-10.00 Lecture 7.

Shock

Class room dr. IGAG. Utara Hartawan, SpAn MARS

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. IGAG. Utara Hartawan,

SpAn MARS 8.

Mon, 19 Sept

2016

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

Tue, 20 Sept

2016

09.00-10.00 Lecture 9.

Emergency Toxicology and

Poisoning

Class room dr. Agus Somya, SpPD

KPTI

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. Agus Somya, SpPD

KPTI 10.

Wed, 21 Sept

2016

09.00-10.00 Lecture 10.

Pregnancy Induce Hypertension

Class room 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. Gede Megaputra,

SpOG(K) 11.

Thue, 22 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.

Fri, 23 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.

Tue, 26 Sept

2016

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 14

Mon, 27 Sept

2016

09.00-10.00 Lecture 14.

Phlegmon

Class room drg. Putu Lestari Sudirman

10.00-11.30 Student Project -

-11.30-12.00 Break Disc room Facilitators

13.30-15.00 SGD

15.00-16.00 Plenary Class room drg. Putu Lestari Sudirman

15 Tue, 28 Sept

2016

09.00-10.00 Lecture 15.

Urologic Concern in Critical Care for NonTrauma

Case

Class room 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. Gede Wirya Kusuma

Duarsa, M.Kes, SpU(K)

16 Wed, 29 Sept

2016

09.00-10.00 Lecture 16.

Urologic Concern in Critical Care for Trauma Case

Class room

dr. Budi Santosa, 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. Budi Santosa, SpU

1 Thu, 30 Sept 2016 08.00-selesai Student Project Presentation and Examination Clinical skill lab Team 2 Fri, 3 Oct 2016 08.00-selesai Student Project Presentation and Examination Clinical skill lab Team 3 Mon, 4 Oct 2016 08.00-Finish

Clinical skill (1) CPR (English Class and Regular Class) Clinical skill lab Team 4 Tue, 5 Oct 2016 08.00-

Finish Clinical skill (2)Basic Trauma Care (English

Class and Regular Class)

Clinical skill

lab Team

Thu 6 Oct 2016 Prepare For Examination Fri,

7 Oct 2016

EXAMINATION

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 2012 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.

Student Project (SP) Emergency Medicine

September-October 2016

 Berikut dibawah ini adalah judul SP yang sudah dibagi pergrup SGD. Masing-masing Grup SGD mendapat satu judul dan Nama Penguji Sudah tercantum.  Pembimbing SP sudah disepakati adalah masing-masing fasilitator tiap Group

SGD yang bersangkutan.

 Pada akhir SP sudah dijadwalkan Ujian-Presentasi SP sesuai Jadwal yang sudah dibuat di Time Table.

No Student Project Group Penguji ₍₂Venuend _floor)

1

Perdarahan Pervaginam Kasus Ginekologi Keganasan

A1

Dr.dr Wayan Megadhana, SpOG(K)

2nd floor: R.2.09

2 Toxic Metabolic Coma A2 dr. Ida Ayu Sriwijayanti,

MBioMed, SpS

2nd floor: R.2.10 3 Kehamilan Dengan _{Hipertensi Kronis} A3 dr. I Gede Mega Putra,_SpOG(K) 2nd floor:_R.2.11 4 Trauma Abdomen A4 Dr.dr. Ketut Suyasa, SpB _{SpOT(K) Spine} 2nd floor:_R.2.12

5 Skizofrenia Hebefrenik A5 Dr. dr. Cokorda Bagus

Jayalesmana, SpKJ

2nd floor: R.2.13 6 Septic Shock Pada Pediatrik A6 dr.Nyoman Budihartawan,_{MSc, SpA} 2nd floor:_R.2.14 7

Dengue Shock Syndrome

Pada Pediatik A7 Dr. dr Dyah Kanya Wati,SpA

(K),

2nd floor: R.2.15

8

Urogenital Trauma Pada

Anak-anak A8

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

2nd floor: R.2.16

9 Laringotrakeobronkitis A9 dr. Wayan Sucipta, SpTHT KL 2nd floor:_R.2.20

10 Pneumonia A10 dr. Putu Andrika, SpPDKIC 2nd floor:

R.2.23 11 Perdarahan Pascaekstraksi

Gigi A11

drg. Putu Lestari Sudirman 3nd floor: R.3.20

12 Petit Mal Seizure A12 dr. IGN Budiarsa,SpS 3nd floor:_R.3.23

English Class (Class B)

No Student Project Group Penguji Venue

(2nd _floor)

1 Emergency Medicine Roles

in Natural Disaster B1

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

2nd floor: R.2.09

2 Radiology Roles in ARDS B2 dr. Srie Laksminingsih, SpR 2nd floor: R.2.10

3 Angiofibroma B3 dr Sari Wulan, SpTHT- KL(K) 2nd floor:_R.2.11

4 Shock In Adult B4 dr. IGAG. Utara Hartawan,

SpAn MARS

2nd floor: R.2.12 5

Sudden Cardiac Death

Rescue B5

dr. IGN. Mahaalit Aribawa, SpAn KAR

2nd floor: R.2.13 6 Alcohol Intoxication B6 dr. I Ketut Agus Somia, SpPD_KPTI 2nd floor:_R.2.14 7 Abdominal and Pelvic Pain_{In The Nonpregnant Female} B7 dr. Endang Sriwidiyanti,SpOG 2nd floor:_R.2.15

8 Toxic Shock Syndrome B8 dr. Nyoman Suryawati Sp.KK 2nd floor:

R.2.16

9 Acute Kidney Injury B9 dr. Kadek Budi Santosa, SpU 2nd floor:_R.2.20

10 Thoraxic Trauma B10 dr. IGN Wien Aryana, SpOT 2nd floor:_R.2.23

11 Acid Base Disorders B11 dr. I Made Agus Kresna

Sucandra, Sp.An

3nd floor: R.3.20

12 Fluid and Electolites B12 dr. I Wayan Aryabiantara,

Sp.An. KIC

3nd floor: R.3.23

LEARNING PROGRAMS

Abstracts of Lectures

Tjokorda Gde Agung Senapathi Objective

To describe

1. Highlight Emergency Medicine

2. Basic principal of Emergency Medicine 3. Triad Emergency Medicine

4. Ethics in critical care

Physicians have been called on to provide emergency care for patients. However, in the house of medicine, the formal specialty of emergency medicine is still relatively young— measured in decades. Emergency medicine developed differently from perhaps many of the other more traditional medical and surgical specialties. In the case of emergency medicine, public demand more than scientifi c inquiry fueled the formation and growth of the specialty. In the 1950s and 1960s, with more physicians seeking specialty training, the number of general practitioners began to decline. At that time, hospitals were becoming more modernized and technologically advanced. Ultimately, these factors, along with the changing demographic and social conditions of the post–World War II era, led to an increased public reliance on hospital emergency departments for the provision of unanticipated medical care. Unfortunately, a uniform system for providing high-quality emergency care did not exist. At that time, junior medical and surgical house offi cers staffed many hospital emergency departments with little or no attending supervision. Most of these physicians did not have the necessary clinical skills to properly care for the increasing complexity of cases seeking medical attention. It was also becoming evident that the physician staffing patterns were inadequate to keep up with the ever increasing patient volume.

Basic principal and triad emergency medicine please read in the lecture power point. Medical ethics is the art of resolving conflicts that arise around treatment and treatment decisions. The conflict may involve the patient, family, caregivers, or society. An approach to these conflicts is as necessary as, say, an approach to hypotension or oliguria. Without an approach we would be ignoring the mechanism that led the conflict or problem in the first place. A little preparation will allow one to be more comfortable when confronting these situations, making responses more likely to be useful (and less likely to make things worse).

There are four basic principles or medical ethics that give us the tools to begin to resolve some of these conflicts : autonomy, beneficence, and justice. The weight we give each of these four different principles is often determined by our individual and societal morals.

LECTURE 1 : HIGHLIGHT

EMERGENCY MEDICINE

Lecture 2

SEIZURE

STATUS EPILEPTICUS

IGN Budiarsa

Status epilepticus is defined as a condition in which epileptic activity persists for 30 minutes more.

The seizures can take the form of prolonged seizures or repetitive attacks without recovery in between. 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 Sri Wijayanti

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.

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.

Learning resources

Kitchener, Hashem, Wahba, Khalaf, Shafir, Mansoor. How to Approach Unconsciousness Patients. In Critical Care in Neurology. Flying Publisher and Kamp; 2012:Chapter 2.

Posner, Saper, Schiff, Plum. Diagnosis of Stupor and Coma. 4th _{ed. Oxford University Press;}

Lecture 4

ACUTE PSYCHIATRIC EPISODE

Cokorda 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.

LEARNING RESOURCES

1. Kaplan & Saddock’s Synopsis of Psychiatry, 10th _ed

Lecture 5

ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE

Putu Andrika

Respiratory distress is a term combining the patient’s subjective sensation of dyspnea with signs indicating difficulty breathing. The acute respiratory distress syndrome (ARDS) is a form of hypoxemic respiratory failure that is characterized by severe impairment of gas exchange and lung mechanics, with a high case fatality rate. In the USA, 150.000 cases were found per year and 50% of them died due to respiratory failure.

ARDS can be triggered by a number of different pulmonary and extrapulmonary insults. The characteristic pathological changes of ARDS include an exudative phase, with the accumulation of fluid within the lung, the release of proinflammatory cytokines and infiltration of inflammatory cells, especially neutrophils, into the lung parenchyma. Damage to the alveolar epithelium and pulmonary capillary endothelium occur and patients develop the characteristic histological appearance of diffuse alveolar damage. This manifests clinically as non-cardiogenic pulmonary edema, which reduces lung compliance and impairs gas exchange.

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:

Fever?

Susp foreign body? Status asthmaticus?

Trauma & unilateral absent breath sounds

Complit obstruction: Back or chest or abdominal blows, laryngoscopy & removal, needle cricothyrotomy

Avoid IV & other potentially agitating or painfull intervention. Evaluate for definitive airway byphysician most skilled in difficull airway

Epinephrine IM, Nebulized albuterol, steroids IV, Terbutaline Prepare for assisted ventilation

Needle thoracotomy followed by tube thoracotomy

Partial obstruction?

NO Allow patient to assume position of comfort. Obtain brief history and begin treatment based on suspected _{disease process. Order labs and imaging as indicated. Continue to reassess patient and obtain additional} history Respiratory distress Respiratory arrest Yes Yes Assess ABC s, ˈ

Place IV, give IVfluid bolus, give oxygen, place on monitor

Immediate resuscitation, Clear airway, Assist ventilations, chest compression, IV,O2, IVF No

Sign of impending respiratory failure?

Airway: Stridor at rest, irregular respirations, apnea.

Breathing: severe retraction, grunting, nasal flaring, poor aeration, progressive fatigue. Circulation: poor color (cyanotic, ashen, Mottled), sluggish capiary refi

Mental status: Decreased level of consciousness, agitation, decreased response to pain

ACUTE RESPIRATORY DISTRESS SYNDROME in Pediatric

Diah Kanyawati

Abstract

ARDS is Acute catastrophic event, develops following either “direct” or “indirect” lung injury. Pneumonia and pulmonary aspiration are among the most common conditions with the potential to inflict direct lung injury and ARDS, but traumatic pulmonary contusion, fat embolism, submersion injury, and inhalational injury are relatively common causes as well. The most common forms of indirect lung injury include systemic conditions, such as sepsis, shock, exposure to cardipulmonary bypass, and transfussion-related lung injury.

Diffuse alveolar disease that meets criteria for ARDS prodeces a predictable sequence of clinical changes. When fluid accumulation in the interstitial space exceeds the absorptive capacity of the pulmonary lymphatics, lung compliance decline and tachypnea ensues as the patient attempts to generate adequate minute ventilation in the face of lower tidal volumes. The eventual leakage of proteinaceous fluid into the alveoral spaces interferes with native surfactant function, creating conditions that favor regional atelectasis and small-airways closure, as well as a decrease in EELV to a point near or bellow closing capacity, as specially in small infants and those with highly compliant chest walls (e.g., patients with neuromuschular dissease). At this point, hypoxia rapidly worsens, and breathing becomes more labored in an effort to generate transpulmonary pressures sufficient first manifests tachypnea. However, as the work of breathing escalates, the PaCO2 will further rise as

respiratory muscle fatigue ensues. At this stage, positive-pressure ventilation is required to open sufficient number of atlectatic lung units for adequate gas exchange. On auscutation, the patient will typically demonstrate rales over areas of atelectasis or aveolar congestion and dicreased air entry over areas that are largely consolidated. Occasionally, it is possible to appreciate wheezes over areas in which intermittent small-airways closure is occurring.

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

Vaginal Bleeding

Wayan Megadhana

OBJECTIVES

1. To recognize life-threatening cause of vaginal bleeding. 2. To develop an approach to the causes of vaginal bleeding.

3. To diagnose and manage vaginal bleeding in pregnant patients (Ectopic pregnancy, Ante partum hemorrhage and Post partum hemorrhage).

Ectopic Pregnancy

Approximately 1% of diagnosed pregnancies are ectopic. Risks factors include PID, IUD, infertility treatment, pelvic surgeries, tubal ligations and endometritis. Mortality is 1 in 850 women if treated, but nearly 100% if untreated. Median time for rupture of a tubal pregnancy is 8 weeks; however interstitial (cornual) ectopic pregnancies can rupture later in pregnancy 12-16 weeks with catastrophic result. The diagnose of ectopic pregnancy is vaginal bleeding, acute abdominal pain. Many of the bleeding ectopic pregnancies are treated surgically and medicamentosa with MTX (Methotrexate).

Ante partum hemorrhage

Diagnostic possibilities for vaginal bleeding in late pregnancy range from trivial to life threatening and include placenta previa, abruption placentae and uterine rupture.

Abruptio placenta is a premature separation of the normally implanted placenta from the uterus. It is associated with various hypertensive, cardiovascular and connective tissue autoimmune disorders. Often, it is associated with various degree of trauma. Abruptio placentae classically presents with a tender contracted uterus, signs of hemorrhage (concealed abruption, there may not be any external bleeding) and fetal distress. Abruptio placentae is often misdiagnosed as preterm labor. Abruptio placentae management based on degree of abruption and labor phase, so it can be expectant vaginal delivery or abdominal delivery.

Placenta previa is the result of implantation and placenta development over the internal cervical os. Risks include multiparity, abnormal uterus, fibroids and prior surgeries. Classically, placenta previa presents with painless bleeding, often preceded by trauma or intercourse. Do not attempt a pelvic examination because it may worsen the hemorrhage in placenta previa. Any patient presenting with vaginal bleeding after the first trimester should have an ultrasound prior to any pelvic exam. Management of placenta previa based on gestational age and it can be conservative management or by surgery.

Uterine rupture occurs in 0.05% of pregnancies. Maternal mortality is 8% while fetal mortality is 50%. It usually seen during labor, so may encounter it in the emergency department when a patient presents following an attempted home delivery. Management of uterine rupture can be conservative management by conservative surgery or by hysterectomy.

Non life threatening causes of third trimester bleeding include: bloody show, cervical traumatic bleeding and marginal sinus rupture.

Postpartum Hemorrhage

Postpartum hemorrhage is seen in varying degrees in 28% of patients. Causes of postpartum hemorrhage: uterine atony, uterine rupture, lacerations/tears, retained placental tissue, uterine inversion, coagulopathy. Careful assessment of uterine tone and the birth

passage is necessary. If atony is present, Oxytocin 30 units in 1 litre of normal saline at 200 cc/hr can be helpful. Ultrasound will assist in ruling out retained products. Make sure that patient is afebrile. Postpartum endometritis may either complicate bleeding or in fact be the contributing factor.

Epistaxis

SARI WULAN

ENT TEAM

Objective

Able to

1. Identify the pathophisiology of the epistaxis, 2. Do proper treatment to protect complication

3. Do ongoing care of epistaxis in order to prevent rebleeding

Preface

Epistaxis is acute bleeding from the nose or nasopharyng. It is not a diseases but the sign of other diseases which is 90% can be stopped spontaneously. Principle of managements are stop bleeding, prevent complication and rebleeding.

Patophisiology

There is a thin and weak area within the bleeding spot area in the younger age that probably caused by mild trauma and ischemia. In the middle age and older can be found changing and thikening of tunica media from capillary endotel that caused the blood vessel loosing their elasticity, so the bleeding usually profuse.

Classification

1. Anterior Epistaxis, usually from pleksus kiesselbach (little’s area) there is anastomosis of capilary in the anterosuperior nasal septum and also from anteroinferior of inferior turbinate

2. Posterior Epistaxis, from a. sfenopalatina and a. posterior ethmoidalis. Diagnosis

Good and complete question should be done as soon as possible about habits and the past history of the systemic diseases if any to recover the caused of the bleeding and also to prevent from rebleeding. Identify the bleeding spot is require in order to give optimal treatment to protect complication.

Anterior epistaxis is usually caused by mild trauma, such as scratching the nose, infection (rhinitis), climate changing. Posterior epistaxis is usually caused by systemic diseases such as hypertension, cardiovascular diseases, fraktur and tumor.

Treatment

Anterior Epistaxis

1. Cauterisation by AgNO3 20-30% or trichloroasetic acid 10% 2. Anterior packing with vaseline

Posterior Epistaxis

1. Posterior packing with vaseline 2. Balloon packing

3. Ligation of posterior ethmoidalis and externa carotid artery 4. Embolisation with intervention radiology to do angiografi

Re ferrence

1. Watkinson JC. Epistaxis. Dalam: Mackay IS, Bull TR. Scott – Brown’s Otolaryngology. Volume 4 (Rhinonology). Ed. 6 th. Oxford: Butterwort - Heinemann, 1997: 1–19. 2. Thornton MA, Mahest BN, Lang J. Posterior epistaxix: Identification of common

bleeding sites. Laryngodcope, 2005. Vol. 115 (4): 588 – 90.

3. Pfaff JA, Moore GP. Otolaryngology. In: Marx et al., editors. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th edition. St Louis: Mosby Elsevier, 2010: 877-887.

Lecture 7

SHOCK

IGAG Utara Hartawan

Objective

1. To describe the term, etio-pathogenesis and pathophysiology of shock

2. To implement a general strategy in the approach to patients with shock through history, physical examination and special tehnique investigations.

3. To manage by assesing, differential diagnosis, provide initial management and refer patient with shock

4. To describe prognosis patient with shock

Shock is a state in which the oxygen (O2) and metabolic demands of the body are not met by the cardiac output. When this process occurs in a single organ, rather than throughout the body, organ ischemia and infarction ensue. When shock occurs on a more global level, multiorgan dysfunction and failure are the consequence, ultimately leading to death if not corrected. Shock is most often accompanied by hypotension, termed decompensated shock. However, shock may also occur with normal or elevated blood pressure. Examples include hypertensive emergency with compromised cardiac output, or carbon monoxide intoxication with the inability to deliver O2 despite normal hemodynamics. The approach to the patient in shock must proceed with the same urgency as the patient suffering from an acute myocardial infarction or cerebral vascular accident.

Shock states are classified according to the underlying physiologic derangement. Hypovolemic shock is defined by decreased circulating blood volume, either due to blood or fluid loss, such that cardiac output is compromised. Impaired cardiac performance characterizes cardiogenic shock. Loss of vasomotor tone with hypotension is the hallmark of distributive shock, as in sepsis, anaphylaxis, or certain intoxications. Anatomic interruption of sympathetic output, usually secondary to spinal cord injury with disruption of the cervical sympathetic chain, leads to bradycardia and hypotension in neurogenic shock. Obstruction of blood flow through the cardiopulmonary circuit is the etiology of obstructive shock, as in tension pneumothorax, cardiac tamponade, or massive pulmonary embolus. Finally, a few patients present with a mixed syndrome, such as a patient with sepsis who develops gastrointestinal (GI) hemorrhage, or who suffers a concomitant myocardial infarction.

If shock is defined by impaired global organ perfusion, then it follows that signs of shock are derived from impaired organ function. Hypotension is an obvious sign of decompensated hemodynamics associated with shock. Alteration in mental status, chest pain, signs of cardiac failure, difficulty breathing, abdominal pain from intestinal ischemia, low urinary output, and mottled skin all suggest shock.

In a proportion of patients, the etiology of the shock state remains in question after initial evaluation. Often, therapeutic intervention must be initiated without a firm diagnosis. The core principle in treatment of such patients is that O2 delivery to the vital organs must be optimized.

Obtaining an accurate history is essential to approaching undifferentiated patients in shock. Deficiencies in the historical database lead to poor treatment choices and increase patient morbidity and mortality. Unfortunately, many patients in shock states are not up to the task of providing an accurate and complete history. Medical records, family members, and friends are invaluable resources in these situations. Time course and progression of illness provide important information regarding the rapidity of decline and may help narrow the differential diagnosis. Pre-existing conditions, particularly limitations of the cardiopulmonary system and immune deficiencies, predispose patients to poor outcomes.

General treatment principles are : oxygenation, cardiac intervention, blood product transfusion, volume intervention, and vasoactive agents intervention.

Goal treatments are :

CVP 8-12 mmHg

PAOP _{8–12 cmH2O}

CO 3.8–7.5 L /min (approximate for normal size adult)

CI 2.4–4.0 L /min/m2

SVR 800–1400 dyne/s/cm5 (approximate for normal size adult)

SVRI 1600–2400 dyne/s/m2/cm5

CVP: central venous pressurePAOP: pulmonary artery occlusion pressure CO: cardiac outputCI: cardiac indexSVR: systemic vascular resistanceSVRI: systemic vascular resistance index

Prognosis depends on early recognition, intervention, source control, and smooth transitions of care help, ensure the most ideal outcomes. Some clinical variables are associated with poor outcome, such as severity of shock, temporal duration, underlying cause, preexisting vital organ dysfunction and reversibility. While associated morbidity and mortality remain high for patients with shock, integration of protocol-based care pathways, with ongoing refinement in response to new information, may lead to continued reductions over time.

Copied from : Sigillito RJ and DeBlieux PMC. Shock. In An Introduction Clinical Emergency Medicine Guide for Practioner in the Emergency Department. Cambridge University Press. 2005. p.85-92

References :

1. Butterworth, J.F., 2013. Fluid Management & Blood Component Therapy. In Morgan & Mikail’s Clinical Anesthesiology. New York: Mc Graw Hill Education, pp. 1161–1181. 2. Nicks, B.A., 2016. Aprroach to Shock. In J. E. Tintinalli, ed. Tintinalli’s Emergency

Medicine. New York: Mc Graw Hill Education, pp. 63–69.

3. Smith, L.M., 2014. Shock. In S. C. ; Joseph M. W. Sherman, ed. Clinical Emergency Medicine. New York: Lange, Mc Graw Hill Education, pp. 42–45.

4. Vincent, J. & Backer, D. De, 2013. Circulatory Shock. The New England Journal of Medicine, 369(18), pp.1726–1734.

SHOCK IN PEDIATRIC

I Nyoman Budihartawan

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 feature.

Lecture 8

CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION

IGN Mahaalit Aribawa

Objective :

1. To describe etio-pathogenesis and pathophysiology of cardiac arrest 2. To know how to identify patients with cardiorespiratory arrest

3. To understand the chain of survival

4. To Understand the principles of treating cardiac arrest incorporate basic life support and advance life support

5. To describe the need for continued resuscitation after return of spontaneous circulation (ROSC )

6. To describe the role of the resuscitation team

Abstract

Cardiac arrest is the cessation of clinically detectable cardiac output. It is unpredictable and rarely occurs with doctors in attendance, can occur anywhere, anytime and to anybody. Cardiac arrest can be because of a disease or due to drowning, poisoning and others that are capable of causing respiratory and cardiac arrest.

The initial rhythm found may be ventricular fibrillation ( VF ), ventricular tachycardia ( VT ), asystole, and pulseless electrical activity ( PEA ). Bystanders need to commence cardiopulmonary resuscitation ( CPR ) immediately if the victim is to survive.

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 / CPR is given immediately and correctly brain death can be avoided and the patient recovers completely.

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. CPR incorporates basic life support ( BLS ), that is, making use of basic equipment or without equipment and advanced life support (ALS), that is, using advanced equipment including drugs, defibrillators and advanced airway management.

The “chain of survival” describes the events needed to achieve a good outcome : early access to emergency services, early bystander CPR, early defibrillation and early ALS. In performing advanced life support, the role of ressucitation team is very important and to achieved good team needed to done routine practical simulation of the team.

Lecture 9

EMERGENCY TOXICOLOGY AND POISONING

I Ketut Agus Somia

BASIC MANAGEMENT OF INTOXICATION

OBJECTIVE: Intoxication or poisoning should be think in patient suddenly onset of disease, with previously healthy condition, and difficult to explain or unclear of the causes. It is complex situation included possibility crime and law, even that the emergency and life threatening. To Underetand of Toxic syndrome is once of method for identification of the toxicant, by specific odor, colour of urine, heart rate, pulse rate, reapiratory rate, body Qransaction and consiousness. Laboratory test is important for to known serum level of the agent,and target organ effect. Osmolar gap and ion gap is also important in toxicology Qransact to support the diagnosis. The time of the first contact with tocicant is very I for determine of prognosis and treatment. The antidote is Qransact therapy for management of patient intoxication, but not always available and should be used carefully because can induced intoxication. The basic treatment of emergency cases is base on ability to control of airways, breathing and circulation( or ABC Qransacti). The specific presedure in intoxication cases beside ABC also DE (Decontamination and Elemination). The heathcare of patient intoxication should be comprehendsive by Team care depend on targen organ damage.

ORGANOPHOSPHAT INTOXICATION

OBJECTIVE : Organophosphorus insecticides are the most common cause of toxicity among all pepticides. Organophosphat bind irreversibly to and inhibit cholinesterase in the nervous system, than accumulation in the synapses and neuromuscular junction. Organophosphate intoxication manifested systemically as a muscarinic,nicotinic and systemic CNS over stimulation effect. Muscarinic overstimulation resulted SLUDGE Syndrome (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal and Emesis), and “ Killer B” effect (Bronchospasm, Bronchorhea and Bradycardia). Additional manifestation was blurred vision associated with miosis. Nicotinic effect included fasciculation, muscle weakness, Qransaction tachycardia and mydriasis. Central Nervous System (CNS) effect : tremor, confusion, seizure and coma. Organophosphate intoxication can caused intermediate and delayed syndrome, with occurs 1-4 days and 1-3 weeks respectively after acute poisoning. Emergency care : Symtomatic patient require emergent attention to airways protection and ventilation, supplement oxygen should administered to maintain oxygen saturation moe than 95%. Decontamination: dermal exposures can be performed using soap and water with dilute blech, Gastric aspiration by nasogastric tube and administration of active charcoal should be performed in significant ingestion. Administration of specific antidote ( Qransact, pralidoxime) my be appropriate for selective patient and selective agent.

CAUSTIC INTOXICATION

OBJECTIVE : Caustic intoxication devide in alkali exposures and acid exposures, the most common caustic exposures is household bleach. The strength of caustic and duration of exposure determine its ability to cause damage. Alkali penetrate deeply into tissue through liquefaction necrosis, alkali ingestion caused more proximal damage to the esophagus rather than to the stomach, Qransac with focal burn in the oropharynx and esophagus. Stong acid tend to produce coagulation necrosis, early eschar formation to protects against deeper injury in esophagus, regadless the esophagus and gastric injury can accur. Alkalis are relatively tasteless and odorless, and caused esophageal perforation and stricture.In the sevire injury manifested by mediastenitis or peritonitis. Acid tend to be more smelling and tasting. Acid can caused injury of the esophagus and they tend to pool in the stomach, leading gastric hemorrhage,necrosis, and perforation. Systemic effect of acid intocication : metabolic acidosis, hemolysis and renal failure. Caustic ingestion can cause distal GI injury without necessarily causing oral burn. Endoscopy is the diagnosis test of choice in evaluation for serious esophageal and gastric injury, it is indicated in vomiting progesive, drooling, dyspnea, stridor and sevire oropharyngal burn. Early endoscopy within several hours of ingestion can be safe and useful in determining the extend of injury as well as the need for admission. Emergency care : Dilutional is the important once. Gastric decontamination with charcoal, ipecac and gastric lavage is contraindicated. Only in cases of strong aci ingestion may NGT be inserted for removal of excessive acid in the stomach( with strong precaution). Dilution is indicated only for solid alkali ingestion. Neutralization cannot be routinely recommended. Steroid are controversial in alkali ingestion, but can be used depend on endoscopic result ( grade II erotion). Antibiotic is reversed for patients with steroid treatment or perforation. Urgent GI consultation should be obtained for any caustic ingestion.

Lecture 10

HYPERTENSION IN PREGNANCY

I Gede Mega Putra

OBGYN Team

Objective :

1. Define hypertension in pregnancy

2. Review appropriate fetal/maternal assessment

3. Discuss appropriate management of hypertension in pregnancy

4. Recognize when and how to transport patient with hypertension in pregnancy

Hypertension in pregnancy occurs in approximately 10% of pregnancies and can be associated with significant maternal and fetal morbidity and mortality. The spectrum of disease is divided into 3 main categories: gestational hypertension, preeclampsia, and eclampsia. Preeclampsia affects 2-6% of pregnancies in the United States, with a higher incidence globally. Eclampsia occurs in < 1 % of patients with preeclampsia.

Gestational hypertension is defined as a blood pressure >140/90 mmHg in a pregnant patient without preexisting hypertension. The hypertension will resolve within12 weeks postpartum. When proteinuria is also present, it is defined as preeclampsia. Preeclampsia typically occurs after 20 weeks' gestation. A subset of patients will develop severe preeclampsia, which is associated with one of more of the following: severe hypertension (>160/110 mmHg on 2 separate occasions >6 hours apart), large proteinuria, neurologic symptoms, epigastric/right upper quadrant (RUQ) pain, pulmonary edema, or thrombocytopenia. Eclampsia is preeclampsia with seizures. HELLP syndrome affects some patients with preeclampsia and eclampsia and is associated with hemolysis, elevated liver enzymes, and low platelets.

Although the exact etiology of preeclampsia is unknown, there are several factors that are thought to contribute.These include maternal immunologic intolerance, abnormal placental implantation, endothelial dysfunction, and genetic factors.

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

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).

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.

3. Comprehend the definition, etiology, special investigation and basic management of colic, urosepsis, hematuri,

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), 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

Budi Santosa

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.

~ CURRICULUM MAP ~

Smstr

Program or curriculum blocks

10

Senior Clerkship

9

Senior Clerkship

8

Senior clerkship

7

Medical Emergency (3 weeks) BCS (1 weeks)

Special Topic: -Travel medicine (2 weeks)

Elective Study III

(6 weeks) Clinic Orientation(Clerkship) (6 weeks) 6 The Respiratory System and Disorders (4 weeks) BCS (1 weeks)

The

Cardiovascular System and Disorders (4 weeks) BCS (1 weeks)

The Urinary System and Disorders (3 weeks) BCS (1 weeks)

The Reproductive System and Disorders (3 weeks) BCS (1 weeks)

5 Elective Study II (1 weeks) Alimentary & hepato-biliary systems & disorders (4 Weeks) BCS (1 weeks)

The Endocrine System, Metabolism and Disorders (4 weeks) BCS (1 weeks)

Clinical Nutrition and Disorders (2 weeks) BCS (1 weeks)

Special Topic : - Palliative medicine -Compleme ntary & Alternative Medicine - Forensic (3 weeks) Elective Study II (1 weeks) 4 Musculoskeletal system & connective tissue disorders (4 weeks) BCS (1 weeks)

Neuroscience and

neurological disorders (4 weeks) BCS (1 weeks)

Behavior Change and disorders (4 weeks) BCS(1 weeks) The Visual system & disorders (2 weeks) BCS (1 weeks) 3 Hematologic system & disor-ders & clinical oncology (4 weeks) BCS (1 weeks)

Immune system & disorders (2 weeks) BCS(1 weeks) Infection & infectious diseases (5 weeks) BCS (1 weeks)

The skin & hearing system

& disorders (3 weeks) BCS(1 weeks)

2

Medical Professionalism (2 weeks) BCS (1 weeks)

Evidence-based Medical Practice (2 weeks)

Health System-based Practice (3 weeks) BCS (1 weeks)

Community-based practice

(4 weeks)

Special Topic - Ergonomi - Geriatri (2 weeks)

Elective Study I (2 weeks)

1

Stadium Generale and Humaniora (3 weeks)

Medical communication (3 weeks) BCS (1 weeks)

The cell as bioche-mical machinery (3 weeks) BCS(1 weeks)

Growth &

development (4 weeks) BCS: (1 weeks) Pendidikan Pancasila & Kewarganegaraan (3 weeks)