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Study Guide Emergency Medicine 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
period of 2012, one of there is The Emergency Medicine Block.
Th
semester,
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
Udayana University Faculty of Medicine, DME, 2016
1
Study Guide Emergency Medicine September 2016
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
Udayana University Faculty of Medicine, DME, 2016
2
Study Guide Emergency Medicine September 2016
PLANNERS
NO.
1.
13.
14.
15
16.
NAME
Dr.dr. Tjok Gde Agung Senapathi, Sp.An KAR
(Coordinator)
Dr.dr. I Ketut Suyasa, SpB,SpOT(K)Spine
dr. IGN Budiarsa,SpS
dr.Sari Wulan,SpTHT-KL(K), dr.Wayan Sucipta,
SpTHT-KL
drg. Putu Lestari Sudirman,M.Biomed
dr. I Ketut Agus Somia, SpPD(KPTI)
dr. Putu Andrika, SpPDKIC
Dr.dr. Dyah Kanyawati, SpA(K)
Dr.dr. Wayan Megadhana, SpOG(K)
dr. Endang Sriwidiyanti, SpOG
dr.I Gede Mega Putra, SpOG(K)
dr. Gede Wirya Kesuma Duarsa, SpU,MKes; dr.
Kadek Budi Santosa, SpU
Dr.dr.Cokorda Bagus Jayalesmana,SpKJ
dr. Nyoman Suryawati, SpKK
dr. Srie Laksminingsih SpR(K)
dr.IGAG Utara Hartawan,SpAn.MARS
17.
dr. IGN Mahaalit Aribawa,SpAnKAR
18.
dr. IA Sriwijayanti,M.Biomed,SpS
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
DEPARTMENT
Anesthesiology and
Intensive Terapy
Surgery
Neurology
ENT
Dentistry
Internal Medicine
Internist
Pediatric
Obstetric-Gynecologic
Obstetric-Gynecologic
Obstetric-Gynecologic
Surgery
Psychiatric
Dermatology
Radiology
Anesthesiology and
Intensive Terapy
Anesthesiology and
Intensive Terapy
Neurology
LECTURERS
NO.
1.
2.
3.
4.
5.
6.
7.
8.
19.
10.
11.
12.
13.
NAME
Dr.dr. Tjok Gde Agung Senapathi,
Sp.AnKAR (Coordinator)
Dr. dr. I Ketut Suyasa, SpB,
SpOT(K)Spine
dr. IGN Budiarsa,SpS
dr.SariWulan,SpTHT-KL(K),
dr.Wayan Sucipta,SpTHT-KL
drg. Putu Lestari Sudirman,
M.Biomed
dr. I Ketut Agus Somia,
SpPD(KPTI)
dr. Putu Andrika,SpPDKIC
Dr.dr. Dyah Kanyawati, SpA(K)
Dr.dr. Wayan Megadana,
SpOG(K)
dr. Endang Sriwidiyanti, SpOG
dr. I Gede Mega Putra, SpOG(K)
dr.Gede Wirya Kesuma Duarsa,
SpU,MKes; dr. Kadek Budi
Santosa, SpU
Dr. dr. Cokorda Bagus
Jayalesmana, SpKJ
Udayana University Faculty of Medicine, DME, 2016
DEPARTMENT
Anesthesiology and
Intensive Terapy
Surgery
PHONE
081337711220
Neurology
ENT
Dentistry
0811399673
081237874447(SW)
08125318941 (WS)
081239885740
Internal Medicine
089617587075
Internist
Pediatric
Obstetric-Gynecologic
08123989192
081285705152
08123917002
Obstetric-Gynecologic
Obstetric-Gynecologic
Surgery (Urology)
081236745839
08123636172
08155753377
(GWK);
081339977799 (BS)
0816295779
Psychiatric
081558724088
3
Study Guide Emergency Medicine September 2016
14.
15
16.
17.
18.
dr. Nyoman Suryawati, SpKK
dr. Srie Laksminingsih SpR (K)
dr. IGAG Utara Hartawan, SpAn.
MARS
dr.IGN Mahaalit Aribawa, SpAn
KAR
dr. IA Sriwijayanti,MBioMed,SpS
Dermatology
Radiology
Anesthesiology and
Intensive Terapy
Anesthesiology and
Intensive Terapy
Neurology
0817447279
08164745561
08123868126
0811396811
081337667939
FACILITATORS
Regular Class (Class A)
No
1
2
3
4
5
6
7
8
9
10
11
12
Name
dr. A.A.Ayu Dwi Adelia
Yasmin, M.Biomed,
Sp.JP.FIHA
dr. I G N Sri Wiryawan,
M.Repro
Ni Putu Wardani, Sp.An,
M.Biomed
dr. Yukhi Kurniawan, Sp.And
dr. Putu Yuliandari, S.Ked
dr. Yuliana, M.Biomed
dr. Ida Bagus Putrawan,
Sp.PD
Dr.dr. Ni Putu Sriwidyani ,
Sp.PA
dr. Ni Luh Putu Ariastuti,
MPH
dr. I Made Suka Adnyana,
Sp.BP-RE
dr. I Dewa Ayu Inten Dwi
Primayanti, M.Biomed
dr. I Made Agus Kresna
Sucandra, Sp.An
Group
Departement
Phone
Cardiology
087861402169
Histology
082341768888
DME
08113992784
Andrology
08123473593
Microbiology
089685415625
Anatomy
085792652363
Interna
081236194672
Clinical
Anatomy
Public Health
081337115012
Surgery
081236288975
Fisiology
081337761299
Anasthesi
081805470888
Departement
Phone
Anasthesi
081337711220
Pharmacology
087861030195
Microbiology
08553711398
A1
A2
A3
A4
A5
A6
A7
A8
A9
A10
A11
A12
0818560008
Venue
(2nd floor)
2nd floor:
R.2.09
2nd floor:
R.2.10
2nd floor:
R.2.11
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
3nd floor:
R.3.20
3nd floor:
R.3.23
English Class (Class B)
No
1
2
3
Name
Dr.dr. Tjok G A Senapathi,
Sp.An. KAR
dr. Agung Nova Mahendra,
M.Sc
Dr.dr. Ni Nyoman Sri
Budayanti, Sp.MK (K)
Udayana University Faculty of Medicine, DME, 2016
Group
B1
B2
B3
Venue
(2nd floor)
2nd floor:
R.2.09
2nd floor:
R.2.10
2nd floor:
R.2.11
4
Study Guide Emergency Medicine September 2016
4
5
6
7
8
9
10
11
12
Dr.rer.Nat. dr. Ni Nyoman
Ayu Dewi, M.Si
I Ketut Mariadi, Sp.PD
Dr.dr. Ni Made Linawati, M.Si
dr. I Wayan Aryabiantara,
Sp.An. KIC
dr. Made Agus Dwianthara
Sueta, Sp.B-KBD
Dr.dr. Susy Purnawati, M.KK
dr. Putu Aryani, MPH
dr. I Made Oka Negara, FIAS
dr. I G A Sri Darmayani,
Sp.OG
Udayana University Faculty of Medicine, DME, 2016
B4
B5
B6
B7
B8
B9
B10
B11
B12
Biochemistry
081337141506
Interna
08123853700
Histology
081337222567
Anasthesi
08123822009
Surgery
081338648424
Fisiology
08123989891
Public Health
082237285856
Andrology
085935054964
DME
081338644411
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
3nd floor:
R.3.20
3nd floor:
R.3.23
5
Study Guide Emergency Medicine September 2016
TIME TABLE
Regular Class (Class A)
DAY/DATE
1.
Thu,
1 Sept
2016
2.
Fri,
2 Sept
2016
TIME
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
3.
Mon,
5 Sept
2016
4.
Fri,
9 Sept
2016
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
LEARNING
ACTIVITY
VENUE
CONVEYER
Highlight in
Emergency
Medicine
(Coordinator)
Individual Learning
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
SGD
Disc room
Facilitators
Plenary
Class room
Lecture 2.
Status Epilepticus
and Other Seizure
Disorders
Individual Learning
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
dr. IGN Budiarsa,SpS
SGD
Disc room
Facilitators
Plenary
Class room
dr. IGN Budiarsa,SpS
Lecture 3.
Coma and
Decrease of
Consciousness
Individual Learning
Class room
dr. Ida Ayu
Sriwijayanti,MBioMed,SpS
SGD
Disc room
Facilitators
Plenary
Class room
Lecture 4.
Acute Psychiatric
Episodes
Individual Learning
Class room
dr. Ida Ayu
Sriwijayanti,MBioMed,SpS
Dr.dr. Tjokorda Bagus
Jayalesmana,SpKJ
-
Break
Student Project
-
Break
Student Project
Break
Student Project
Udayana University Faculty of Medicine, DME, 2016
6
Study Guide Emergency Medicine September 2016
5.
Tue,
13 Sept
2016
6.
Wed,
14 Sept
2016
7.
Thu,
15 Sept
2016
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
SGD
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
Individual Learning
08.0009.00
Lecture 6.
Class room
Bleeding
Disorder(Epistaxis,
Hemorrhage In
Pregnancy)
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
Individual Learning
Facilitators
Class room
Dr.dr. Tjokorda Bagus
Jayalesmana,SpKJ
dr. Putu Andrika,
SpPDKIC, Dr. dr Dyah
Kanya Wati,SpA (K), dr.
Sucipta, SpTHT KL
dr. Srie Laksminingsih,
SpR
Break
Student Project
Plenary
Lecture 5.
Class room
Acute Respiratory
Distress Syndrome
and Failure
SGD
Disc room
Facilitators
Class room
ENT,
Pulmo, Pediatric,
Radiology
dr Sari Wulan, SpTHTKL(K),( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
-
Break
Student Project
Plenary
SGD
Disc room
Facilitators
Class room
dr Sari Wulan, SpTHTKL(K), ( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
dr. IGAG. Utara Hartawan,
SpAn MARS
dr.Nyoman
Budihartawan,MSc,SpA
-
Break
Student Project
Plenary
Lecture 7.
Shock
08.0009.00
09.0010.30
10.3012.00
12.0012.30
Disc room
Class room
Individual Learning
SGD
Disc room
Facilitators
Break
Udayana University Faculty of Medicine, DME, 2016
7
Study Guide Emergency Medicine September 2016
8.
Mon,
19 Sept
2016
9
Tue,
20 Sept
2016
10.
Wed,
21 Sept
2016
11.
Thu,
22 Sept
2016
12.3014.00
14.0015.00
Student Project
Plenary
Class room
08.0009.00
Lecture 8.
Cardiac Arrest and
+
Cardiopulmonary
Resuscitaton
Individual Learning
Class room
SGD
Disc room
Facilitators
Plenary
Class room
Lecture 9.
Emergency
Toxicology and
Poisoning
Individual Learning
Class room
dr. IGN. Mahaalit Aribawa,
SpAn KAR
dr. IKetut Agus Somia,
SpPD KPTI
SGD
Disc room
Facilitators
Plenary
Class room
Lecture 10
Hypertension In
Pregnancy
Individual Learning
Class room
dr. I Ketut Agus Somia,
SpPD KPTI
dr. I Gede Mega Putra,
SpOG(K)
SGD
Disc room
Facilitators
Plenary
Class room
Lecture 11.
Shoulder Dystocia
Class room
dr. I Gede Mega Putra,
SpOG(K)
dr. Endang
Sriwidiyanti,SpOG
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.30-
dr. IGAG. Utara Hartawan,
SpAn MARS
dr.Nyoman
Budihartawan,MSc,SpA
dr. IGN. Mahaalit Aribawa,
SpAn KAR
-
Break
Student Project
Break
Student Project
-
Break
Student Project
Individual Learning
SGD
Udayana University Faculty of Medicine, DME, 2016
Disc room
Facilitators
8
Study Guide Emergency Medicine September 2016
12.
Fri,
23 Sept
2016
13.
Tue,
26 Sept
2015
12.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
14
Mon,
27 Sept
2016
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
Break
Student Project
Plenary
Class room
Lecture 12.
Acute Blistering
and Exfoliative
Skin
Individual Learning
dr. Endang
Sriwidiyanti,SpOG
dr. Nyoman Suryawati
Sp.KK
-
SGD
Fasilitator
Break
Student Project
dr. Nyoman Suryawati
Sp.KK
Dr.dr. Ketut Suyasa, SpB
SpOT(K) Spine
dr. IGN Wien Aryana,
SpOT
Plenary
Lecture 13.
Trauma Which
Potentially
Disabling and life
Threatening
Conditions
Individual Learning
SGD
Disc room
Fasilitators
Break
Student Project
Plenary
Lecture 14.
Phlegmon
Individual Learning
SGD
Class room
Dr.dr. Ketut Suyasa, SpB
SpOT(K) Spine
dr. IGN Wien Aryana,
SpOT
drg. Putu Lestari
Sudirman
-
-
Disc room
Facilitators
Class room
drg. Putu Lestari
Sudirman
Break
Student Project
Plenary
Udayana University Faculty of Medicine, DME, 2016
9
Study Guide Emergency Medicine September 2016
15
Tue,
28 Sept
2016
16
Wed,
29 Sept
2016
1
Thu,
30 Sept
2016
08.0009.00
Lecture 15.
Urologic Concern
in Critical Care for
NonTrauma Case
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
Individual Learning
08.0009.00
09.0010.30
10.3012.00
12.0012.30
12.3014.00
14.0015.00
08.00selesai
SGD
Class room
dr. Gede Wirya Kusuma
Duarsa, M.Kes, SpU(K)
Disc room
Facilitators
Plenary
Class room
dr. Gede Wirya Kusuma
Duarsa, M.Kes, SpU(K)
Lecture 16.
Urologic Concern
in Critical Care for
Trauma Case
Individual Learning
Class room
SGD
Disc room
Facilitators
Class room
dr. Budi Santosa, SpU
Student Project
Presentation and
Examination
Theater
Room FK
UNUD
Team
Theater
Room FK
UNUD
Team
Break
Student Project
dr. Budi Santosa, SpU
-
-
Break
Student Project
Plenary
2
Fri,
3 Oct
2016
08.00selesai
Student Project
Presentation and
Examination
3
Mon,
4 Oct
2016
08.00Finish
Basic clinical skill
(1)
CPR (English
Class and Regular)
Clinical skill
lab
Team
4
Tue,
5 Oct
2016
08.00Finish
Basic clinical skill
(2)
Basic Trauma Care
(English Class and
Regular)
Prepare For
Examination
Clinical skill
lab
Team
Thu,
6 Oct
2016
Udayana University Faculty of Medicine, DME, 2016
10
Study Guide Emergency Medicine September 2016
Fri,
7 Oct
2016
EXAMINATION
English Class (Class B)
DAY/DAT
E
TIME
LEARNING
ACTIVITY
VENUE
1.
Thu,
1 Sept
2016
09.00-10.00
Highlight in
Emergency
Medicine
(Coordinator)
Student Project
Break
Individual Learning
SGD
Plenary
Class room
Lecture 2.
Status Epilepticus
and Other Seizure
Disorders
Student Project
Break
Individual Learning
SGD
Plenary
Lecture 3.
Coma and
Decrease of
Consciousness
Student Project
Break
Individual Learning
SGD
Plenary
Class room
Lecture 4.
Acute Psychiatric
Episodes
Student Project
Break
Individual Learning
SGD
Plenary
Class room
Lecture 5.
Acute Respiratory
Distress
Syndrome and
Class room
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
2.
Fri,
2 Sept
2016
09.00-10.00
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
09.00-10.00
3.
Mon,
5 Sept
2016
4.
Fri,
9 Sept
2016
5.
Tue,
13 Sept
2016
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
09.00-10.00
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
09.00-10.00
Udayana University Faculty of Medicine, DME, 2016
CONVEYER
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
-
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
dr. IGN Budiarsa,SpS
Disc room
Facilitators
Class room
Class room
dr. IGN Budiarsa,SpS
dr. Ida Ayu
Sriwijayanti,MBioMed,SpS
Disc room
Facilitators
Class room
dr. Ida Ayu
Sriwijayanti,MBioMed,SpS
Dr.dr. Tjokorda Bagus
Jayalesmana,SpKJ
Disc room
Facilitators
Class room
Dr.dr. Tjokorda Bagus
Jayalesmana,SpKJ
dr. Putu Andrika, SpPDKIC,
Dr. dr Dyah Kanya
Wati,SpA (K), dr. Sucipta,
SpTHT KL
11
Study Guide Emergency Medicine September 2016
Failure
6.
Wed,
14 Sept
2016
7.
Thu,
15 Sept
2016
8.
Mon,
19 Sept
2016
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 6.
Bleeding
Disorder(Epistaxi
s, Hemorrhage In
Pregnancy)
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 7.
Shock
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
09.00-10.00
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
9
Tue,
20 Sept
2016
09.00-10.00
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
dr. Srie Laksminingsih,
SpR
Disc room
Facilitators
Class room
ENT
Pulmo, Pediatric,
Radiology
dr Sari Wulan, SpTHTKL(K),( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
Facilitators
Class room
Disc room
Class room
Class room
dr Sari Wulan, SpTHTKL(K),( and ENT Team)
Dr.dr Wayan Megadhana,
SpOG(K) (and OBGYN
Team)
dr. IGAG. Utara Hartawan,
SpAn MARS
-
Disc room
Facilitators
Plenary
Class room
Lecture 8.
Cardiac Arrest
and +
Cardiopulmonary
Resuscitaton
Student Project
Break
Individual Learning
SGD
Plenary
Class room
dr. IGAG. Utara Hartawan,
SpAn MARS
dr. IGN. Mahaalit Aribawa,
SpAn KAR
Lecture 9.
Emergency
Toxicology and
Poisoning
Student Project
Break
Individual Learning
SGD
Class room
Udayana University Faculty of Medicine, DME, 2016
Disc room
Facilitators
Class room
dr. IGN. Mahaalit Aribawa,
SpAn KAR
dr. Agus Somya, SpPD
KPTI
Disc room
Facilitators
12
Study Guide Emergency Medicine September 2016
10.
Wed,
21 Sept
2016
11.
Thue,
22 Sept
2016
12.
Fri,
23 Sept
2016
15.00-16.00
Plenary
Class room
09.00-10.00
Lecture 10.
Pregnancy Induce
Hypertension
Student Project
Break
Individual Learning
SGD
Plenary
Class room
09.00-10.00
Lecture 11.
Shoulder
Dystocia
Class room
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 12.
Acute Blistering
and Exfoliative
Skin
Student Project
Break
Individual Learning
SGD
Plenary
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
13.
Tue,
26 Sept
2016
14
Mon,
27 Sept
2016
15
09.00-10.00
Lecture 13.
Trauma Which
Potentially
Disabling and life
Threatening
Conditions
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
dr. Agus Somya, SpPD
KPTI
dr. Gede Megaputra,
SpOG(K)
-
Disc room
Facilitators
Class room
dr. Gede Megaputra,
SpOG(K)
dr. Endang
Sriwidiyanti,SpOG
Disc room
Facilitators
Class room
dr. Endang
Sriwidiyanti,SpOG
dr. Nyoman Suryawati
Sp.KK
Fasilitator
dr. Nyoman Suryawati
Sp.KK
Dr.dr. Ketut Suyasa, SpB
SpOT(K) Spine
dr. IGN Wien Aryana, SpOT
Disc room
Fasilitators
Class room
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Lecture 14.
Phlegmon
Student Project
Break
Individual Learning
SGD
Plenary
Dr.dr. Ketut Suyasa, SpB
SpOT(K) Spine
dr. IGN Wien Aryana, SpOT
drg. Putu Lestari Sudirman
Disc room
Facilitators
Class room
drg. Putu Lestari Sudirman
09.00-10.00
Lecture 15.
Class room
dr. Gede Wirya Kusuma
Udayana University Faculty of Medicine, DME, 2016
-
13
Study Guide Emergency Medicine September 2016
Tue,
28 Sept
2016
16
Wed,
29 Sept
2016
Urologic Concern
in Critical Care for
NonTrauma Case
Duarsa, M.Kes, SpU(K)
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
Student Project
Break
Individual Learning
SGD
15.00-16.00
Plenary
09.00-10.00
Lecture 16.
Class room
Urologic Concern
in Critical Care for
Trauma Case
Student Project
Break
Disc room
Individual Learning
SGD
Plenary
Class room
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Disc room
Facilitators
Class room
dr. Gede Wirya Kusuma
Duarsa, M.Kes, SpU(K)
dr. Budi Santosa, SpU
Facilitators
dr. Budi Santosa, SpU
1
Thu,
30 Sept
2016
08.00selesai
Student Project
Presentation and
Examination
Clinical skill
lab
Team
2
Fri,
3 Oct
2016
3
Mon,
4 Oct
2016
08.00selesai
Student Project
Presentation and
Examination
Clinical skill
lab
Team
08.00Finish
Clinical skill (1)
CPR
(English Class
and Regular
Class)
Clinical skill
lab
Team
4
Tue,
5 Oct
2016
08.00Finish
Clinical skill (2)
Basic Trauma
Care (English
Class and
Regular Class)
Prepare For
Examination
Clinical skill
lab
Team
Thu
6 Oct
2016
Fri,
7 Oct
2016
EXAMINATION
Udayana University Faculty of Medicine, DME, 2016
14
Study Guide Emergency Medicine September 2016
ASSESSMENT METHOD
Assessment will be carried out on the 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
Student Registration Number
Faculty of Medicine, Udayana University 2012
2.
3.
4.
5.
Green coloured cover
Introduction
Journal critism/literature review
Conclusion
References
Example :
Journal
Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA Protection from
Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79-84.
Textbook
Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 4th ed.
Pennysylvania: WB Saunders Co. Pp 1636-1642.
Note.
Minimum 10 pages; line spacing 1.5; Times new roman 12
Udayana University Faculty of Medicine, DME, 2016
15
Study Guide Emergency Medicine September 2016
Student Project (SP) Emergency Medicine
September-October 2016



No
1
2
3
4
5
6
Berikut dibawah ini adalah judul SP yang sudah dibagi pergrup SGD. Masingmasing 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.
Student Project
Perdarahan Pervaginam
Kasus Ginekologi
Keganasan
Toxic Metabolic Coma
Kehamilan Dengan
Hipertensi Kronis
Trauma Abdomen
Skizofrenia Hebefrenik
Septic Shock Pada Pediatrik
Group
Penguji
A1
Dr.dr Wayan Megadhana,
SpOG(K)
A2
A3
A4
A5
A6
7
Dengue Shock Syndrome
Pada Pediatik
A7
8
Urogenital Trauma Pada
Anak-anak
A8
9
10
11
12
Laringotrakeobronkitis
Pneumonia
Perdarahan Pascaekstraksi
Gigi
Petit Mal Seizure
A9
A10
A11
A12
dr. Ida Ayu Sriwijayanti,
MBioMed, SpS
dr. I Gede Mega Putra,
SpOG(K)
Dr.dr. Ketut Suyasa, SpB
SpOT(K) Spine
Dr.
dr.
Cokorda
Bagus
Jayalesmana, SpKJ
dr.Nyoman
Budihartawan,
MSc, SpA
Dr. dr Dyah Kanya Wati,SpA
(K),
dr. Gede Wirya Kusuma
Duarsa, M.Kes, SpU(K)
dr. Wayan Sucipta, SpTHT KL
dr. Putu Andrika, SpPDKIC
drg. Putu Lestari Sudirman
dr. IGN Budiarsa,SpS
Venue
(2nd floor)
2nd floor:
R.2.09
2nd floor:
R.2.10
2nd floor:
R.2.11
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
3nd floor:
R.3.20
3nd floor:
R.3.23
English Class (Class B)
No
1
2
3
4
Student Project
Emergency Medicine Roles
in Natural Disaster
Radiology Roles in ARDS
Angiofibroma
Shock In Adult
Udayana University Faculty of Medicine, DME, 2016
Group
B1
B2
B3
B4
Venue
(2nd floor)
Dr.dr.
Tjok
Gde
Agung 2nd floor:
Senapathi, Sp.AnKAR
R.2.09
dr. Srie Laksminingsih, SpR
2nd floor:
R.2.10
dr Sari Wulan, SpTHT- KL(K)
2nd floor:
R.2.11
dr. IGAG. Utara Hartawan, 2nd floor:
SpAn MARS
R.2.12
Penguji
16
Study Guide Emergency Medicine September 2016
5
6
7
8
9
10
11
12
Sudden
Rescue
Cardiac
Death
Alcohol Intoxication
Abdominal and Pelvic Pain
In The Nonpregnant Female
Toxic Shock Syndrome
Acute Kidney Injury
Thoraxic Trauma
Acid Base Disorders
Fluid and Electolites
Udayana University Faculty of Medicine, DME, 2016
B5
B6
B7
B8
B9
B10
B11
B12
dr. IGN. Mahaalit
SpAn KAR
Aribawa,
2nd floor:
R.2.13
dr. I Ketut Agus Somia, SpPD
KPTI
dr. Endang Sriwidiyanti,SpOG
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
3nd floor:
R.3.20
3nd floor:
R.3.23
dr. Nyoman Suryawati Sp.KK
dr. Kadek Budi Santosa, SpU
dr. IGN Wien Aryana, SpOT
dr. I Made Agus Kresna
Sucandra, Sp.An
dr. I Wayan Aryabiantara,
Sp.An. KIC
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Study Guide Emergency Medicine September 2016
LEARNING PROGRAMS
Abstracts of Lectures
LECTURE 1 : HIGHLIGHT
EMERGENCY MEDICINE
Tjokorda Gde Agung Senapathi
Objective
To describe
1.
2.
3.
4.
Highlight Emergency Medicine
Basic principal of Emergency Medicine
Triad Emergency Medicine
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.
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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;
2007.
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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
2. Kaplan & Saddock’s Study Guide and Self Examination Review in Psychiatry, 7th ed.
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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.
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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:
Assess ABCˈs,
Place IV, give
IVfluid bolus, give
oxygen, place on
monitor
Respiratory distress
No
Respiratory arrest
Yes
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
Susp foreign body?
Complit obstruction:
Back or chest or
abdominal blows,
laryngoscopy &
removal, needle
cricothyrotomy
Partial obstruction?
NO
Immediate resuscitation, Clear
airway, Assist ventilations, chest
compression, IV,O2, IVF
Yes
Immediate intervention needed
Fever?
Status asthmaticus?
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
Trauma &
unilateral absent
breath sounds
Needle
thoracotomy
followed by tube
thoracotomy
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
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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 smallairways 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.
Udayana University Faculty of Medicine, DME, 2016
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Study Guide Emergency Medicine September 2016
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
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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
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Referrence
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.
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.
3.
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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.
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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 pressure
PAOP: pulmonary artery
occlusion pressure CO: cardiac output
CI: cardiac index
SVR: systemic vascular resistance
SVRI: 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.
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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.
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Lecture 8
CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION
IGN Mahaalit Aribawa
Objective
:
1.
2.
3.
4.
To describe etio-pathogenesis and pathophysiology of cardiac arrest
To know how to identify patients with cardiorespiratory arrest
To understand the chain of survival
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.
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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
33ransaction 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
33ransact to support the diagnosis. The time of the first contact with tocicant is very I for
determine of prognosis and treatment. The antidote is 33ransact 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 33ransacti). 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, 33ransaction 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 ( 33ransact, 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
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rather than to the stomach, 34ransac 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.
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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
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Lecture 11
SHOULDER DYSTOCIA
Endang Sriwidiyanti
OBGYN Team
Objective
1. Define shoulder dystocia
2. Review appropriate fetal/maternal assessment
3. Discuss the risk factors of shoulder dystocia
4. Discuss the complications of shoulder dystocia
5. Discuss appropriate management of shoulder dystocia
Shoulder dystocia is one of emergency problems during delivery. Following the
delivery of the head, there is impaction of the anterior shoulder on the symphysis pubis in
the AP diameter, in such a way that the remainder of the body cannot be delivered in the
usual manner. More than 50% of cases shoulder dystocia occur in the absence of any
identified risk factor. The student will discuss the assessment of shoulder dystocia, the
complication for fetus and mother, identification of risk factor, diagnosis and management
Definition
After the birth of the head, external rotation will take place which causes axis of the head to
be on the normal axis to the spine. Generally shoulder will be on the oblique axis under the
pubic ramus. Pushing of the mother will cause the anterior shoulder become under the
pubis. If the shoulder fails to hold a rotation of adjusting to the axis of tilted pelvis and
remain in the anteroposterior position, the baby will most collision front shoulder to the
symphysis.
Shoulder dystocia is mainly caused by deformities of the pelvis, the failure of the shoulder to
"folded" into the pelvis (eg on macrosomia) caused by active phase and short second stage
of labor in multiparas so the descence of the head is too quickly, causing the shoulder does
not fold through the birth canal or head has through the middle pelvis after a prolong of the
second stage of labor before the shoulder successfully folded into the pelvis.
Incidence
• 1 - 2 in 1000 Birth
• 16 in 1000 baby weight > 4000 g
Complication :
• Baby
- Death
- Asphysxia and its complications
- Fracture of Clavicula, humerus
- Brachial Plexus Injury
• Mother
- Postpartum haemorrhage
- Uterine Rupture
Risk Factors :
• Post date pregnancy
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•
•
•
•
•
•
Maternal Obesity
Macrosomia baby
History of prior shoulder dystocia
Operative vaginal delivery
Prolong second stage of labour
Uncontrolled Maternal Diabetes
•
•
•
Turtle’ sign
Prolonged second stage of labour
Fail to deliver the baby with maximal effort and proper management
Diagnosis
Management
Requirement :
 Maternal vital condition is sufficient to work together to completing deliveries
 The mother has the ability to pushing
 The passage and the pelvic outlet are adequate for the baby's body accommodation
 The baby is still alive or are expected to survive
 Not monstrum or congenital abnormality that prevents the delivery of baby
The management : "ALARMER"
1. Principles : Do not 4 “P” :
 Panic
 Pulling (the head of the baby)
 Pushing (the fundal of uterine)
 Pivoting (the head of the baby with coccygeus as fulcrums
2. Ask For Help :
 The mother of patient
 Husband
 Midwife
 Physician in charge or other paramedic
3. Lift the buttock- McRobert’s Maneuver
Figure 1. McRobert's Maneuver
4. Anterior Disimpaction 4.1. Suprapubic Pressure (Manuver Massanti )
• Suprapubic pressure on the baby's anterior shoulder toward the chest of the
baby.
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Figure 2. Suprapubic Pressure
4.2. Rubin Manouver
• vaginal approach
• adduction anterior shoulder by pressing the posterior shoulder towards the
chest
• Consider episiotomy
Figure 3. Rubin Manouver
5. Rotate the posterior shoulder- Corkscrew/ Wood Maneuver
Figure 4. Wood Maneuver
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6. Manual removal of posterior arm / Schwartz and Dixon Maneuver
 Pressure on antecubital fosa to flexi the forearm
 move the forearm anteriorly.
 Reach the forearm or the fingers
 Deliver the posterior shoulder
Figure 5. Schwart and Dixon Maneuver
7. Episiotomy-consider
 Help Wood Manouver or giving more space to deliver the posterior arm, rotate
the chest and ease reaching the posterior shoulder
8. Roll over
9. Last Efforts :
 Break the clavicle
 Cephalic replacement (Zavenelli Manouver)
 Symphisiotomy
10. After procedure :
• Post partum haemorrhage anticipation
• Exploration of lasceration and tear
• Examination of the baby
• Explain to the patient
• Record the procedure
Reference
1. Cunningham FG, Leveno KJ, Bloom SL, Spong, CY, Dashe JS, Hoffman BL, Casey
BM, Sheffield JS. 2014. William Obstetrics, 24 edition. Mc Graw Hill.
2. Buku Acuan Modul PONEK. 2008. JNPK-KR.
3. ALARM International Course
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Lecture 12
DERMATO - EMERGEMENCIES
ACUTE BLISTERING AND EXFOLIATIVE SKIN
Nyoman Suryawati
Objective
 To understand the basic principle of acute blistering and exfoliative skin
 Able to identify a case with acute blistering and exfoliative skin
 Able to manage and referral a case with acute and exfoliative skin
Abstract
Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis
Stevens–Johnson syndrome (SJS) and Toxic epidermal necrolysis (TEN) are acute lifethreatening mucocutaneous reactions characterized by extensive necrosis and detachment
of the epidermis, with a mortality rate reaching 30%. The pathophysiology of EN is still
unclear; however, drugs are the most important etiologic factors. Both SJS and TEN are
differs only in the final extent of body surface involved: (1) SJS, less than 10% of body
surface area (BSA); (2) SJS/TEN overlap, between 10% and 30%; (3) TEN, more than 30%
of BSA.
Nonspecific symptoms such as fever, headache, rhinitis, cough, or malaise may
precede the mucocutaneous lesions by 1 to 3 days. Pain on swallowing and burning or
stinging of the eyes progressively develop, heralding mucous membrane involvement. The
eruption is initially symmetrically distributed on the face, the upper trunk, and the proximal
part of limbs. The initial skin lesions are characterized by erythematous, dusky red, purpuric
macules, irregularly shaped, which progressively coalesce. Nikolsky’s sign (dislodgement of
the epidermis by lateral pressure) is positive on erythematous zones. At this stage, the
lesions evolve to flaccid blisters, which spread with pressure and break easily. The necrotic
epidermis is easily detached at pressure points or by frictional trauma. Mucous membrane
involvement (nearly always on at least two sites) is observed in approximately 90% of cases
and can precede or follow the skin eruption.
SJS and TEN are a life-threatening disease that requires optimal management: early
recognition and withdrawal of the offending drug and supportive care in an appropriate
hospital setting. The patient must be transferred to an intensive care unit or a burn center.
Prompt referral reduces risk of infection, mortality rate, and length of hospitalization. Specific
therapy including immunosuppressive and/or anti-inflammatory therapies, antibiotic therapy
only if clinical infection is suspected. Supportive care consists of fluid replacement, early
nutritional support, aseptic and careful handing to reduce the risk of infection.
Staphylococcal Scalded Skin Syndrome
Staphylococcal Scalded Skin Syndrome (SSSS) is the term used to define a potentially lifethreatening, blistering skin disease caused by exfoliative toxins (ETs) of certain strains of
Staphylococcus aureus (usually phage group 2). ETs are serine proteases that bind to the
cell adhesion molecule desmoglein 1 and cleave it, resulting in a loss of cell–cell adhesion.
The onset of SSSS may either be acute with fever and rash or be preceded by a
prodrome of malaise, irritability, and cutaneous tenderness, often accompanied by purulent
rhinorrhea, conjunctivitis, or otitis media. Within 1–2 days the rash progresses from an
exanthematous scarlatiniform to a blistering eruption. Very superficial tissue paper-like
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wrinkling of the epidermis, which is characteristic, progresses to large flaccid bullae in
flexural and periorificial surfaces. A positive Nikolsky sign can be elicited by stroking the
skin, which results in a superficial blister. One or two days later, the bullae rupture and their
roofs are sloughed, leaving behind a moist, glistening, red surface along with varnish-like
crusts. At this stage, the clinical appearance closely resembles that of extensive scalding.
Mucous membranes are usually spared by bullae and erosions. Days later, due to
generalized shedding of the epidermis, scaling and desquamation progressively occur. The
skin returns to normal in 2–3 weeks.
Patients with SSSS require hospitalization because, besides the appropriate
systemic antibiotic therapy, intensive general supportive measures are needed. The
mainstay of treatment is to eradicate staphylococci from the focus of infection, which in most
cases requires intravenous (IV) antistaphylococcal antibiotics. The use of suitable
antibiotics, combined with supportive skin care and management of potential fluid, and
electrolyte abnormalities due to the widespread disruption of barrier function, will usually be
sufficient to ensure rapid recovery. Major complications of SSSS are serious fluid and
electrolyte disturbances. The mortality in uncomplicated pediatric SSSS is very low (2%)
and is not usually associated with sepsis.
References
-
-
-
-
-
Roujeau C-Jean, Valeyrie L- Allanore. Epidermal Necrolysis (Stevens–Johnson
Syndrome and Toxic Epidermal Necrolysis). In Goldsmith LA, Katz SI, Gilchrest BA,
Paller AS, Leffel DJ, Wolff K, eds. Fitzpatrick’s Dermatology In General Medicine. 8 th
ed. New York : McGraw-Hill, Medical 2012. Ch 40. P. 846-862
Wolf R, Davidovici BB. Severe, Acute Adverse Cutaneous Drug Reactions I: Stevens–
Johnson Syndrome and Toxic Epidermal Necrolysis. In Wolf R, Davidovici BB, Parish
JL, Parish LC, eds. Emergency Dermatology. Cambridge University Press 2010. Ch15.
p.154-161
Travers BJ, Mousdicas N.Gram-Positive Infections Associated with Toxin Production. In
Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffel DJ, Wolff K, eds. Fitzpatrick’s
Dermatology In General Medicine. 8 th ed. New York : McGraw-Hill, Medical 1012. Ch
177. p 4028-4037
Eleonora Ruocco E, Baroni A, Sangiuliano S, Donnarumma G, Ruocco V.
Staphylococcal Scalded Skin Syndrome. In Wolf R, Davidovici BB, Parish JL, Parish
LC, eds. Emergency Dermatology. Cambridge University Press 2010. Ch. 11:109-114
Trauma, burns and skin injury. In Beed M, Sherman R, Mahajann R, eds. Emergency in
Critical Care. 2 nd ed. Oxford University Press 2013. Ch 12. P 422-23
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Lecture 13
TRAUMA WHICH POTENTIALLY DISABLING AND LIFE THREATENING
CONDITIONS
I Ketut Suyasa, IGN Wien Aryana
Objectives :
 To implement a general strategy in the approach to patient with trauma which
potentially disabling and life threatening conditions through history, physical
examination and special technique investigations
 To manage by assessing, provide initial management and refer patient with trauma
which potentially disabling and life threatening conditions
 To describe prognosis patient with trauma which potentially disabling and life
threatening conditions
The field of trauma, or injury, is continuously evolving as knowledge is gained in to
therapeutic management. There is a trimodal distribution of death due to trauma, Early or
immediate death (45%) occurs at the scene of the incident and is related to a devastating
and catastrophic injury such as cerebral herniation, aortic 42ransaction or cardiac rupture.
Other than preventive measures, there is little medically that can be done. Although rapid
transport from the scene has allowed some of these patients to arrive in extremis in the
emergency room, lethality is uniform. The second group (35%) are those that arrive in the
emergency department. And require aggressive evaluation and therapy. The third mode of
death (20%) occurs days or weeks after admission in patient who usually reside in the ICU.
In the following section on trauma assessment and resuscitation, methods of care
are discussed so as to prevent the progression to this most serious of clinical conditions.
Key Points
• Assess all trauma patients with a rapid primary survey followed by a more comprehensive
secondary evaluation.
• Address all emergent l ife threats in a stepwise manner during the
primary survey before progressing to the next stage.
• Treat hemodynamically unstable patients as hemorrhagic shock until proven otherwise.
•
Initiate aggressive volume resuscitation in all unstable patients while concurrently searching
for active sources of hemorrhage.
INTRODUCTION
Trauma is currently the fourth leading cause of death in the United States across all age
groups and the leading cause of death in patients under the age of 44 years. It is
responsible for more deaths in patients under the age of 19 years than all other causes
combined. Approximately 40% of all emergency department (ED) visits are for traumarelated complaints, and the annual costs exceed $400 billion. Adding to these costs,
permanent disability is actually 3 times more likely than death in this cohort.
Trauma is broadly classified by mechanism into blunt and penetrating varieties, with the
former more than twice as common as the latter. Regardless of mechanism, victims of
significant trauma present with a wide range of complex problems, and their proper care
necessitates a multidisciplinary approach, including emergency physicians, trawna
surgeons, and the appropriate subspecialties. Most trawna care delivery systems follow the
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Advanced Trawna Life Support guidelines developed and maintained by the American
College of Surgeons.
The mortality rates for traumatic injuries typically follow a trimodal distribution. Certain injury
patterns including major vascular injuries and high cervical cord disruption with secondary
apnea result in near immediate death. The second cohort of injuries, including conditions
such as pneumothorax and pericardial tamponade, typically evolve over a duration of
minutes to hours and are generally responsive to aggressive emergent intervention.
Septicemia and multisystem organ failure account for the third peak of fatalities and typically
occur weeks to months after injury.
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Lecture 14
PHLEGMON / LUDGIG’S ANGINA
Putu Lestari Sudirman
Objective
:
1. To describe etio-pathogenesis and pathophysiology of phlegmon
2. To implement a general strategy in the approach to patients with phlegmon, physical
examination and special technique investigations.
3. To manage by assessing and refer patient phlegmon
4. To describe prognosis patient with phlegmon
Abstract
Phlegmone / Ludwig's angina is a diffuse cellulitis is on spasia sublingual, submental
and submandibular bilateral, sometimes up about spasia pharingeal. Cellulitis starts from
the bottom up. Often bilateral, but when just about one side / unilateral called
Pseudophlegmon. Often caused by primary infection of cellulitis come from M1, M2 lower
jaw, other causes (Topazian, 2002): sialodenitis submandibular gland, compund mandibular
fractures, lacerations of the soft mucosa of the mouth, stab wounds basic secondary
infection of the mouth and oral malignancy.
Clinical symptoms of phlegmon, such as edema on both sides floor of the mouth,
walked quickly spread to the neck just a few hours, the tongue uplifted, progressive trismus,
chewy consistency - stiff as a board, swelling redness, neck loses its normal anatomy, often
febrile / increase in body temperature, pain and difficulty in swallowing, droling, sometimes
up tough talk and breathe and stridor (inspiratory rough sound, because the narrowing of
the airways in the oropharynx, subglottic or tracheal) Phlegmone / Ludwig's angina requiring
treatment as soon as possible, in the form of: referral for hospitalization, intravenous
antibiotics high doses, typically used for initial therapy in combination with Ampisillin
metronidazole, intravenous fluid replacement, drainage, as well as the handling of the
airway, such as endotracheal intubation or tracheostomi if needed.
Local symptoms include swelling of the soft tissue / spasia, pain, heat and redness in
the area of swelling, swelling caused by edema, cellular infiltration, and sometimes because
of pus, diffuse swelling, chewy consistency - hard as a board, sometimes accompanied by
trismus and sometimes floor of the mouth and tongue raised. Systemic symptoms such as
high temperature, rapid and irregular pulse, malaise, lymph nodes, increasing the number of
leukocytes, rapid breathing, face reddish, dry tongue, delirium, especially at night,
dysphagia and dyspnoea and stridor. Prognosis in case of phlegmon depending on patient
age, the condition of the patient come first to get treatment and also depending on
conditions Systemic patients.
If there are signs of systemic conditions such as malaise and high fever, presence of
dysphagia or dyspnoea, dehydration or drinking less patient, thought to decrease resistance
to infection, septicemia, and toxic infiltration into anatomic regions are dangerous and
require general anesthesia for drainage, required serious treatment and hospital care as
soon as possible. Should always be controlled airway, endotracheal intubation or
tracheostomy. Four basic principles infection treatments (Falace, 1995), namely: eliminating
causa (If the patient's general condition possible to be done This procedure, by way of
cause tooth extraction), drainage (drainage Incision can be done intra and extra oral, or can
be done simultaneously in the case - severe cases. Determining the location of the incision
by spasium involved). In the administration of antibiotics to consider whether the patients
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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).
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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
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cord. The spermatogenic cells are the most sensitive to ischemia, whereas the testosteroneproducing 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.
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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.
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~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
9
Senior Clerkship
8
Senior clerkship
7
Medical
Emergency
(3 weeks)
Special Topic:
-Travel medicine
(2 weeks)
Elective Study III
(6 weeks)
Clinic Orientation
(Clerkship)
(6 weeks)
6
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The
Cardiovascular
System and
Disorders
(4 weeks)
The Urinary
System and
Disorders
(3 weeks)
The Reproductive
System and
Disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary 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)
BCS (1 weeks)
Musculoskeletal
system &
connective
tissue disorders
(4 weeks)
Neuroscience
and
neurological
disorders
(4 weeks)
Behavior Change
and disorders
(4 weeks)
BCS (1 weeks)
Hematologic
system & disorders & 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)
Medical
Professionalism
(2 weeks)
BCS(1 weeks)
Evidence-based
Medical Practice
(2 weeks)
BCS (1 weeks)
Health Systembased Practice
(3 weeks)
BCS(1 weeks)
Community-based
practice
(4 weeks)
-
BCS (1 weeks)
Stadium
Generale and
Humaniora
(3 weeks)
Medical
communication
(3 weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(3 weeks)
Growth
&
development
(4 weeks)
BCS (1 weeks)
BCS(1 weeks)
BCS: (1 weeks)
BCS (1 weeks)
Elective Study
II
(1 weeks)
5
4
3
2
1
BCS (1 weeks)
Special Topic :
- Palliative
medicine
-Compleme
ntary &
Alternative
Medicine
- Forensic
(3 weeks)
Elective
Study II
(1 weeks)
Special Topic
- Ergonomi
- Geriatri
(2 weeks)
Elective
Study I
(2 weeks)
The Visual
system &
disorders
(2 weeks)
Pendidikan Pancasila & Kewarganegaraan (3 weeks)
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