Hayo Apa Ini

Study Guide Emergency Medicine
STUDY GUIDE THE EMERGENCY MEDICINE
First Edition March 2019

All rights reserved. No part of this publication may be reproduced, stored in a
retrieval system, or transmitted in any form or by any means, electronic, mechanical,
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publisher.
Published by Medical Health and Education Development Unit, Faculty of Medicine,
Universitas Udayana.
Medical Health and Education Development Unit - Faculty of Medicine Udayana University – March 2019 1
CONTENTS
STUDY GUIDE THE EMERGENCY MEDICINE.................................................................1
CONTENTS..............................................................................................................................2
PREFACE..................................................................................................................................3
CURRICULUM CONTENTS..................................................................................................4
PLANNERS/ LECTURES TEAM............................................................................................5
FACILITATORS........................................................................................................................6
ASSESSMENT METHOD.......................................................................................................7
STUDENT PROJECT...............................................................................................................7
Student Project (SP) Emergency Medicine...............................................................................8
FORM BIMBINGAN STUDENT PROJECT........................................................................10
LEARNING PROGRAMS.....................................................................................................12
Lecture 1..............................................................................................................................12
Lecture 2..............................................................................................................................15
Lecture 3..............................................................................................................................17
Lecture 4..............................................................................................................................18
Lecture 5..............................................................................................................................20
Lecture 6..............................................................................................................................21
Lecture 7..............................................................................................................................22
Lecture 8..............................................................................................................................23
Lecture 9..............................................................................................................................25
Lecture 10............................................................................................................................30
Lecture 11............................................................................................................................31
Lecture 12............................................................................................................................41
Lecture 13............................................................................................................................42
Lecture 14............................................................................................................................43
Lecture 15............................................................................................................................45
Lecture 16............................................................................................................................48
Lecture 17............................................................................................................................50
Lecture 18............................................................................................................................51
Lecture 19............................................................................................................................61
Lecture 20............................................................................................................................66
Lecture 21............................................................................................................................78
Lecture 22............................................................................................................................82
Lecture 23............................................................................................................................84
Lecture 24............................................................................................................................86
LEARNING TASK FOR SGD................................................................................................87
DAFTAR DOSEN PENGAJAR BLOK EMERGENCY MEDICINE 2019........................101
TIME LINE BLOK EMERGENCY MEDICINE MARET-APRIL 2019............................105
JADWAL BCS.......................................................................................................................109
PREFACE
Emergency Medicine has long been established especially in Australasia, Canada, Ireland,
the United Kingdom and the United States, in Asiaothe emergency medicine officially
inauguration of Asian Society of Emergency Medicine in Singapore on the 24th of October
1998 at the first Asian Conference on Emergency Medicine which as Prof. DR. dr. Eddy
Rahardjo, Sp.An.KIC and dr. Tri Wahyu Murni sat as member of Board Director.
It is thus sometimes seen to be synonymous with emergency medical careand within the
province and expertise of almost all medical practitioners. However, 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 see kto compete with other medical
specialties.
Basic science concepts to help in the understanding of the pathophysiology and treatment
of disease. The medical curriculum has become increasingly vertically integrated, with a
much greater use of clinical examples and cases to help in the understanding of the
relevance of the underlying basic science, The Emergency Medicine block has been written
to take account of this trend, and to integrate core aspects of basic science,
pathophysiology and treatment into a single, easy to use revision aid.
In accordance the lectures that have been full integrated for studens in 6Th semester, period
of 2012, one of there is The Emergency Medicine Block.
There are many topics will be discussed 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.
Planner
CURRICULUM CONTENTS
Mastering of basic knowledge with its clinical and practical implication.
Establish tentative diagnosis, provide initial management and refer patient with:
 Seizure and mental status changes
 Coma and decrease of conciousness
 Psychiatric Disorder
 Radiology imaging emergency setting
 Acute respiratory distress syndrome and failure
 Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding)
 Shock (adult and pediatric patient)
 Cardiac critical care (Cardiac arrest and CPR)
 Neonatal resuscitation
 Emergency toxicology and poisoning
 Pregnancy induce Hypertension, Shoulder dystocia
 Urologic concern in critical and non critical care
 Phlegmon
 Brain Resusscitation
 Acute Blistering and Expoliative skin
 Trauma which potentially disabling and Life threatening condition
 Environmental injury
 Pain management
 Emergency in pediatric (non trauma)
Skills
 To implement a general strategy in the approach to patients with critical ill through
history and physical examination and special technique investigations
 To manage by assessing, provide initial management and refer patient with critical ill
Personal Development/ Attitude

Awareness to:
 Ethic in critical care
 Basic principle of critical care
 The importance of informed consent to patient and family concerning critical ill
situations
 Risk of patient with critically ill and its prognosis
Community Aspect
 Communicability of the critical cases
 Cost effectiveness
 Utilization of health system facilities
 Critical ill patient
PLANNERS/ LECTURES TEAM
NO. NAME DEPARTMENT

1. Dr.dr.Tjok Gde Agung Senapathi,Sp.AnKAR Anesthesiology and Intensif Terapy
(Coordinator) HP 081337711220
2. Dr.dr. Gd Wirya Kesuma Duarsa, SpU(K),MKes Urologic Surgery
HP 08155753377
3. dr. IGN Budiarsa,SpS HP 0811399673 Neurology
4. dr. Sari Wulan,SpTHT KL HP 081237874447 ENT
5. Drg. Lestari Sudirman HP 08155764446 Dentistry
6. Dr.dr. I Putu Pramana Anesthesiology and Intensif Terapy
Suarjaya,SpAn.M.Kes.KMN.KNA
HP 0811394811
7. Dr.dr. Agus Somya, SpPD. KPTI Internal Medicine
HP 08123989353
8. Dr.dr.Dyah Kanyawati, SpA(K) Pediatric
HP 081285705152
9. Dr.dr. Wayan Megadana, SpOG(K) Obstetric-Gynecologic
HP 08123917002
10. dr. Endang Sriwidiyanti, SpOG Obstetric-Gynecologic
HP 081558314827
11. Dr.dr. Gede Megaputra, SpOG(K) Obstetric-Gynecologic
HP 08123636172
12. dr. Wayan Yudiana, SpU Urologic Surgery
HP 081338708195
13. Dr.dr.Tjokorda Bagus Jayalesmana,SpKJ Psychiatric
HP 0816295779
14. dr. Nyoman Suryawati, SpKK Dermatology
0817447279
15. dr. Sri Laksminingsih SpR (K) Radiology
HP 08164745561
16. dr. IA Sriwijayanti,MBioMed,SpS Neurology
HP 081337667939
17. dr. IGAG Utara Hartawan,SpAn.MARS Anesthesiology and Intensif Terapy
18. dr. Nyoman Budihartawan,M.Sc,SpA Pediatrician
HP 081236333221
19. dr. Pontisomaya Parami, SpAn MARS Anesthesiology and Intensif Terapy
HP 08113800107
20. Dr.dr. Ketut Suyasa, SpB. SpOT(K)Spine Ortophedic Surgery
HP 081558724088
21. dr. IGN. Wien Aryana,SpOT Ortophedic Surgery
HP 0811385263
22. dr. Wayan Sucipta,SpTHT KL ENT
HP 08125318941
23. dr. Ida Bagus Krisna Jaya Anesthesiology and Intensif Terapy
Sutawan,SpAn.M.Kes HP 08123836470
24. dr. Made Agus Kresna Sucandra, SpAn KIC Anesthesiology and Intensif Terapy
HP 081236214222
25. dr. I Made Darmajaya, SpB, SpBA, MARS Pediatric Surgery
HP 08123959701
26. dr. AA Gde Yuda Asmara, SpOT Orthopedic Surgery
HP 081337870347
27. dr. Agus Roy Ruly Hariantana Hamid, SpBP- Plastic Surgery
RE(K) HP 08123511673
dr. Made Agus Dwianthara Sueta, SpB KBD Digestive Surgery
28. HP 081338648424
FACILITATORS
Regular Class (Class A)

Venue
No Name Group Departement Phone
(2ndfloor)
dr. IA Sri Wijayanti, Sp.S, 3rd floor:
1 A1 Neurologi 081337667939
M.Biomed R.3.09
dr. Ni Gusti Ayu Agung Manik 3rd floor:
2 A2 Surgery 08123214075
YW, Sp.B(K)Onk R.3.10
Dr rer nat dr Ni Nyoman Ayu 3rd floor:
3 A3 Biochemistry 081337141506
Dewi M.Kes R.3.11
dr. Ni Luh Gede Yoni 3rd floor:
4 A4 Histology 0817569493
Komalasari, S.Ked R.3.12
dr. Pontisomaya Parami, 3rd floor:
5 A5 Anesthesiology 08113800107
Sp.An, MARS R.3.13
3rd floor:
6 dr Putu Cintya DY MPH A6 Public Health 081353380666
R.3.14
dr Agung Nova Mahendra 3rd floor:
7 A7 Pharmacology 087861030195
M.Sc R.3.15
dr. Kadek Ayu Candra Dewi, Orthopaedi & 3rd floor:
8 A8 081510025778
Sp.OT Traumatology R.3.16
3rd floor:
9 dr. Nila Wahyuni, M.Fis A9 Physiology 081805469684
R.3.17
Orthopaedi & 3rd floor:
10 dr. I Wayan Subawa, Sp.OT A10 081337096388
Traumatology R.3.19
English Class (Class B)

Venue
No Name Group Departement Phone
(2ndfloor)
dr Kadek Agus Heryana 3rd floor:
1 B1 Anesthesiology 081338568883
Putra, Sp.An R.3.09
3rd floor:
2 dr Yuliana, M.Biomed B2 Anatomy 085792652363
R.3.10
dr Ida Bagus Budiarta, 3rd floor:
3 B3 Surgery 081338760640
Sp.B(K)V R.3.11
dr Made Bramantya Karna Orthopaedi & 3rd floor:
4 B4 08113891506
Sp.OT(K) Traumatology R.3.12
Dr. dr. Ni Nyoman Sri 3rd floor:
5 B5 Microbiology 08553711398
Budayanti, Sp.MK(K) R.3.13
dr Ni Luh Putu Eka Diarthini, 3rd floor:
6 B6 Parasitology 087860028001
M.Si R.3.14
dr I Gede Budhi Setiawan, 3rd floor:
7 B7 Surgery 08123923956
Sp.B(K)Onk R.3.15
3rd floor:
8 Dr. Agus Eka Darwinata, PhD B8 Microbiology 081993933144
R.3.16
3rd floor:
Dr dr Luh Putu Ratna
9 B9 Physiology 081933070077 R.3.17
Sundari, M.Biomed
dr IB Krisna Jaya Sutawan, 3rd floor:
10 B10 Anesthesiology 08123836470
Sp.An, M.Kes, KNA R.3.19
Student Project (SP) Emergency Medicine
 Pembimbing dan penguji SP disesuaikan dengan tabel di bawah ini.

 Bimbingan SP dengan pembimbing harus dilakukan tatap muka dengan pembimbing
minimal 2 kali pertemuan, yang dibuktikan dengan tanda tangan form bimbingan SP.
Mahasiswa yang tidak memenuhi bimbingan 2 kali, dianggap tidak ikut SP. Form
bimbingan ada di halaman terakhir pengumuman ini.
 Ujian SP (presentasi SP) disesuaikan dengan time table yang sudah ada. Setiap
kelompok akan mendapatkan alokasi waktu 60 menit (sudah termasuk presentasi dan
tanya jawab).
 Masing-masing kelompok menghubungi pembimbing dan pengujinya. Pelaksanaan
ujian bisa disepakati dengan penguji, tidak harus sesuai dengan jadwal.
 Lokasi Ujian SP adalah di Ruang Kuliah dr. Mangku Departemen Anestesiologi dan
Terapi Intensif RS Sanglah Denpasar
Jadwal Ujian SP
SMT 6 1/4/2019 2/4/2019 4/4/2019
08.00-09.00 A1 A4 A7
09.00-10.00 B1 B4 B7
10.00-11.00 A2 A5 A8
11.00-12.00 B2 B5 B8
12.00-13.00 A3 A6 A9
13.00-14.00 B3 B6 B9
14.00-15.00 - - A10
15.00-16.00 - - B10
Note: mahasiswa yang tidak mendapatkan ujian SP mendapatkan waktu Individual
Learning untuk persiapan ujian blok.
SP Regular class
No Student Project Group Pembimbing dan Penguji
1 Abrupsio Plasenta A1 Dr.dr. Wayan Megadhana, SpOG(K) (HP
08123917002)
2 Septic Shock A2 dr. I G A G Utara Hartawan, SpAn
MARS (08113891490)
3 Resuscitation in Pregnancy A3 dr. IB Krisna Jaya Sutawan,
SpAn.MKes(HP 08123836470)
4 Intoksikasi Organofosfat A4 Dr.dr. I Ketut Agus Somia, SpPD KPTI
(HP 08123989353/089617587075)
5 Steven Johnson-Syndrome A5 dr. Nyoman Suryawati, SpKK (HP
0817447279)
6 Hipertensi Dalam Kehamilan A6 Dr.dr. Gede Megaputra, SpOG(K)
(HP 08123636172)
7 Trauma Sendi A7 dr. IGN Wien Aryana, SpOT (HP
0811385263)
8 Carcinoma Nasofaring A8 dr. dr. Sari Wulan,SpTHT KL (HP
081237874447)
9 Retentio Urine in Emergency A9 Dr.dr. Gd Wirya Kesuma Duarsa,
Setting SpU,MKes
HP 08155753377
10 Angina Ludwig A10 dr. Made Agus Dwianthara Sueta, SpB
KBD
(HP 081338648424)
SP English Class
No Student Project Group Pembimbing/penguji
1 Spine: Fracture and Dislocation B1 Dr.dr Ketut Suyasa, Sp.B,
SPOT(K)Spine
(HP 081558724088)
2 Post Traumatic Stress Disorder B2 Dr.dr. Tjokorda Bagus Jayalesmana,
SpKJ
(HP 0816295779)
3 Dengue Shock Syndrome in B3 dr. Nyoman Budi Hartawan, MSc, SpA
Pediatric Patient (HP 081236333221)
4 Febris Seiuzures in Pediatric B4 Dr.dr Dyah Kanya Wati, SpA(K) (HP
Patient 081285705152)
5 Pelvic Injury B5 dr. Wayan Yudiana, SpU
(HP 081338708195)
6 Blust Injury B6 dr. Agus Roy Rusly Hariantana Hamid,
SpBP-RE(K)
(HP 08123511673)
7 Subarachnoid Hemoragic B7 Dr.dr I Pt Pramana Suarjaya, SpAn
KMN KNA (HP 0811394811)
8 Malaria Serebral B8 dr. IA Sriwijayati, MBiomed, SpS (HP
081337667939)
9 Distosia B9 dr. Endang Sriwidiyanti, SpOG
HP 081558314827
10 Haematothorax B10 dr. AA Gde Yuda Asmara, SpOT
HP 081337870347
FORM BIMBINGAN STUDENT PROJECT

BLOK EMERGENCY MEDICINE
MARET - APRIL 2019
Nama Mahasiswa :
Kelas :
NIM :
Grup :
Topik Student Project :
Pembimbing :
Bimbingan/tanggal Pembahasan Tanda tangan pembimbing
I tanggal …..
II tanggal …..
III tanggal …..
IV tanggal …..
V tanggal ……
Mahasiswa, Pembimbing,
( ) ( )
FORM PENILAIAN STUDEN PROJECT

BLOK EMERGENCY MEDICINE
MARET-APRIL 2019
Nama Mahasiswa :
Kelas :
NIM :
Grup :
Topik Student Project :
Pembimbing :
Tanggal Ujian :
No. Penilaian Nilai maksimal Nilai

1 Penulisan makalah 20
2 Teknik penyajian 20
3 Penguasaan materi 25
4 Kemampuan diskusi 25
5 Daftar pustaka 10
Total
Penguji,
(………………………)
LEARNING PROGRAMS
Lecture 1
HIGHLIGHT EMERGENCY DISASTER PREPAREDNESS
Tjokorda Gde Agung Senapathi
Disasters have claimed millions of lives and cost billions of dollars world-wide in the past
few decades. Examples of large-scale disasters include the terrorist attacks of September
11, 2001; the 2004 Pacific Ocean tsunami; the 2010 earthquake in Haiti; the 2011
earthquake and tsunami in Japan; and Superstorm Sandy of 2012. Emergency physicians
frequently have extensive responsibilities for community and hospital-level disaster
preparedness and response.
DISASTER DEFINITION
The World Health Organization defines a disaster as a sudden ecologic phenomenon of
sufficient magnitude to require external assistance. A disaster is an event that overwhelms
the resources of the region or location in which it occurs. Furthermore, a hospital disaster
may similarly be defined as an event that overwhelms the resources of the receiving
hospital. A hospital disaster may be of any size and is not limited to mass casualty incidents.
A single patient who ingested an organic phosphorous pesticide may overwhelm the
resources of a hospital if that hospital is not prepared to decontaminate external to the ED.
A single patient with suspected small-pox or a single influential patient (e.g., world leader or
a celebrity) may use so many ED resources that it affects the care of other patients.
Whether an event is a disaster further depends on the time of day, nature of the injuries,
type of event, and the amount of preparation time before the arrival of patients. The ED
“surge capacity” (ability of the ED to care for more patients than is typical) may be severely
limited by hospital overcrowding.
When it appears that the normal procedures of an ED may be interrupted by an event, there
must be policies and procedures in place to activate a disaster response, direct the
mobilization of personnel and equipment, and permit the rapid triage, assessment,
stabilization, and definitive care of victims.
TYPES OF DISASTERS
Disasters are subdivided into several categories (Table 1). External disasters occur at
locations that are physically separate from the hospital (e.g., transportation accident,
industrial accident). An internal disaster is an event that occurs within the confines of the
hospital (e.g., bomb scare, laboratory accident involving radiologic agents, power failure).
Disasters can be both internal and external (e.g., earthquake with mass casualties as well
as damage to the internal hospital).
Table 1 Types of Disarter

Disaster Type Definition Examples
Natural disaster Disaster caused by a naturally Earthquakes, tsunamis, tornadoes,
occurring event hurricanes/typhoons, volcanic
eruption, pandemic influenza
Man-made Nonnatural events that are not Vehicle crashes (e.g., car, plane,
disaster purposefully produced bus), mass casualty events,
explosions, fires, industrial
accident/chemical release
Terrorist-related Events that are purposefully Events of September 11, 2001, as
disaster produced in an effort to cause well as intentional chemical,
terror biological, radiologic, or toxin
releases
Internal disaster An event that occurs within the Hazardous materials spill in hospital
hospital laboratory, fire or explosion within
hospital, power failure
External An event that occurs external to Transportation accident, industrial
disaster the hospital accident
Acute disaster Disaster that occurs in a narrow Explosion, industrial release,
and well-defined time frame earthquake
Nonacute Disaster with no well- defined Pandemic infectious disease,
disaster start point or continuous incremental release of a biological or
production of casualties over a toxin (e.g., anthrax sent through
broad time frame mail)
DISASTER CHARACTERISTICS
Regardless of the cause, most disasters have common characteristics that are important for
disaster preparedness and planning. In an acute disaster, or a disaster with an identifiable
time of onset that produces casualties (e.g., explosion, chemical release, fire, earthquake),
the event is followed by a large number of minimally injured patients presenting to the
nearest hospitals, usually without prehospital triage or evaluation. This is typically followed
by prehospital transport of the most affected patients to the same hospitals. Initial patients
can be expected within minutes, and peak volumes can be expected at 2 to 3 hours after
the event. The vast majority (~80%) of patients are not transported by prehospital agencies,
but instead self-transport by car, van, police vehicle, cabs, foot, or any means available to
the nearest ED. Even in acute events, ED volumes tend to remain elevated for days to
weeks after events. In nonacute events, such as a pandemic of an infectious disease, ED
volumes have a slower onset of surge, but ED and hospital volumes remain elevated for
extended periods.
Based on previous events, common factors that may hinder ED response are listed in Table
2. A large amount of federal funding has been supplied to address these issues, but they
likely remain as the major common limitations to effective ED disaster response.
Table 2 Factors That May Hinder ED Response to Disasters

Poor communication between ED and disaster scene
Poor communication within the hospital (e.g., ED to emergency operations center, emer-
gency operations center to patient care areas)
Inability to control volunteer healthcare personnel who are unfamiliar with the ED
function and their roles in disaster response
Inability to engage and control convergence of media to the ED
Inability to engage, control, and direct visitors who are searching for loved ones Inability
to control large numbers of patients (i.e., crowd control)
Difficulty maintaining high staffing needs for extended periods
DISASTER PREPAREDNESS AND PLANNING

Planning for any type of disaster consists of common elements. A hospital disaster planning
group is responsible for generating the hospital’s emergency operations plan. Include a
diverse membership of hospital employees and decision makers. The group should meet on
a regular basis to assess hazards, develop and update short- and long-term disaster plans,
plan exercises and training, and redesign the disaster plan based on evaluations of
exercises and real events.
The general components of the disaster plan include hazard vulnerability analysis,
compliance with agency requirements, hospital–community coordination, integration with
national response assets, and training and disaster drills. Develop specific plans (for
radiation, explosions, mass casualties, decontamination) based on an assessment of the
potential disasters in the area as well as study of the events that would cause the most
disruption to the ED and hospital.
Lecture 2
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
had history of allergy to certain antibiotics, especially if given in Intravenous it is necessary
to do skin test beforehand. antibiotics are given for 5-10 days (Milloro, 2004) Suppotive
Care, such as rest and adequate nutrition, administration analgesic and anti-inflammatory
(nonsteroidal anti-inflammatory painkillers such as diclofenac (50 mg / 8 hours) or Ibuprofen
(400-600 mg / 8 hours) and if Corticosteroids granted, it should be added pure analgesics,
such as paracetamol antiinflammatory given in (650 mg / 4-6 hours) and / or low opioids
such as codeine (30mg / 6 h)), granting the application of external heat (hot compresses) or
orally (mouthwash).
Lecture 3
SEIZURE AND MENTAL CHANGES DISORDER STATUS EPILEPTICUS
IGN Budiarsa
Status epilepticus is defined as a continuous or intermittent seizure activity for more than 5
minutes without regaining consciousness. It means the seizure can take the form of
prolonged seizure or repetitive attack without recovery in between. The etiology of status
epilepticus approximately 30% of all cases is caused by withdrawal of anticonvulsant,
cerebrovascular diseases and alcohol withdrawal.
There are various types of status epilepticus and a classification:
Status epilepticus confined to early childhood

1. Neonatal status epilepticus
2. Status epilepticus in specific neonatal epilepsy syndrome
3. Infantil spasms
Status epilepticus confined to later childhood

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

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

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

1. Lifesaving (ABC)
2. Stop seizures immediately
3. Manage in ICU
Lecture 4
COMA AND DECREASE OF CONCIOUSNESS
IA Sriwijayanti
AIM:
Describe condition of coma and altered states of consciousness, know the current definition
of coma and altered states of consciousness, etiology, mechanism based of altered states
of consciousness, clinical presentation, diagnostic work-up including history, clinical
examination and early management of altered states of consciousness.
LEARNING OUTCOMES:
1. Know current definition of coma and altered states of consciousness
2. Understand and be able explain etiology and mechanism based of coma and
altered states of consciousness
3. Be able to explain a comprehensive history, clinical examination and assessment of
comatose patients and altered states of consciousness.
4. Understand early management of altered states of consciousness
ABSTRACT
Impaired consciousness is among the most difficult and dramatic of clinical problems. The
ancient Greeks knew that normal consciousness depends on an intact brain, and that
impaired consciousness signifies brain failure. The brain tolerates only limited physical or
metabolic injury, so that impaired consciousness is often a sign of impending irreparable
damage to the brain.
Consciousness can be defined by two components: arousal and awareness. Disorders of

Consciousness (DOC) are characterized by disrupted relationship between these two
components. Coma is described by the absence of arousal and, hence of awareness
whereas the vegetative state is defined by recovery of arousal in the absence of any sign of
awareness. In the minimally consciousness state, patient show preserved arousal level and
exhibit discernible but fluctuating signs of awareness.
At the bedside, arousal (also called vigilance or alertness) is observed by looking at the
presence of eye opening. At neuroanatomical level, the level of arousal is mainly supported
by the brainstem and thalami. Awareness, the second component of consciousness, refers
to consciousness perception which include cognition, experience from the past and present
and intentions. At neuroanatomical level, awareness is underpinned by the cerebral cortex,
and mainly through a wide frontoparietal network. Awareness can be further divided into
awareness of the environment and awareness of self. Awareness of the environment can be
defined as the conscious perception of one’s environment through the sensory modalities,
whereas awareness of self is a mental process that does not require the mediation of the
senses and is not related to external stimuli for its presence.
Altered states of consciousness may have an organic or functional cause. This condition
represents a spectrum of disease presentations from profoundly depressed arousal
requiring emergent intubation to severe agitation and confusion requiring restraint and
sedation. Initial stabilizing measures are often needed before complete history and physical
examination can be performed (Lee, 2014).
All unconscious patients should have neurological examinations to help determine the site
and nature of the lesion, to monitor progress, and to determine prognosis. Neurological
examination is most useful in the well-oxygenated, normotensive, normoglycemic patient
with no sedation, since hypoxia, hypotension, hypoglycemia and sedating drugs profoundly
affect the signs elicited. Therefore, immediate therapeutic intervention is a must to correct
aberrations of hypoxia, hypercarbia and hypoglycemia. Medications recently taken that
cause unconsciousness or delirium must be identified quickly followed by rapid clinical

assessment to detect the form of coma either with or without lateralizing signs, with or
without signs of meningeal irritation, the pattern of breathing, the size and reactivity of pupils
and ocular movements, the motor response, the airway clearance, the pattern of breathing
and circulation integrity, etc.
Coma may result from a variety of conditions including intoxication, metabolic abnormalities,
central nervous system diseases, acute neurologic injuries such as stroke, hypoxia or
traumatic injuries including head trauma caused by falls or vehicle collisions. Looking for the
pathogenesis of coma, two important neurological components must function perfectly that
maintain consciousness. The first is the gray matter covering the outer layer of the brain and
the other is a structure located in the brainstem called the reticular activating system (RAS
or ARAS), a more primitive structure that is in close connection with the reticular formation
(RF), a critical anatomical structure needed for maintenance of arousal. It is necessary to
investigate the integrity of the bilateral cerebral cortices and the reticular activating system
(RAS), as a rule. Unilateral hemispheric lesions do not produce stupor and coma unless
they are of a mass sufficient to compress either the contralateral hemisphere or the brain
stem (Bateman 2001). Metabolic disorders impair consciousness by diffuse effects on both
the reticular formation and the cerebral cortex. Coma is rarely a permanent state although
less than 10% of patients survive coma without significant disability (Bateman 2001); for
ICU patients with persistent coma, the outcome is grim. Maneuvers to be established with
an unconscious patient include cardiopulmonary resuscitation, laboratory investigations, a
radiological examination to recognize brain edema, as well as any skull, cervical, spinal,
chest, and multiple traumas. Intracranial pressure and neurophysiological monitoring are
important new areas for investigation in the unconscious patient.
Lecture 5
ACUTE PSYCHIATRIC EPISODE
Tjokorda Bagus Jayalesmana
Objective:
1. To describe etio-pathogenesis and pathophysiology of acute psychiatric episodes
2. To implement a general strategy in the approach to patients with acute psychiatric
episodes through history and special technique investigations
3. To manage by assessing, provide initial management and refer patient with acute
psychiatric episodes
4. To describe prognosis patient with acute psychiatric episodes
Emergency occur in psychiatric just as we do in every field of medicine. However,

psychiatric emergencies are often particularly disturbing because we do not just involve the
body’s reactions to an acute disease state, as must as actions directed against the self or
others. These emergencies, such as suicidal acts, homicidal delusions, or a serve in ability
to care for oneself, are more likely than medical ones to be sensationalized when they are
particularly dramatic or bizarre. Frequently identified medical causes of abnormal behavior
include hypoglycemia, hypoxia, seizures, head trauma, and thyroid abnormalities. Patients
should also be assessed for the presence of delirium or dementia, as both have potentially
treatable causes.
Psychosis is difficult term to define and is frequently misused, not only in the newspaper,
movies, and on television, but unfortunately among mental health professionals as well.
Stigma and fear surround the concept of psychosis and the average citizens’ worries about
long-standing myths of mental illness, including psychotic killers, psychotic rage, and
equivalence of psychotic with the pejorative term crazy. Aggressive and hostile symptoms
can overlap with positive symptoms but specifically emphasize problems in impulse control
History and physical examination, including a neurologic and mental status examination,
may be sufficient to determine whether the patient has an acute psychiatric illness.
However, any abnormality noted from the history and physical exam warrants further
evaluation and treatment looking for a medical etiology. Once medical issues have been
addressed, patients with presentation of psychosis, depression, anxiety, suicidal, or
homicidal ideation need an appropriate psychiatric evaluation and disposition. Clinical
judgment is often necessary to determine the need for admission in patients with chronic
suicidal or homicidal ideation, and patients with other psychiatric illnesses and the potential
inability to care for oneself.
Lecture 6
RADIOLOGY IMAGING
Srie Laksminingsih
Learning Objective
At the end of meeting, the student will be able to :
1. Describe the radiology imaging of thorax photo for IRDS (Idiopathic Respiratory Distress
Syndrome) case, Bronchopneumonia, CHD, Pericardial Effusion, Lung Edema,
Pneumothorax, Pleural Effusion, Vena Cava Superior Syndrome.
2. Describe the imaging of abdominal plain photo in : Illeus Obstruction, Paralytic Illeus,
Stone in the Urinary Bladder, Peritonitis, NEC, Cholelithiasis & Acute Cholecystitis.
Lecture 7
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:
Lecture 8
EPISTAXIS
SARI WULAN
Objective
Able:
1. To explained anatomi, histologi and phisiology of the nose
2. To explained etiology that cause epistaksis
3. To explained patophisiology & the simtomp of epistaksis
4. To explained and choose the adding examination ( lab, x-ray, nasoendoscopi)
5. To make diagnosis base on phisical diagnostic
6. To explained the therapy of epistaksis
7. To do work-up to epistaksis
Abstract
Epistaksis is one of emergency case in ENT field, that can be fatal if not threaten well. The
bleeding comes from the nose n mouth, because epistaksis caused by an alteration of
normal hemostasis whitin the nose. Hemostasis is compromised by mucosal abnormalities,
vessel pathology or disorders of coagulation. Etiology of epistaxis may be local or systemic.
The local epistaxis commonly causes by mild trauma, climate changing, infection. The
systemic can be caused by systemic ds, ex. hypertension, malignancy, dengue fever,
hemophilia. Epistaksis mostly can stopped spontaneously, only 1-2% patient must be
refered to hospital. Management of epistaxis is stop the bleeding, avoid complication
treatment of initial disorders.
Gambar 1. Vaskularisasi septum nasi

Tabel 1. Etiologi epistaksis
Penyebab lokal Penyebab sistemik

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

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

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

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

48-72 jam
Perdarahan tidak berhenti

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

Koreksi gangguan koagulopati:
-FFP - vit K
-cryprecipitate -trombosit
Penatalaksanaan dengan fibrin glue
Lecture 9
BLEEDING DISORDER HEMORRHAGE IN PREGNANCY:
ANTEPARTUM AND POST PARTUM
Wayan Megadhana
ANTEPARTUM HEMMORRHAGE
COMPETENCE
Manage pregnancy with Placenta previa and abruption placenta
Placenta Previa
Definition
A condition where the placenta intrudes the lower uterine segment, which resulted in it
covering the internal uterine os partialy or completely during the 20th week of pregnancy or
further.
Classification
- Placenta previa: the placenta covers the internal oral ostium partially or completely.
- Low placenta: placenta implanted in the lower uterine segment where the placental tip
does not reach the edges of the internal uterine os and there is peripheral spacing of
more than 2 cm around the internal uterine os. Formerly called marginal placenta previa.
Epidemiology
- Incidence of Placenta previa is 1 in 300 - 400 deliveries.
- Etiology is still unknown, incidence increases with age, multiparity, parity, history of
cesarean section, smoking.
Pathophysiology
- The low-lying placenta is present in 28% of pregnancies <24 weeks, as the lower uterine
segment is not established. In accordance with the enlargement of the upper segment of
the uterus and the formation of the lower uterine segment, the placenta will move its
position upward (placental migration). Thus, ultrasound should be repeated at 32-34
weeks of pregnancy.
- Risk of maternal and fetal: postnatal bleeding, anesthesia and surgical complications, air
embolism, postpartum sepsis, placenta accreta, recurrence 4-8%, prematurity, IUGR,
congenital malformation, malpresentation, fetal anemia.
- Initial bleeding is mild, recurrent bleeding is more severe and can lead to shock, early
bleeding in general occurs at 33 weeks. At bleeding in <32 weeks, beware for infection
of the urine tract, vaginitis and cervicitis
Diagnosis
- Bright red vaginal haemorrhage without any pain in the second or third trimester of
pregnancy, with peak incidence in 34 weeks of pregnancy.
- Speculum examination, palpation of fornices and internal examination on the operating
table (double set up)
- Sterile internal examination should not be done.
- Ultrasound, a quick and standard examination to determine the location of the placenta.
- MRI
Management
- Abdominal termination in case of massive vaginal bleeding or life threatening condition
especially for mother and fetus
- If the fetus is preterm and there is no persistent active bleeding, conservative
management with close observation in the obstetric room.
- Tocolytic therapy is administered up to 48 hours after admission.

- For pregnancies approaching full term without bleeding, make schedule for cesarean
section.
- Elective SC at 37th weeks of pregnancy, vertical incision is recommended.
- Special attention to placenta previa in post SC wound scarring for possible placenta
accreta / increta / percreta (incidence increases 30%)
Solusio Placenta (placenta abruption)
Definition
Detachment of placenta partially or completely from its normal implant site on the uterine
wall after 20th weeks of gestation and prior to delivery.
Epidemiology
- Incidence increases in accordance to advanced maternal age, multiparity, history of
maternal shock, poor nutrition, hypertension, chorioamnionitis, sudden decompression
after ruptured membranes in overdistended uterus such as twin and polyhydramnios,
abdominal trauma, external cephalic versus circular placenta, folic acid deficiency,
Compression of the inferior vena cava and lupus anticoagulant. In smoker and cocaine
users, decidual necrosis on the edge of the placenta.
- 5-17% recurrence after 1 episode in previous pregnancy and 25% after 2 previous
episodes of pregnancy.
Pathophysiology
- The primary etiology is still unknown.
- The risk of hypovolemic shock, acute renal failure, DIC, postnatal bleeding and
fetomaternal haemorrhage.
Predisposing factors
- Demographic factors
- Hypertension and preeclampsia
- Premature rupture of membranes
- Smoking
- Cocaine
- SLE
- Thrombophilia
- Mioma uteri
- A previous placenta abruption
Diagnosis
- Placental abruption has a rapid onset with abdominal pain, vaginal bleeding and
tenderness.
- Clinical symptoms are often followed by increased contraction and persistent hypertonia.
- Clinical symptoms: fetal tachycardia / IUFD, Virchow's triad of focal or common uterine
pain, increased tone, and vaginal bleeding (85%), 15% in concealed type. Ultrasound:
helps in concealed types which is retroplacental sonolucent areas, placental site to
differentiate with placenta previa.
Management
- Management of placental abruption depends on clinical conditions, gestational age and
amount of bleeding.
- Perform blood / fluid resuscitation as needed
- If the fetus dies or not mature enough to live outside the uterus, vaginal delivery may be
considered.
- Cesarean section, respond time is important for perinatal outcome.
POSTPARTUM HEMMORRHAGE
COMPETENCE
1. Management of postpartum hemorrhage
Definition and classification
Postpartum hemorrhage (PPS) is generally defined as blood loss from the genital tract of >
500 ml after vaginal delivery or > 1000 ml after delivery by cesarean section. This limitation
has become difficult, given the estimated loss of blood is usually not as much as it actually
is, sometimes only half from the truth. The blood mixes with amnionic fluid or with urine.
Blood is also absorbed by sponges, towels, and cloths, in buckets and on the floor.
Therefore, an estimated loss of blood that exceeds "average" or 500 mL should be an
obstetric concern for the possibility of excessive bleeding.
Postpartum hemorrhage may be minor (500-1000 ml) or major (> 1000 ml). Major bleeding
can be divided into moderate (1000-2000 ml) or heavy (> 2000 ml). Postpartum hemorrhage
may be caused by four factors: weakness of uterine tone to stop bleeding from placental
insertion (tone), rupture of the perineum, vagina, to uterine lining (trauma), placental
remains or blood clots that block adequate uterine contractions (tissue), and clotting factor
disorders (thrombin).
Postpartum hemorrhage is divided into 2, namely:

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

- Episiotomy
- Obstetric surgery
- Sectio cesarea
- Hysterectomy
- uterine rupture
Obstetric factors
- Obesity
- Previous post-natal bleeding
- Sepsis syndrome
- preeclampsia
Atonia uteri
- Overdistention
- Labor induction
- Abnormal labor
Concomitant coagulopathy
- Placental Solution
- IUFD
- Massive transfusion
Etiology
- Primary postpartum hemorrhage is often caused by placental retention, laceration of
birth canal, rest placenta, uterine atony, uterine inversion, uterine rupture, clotting
disorders.
- Secondary postpartum bleeding is often caused by rest placenta, from a former
cesarean section, infection / endometritis.
General prevention and treatment

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

- Ask for HELP. Immediately request help or be referred to the hospital if the birth is
midwife / public health. The presence of obstetricians, midwives, anesthesiologists, and
hematologists is very important.
- Assess (vital parameters, blood loss) and Resuscitate. It is important to immediately
assess the amount of blood that comes out as accurately as possible and determine the
degree of hemodynamic change. The value of the level of consciousness, pulse, blood
pressure, and when facility permits, oxygen saturation should be monitored. When
installing an intravenous line with a 14G-16G albocath, immediate blood samples should
be taken to check for hemoglobin, clotting profiles, electrolytes, blood type
determination, and crossmatch
- Establish Etiology, Ensure Availability of Blood, Ecbolics (Oxytocin, Ergometrin or
Syntometrine bolus IV / IM). While resuscitation is ongoing, attempts are made to
determine the etiology. Evaluate uterine contractions, look for free fluid in the abdomen,
if there is a risk of trauma (former cesarean section, difficult artificial delivery) or when
the patient's condition is worse than the amount of blood coming out. When placental
retention occurs after vaginal delivery, uterine tamponade may be conducted while
waiting for surgery / laparotomy
- Massage the uterus. Massive bleeding that occurs after the birth of placenta should be
treated promptly with uterine massage and uterotonic drug delivery. If the uterus
remains soft, internal bimanual compression should be performed using the fist inside to
suppress the anterior fornix so that it is pushed upward and the outer palm presses on
the back of the fundus so that the uterus is compressed.
- Oxytocin infusion / prostaglandins - IV / per rectal / IM / intramyometrial 40 units of
Oxytocin in 500 cc of normal saline can be administered with the speed of 125 cc / hour.
Avoid excess fluid because it can cause pulmonary edema to cerebral edema which can
eventually cause seizures due to hyponatremia. Administration of ergometrine as a

second line of oxytocin may be given intramuscularly or intravenously. Initial dose is 0.2
mg (slowly), additional dose of 0.2 mg can be given after 15 minutes if still needed. The
dosage may be repeated every 2-4 hours if necessary.
- Shift to theater - exclude retained products and trauma / bimanual. If massive bleeding
persists, immediately evacuate the patient to the operating room. Ensure examination to
exclude any residual placenta or amniotic membrane. If there is suspicion of remaining
tissue, do the curettage action immediately. Bimanual compression can be done as long
as the mother is taken to the operating room.
- Tamponade balloon / uterine packing (conservative, non-surgical). If bleeding persists,
consider the possibility of coagulopathy accompanying refractory atony. Uterine
tamponade may help reduce bleeding. This action can also allow for freezing factor
correction. Tamponade test can be done by using Tube Sengstaken which has a positive
predictive value of 87% to assess the success of management Postpartum
hemmorrhage.
- Apply compression sutures - B-Lynch / modified (conservative surgery). In making
decisions, consideration between sustaining life and the desire to maintain fertility
should always be made. Before attempting any conservative surgical procedure, the
patient should be reassessed based on the estimation of the amount of blood coming
out, ongoing bleeding, hemodynamic state, and parity.
- Systematic pelvic devascularization - uterine / ovarian / quadruple / internal iliac.
Ligation a. Uterine and ligation a. Hypogastrics
- Interventional radiologist, if appropriate, uterine artery embolization
- Subtotal / total abdominal hysterectomy
Lecture 10
NEONATAL RESUSCITATION and ARDS (PEDIATRIC)
Diah Kanyawati
Abstract
Ninety percent of asphyxia insults occur in the antepartum or intrapartum periods a a result
of placental insufficiency. After delivery, the baby’s ineffective respiratory effort and decrease
cardiac output. Hypoxic tissues begin anaerobic metabolism, producing metabolic acids that
are initially buffered by bicarbonate.
The incidence of perinatal asphyxia usually related to gestational age and birth weight. The
basic goal of resuscitation are: to expend the lungs and maintain adequate ventilation and
oxygenation, to maintain adequate cardiac output and tissue perfusion. Neonatal
resuscitation equipment and emergency medications should be immediately available.
Lecture 11
SHOCK IN ADULT
IGAG Utara Hartawan
OBJECTIVE
1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patient's approach to shock through symptoms,
physical examination and special technique examination.
3. Able to perform assessment, differential diagnosis, provide early treatment and refer
patients with shock
4. Knowing the patient's prognosis with shock
INTRODUCTION
Shock is a clinical expression of circulatory failure that results in inadequate cellular oxygen
utilization. Shock is a common condition that often occurs in critical conditions, which occurs
in more than one-third of patients treated in intensive care. The diagnosis of shock can be
established based on clinical, haemodynamic and biochemical criteria, which can generally
appear in 3 forms. The first is arterial hypotension, but the magnitude of hypotension can
vary widely, especially in patients with chronic hypertension. Typically, in adults, the systolic
arterial pressure is less than 90 mmHg or an average arterial pressure less than 70 mmHg,
with tachycardia. Secondly, there is a clinical sign of tissue hypoperfusion, seen through the
three "Windows" of the body: skin (cold and moist skin, with vasoconstriction and cyanosis),
kidney (urine output <0.5 ml per kilogram body weight per hour), and neurologic (changed
mental state, which usually includes obtundation, disorientation, and confusion). Third,
accompanied by conditions of hyperlactatemia, which indicate abnormal cellular oxygen
metabolism (> 1.5 mmol per liter). Shocks are classified as: hypovolemic, cardiogenic,
obstructive and distributive.
PATHOPHYSIOLOGY
Shock may originate from four conditions of pathophysiological mechanisms: hypovolemia
(from internal or external fluid loss), cardiogenic factors (eg, acute myocardial infarction,
end-stage cardiomyopathy, advanced heart valve disease, myocarditis, or cardiac
arrhythmias), obstructive (eg embolism Lung, cardiac tamponade, or tension
pneumothorax), and distributive factors (such as severe sepsis or anaphylaxis with the
release of inflammatory mediators). The first three mechanisms are characterized by low
cardiac output and, therefore, inadequate oxygen transport. In distributive shocks, the major
deficits are located on the peripheral, accompanied by decreased systemic vascular
resistance and oxygen extraction disorders. Usually, in such cases cardiac output increases,
although it may be low due to associated myocardial depression. Patients with acute
circulatory failure often have this combination. For example, patients with distributive shock
from severe pancreatitis, anaphylaxis, or sepsis also experience hypovolemia and
cardiogenic shock in the form of myocardial depression.
The three main factors that determine the delivery of oxygen to the tissues are cardiac
output, defined as the stroke volume of heart rate; oxygen saturation bound to Hgb / O2
X100 capacity and the amount of dissolved oxygen in the blood, defined as O2 content
(ml/dl blood) = ( Hgb x 1.39 X% sat O2 + (0.003 x PaO2).
Any or all of these factors may be disrupted resulting in a decrease in the release of oxygen
to tissue levels in the vital organs. The result of a disturbance in these vital organs is called
shock. Shock begins with a simple state, to the very severe state of the imbalance between
the supply and the need for oxygen.
Hypovolaemia leads to increased activity of baroreceptor of the aortic arch and carotid.
There is also an increase in baroreceptor activity in the right atrium. The activity of the
sympathetic nervous system increases and results in stimulation of the heart and peripheral
vasoconstriction. The pituitary gland releases ACTH and ADH, resulting in increased cortisol
levels in the blood and sodium and water retention. Increased adreno-cortical activity was
soon followed by epinephrine and norepinephrine release. Increased plasma renin-
angiotensin-aldosterone results in greater water and sodium retention and peripheral
vasoconstriction occurs more severely. As the hypovolemia weighs up, the compensation
mechanism becomes lost and the organ functional disorder becomes more severe.
In addition, the vasoactive hormone is released during shock syndrome, such as

prostaglandin, histamine, bradykinin, serotonin, β-endorphin, MDF (myocardial depressant
factor) and cachectin. All of these substances will affect the perfusion of internal organs and
may increase the permeability of blood vessels and myocardium and platelet function.
SYMPTOMPS
Hypotension and vasoconstriction appear in hemorrhagic shock, hypovolemic shock and
cardiogenic shock due to decreased perfusion and abnormalities of vital organs. Where
there is a change of the regional vascular resistance thereby reducing the perfusion
pressure, thus perfusion to the vital organs can be maintained. In general, the skin becomes
cold, moist and wrinkled. Superficial veins will collapse. Brain circulation is also disrupted as
well as skin and other organs, which can lead to classic symptoms of confusion and
disorientation. Cerebral perfusion pressure is the difference between mean arterial pressure
and intracranial pressure or right atrial pressure, which is higher (CPP = MAP - ICP). Brain
auto regulation is still good at mean arterial pressure between 50 mmHg and 150 mmHg
with a rightward shift in chronic hypertension. In hypotension that accompanies shock
occurs mental status changes ranging from agitation, anxiety accompanied by feelings of
hovering, then going into a coma. This occurs due to the decrease of cerebral perfusion
below the critical value. Of course the patient's response will be clear and appropriate after
resuscitation action to improve the hemodynamic state in shock.
Table 1. Early symptoms on shock

Organ Clinical signs / symptoms Cause
System
CNS Decrease of consciousness Decrease in CPP
CVS Tachycardia The Adrenergic Stimulus
Dysrhythmias Ischemic Coronary
Hypotension Decreased contractility, MDF ischaemia, or RVF,

also decreased SVR or preload
Murmurs Valvular dysfunction
JVP increase / decrease Decrease in volume / preload or RV failure
Respiration Takipneu Pulmonary edema, respiratory muscle failure,

sepsis, acidosis, hypoxemia
Renal Oliguria Decreased perfusion, constriction of afferent

arterioles
Skin Cold, pale, sweat Vasoconstriction, sympathetic stimulation
Other Lactic acidosis Anaerobic metabolism
Fever Infection of hepatic dysfunction
CNS=central nervous system; CVS=cardiovascular system; CPP=cerebral perfusion pressure;

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

reflected from cold skin, changing from pale to grayish to cyanosis. The activity of the
sympathetic nervous system results in increased production of sweat (a cholinergic
sympathetic response).
Metabolic acidosis almost always accompanies shock with the accumulation of lactic acid
into hypoxemia. Anaerobic metabolism as a complication due to decreased liver function
that can produce lactic acid.
Thus, shock indicates a perfusion disorder characterized by decreased cardiac output or

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

In general, there are four phases in shock treatment. Target therapy and monitoring need to
be adapted to each phase. In the first phase (salvage), the goal of therapy is to achieve
minimum blood pressure and adequate cardiac output for minimal survival. Close
monitoring is required; in many cases, invasive monitoring can also be used in arterial and
central venous catheters. Lifesaving procedures (e.g., surgery for trauma, pericardial
drainage, revascularization for acute myocardial infarction, and antibiotics for sepsis) are
needed to treat the underlying cause. In the second phase (optimization), the goal is to
increase the availability of cellular oxygen, as well as interventions that target hemodynamic
status. Adequate hemodynamic resuscitation reduces inflammation, impaired mitochondrial
function, and caspase activation. Measurement of SvO2 and lactate can help guide therapy.
Cardiac monitoring should be considered. In the third phase (stabilization), the goal is to
prevent permanent organ dysfunction, even after hemodynamic stability has been achieved.
The supply of oxygen to the tissues is no longer a major problem, and the organ of support
becomes more relevant. Finally, in the fourth phase (de-escalation), the goal is to wean
patients from vasoactive agents and achieve spontaneous polyuria conditions or provoke
fluid elimination through the use of diuretics or ultrafiltration to achieve a negative fluid
balance. However, specific treatment of course depends on the type of shock and
pathophysiology causes the shock.
Shock Hipovolemik/Hemoragik
In hypovolemic shock indicates the occurrence of bleeding. It is important to know the
percentage of blood volume lost as a basis in providing appropriate therapy. In general,
physical examination alone is not enough, but by following the scheme this can be helped.
As an assumption that the perceived normal blood volume is 7.5 ml / kgbb, the hypovolemic
shock is divided into four groups based on the estimated number of bleeds:
I. 10-15% blood loss from Estimate Blood Volume (EBV) causes mild tachycardia and
shock has not occurred.
II. Blood loss of 15-25% of EBV (1000-1250ml / 70kg) arises moderate shock, with
tachycardia, systolic pressure and pulse pressure drop, slightly increased diastolic
pressure, slow capillary refill. Urine production is still within normal limits.
III. Blood loss 25-35% EBV (1250-1750 ml / 70kg) causes severe shock, with prominent
symptoms: the skin is cold, wrinkled, and pale. Blood pressure decreased between 30-
40% (systolic pressure and pulse pressure) and an increase in diastolic pressure of
about 15-20%. Vasoconstriction stands out and oliguria develops. Prominent CNS
disorder is confusion, which is severe until stupor occurs. Tachypnea results from
secondary metabolic acidosis to hypoxemia, tissue hypo perfusion and anaerobic
metabolism. The pulse rate is greater than or equal to 120x / min.
IV. Blood loss of 35-45% of EBV (1750-2250 ml / 70 kg) causes very severe shock, usually
a preterminal condition. Unmeasured blood pressure, peripheral pulses are not
palpable and carotid pulse is also may not palpable.
Hemorrhagic shock is accompanied by hemodilution and widespread plasma volume
expansion at any given time and therefore, the hematocrit does not change for 3 to 4 hours
in acute bleeding.
SHOCK CARDIOGENIC
Cardiogenic shock (CGS) is a shock characterized by many factors that interfere with the
normal functioning of the heart, or (in particular) adverse factors to preload, afterload,
contractility, heart rate or heart rhythm. For example right or left ventricular myocardial
infarction, and in situations where cardiac pump failure, or ventricular filling or impaired
cardiac discharge.
The above changes occur in hypovolemic / hemorrhagic shock and also in cardiogenic
shock. In cardiogenic shock caused by myocardial infarction, there is a decrease in mean
arterial pressure, cardiac output, stroke work index, left ventricular diastolic end pressure
and volume and venous oxygen content. Heart rate, central venous pressure and increased
arterial and venous oxygen content, and peripheral vascular resistance also increase as a
result of compensation. The basic problem is the failure of the heart to pump blood to
peripheral tissue, whatever the cause. Therapy in all types of shock, aimed at the underlying
cause while conducting circulatory resuscitation efforts. What is more important is to save
myocardial ischemia and limit the size of infarction through improvement of hemodynamic
abnormalities and dysrhythmias. Myocardial revascularization, balloon angioplasty and
thrombolytic therapy are all part of the treatment plan.
SEPTIC SHOCK
Incident and Etiology

One of the most common forms of distributive shock is septic shock. The complication of
this shock is about 40% of cases by bacteremia gram negative, with a mortality rate of
around 40-90%. Septic shock may be caused by bacteria, both gram-negative and gram-
positive (gram - endotoxin and gram + endotoxin); For example, staphylococci, S.
pneumonia, N.meningitidis, H.gonorrhea or Clostridia, sepsis; Fungi, rickettsia or viruses.
Lipopolysaccharides from endotoxin released from gram-negative cell wall bacteria may be
a major part of this syndrome. Septic shock is caused by sequester or misdistribution of
normal or high cardiac output in different parts of the body. Tumor necrosis factor
(cachectin) is known to be a very important mediator of clinical and humoral manifestations
in shock caused by endotoxins (A- and -O lipid chains) or by all gram-negative bacteria.
Vasoactive mediators such as histamine, complement activation, quinine activation
(especially precancerrein), prostaglandins and possibly other substances that give rise to
vasodilation without compensation to maintain cardiac output. Leucocyte aggregation may
cause capillary blockage with inadequate blood flow results in capillaries. Micro vascular
thrombosis is determined by the amount of platelets and clotting factors and manifestations
of stimuli of fibrinolysis systems such as DIC and resulting bleeding. DIC is caused by
sepsis associated with a decrease of factor XII, but endotoxin is triggered by intrinsic and
extrinsic blood clotting systems.
One theory says that hemorrhagic shock can develop into septic shock as a result of
increased permeability of mucous membranes that facilitate enteric bacteria entering the
bloodstream. In this model, severe cellular damage increases the permeability of cell
membranes and extracellular fluid displacement into cells associated with impaired cell
barrier function and disrupts the entry of gram negative or gram-positive bacteria into the
bloodstream. This cellular damage can be overcome if resuscitation is successful,
secondary phase bacteremia can be delayed. Survival may be improved if pre shock
therapy is anticipated with broad-spectrum antibiotics. Both gram-positive and gram-
negative bacteria appear to cause both cardiovascular abnormalities.
Clinical Manifestations
The cardiovascular system is affected by septic shock, at both the myocardial and
peripheral levels. Misdistribution of blood flow followed by myocardial depression, with
normal or increased bulk followed by decreased systemic vascular resistance (SVR). Heart
rate increased, meanwhile mean arterial pressure, stroke volume, stroke work, oxygen
consumption and arterial venous oxygen content all decreased. As already explained,
cardiac output may have been normal or increased. Patients with this condition require large
amounts of fluids due to peripheral vasodilation. The decrease of Left Ventricular Ejection
Fraction (LVEF) and Right Ventricular Ejection Fraction (RVEF) especially biventricular
dilatation occurs 2-4 days after onset of hypotension. Patients who can be rescued from a
septic shock their hemodynamic value will return to their original state of 7-10 days from the
onset of septic shock. It has been argued that what can be saved in septic shock is more
likely than cannot be saved with decreased LVEF and left ventricular dilatation, where left
ventricular dilatation gives the impression of a compensatory effort through the Frank-
Starling mechanism. The irreversible to normal heartbeat, cardiac output or systemic
vascular resistance (SVR), whereas improvement can occur within 24 hours. Mortality can
generally be seen from hypotension that is irreversible due to depression of systemic
vascular resistance (SVR) and cardiac depression so that normal values cannot be
maintained within normal limits or above normal until the patient dies. So at first hyper
dynamic state with high and normal cardiac output with low cardiac filling pressure and
decreased systemic vascular resistance. The oxygen saturation of the mixed-vein may be
normal or low. In high cardiac output, where abnormal systolic function (decreased stroke
volume and decreased ejection of left ventricular fraction) and ventricular compliance. The
relationship between pulmonary capillary pressure (PCWP) and left ventricular diastolic end
(LVEDV) volume is not normal. At the next stage, there is a decrease in dynamic state and
the picture resembles a cardiogenic shock. Regarding respiration, where respiratory
frequency increases, hyperpnoea, tachypnea and respiratory alkalosis. The antigen-

antibody complex activates the complement system. Septicemia is often followed by ARDS
as a complication. Patients with manifest dyspnea, hypoxemia, bilateral diffuse pulmonary
infiltrate, reduction of lung compliance and have usually unchanged pulmonary capillary
pressure from the baseline (especially if lung function before shock is normal).
Therapy
The primary goal of treating patients with septic shock is eradication / removal of causal
factors, such as infection, the harmful effects of bacterial toxins or endogenous toxins from
the host and attempts to improve the cardiovascular system and other systems.
Many ongoing research experiments to study drugs to counteract the effects of toxins on
septic shock. For the practical use of anesthesia, most of these are clinically unimportant
and are mentioned only for the completeness of the data. Currently, monoclonal antibodies
as part of gram-negative bacteria, naloxone, prostaglandin inhibitors, lipid X, tumor necrosis
factor antibodies (TNF), genetically engineered protease inhibitors and other recombinants
or synthetic protease inhibitors. Cardiovascular support for septic shock patients consists of
fluids and vasopressors required.
Fluid is required for optimization of preload and cardiac output above normal values so that
MAP returns to the baseline if possible or at least initially 60 mmHg. Pulmonary capillary
pressure (PCWP) is optimally 12-15 mmHg and should be monitored by invasive techniques
with pulmonary artery catheter. The selected fluid type did not seem to provide much benefit
with respect to the expected results, although experimental experiments in experimental
animals with septic shock resulted in a significant improvement in cardiac output, Lung
Water Extravascular Extension (PVR) and Venous Admixture (VR) vascular cavity when
given Dextran 70 compared to Ringer's Lactate. Fluid resuscitation has shown effective
results for increasing oxygen delivery (DO2) and oxygen consumption (VO2) in septic
shock.
The arrangement of ventricular function following Frank-Starling law and the category of
patients corresponding to the functional can assist in decision-making of inotropic drugs,
diuretics and vasopressors for patient resuscitation. Optimal oxygen transport through
correction of anemia and also followed by improvement in serum albumin levels of at least 2
g / 100 ml is important as adjunctive therapy. If only with volume correction alone the
hypotension is not corrected, while maintaining the pulmonary capillary pressure (PCWP)
greater than or equal to 15mmHG, the vasopressor may be added cautiously, starting with
low dopamine doses (1-3μg / kg / min) and norepinephrine If large doses of dopamine are
ineffective to increase mean arterial pressure (MAP) or side effects (tachycardia,
dysrhythmias). If norepinephrine is also ineffective, it should be substituted with epinephrine
or dobutamine or when low cardiac output is required to use beta-mimetic adrenergic
agonism.
OBSTRUCTIVE SHOCK
Obstructive shock is a form of shock associated with physical obstruction of the great
vessels or the heart itself. Pulmonary embolism and cardiac tamponade are considered
forms of obstructive shock. Obstructive shock has much in common with cardiogenic shock,
and the two are frequently grouped together. It was described as involving obstruction to
flow in the cardiovascular circuit and characterized by impairment of diastolic filling or
excessive afterload. The consequent obstruction of blood flow into or out of the heart
causes a decrease in cardiac output, and hence inadequate oxygen delivery, which is
manifest by the classic signs and symptoms of the shock state. Obstructive shock is rare in
pediatrics, though the most common causes generally include tension pneumothorax,
cardiac tamponade, and pulmonary embolism. Also included in this category physiologically,
and more specific to pediatrics, are congenital heart lesions characterized by left ventricular
outflow tract obstruction, including critical aortic stenosis, coarctation of the aorta,
interrupted aortic arch, and hypoplastic left heart syndrome. Herein, we will briefly review
the major causes of obstructive shock found in children.
Tension Pneumothorax
A pneumothorax is defined as the accumulation of air in the pleural space, a cavity that is
normally filled with a small amount of pleural fluid. It can be spontaneous (more common in
adolescent males) or secondary to underlying lung pathology, such as trauma (both
penetrating and blunt trauma), asthma, cystic fibrosis, and pneumonia. Also included in this
subcategory are iatrogenic causes such as barotrauma during positive pressure ventilation
or during placement of central venous catheters in the chest vessels.
The incidence of secondary pneumothorax in pediatric patients is not well described,

however, in critically ill children requiring mechanical ventilation it is reported to be 4-15%.
Notably, the incidence of secondary pneumothorax in mechanically ventilated pediatric
patients has declined markedly since the introduction of protective lung strategies.
Pneumothoraces can be well tolerated in some patients, though signs and symptoms of
obstructive shock can develop if the pneumothorax is under tension. In this scenario, the air
in the pleural space continues to collect under a one-way or ball valve effect, such that air
enters during inhalation, but cannot exit during exhalation. Eventually, enough air
accumulates such that the intrathoracic pressure of the affected hemi-thorax equilibrates
with atmospheric pressure, leading to complete lung collapse or atelectasis. Air under
tension also causes a shifting of the mediastinum, compression and total collapse of the
lung and great vessels, thereby compromising both cardiovascular and respiratory
function. Studies in animal models have shown that the early clinical features of a tension
pneumothorax include hypoxemia, tachycardia, and respiratory distress due to
compression and collapse of lung segments. As mechanical compromise of venous
structures develops, there is a drastic and profound reduction in venous return to the heart
as well, clinically manifested by symptoms of shock and poor perfusion. Thus, overt
hypotension may be a late sign. Complete occlusive mechanical compression is suggested
by equalization of the Mean Intrathoracic Pressure (MIP) and Central Venous Pressure
(CVP), which is a very late event and results in cardiovascular collapse. Treatment of a
tension pneumothorax requires emergent needle decompression, usually performed by
placing a sterile needle in the second intercostal space along the midclavicular line.
Definitive treatment requires thoracostomy tube placement.
Cardiac Tamponade
The pericardial sac around the heart is relatively noncompliant, and the accumulation of
even small amounts of fluid can be sufficient to produce cardiac tamponade
physiology. While acute pericardial fluid changes are usually symptomatic, the chronic
accumulation of fluid may occur with little to no hemodynamic derangements, as the
pericardium slowly stretches to accommodate the excess volume over time. Pericardial
effusions can develop as a result of any type of pericardial inflammation (i.e., pericarditis),
causing a range of physiologic perturbations along the spectrum of minor flu-like symptoms
(i.e., manifestations of the pericarditis itself) to a life-threatening state characterized by
cardiac tamponade and obstructive shock. Historically, the most common cause of
pericardial effusions was infectious pericarditis, though a recent review suggests that
idiopathic and neoplastic causes are much more frequent due to the success of childhood
vaccinations. Other common causes include postpericardiotomy syndrome (following
cardiac surgery for congenital heart disease) and trauma, most often causing
hemopericardium. Effusions may also develop as a result of a central line that erodes
through the thin wall of the right atrium, a phenomenon that appears primarily limited to
neonates and young infants. The pathophysiology of cardiac tamponade is welldescribed.
Briefly, increased intrapericardial pressure limits venous return to the heart and causes right
ventricular compression. There is a progressive decline in right ventricular end-diastolic
volume as diastolic filling lessens, worsening cardiac output. In severe tamponade, venous
return during inspiration into the compressed right ventricle bows the interventricular septum
into the left ventricle, further diminishing systemic cardiac output. As pericardial
pressure increases and surpasses ventricular end-diastolic pressure, the ventricular
volumes grow smaller and smaller and cardiac output worsens. Tamponade is a clinical
diagnosis and classically, patients with critical cardiac tamponade present with Beck’s triad
of symptoms including hypotension, quiet (“muffled”) heart sounds, and raised jugular
venous pressure. Patients may present with dyspnea, compensatory tachycardia, and poor
perfusion. On auscultation, a friction rub and distant heart sounds may be present. Pulsus
paradoxus, defined as a decline in systolic blood pressure greater than or equal to 10 mm
Hg during inspiration, results from the inspiratory reduction in pleural pressure that
produces a fall in left ventricular output and arterial systolic pressure. An electrocardiogram
may show electrical alternans due to the heart swinging within the large effusion. Formal
evaluation with an urgent echocardiogram should be performed in those patients with
symptoms suspicious for cardiac tamponade. However, emergent management should not
wait for echocardiography and is frequently based upon the recognition of tamponade
physiology in the appropriate clinical context. Pericardiocentesis is the lifesaving procedure
of choice for children with cardiac tamponade and can safely be done with bedside
echocardiographic guidance. Medical stabilization with fluid resuscitation and inotropic
support is temporary at best and somewhat controversial as fluid resuscitation may worsen
tamponade physiology, especially in children who are either normovolemic or hypervolemic.
In the latter scenario, fluid administration will increase intracardiac pressures further, hence
increasing intrapericardial pressures and worsening tamponade.
Pulmonary Embolism
Pulmonary embolism (PE) is uncommonly diagnosed in children, making its true incidence
difficult to determine. However, the incidence of PE does appear to be on the rise, though
this may be due to a heightened index of clinical suspicion and better recognition by
pediatric providers. Alternatively, it may be due to the fact that more children are
surviving from previously fatal conditions that place them at an increased risk for developing
PE, such as congenital heart disease and malignancy. In addition, more children are
requiring central venous catheterization for vascular access, a major risk factor for venous
thromboembolism (VTE), which can lead to a PE. PE is frequently fatal and difficult to
diagnose. In a recent literature review comparing pediatric PE with adult PE, pediatric cases
were more often diagnosed at autopsy and were associated with a higher mortality rate than
adults. The clinical presentation often is confusing, perhaps compounded by the fact that
very few pediatricians have much experience with this disorder. Results of screening
tests, such as oxygen saturation, electrocardiography, and chest radiography, may be
normal. Thus, a high index of clinical suspicion is necessary. Evaluation should be
performed with spiral computed tomography (CT) venography, which is now widely
considered the study of choice due to its >90% sensitivity and specificity in adults.
Ventilation/ Perfusion (V/Q) scans are also available but are more difficult to obtain and to
interpret in pediatrics. As a cause of cardiogenic shock, a massive PE has a profound
impact upon gas exchange and hemodynamics. Obstruction to flow through the pulmonary
artery results in increased dead space ventilation where affected lung segments are
ventilated but not perfused, observed clinically as a substantial decrease in the end-tidal
CO2 (ETCO2) that no longer reflects arterial PCO2. A widened alveolar-arterialgradient (A-
a) is present as well. The mechanism for hypoxemia likely involves several mechanisms. In
some pediatric patients, an intracardiac right-to-left shunt through a patent foramen ovale
may be present and as right atrial pressure increases and eventually exceeds the left atrial
pressure, deoxygenated blood can shunt directly into the systemic circulation. In addition,
V/Q mismatching is compounded by the accompanying fall in cardiac output that results
from massive PE, leading to mixed venous desaturation. PE increases the right ventricular
(RV) afterload, resulting in an increase in the RV end-diastolic volume (EDV). The increase
in RVEDV adversely affects left ventricular hemodynamics through ventricular
interdependence. Specifically, the interventricular septum bows into the left ventricle (LV)
and impairs diastolic filling, resulting in decreased LV preload and subsequently diminished
cardiac output and hypotension. These physiologic phenomenon are manifested by

respiratory distress, hypoxia, and decreased cardiac output with signs of shock.
Treatment of an acute pulmonary embolus in children should begin with initiation of a

heparin infusion with or without fibrinolytic agents such as tPA, depending on the
child and the extent of the clot. In the resolution period, the child will then warrant at least 3-
6 months of anticoagulation with low molecular weight heparin (LMWH) or warfarin.
MONITORING SHOCK
Hemodynamic Monitoring
Patients with shock are a critical condition and require invasive hemodynamic monitoring
especially in cases where vasoactive drugs are used for resuscitation or are used to support
the cardiovascular system. Generally, it is classified into routine and exceptional or non-
routine monitoring. Regular monitoring are used in patients with critical condition who
receive / get state of the art care in the intensive care room. Extraordinary or non-routine
monitoring are used in patients who need to be monitored continuously in the ICU, for
example in the extravascular lung water.
Meanwhile, blood pressure changes must be correctly measured in shock because blood
flow is determined by the relationship between cardiac output and systemic vascular
resistance, but in shock, blood pressure should be measured by continuous monitoring with
beat to beat arterial pressure. To be able to see the rapid changes can be installed
sphygmomanometer or Doppler placed on the artery line. In addition, monitoring of all
patients includes: heart rate and rhythm, breath frequency, body temperature, right and left
heart pressure, ECG and hematocrit. In the installation of arterial catheters that settle
arterial blood samples can be taken in a peiodic manner to determine the state of
electrolytes and the properties of blood clotting and arterial lactate levels. The catheter
insertion into the pulmonary artery may be excellent for assessing pulmonary artery
pressure, pulmonary artery occlusion pressure, cardiac output and other parameters
including vascular resistance. Pulmonary artery catheters have the ability to assess venous
blood saturation, particularly in patients with cardiogenic shock. Central venous pressure
monitoring is sometimes used to determine or determine the amount of blood lost, given
that a 500-800ml blood loss for 70kg weight will lower central venous pressure by about
7cmH2O.
Patients with shock who also get general anesthesia, decreased arterial blood pressure
may be faster than patients who are not publicly anesthetized because the compensation of
tone sympathetic nervous system is removed by anesthesia and in this patient, invasive
blood pressure monitoring by continuously beat to beat, will be very helpful. Korotkoff
sounds decreased or inaudible in severe shock which received general anesthesia and
subsequently assisted with an invasive monitor.
Assessment of electrolytes and hematocrit from arterial blood samples can provide
important information during resuscitation and shock management. Assessment of blood
volume and circulatory function can be better assessed in patients who have serial
laboratory results. Blood loss of about 3-4 times in acute bleeding can lead to significant
changes in hematocrit. The decrease in capillary hydrostatic pressure with bleeding is
characterized by increased intravenous interstitial fluid absorption. As a result, intravascular
fluids multiply and hematocrit decreases as a result of fewer percentage of red blood cells in
intravascular fluid. It should still be assessed during shock therapy and monitoring of fixed
hemodynamic variables, and there is no evidence to suggest that simple correction by
assessment of common parameters can result in greater outcomes or lower morbidity.
Of the hemodynamic variables, two things that need attention in the assessment of shock
sufferers are: oxygen delivery and oxygen consumption.
Oxygen delivery (DO2) is the result of arterial oxygen content and cardiac index. DO2 =
CaO2 x CI x 10, where CaO2 = 1.39 x Hgb x% saturation + (PaO2 x 0.003) and CI =
cardiac output / body surface area. The normal value for DO2 is 520-720ml / min / m2.
Oxygen consumption (VO2) is the result of arterial oxygen content minus venous oxygen
content and cardiac index times 10 (VO2 = CaO2 - CVO2 x CI x 10). The normal value for
VO2 is 100-180ml / min / m2. VO2 describes the sum of all oxidative metabolic outcomes
and thus is a measure of total body metabolism.
Of the hemodynamic variables that need attention include the counting of shunt fraction
Q2 / Qt and A-aDO2 or the oxygen difference between alveolar and arterial. The direct flow
of the pulmonary artery catheter is a therapeutic change in shock sufferers with modification
of Starling's law. In general, it is used given that the mean pulmonary artery pressure of
about 5-10mmHg is greater than the pulmonary capillary wedge pressure (PCWP), and the
pulmonary arterial diastolic pressure is approximately 0-3mmHg greater than PCWP. PCWP
is almost identical with left atrial pressure or diastolic final pressure except in cases with
mitral stenosis, where the left ventricular end diastolic pressure (LVEDP) can not be
determined or estimated from pulmonary capillary wedge pressure (PCWP). Cardiac output
may also be demonstrated by using thermodilatory techniques if there is no intracardiac
shunt (left to right or right to left).
Central Vein Pressure

Interpreting Central Venous Pressure (CVP) separately on the shock has a small value of
significance. Central venous pressure response to fluids is questionable, although important
as a guide in therapy. If the central venous pressure changes little or does not change with
the increase in pulse pressure after fluid administration, subsequent fluid administration may
be indicated. If CVP increases after fluid bolus or doubt, subsequent fluid administration
may be discontinued and to achieve the desired blood pressure, need to be
pharmacologically or otherwise.
Pulmonary Arterial Diastolic Pressure (PAdP)

PAdP is usually worth about 1-2mmHg greater than pulmonary capillary pressure (PCWP) in
the absence of pulmonary hypertension. If PAdP is reduced PCWP greater than 5mmHg, it
means pulmonary hypertension. PAdP changes are used to assess the benefits of the
effects of fluid therapy on shock.
Lactate levels
Monitoring arterial lactate levels is important in shock and associated with prognosis. In
shock, lactate levels increase and the lactate-pyruvate ratio also increases. Arterial blood
lactate levels are greater than 2.5mM / L, statistically the likelihood of survival decreases
dramatically and at 4.5mM / L, the chance of survival is only about 50%. When more than
7.0mM / L the chance to survive less than 10%.
Patients who can be rescued from shock seem to have low lactate levels compared with
those that do not and also appear to decrease lactic acid at least 10% per hour immediately
after therapy, while patients who can not be saved by therapy, lactate levels do not
decrease. The level of lactate is expressed in milligrams of milliliters or milliliters of perliter.
Apparently, lactate levels may be measured from arterial blood or from a central vein of the
pulmonary artery with the same degree of accuracy. One study showed that there was no
correlation between arterial blood lactate levels and oxygen delivery changes in septic
shock or non septic shock. However, continuous monitoring of lactate levels is very useful to
know the severity of shock.
Lecture 12
SHOCK IN PEDIATRIC
I Nyoman Budi Hartawan
Abstracts
Shock is divided into three major categories: hypovolemic, cardiogenics, and distributive,
with a degree of overlap. Hypovolemic shock is result of inadequate circulating blood
volume owing to blood or fluid loss or of insufficent fluid intake. Cardiogenic shock occurs
when cardiac compensatory mechanisms fail and may occur in infants and young children
and in patients with preexisting myocordinal disease or injury. Distributive shock, such as
septic and anaphylactic shock, is associated with peripheral vasodilations, arterial and
capillary shunting past tissue beds with pooling of venous blood, and decreased venous
return to the heart. Shock is clinical diagnosis, but its recognition remain problematic in
children. Shock may be present long before hypotention occurs. Children will often maintain
their blood pressure until late stage of shock; therefore, the presence of systemic
hypotention is not required to make the diagnosis of shock in chldren, as it is an adult. For
example septic shock in pediatric patients has been define as tachycardia (which may be
absent in the hypothermic patient) with signs of decreased perfusion, including decreased
peripheral pulses, compared with central pulses, altered alertnes, flash capillary refill or
capillary refill > 2secs, mottled or cool extremities, and decrease urine output. Hypotention
ia a sign of late and decompensated shock in children. If present in a child with these other
features.
Lecture 13
CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION
Pontisomaya Parami
Objective:
1. To describe etio-pathogenesis and pathophysiology of cardiac arrest
2. To implement a general strategy in the approach to patients with cardiac arrest
through history, physical examination and special tehnique investigations.
3. To manage by assesing, provide initial resuscitation and refer patient with post
resuscitation cardiac arrest
4. To describe prognosis patient with post cardiac arrest
Abstract
Medical emergencies that threaten lives can occur anywhere, anytime and to anybody. It
can be because of a disease or due to road accident, drowning, poisoning and others that
are capable of causing respiratory and cardiac arrest.
Air way obstruction such as hypoventilation, respiratory arrest, shock, even cardiac arrest,
causes death quickly if fast and appropriate help is not given. Death of patients due to the
causes mentioned above can be avoided if resuscitation is done immediately on the spot.
Permanent brain damage can occur if blood circulation has stopped for more than a few
minutes (now it has been agreed more than 4-6 minutes) or after a trauma with severe
hypoxia or loss of lots of blood which are not corrected. If resuscitation is given immediately
and correctly brain death can be avoided and the patient recovers completely.
General strategy to obtain the diagnosis of acute respiratory failure and cardiac arrest, is
done by a subjective approach or anamnesis and objective approach with physical
examinations and few other diagnostic criteria to find the primary signs and symptoms of
respiratory and cardiac arrest. The diagnosis of respiratory and cardiac arrest should be
done immediately and accurately. Delay in diagnosis will cause delay in resuscitation and
this will cause death to even the patients with higher living chances.
Resuscitation can be done anywhere, anytime, with or without equipment by trained

whether public or health personnel. CPR (cardiopulmonary resuscitation) is an effort of
medical emergency to cure respiratory function and circulation which has failed drastically
on a patient that has the chances of living.
For an immediate failure, the lung and heart are in good shape, compared to those due to
chronic diseases, that cure is possible. Besides that, how are we to know a patient’s
condition that still has a chance of living? To know the prognosis, a senior doctor/consultant
with knowledge, experience and mature considerations is needed.
Lecture 14
PAIN MANAGEMENT
Made Agus Kresna Sucandra
Pain is not just a sensory modality but an experience. The International Association for the
Study of Pain defines pain as “an unpleasant sensory and emotional experience associated
with actual or potential tissue damage, or described in terms of such damage.” This
definition recognizes the interplay between the objective, physiological sensory aspects of
pain and its subjective, emotional, and psychological components. The response to pain can
be highly variable among different individuals as well as in the same person at different
times.
The term nociception is derived from noci (Latin for harm or injury) and is used to describe
neural responses to traumatic or noxious stimuli. All nociception produces pain, but not all
pain results from nociception. Many patients experience pain in the absence of noxious
stimuli. It is therefore clinically useful to divide pain into one of two categories: (1) acute
pain, which is primarily due to nociception, and (2) chronic pain, which may be due to
nociception, but in which psychological and behavioral factors often play a major role.
Chronic pain is a painful condition that lasts >3 months, pain that persists beyond the
reasonable time for an injury to heal, or pain that persists 1 month beyond the usual course
of an acute disease. Chronic pain lacks the essential function of acute pain. Whereas acute
pain is a vital biologic signal to stop the individual from a potentially injurious activity or to
pursue medical care, chronic pain serves no obvious biologic function. Complete pain relief
is unrealistic in cases of chronic pain. Rather, the goal of therapy is pain reduction and
return to functional status.
Chronic pain is a common problem affecting 30.7% of the U.S. population and is more
prevalent in women (34.3%) than in men (26.7%). Back pain is the most common site for
chronic pain, followed by the knee and neck. The prevalence of neuropathic pain is 6.9% to
10% of the population. Risk factors for chronic pain include increasing age, female gender,
higher body mass, and chronic illness. An exacerbation of chronic pain is part of the
presentation of 11% to 15% of ED visits. Compared to patients with acute pain, chronic pain
patients are more likely to report their pain as severe and more likely to be frequent visitors
to the ED.
Pathophysiologi of Chronic Pain

Scientists study pain at several levels of the nervous system. At the site of injury special
nerve cell endings called nociceptors, which have been waiting for exactly this moment,
respond to one of a myriad of unpleasant stimuli such as heat, pressure and inflammation,
by sending a rapid and urgent signal that something is wrong. Shortly afterwards potent
chemicals are released by crushed and broken cells which are detected by other nerves
and amplify the pain signal. This whole process is called nociception, the change in the
senses induced by a noxious stimulus. Activation of nociceptors can often lead to pain, but
this is not always the case. A person may perceive a given event as merely annoying, mildly
painful, or excruciating, based not only on the size of the trauma, but also on their thoughts,
attitudes and context. An elite athlete or soldier in battle, for example, may be so focussed
on the task at hand that he or she does not even notice his broken finger until the moment
has long passed. Pain is thus the result of integrated neural input. It is highly individual and
subjective in nature, often making pain difficult to define scientifically. From an experimental
perspective, pain can be broken down into three types, each mediated by different
mechanisms.Nociceptive pain results from activation of nociceptors in peripheral tissues.
Neuropathic pain results from injury or irritation to the nerves themselves such as in
shingles or diabetic neuropathy. Inflammatory pain arises from inflamed joints or other
tissues. On a day-to-day basis pain subsides after the recovery from tissue injury, such as a
burn, a cut or even a broken bone. However, in some cases pain does not subside even
despite healing of the injury. This is the pathologic condition known as chronic or persistent
pain. In this case the individual may experience one or more of the following: spontaneous
pain (pain for no apparent reason), hyperpathia (more pain than would be expected after a
painful event)), hyperalgesia (increased intensity of pain to a further noxious stimulus),
secondary hyperalgesia (spreading of sensitivity or pain to nearby, uninjured tissue) and
allodynia (sensation of pain from a normally innocuous stimulus).
Chronic Pain Management

There is evidence for the use of a range of non-drug therapies in pain control. Some
therapies have a stronger evidence base than others. Most evidence exists for the efficacy
of Cognitive Behavioural Therapy (CBT). For some people spiritual support, prayer or
meditation may be an important aspect of their overall pain management, as may self-help
and relaxation techniques.
Complementary therapies for chronic and cancer pain.

Complementary Therapy must be distinguished from ‘Alternative Medicine’ which, by
definition, is offering a different system of ‘medicine’ to conventional medicine;
complementary therapies can be used alongside conventional medicine; not in competition
with it. Complementary therapies include: Acupuncture, Therapeutic hypnosis,
Aromatherapy, Homoeopathy, Reflexology, Reiki,Therapeutic Touch, Therapeutic Massage.
Specific Drug Therapies For Pain Management

Analgesics act at many different sites and therefore not all types of pain respond to all
analgesics. Non-Opioid Analgesics : Paracetamol, Non-Steroidal Anti-inflammatory Drugs
(NSAIDs) including COX-2-Selective NSAIDs. Opioid Analgesics : The term ‘opioid’ is
applied to any substance that produces morphine-like effects and can be classified into:
Pure agonists (morphine, diamorphine, oxycodone), Weak agonists (codeine,
dihydrocodeine, tramadol), Partial agonist or mixed-agonist antagonists, Pure antagonists.
Lecture 15
EMERGENCY TOXICOLOGY AND POISONING
Agus Somya
LEARNING OBJECTIVE
1. To describe general approach of acute intoxication/poisoning
2. To describe general management of acute intoxication/poisoning
3. To describe management of methanol intoxication
4. To describe management of opiate intoxication
5. To descripe management of organophospate intoxication
6. To describe management of caustic intoxication
ABSTRACT
General approach and management of acute intoxication/poisoning
Acutely poisoned patients are commonly encountered in Emergency Centres. Acute
intoxication/poisoning (accidental or intentional) requires accurate assessment and prompt
therapy. Early identification of the involved toxin/s is crucial and the majority will be identified
by a thorough history and physical examination. An ABC-approach should be followed
ensuring a protected airway, adequate ventilation and hemodynamic stability. Supportive
and symptomatic care remains the cornerstone of treatment. A stepwise approach may be
followed to decrease the bioavailability of toxins. Indications, contra-indications, risks and
dosage regimens are describe for decontamination procedures including both termination of
topical exposures and decreasing exposure to ingested toxins. Furthermore, procedures to
increase the elimination of toxins and a short section covering specific toxins and their
antidotes are also included
Organophosphat poisoning
Organophosphorus pesticide self-poisoning is a major clinical and public-health problem
across much of rural Asia. Of the estimated 500 000 deaths from self-harm in the region
each year, about 60% are due to pesticide poisoning.
Organophosphorus pesticides inhibit esterase enzymes, especially acetylcholinesterase in

synapses and on red-cell membranes, and butyrylcholinesterase in plasma. Although acute
butyrylcholinesterase inhibition does not seem to cause clinical features,
acetylcholinesterase inhibition results in accumulation of acetylcholine and overstimulation
of acetylcholine receptors in synapses of the autonomic nervous system, CNS, and
neuromuscular junctions. The subsequent autonomic, CNS, and neuromuscular features of
organophosphorus poisoning are well known
Clinical features of organophosphorus pesticide poisoning including:

- overstimulation of muscarinic acetylcholine receptors in the parasympathetic system
Bronchospasm, Bronchorrhoea, Miosis, Lachrymation, Urination, Diarrhoea,
Hypotension, Bradycardia, Vomiting, Salivation.
- overstimulation of nicotinic acetylcholine receptors in the sympathetic system:
Tachycardia, Mydriasis, Hypertension, Sweating.
- overstimulation of nicotinic and muscarinic acetylcholine receptors in the CNS:
Confusion, Agitation, Coma, Respiratory failure.
- overstimulation of nicotinic acetylcholine receptors at the neuromuscular junction:
Muscle weakness, Paralysis and Fasciculations
Treatment includes resuscitation of patients and giving oxygen, a muscarinic antagonist

(usually atropine), fluids, and an acetylcholinesterase reactivator (an oxime that reactivates
acetylcholinesterase by removal of the phosphate group). Respiratory support is given as
necessary. Gastric decontamination should be considered only after the patient has been
fully resuscitated and stabilised. Patients must be carefully observed after stabilisation for
changes in atropine needs, worsening respiratory function because of intermediate

syndrome, and recurrent cholinergic features occuring with fat-soluble organophosphorus.
Caustic agent intoxication

Caustic ingestions may cause widespread injury to the lips, oral cavity, pharynx, and the
upper airway. The effect that these agents have on the esophagus accounts for most of the
serious injuries and long-term complications. The nature of the injury caused by caustic
ingestion is determined by a number of factors including the identity of the agent, the
amount consumed, the concentration, and the length of time the agent is in contact with a
given tissue. Caustic materials cause tissue injury by chemical reaction. These materials are
generally acidic or alkali. Usually, acids with pH less than 3 or bases with pH greater than 11
are of the greatest concern for caustic injury.
The esophagus is the site of most long-term sequelae from caustic ingestion. Injury to the
esophagus is rapid, as described above, for both acids and alkalis, but this acute tissue
disintegration and deep tissue penetration may continue for hours. Injury progresses within
the first week after ingestion, with inflammation and vascular thrombosis. A developing ulcer
with fibrin crust will be seen in a few days. Granulation tissue develops between 2 to 4 days
and is revealed under shed necrotic tissue by days 15 to 20.
After caustic ingestion, patients may present with a combination of many symptoms or none
at all depending on the nature of the agent, the specifics of the ingestion (quantity, intent,
timing), and what tissues were affected.
Induction of emesis should be avoided to prevent further injury as the agent is vomited.
Neutralization of the caustic material should be avoided because of the potential for causing
an exothermic injury, which may worsen an existing injury.
Opioid intoxication
Opioid analgesic overdose is a preventable and potentially lethal condition that results from
prescribing practices, inadequate understanding on the patient's part of the risks of
medication misuse, errors in drug administration, and pharmaceutical abuse. Three features
are key to an understanding of opioid analgesic toxicity. First, opioid analgesic overdose can
have life-threatening toxic effects in multiple organ systems. Second, normal
pharmacokinetic properties are often disrupted during an overdose and can prolong
intoxication dramatically. Third, the duration of action varies among opioid formulations, and
failure to recognize such variations can lead to inappropriate treatment decisions,
sometimes with lethal results.
Opioids increase activity at one or more G-protein–coupled transmembrane molecules,

known as the mu, delta, and kappa opioid receptors.
The presence of hypopnea or apnea, miosis, and stupor should lead the clinician to
consider the diagnosis of opioid analgesic overdose, which may be inferred from the
patient's vital signs, history, and physical examination. In patients with severe respiratory
depression, restoration of ventilation and oxygenation takes precedence over obtaining the
history of the present illness or performing a physical examination or diagnostic testing
Naloxone, the antidote for opioid overdose, is a competitive mu opioid–receptor antagonist

that reverses all signs of opioid intoxication.
Metanol Intoxication
Methanol (methyl alcohol, CH3OH) is the simplest type of alcohol, very light, volatile,
colorless, flammable, distinctive smell a little sweeter than etanol.3 methanol is used for
industrial products, and also as a mixture with ethanol to drink Traditional hard. Industrial
products that use methanol is a liquid car cleaner, solvent paints, cleansers, perfumes, car
fuel and other industrial products.
Methanol poisoning is a major disruption to the central nervous system, the optic nerve and
basal ganglia. The formic acid acts cause toxicity to the eye by inhibiting cytochrome
oxidase in the optic nerve, interrupting the flow axoplasma. While substances that contribute
to the occurrence of metabolic acidosis and decreased plasma bicarbonate is
formaldehyde, formic acid and lactic acid.
Toxic doses of methanol ranges between 15-500 cc of methanol solution containing 40% to
60-600 cc of methanol. Methanol poisoning begins with mild drunk and sleepy. Followed by
a latent phase (40 minutes - 72 hours) which is the period without symptoms, due to the
slow production of formaldehyde and formic acid. This phase was followed by the
appearance of metabolic acidosis, anion gap and impaired of vision. Visual disturbances
such as blurred to decrease visual acuity. In the later phase of seizures, coma and death.
Slower onset of methanol poisoning if the patient is also taking ethanol simultaneously.
On laboratory examination found an increase in serum osmolality, anion gap, serum lactic
acid and metabolic acidosis. Definitive diagnosis and monitoring of treatment response
based on the examination of serum methanol levels.
Specific Management of acute methanol poisoning include:

- Inhibitors of alcohol dehydrogenase
- Treatment with Co-factor: folinic acid 50 mg IV or folic acid 50 mg IV every 6 hours.
- Sodium Bicarbonate
- Hemodialis: Hemodialis is the fastest way of issuing metabolic toxic acid and methan
Lecture 16
DERMATO - EMERGEMENCIES
Nyoman Suryawati
Objective
 To understand the basic principle of acute blistering and exfoliative skin
 Able to identify a case with acute blistering and exfoliative skin
 Able to manage and referral a case with acute and exfoliative skin
Abstract
Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis
Stevens–Johnson syndrome (SJS) and Toxic epidermal necrolysis (TEN) are acute life-
threatening mucocutaneous reactions characterized by extensive necrosis and detachment
of the epidermis, with a mortality rate reaching 30%. The pathophysiology of EN is still
unclear; however, drugs are the most important etiologic factors. Both SJS and TEN are
differs only in the final extent of body surface involved: (1) SJS, less than 10% of body
surface area (BSA); (2) SJS/TEN overlap, between 10% and 30%; (3) TEN, more than 30%
of BSA.
Nonspecific symptoms such as fever, headache, rhinitis, cough, or malaise may precede the
mucocutaneous lesions by 1 to 3 days. Pain on swallowing and burning or stinging of the
eyes progressively develop, heralding mucous membrane involvement. The eruption is
initially symmetrically distributed on the face, the upper trunk, and the proximal part of limbs.
The initial skin lesions are characterized by erythematous, dusky red, purpuric macules,
irregularly shaped, which progressively coalesce. 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 life-
threatening, blistering skin disease caused by exfoliative toxins (ETs) of certain strains of
Staphylococcus aureus (usually phage group 2). ETs are serine proteases that bind to the
cell adhesion molecule desmoglein 1 and cleave it, resulting in a loss of 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 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 40:846-862.
- 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.
Ch15:154-161.
- 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
177:4028-4037.
- 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 12:422-23.
Lecture 17
PREGNANCY INDUCED HYPERTENSION
Gede Megaputra
Objective:
1. Define pregnancy induced hypertension
2. Review appropriate fetal/maternal assessment
3. Discuss appropriate anti – hypertension and anti – seizure therapy
4. Recognize when and how to transport patient with pregnancy induced hypertension
Hypertensive disorders in pregnancies are the leading causes of maternal death in

emerging countries. All caregivers must be able to promptly recognized the signs,
symptoms and laboratory findings of gestational hypertension with or without proteinuria
and with other adverse manifestation. Caregivers must appreciate fully the seriousness of
gestational hypertension, its potential for multi – organ involment and the risk for perinatal
and maternal morbidity and mortality. The appropriate management of gestational
hypertension may vary based on the availability of resources. In this lecture student will
discuss such as : the classification and definition of hypertensive disorders in pregnancy;
management and treatment of gestational hypertension.
Severe gestational hypertension is an obstetrical emergency, which requires prompt

recognition, stabilization of mother and fetus and multi – disciplinary approach to
management and treatment
Lecture 18
SHOULDER DYSTOCIA
Endang Sriwidiyanti
Objective
1. Define shoulder dystocia
2. Review appropriate fetal/maternal assessment
3. Discuss the risk factors of shoulder dystocia
4. Discuss the complications of shoulder dystocia
5. Discuss appropriate management of shoulder dystocia
Shoulder dystocia is one of emergency problems during delivery. Following the delivery of
the head, there is impaction of the anterior shoulder on the symphysis pubis in the AP
diameter, in such a way that the remainder of the body cannot be delivered in the usual
manner. More than 50% of cases shoulder dystocia occur in the absence of any identified
risk factor. The student will discuss the assessment of shoulder dystocia, the complication
for fetus and mother, identification of risk factor, and management
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.
The main mechanism behind the occurrence of shoulder dystocia is the retention of the
anterior shoulder behind the pubic symphysis, while the posterior shoulder is usually located
in the maternal pelvis (Figure 1). In rare situations, both shoulders are retained above the
pelvic brim.
Figure 1. The main mechanism behind the occurrence of shoulder dystocia –

retention of the anterior fetal shoulder above the pubic symphysis
INCIDENCE
An overall incidence between 5.8-7 in 1000 of vaginal deliveries is reported in the largest
observational studies 4, while others studies find incidence of 1-2 in 1000 birth and 16 in
1000 birth of baby weight more than 4000 gram.
RISK FACTORS
The main risk factors for shoulder dystocia are listed in Table 1. Previous shoulder
dystocia stands out as a major risk factor for recurrence, and it is reported to be 10 times
higher than in the general population, for an overall incidence of 1–25%. The anatomical
characteristics of the maternal pelvis that predispose to shoulder dystocia and may cause it
to be recurrent in nature are poorly understood. When additional risk factors are present,
such as maternal diabetes or suspected fetal macrosomia or when previous fetal injury
occurred in association with shoulder dystocia, serious consideration should be given to
elective caesarean delivery, and this option should be discussed with the mother.
Another major risk factor is fetal macrosomia, and when coexistent with poorly controlled
maternal diabetes, an additional 2–4-fold risk is present, posed by the increased diameter
of the fetal shoulders.
Table 1. Main Risk Factors for Shoulder Dystocia

Risk Factor
Previous shoulder dystocia
Fetal macrosomia and its associated risk factors
Pre-existing or gestational diabetes
Maternal obesity
Excessive weight gain during pregnancy
Post-term pregnancy
Slow progress of labour vaginal delivery
Prolonged first and/or second stage
Need for labour acceleration
Instrumental
The majority of cases of shoulder dystocia occur in pregnancies that have no risk factors,
and when one is present, the majority of cases do not develop this complication. There is
therefore wide agreement within the medical community that shoulder dystocia is generally
an unpredictable situation. Nevertheless, identification of risk factors is useful for
anticipating of the situation, so that an experienced team can be on hand at the time of
delivery.
COMPLICATIONS
Complications of shoulder dystocia are described in Table 2. The most frequent
complication of shoulder dystocia is brachial plexus injury, of which Erb’s palsy is the
usual presentation. The latter manifests by a characteristic position of the affected arm that
hangs by the side of the body and is rotated medially. The forearm is usually extended and
pronate (Fig. 2). It affects about 0.15 % of all births, and in some countries, the incidence
appears to be decreasing. Older studies report brachial plexus injury to occur in 2–16 % of
shoulder dystocias, but recent data from centres performing regular staff training refer that
this can be reduced to about 1.3 %. Brachial plexus injury appears to be related mainly to
the traction force applied on the fetal head. Improved awareness of the fact and simulation-
based training of the force that can be safely applied to the fetal head may be responsible
for the decreasing incidence of this complication.
Of all brachial plexus injuries diagnosed at birth, the majority disappear after treatment, and
only 10–23% remain after 12 months. In the majority of cases of residual paralysis, some
degree of recovery is achievable after surgery.
Shoulder dystocia is also a cause of perinatal mortality, although the incidence appears to
have decreased in the last decades. Confidential enquiries carried out in the United
Kingdom indicate that it may be responsible for about 8% of intrapartum fetal deaths. The
main cause of perinatal death is acute fetal hypoxia/acidosis.
There is uncertainty about how many minutes may elapse before the fetus is at risk of injury
from acute hypoxia/ acidosis. The phenomenon is probably faster when there are nuchal
cords and when cord clamping takes place before the shoulders are released.
Figure. 2 Newborn with a right arm position typical of Erb’s paralysis.
Compression of fetal neck vessels may also play an important part in the patho-
physiological mechanism, and it may be the main cause of cerebral injury when no nuchal
cords are present. Again, umbilical blood gas values may not translate the severity of
hypoxia/acidosis occurring in the brain, and hypoxic-ischaemic encephalopathy has been
documented in cases with only moderate acidemia on cord gas analysis. In a small but well-
documented observational study, no cases of hypoxic- ischaemic encephalopathy were
found when resolution took less than 5 min, and only mild cases of hypoxic-ischaemic
encephalopathy were reported when it lasted 5–9 min. Serious complications of
hypoxia/acidosis were only described in one case where more than 12 min elapsed.
Table 2. Complications of Shoulder Dystocia

Newborn Complications
Death (8%)
Asphysxia and its complications
Fracture of Clavicula, humerus
Brachial Plexus Injury (most common)
Maternal Complications
Postpartum haemorrhage (11%)
Uterine Rupture
Bladder rupture
Dehiscence of pubic symphisis
Sacro-iliac joint dislocation
Although there are no certainties as to the time that may elapse before the fetus is at risk of
injury from hypoxia/acidosis, it seems wise not to clamp nuchal cords after the head is
delivered unless there is no other alternative and to attempt resolution preferably within 5
min. When 12 min have elapsed, fetal prognosis is likely to be poor. Different timings must
be considered when fetal oxygenation is already compromised before the occurrence of
shoulder dystocia or when there is fetal growth restriction.
Rarer complications of shoulder dystocia are fractures of clavicle and humerus, the
majority of which are iatrogenic in nature, consequent to the manoeuvres used for resolution
of the situation, and they usually heal without sequelae after immobilisation.
The most frequent maternal complications are vaginal and perineal lacerations, and some
studies report anal sphincter lacerations to occur in about 4% of shoulder dystocia cases.
Postpartum haemorrhage affects about 11% of cases and can be caused by birth canal
lacerations and more frequently by uterine atony. Rare cases of uterine rupture, bladder
rupture, dehiscence of the pubic symphysis and sacroiliac joint dislocation have also been
described.
DIAGNOSIS
• Turtle’ sign
• Prolonged second stage of labour
• Fail to deliver the baby with maximal effort and proper management
Figure. 3 Turtle sign, with the lower structures of the fetal head depressing the maternal
perineum
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 mnemonic "ALARMER"

1. Principles : Do not 4 “P” :
- Panic
- Pulling (the head of the baby)
- Pushing (the fundal of uterine)
- Pivoting (the head of the baby with coccygeus as fulcrums
2. Ask For Help :

- The mother of patient
- Husband
- Midwife
- Physician in charge or other paramedic
3. Lift the buttock- McRobert’s Maneuver

The McRoberts maneuver was described by Gonik and associates (1983) and named
for William A. McRoberts, Jr., who popularized its use at the University of Texas at
Houston. The maneuver consists of removing the legs from the stirrups and sharply
flexing them up onto the abdomen (Figure 4). Gherman and associates (2000) analyzed
the McRoberts maneuver using x-ray pelvimetry. They found that the procedure caused
straightening of the sacrum relative to the lumbar vertebrae, rotation of the symphysis
pubis toward the maternal head, and a decrease in the angle of pelvic inclination.
Although this does not increase pelvic dimensions, pelvic rotation cephalad tends to
free the impacted anterior shoulder. Gonik and coworkers (1989) tested the McRoberts
position objectively with laboratory models and found that the maneuver reduced the
forces needed to free the fetal shoulder.
a b
Figure 4. a. McRobert's Maneuver, the maneuver consists of removing the legs from
the stirrups and sharply flexing the thighs up onto the abdomen. b. “The McRoberts
maneuver and the assistant is also providing suprapubic pressure simultaneously
(arrow). 2,4
4. Anterior Disimpaction
4.1. Suprapubic Pressure (Manuver Massanti )
• Suprapubic pressure on the baby's anterior shoulder toward the chest of the
baby.
Figure 5. Suprapubic Pressure
4.2. Rubin Manouver

• vaginal approach
• adduction anterior shoulder by pressing the posterior shoulder towards the
chest
• Consider episiotomy
Rubin (1964) recommended two maneuvers. First, the fetal shoulders are rocked
from side to side by applying force to the maternal abdomen. If this is not
successful, the pelvic hand reaches the most easily accessible fetal shoulder, which
is then pushed toward the anterior surface of the chest. This maneuver most often
abducts both shoulders, which in turn produces a smaller shoulder-to-shoulder
diameter. This permits displacement of the anterior shoulder from behind the
symphysis. 4
Figure 6. Rubin Manouver. A. The shoulder-to-shoulder diameter is aligned vertically. B.

The more easily accessible fetal shoulder (the anterior is shown here) is pushed toward
the anterior chest wall of the fetus (arrow). Most often, this results in abduction of both
shoulders, which reduces the shoulder-to-shoulder diameter and frees the impacted
anterior shoulder
5. Rotate the posterior shoulder- Corkscrew/ Wood Maneuver
Woods (1943) reported that by progressively rotating the posterior shoulder 180
degrees in a corkscrew fashion, the impacted anterior shoulder could be released. This
is frequently referred to as the Woods corkscrew maneuver.
Figure 7. Wood Maneuver. The hand is placed behind the posterior shoulder of the
fetus. The shoulder is then rotated progressively 180 degrees in a corkscrew manner so
that the impacted anterior shoulder is released
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
Figure8. 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 / All-Fours Manoeuvre / Gaskin’s Manouvre

This manoeuvre consists of placing the labouring woman on her hands and knees
and applying continuous and gentle axial traction on the fetal head, to release what was
previously the posterior shoulder (Fig. 9). Its place in the shoulder dystocia
management protocol is currently unclear, particularly in hospital environments. It is
mostly used in community settings when only one birth attendant is present and where
an 83 % success rate has been reported. In hospital settings, it may be attempted
before the exceptional manoeuvres described below are considered.
Figure.9 All-fours manoeuvre with axial traction being applied on the fetal head.
9. Last Efforts
9.1. Break The Clavicle

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

Zavanelli’sManoeuvre (Cephalic replacement followed by caesarean section was
described for the first time in 1978, and it is performed in the operating theatre under
general anaesthesia with halogenated agents. The manoeuvre starts with slow rotation
of the fetal head to an occiput-anterior position, followed by flexion of the fetal neck and
application of firm and continuous pressure for the reintroduction of the fetal head in the
maternal pelvis (Fig. 10). An immediate caesarean section follows. A small number of
case series are reported in the literature with varying success rates and usually low
maternal morbidity, but uterine rupture and subsequent need for hysterectomy have also
been described. When fetal prognosis is reserved, maternal morbidity becomes the
main priority, and this is probably the less traumatic alternative for her.
Figure 10. Zavanelli’s manoeuvre.

9.3. Symphysiotomy
This technique has been described for the resolution of obstructed labour since the
nineteenth century, but its current use in high-resource countries is limited to cases of
shoulder dystocia and retention of the after-coming head. Symphysiotomy is associated with
important maternal morbidity, so it should probably be the last option when fetal prognosis is
poor. The procedure can be performed under regional, general and local anaesthesia with
opiate sedation. It should be preceded by antibiotic prophylaxis, bladder catheterisation,
shaving and disinfection of the pubic area. Before incision, two assistants hold the mother’s
legs 60–80° apart, after removing them from the bed stirrups. This avoids sudden leg
abduction when the symphysis is opened, which can cause urethral injury.
Figure 11 The main steps of symphysiotomy
With a hand introduced in the vagina to push the urethra aside, a transabdominal vertical
incision is performed with a long scalpel between the lower two-thirds and the upper third of
the pubic symphysis (Fig. 11). Pushing the handle upwards will open the lower two-thirds.
The scalpel is then reintroduced into the incision with the blade facing upwards and the
handle pushed downwards to open the remaining upper third. It is usually possible to
separate the pubic bones by about 2–3 cm, and this allows the shoulders to be released.
After closing the abdominal skin, the maternal pelvis is bound with an orthopaedic strap,
and bladder catheterisation is maintained for 48 hours.
In the absence of complications, the patient is maintained in lateral decubitus for two days,
and assisted walking starts on the third. Among the reported complications are para-urethral
lacerations, vulval oedema and skin incision haematomas. Difficulties in mobilisation may
persist for several months in 1–2 % of cases.
10. After procedure
- Post partum haemorrhage anticipation
- Exploration of lasceration and tear
- Examination of the baby
- Explain to the patient
- Record the procedure
Lecture 19
TRAUMA WHICH POTENTIALLY DISABLING AND LIFE THREATENING CONDITIONS
I Ketut Suyasa, IGN Wien Aryana, AA Gde Yuda Asmara
AIMS:
Establish tentative diagnosis, provide initial management and/or refer patient with: Trauma
Which Potentially Disabling and Life Threatening Condition.
LEARNING OUTCOMES:
Establish tentative diagnosis, provide initial management and/or refer patient with: Trauma
Which Potentially Disabling and Life Threatening Condition
CURRICULUM CONTENTS:
1. Trauma Which Potentially Disabling and Life Threatening Condition
2. Diagnosis, provide initial management and/or refer patient with: Trauma Which
Potentially Disabling and Life Threatening Condition
ABSTRACTS
The initial assessment and management of seriously injured patients is a challenging task
and requires a rapid and systematic approach. This systematic approach can be practised
to increase speed and accuracy of the process but good clinical judgement is also required.
Although described in sequence, some of the steps will be taken simultaneously. The aim of
good trauma care is to prevent early trauma mortality. Early trauma deaths may occur
because of failure of oxygenation of vital organs or central nervous system injury, or both.
Injuries causing this mortality occur in predictable patterns and recognition of these patterns
led to the development of advanced trauma life support (ATLS) by the American College of
Surgeons. A standardised protocol for trauma patient evaluation has been developed. The
protocol celebrated its 25th anniversary in 2005.[ Good teaching and application of this
protocol are held to be important factors in improving the survival of trauma victims
worldwide.
Initial assessment
 Resuscitation and primary survey.
 Secondary survey.
 Definitive treatment or transfer for definitive care.
1. Resuscitation and primary survey

For speed and efficacy a logical sequence of assessment to establish treatment priorities
must be gone through sequentially although, with good teamwork, some things will be done
simultaneously (resuscitation procedures will begin simultaneously with the assessment
involved in the primary survey, ie lifesaving measures are initiated when the problem is
identified). Special account should be taken of children, pregnant women and the elderly as
their response to injury is modified.
The primary survey is according to: A = Airway maintenance cervical spine protection
The key = Look, Listen, Feel. Ensure the airway is open obstructions, airway is clear,
Trachea is midline and Mandibular or maxillofacial fracture. Assume a cervical spine injury
with any multisystemtrauma, especially with an altered level of consciousness or blunt injury
above the clavicle.
- Recognition of: Stridor, change of voice quality, obvious trauma
- Major problems:
1. obstructions,
2. Laryngeal injury,
3. Posterior dislocation / fracture dislocation of the sternoclavicular joint.
- Management: Establishing a patent airway/ ET intubation; closed reduction.
B = Breathing and ventilation

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

Blood loss is the main preventable cause of death after trauma. To assess blood loss rapidly
observe:
- Assessment: Pulse quality, rate and regularity. BP, pulse pressure, observing and
palpating the skin for color and temperature. Neck veins.
- Important notes: Neck veins may not be distented in the hypovolemic patient with
cardiac tamponade, tension pneumothorax,or traumatic diaphragmatic injury.
- Monitor with: Cardiac monitor/pulse oximeter.
- Major problems:
1. Massive hemothorax:
 Rapid accumulation of > 1500 mL o blood in the chest cavity.
 Hypoxia
 Neck veins may be flat secondary to hypovolemia
 Absence of breath sounds and/or dullness to percussion on one side of the
chest
 Management: Restoration of blood volume and decompression of the chest
cavity.
 Indication of thoracotomy: a. Immediately 1500 mLof blood evacuated. b.
200mL/hr for 2-4 hrs. c. Patient’s physiology status. d. Persistent blood
transfusion requirements.
2. Cardiac Tamponade
 Cardiac tamponade is usually due to penetrating cardiac injuries and are a
leading cause of traumatic death.
 Diagnosis : Cardiac tamponade requires prompt recognition and treatment.

Signs and symptoms range from rarely stable to Beck’s triad of hypotension,
CVP above 12cc of water and muffled heart sounds
 Auscultation of the thorax is performed specifically to evaluate the clarity of heart
tones and breath sounds. Muffled heart tones are an indication of blood in the
pericardium. A systolic - to diastolic gradient of less then 30 mmHg, associated
with hypotension is consistent with cardiac tamponade.
 Neck veins are distended. Central venous pressure is elevated.
 The X-ray film may demonstrate a widening of the cardiac silhouette. The
ultrasound scan shows presence of blood in pericardial space.
 Electrocardiograph is not particularly helpful.
 Prompt definitive therapy is imperative. This includes antishock therapy,
pericardiocentesis (possibly under U.S. guide), emergency thoracotomy and
suture of the wound.
3. Tension Pneumothorax
 Tension pneumothorax develops when air enters the pleural space but cannot
exit and as a result there is a progressively increasing intrathoracic pressure in
the affected hemithorax resulting in impaired central venous return and
mediastinal shift.
 Clinically, the patient experiences dyspnea, complains of chest pains, and
becomes cyanotic because of shunting in the collapse of lung and has
hemodynamic instability because decrease is venous return for endopleural
hypertension.
 The presence of hyper-resonance and the absence of breath sounds, together
with X-ray examination, should be useful in confirming the cause of the
emergency.
 A chest X-ray film indicates that the trachea and mediastinum are deviated to the
side opposite the tension pneumothorax, while on the ipsilateral side intercostal
spaces are widened and the diaphragm is pushed downward.
 The emergency require immediate thoracosintesis and thoracostomy with
underwater-seal drainage.
4. Blunt Abdominal trauma

 Mechanism of Injury:
1) Blunt Trauma: Spleen, liver, retroperitoneal hematoma
2) Penetrating Trauma:
o Stab: Liver, small bowel, diaphragm, colon
o Gunshot: small bowel, colon, liver, abdominal vascular structures.
 Assessment:
1) History.
2) PE:
o Inspection
o Auscultation: Bowel sounds
o Percussion
1. signs of peritonitis
2. Tympanic/ diffuse dullness
o Palpation: Involuntary muscle guarding
3) Evaluation of penetrating wounds: Determine the depth
4) Assessing pelvic stability: Manual compression
5) Penile, perineal and rectal examination:
o Presence of urethral tear.
o Rectal exam: Blunt (sphincter tone, position of the prostate, pelvic bone
fractures), Penetration (sphincter tone, gross blood from a perforation)
6) Vaginal examination
7) Gluteal examination
8) Intubation:
o Gastric tube:
1. Relieve acute gastric dilatation.
2. Presence of blood
o Urinary catheter:
1. Relieve urine retention
2. Monitoring urine output.
3. Caution: The inability to void, unstable pelvic fracture,blood in the
meatus, a scrotal hematoma, perineal ecchymoses, high-riding
prostate.
9) X-rays studies:
10) Special diagnostic studies in blunt trauma:
o DPL
o Ultrsonography
o Computed tomography
11) Special diagnostic studies in penetrating trauma:
o Lower chest wounds
o Anterior abdominal
o Flank/back
12) Indications for Celiotomy. Based on abdominal evaluation
o Blunt: Positive DPL/ ultrasound
o Blunt: Recurrent hypotension despite adequate resuscitation
o Peritonitis
o Penetrating: Hypotension
o Penetrating: Bleeding from the stomach, rectum, GU tract.
o Gunshot wounds: Traversing the peritoneal cavity
o Evisceration
5. Pelvic Fractures:
 Assessment:
1) The flank, scrotum and perianl area should be inspected
2) Blood at the urethral meatus, swelling/bruishing/laceration in the peritoneum,
vagina, rectum, or buttock, open pelvic facture
3) Palpation of a high-riding prostate gland.
4) Manual manipulation of the pelvis should be performed only once.
Management Pelvic fracture:

Exsanguination with/without Blood pressure stabilizees Blood Pressure normal
open pelvic fracture with difficulty and and closed/unstable or
(BP<70mmHg) closed/ unstable fracture stable fracture (BP 120
(BP 90-110mmHg) mmHg)
Initiate ABCDEs Initiate ABCDEs Initiate ABCDEs
If transfer neccessary, apply If transfer neccessary, apply

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

reduce & apply & apply
Positive Negative fixation device fixation
as appropriate device as
After operation Red uce & appropriate
reduce & apply apply
fixation device fixation device
as appropriate as appropriate
Hemodynamically
Hemodynamically Abnomal
Abnomal
Angiography
Angiography
D = Disability: neurological status. Rapid neurological assessment is made to establish:

 Level of consciousness, using Glasgow Coma Scale
 Pupils: size, symmetry and reaction.
 Any lateralising signs.
 Level of any spinal cord injury (limb movements, spontaneous respiratory effort).
E = Exposure/environmental control. Undress the patient, but prevent hypothermia.

Additional considerations to primary survey and resuscitation
ECG monitoring:
Urinary/gastric catheters:
Other monitoring:
 Pulse rate blood pressure, ventilatory rate, arterial blood gases, body temperature
and urinary output.
 Carbon dioxide detectors may identify dislodged endotracheal tubes.
 Pulse oximetry measures oxygenation of haemoglobin colorimetrically (sensor on
finger, ear lobe, etc.).
Diagnostic procedures: X-rays most likely to guide resuscitation early on, especially in
blunt trauma, include:
 CXR.
 Pelvic X-ray. It has been suggested that CT scans may be used in some stable
patients.
 Lateral cervical spine X-ray.
 FAST (= focused assessment with sonography for trauma), eFAST (= extended
focused assessment with sonography for trauma) and/or CT scanning to detect
occult bleeding.
Lecture 20
Emergency in Pediatric (Non Trauma)
I Made Darmajaya
Tujuan pembelajaran
1. Mengetahui definisi gawat darurat bedah pasien anak-anak.
2. Mampu melakukan asessement dan penanganan awal kasus kedaruratan bedah
anak.
3. Mengetahui manajemen definitive kedaruratan bedah pasien anak-anak
4. Mengetahui prognosa pasien anak-anak dengan kedaruratan bedah.
Latar Belakang
Gawat darurat pada kasus bedah anak adalah suatu keadaan yang terjadinya mendadak
mengakibatkan seorang anak atau bayi memerlukan penanganan atau pertolongan segera
dalam arti pertolongan secara cermat, tepat dan cepat. Apabila tidak mendapatkan
pertolongan penderita dapat meninggal atau cacat atau kehilangan anggota tubuhnya
seumur hidup.
Kasus gawat darurat bedah anak tidak sama dengan kasus gawat darurat pada penderita
dewasa. Neonatus dan anak-anak bukan penderita dewasa yang mini. Neonatus dan anak-
anak sangat berbeda dengan orang dewasa dalam aspek bentuk dan ukuran, luas
permukaan tubuh, kapasitas stress, maturasi organ maupun adaptasi dengan lingkungan
sekitarnya. Pada neonatus dan anak-anak juga didapatkan pola penyakit yang berbeda
dengan dewasa. Pada neonatus dan anak-anak lebih sering didapatkan kelianan bedah
yang ada merupakan kelainan bawaan. Dengan perbedaan tersebut maka diperlukan
cara menegakkan diagnosis yang juga berbeda serta penanganan yang sangat berbeda
dengan orang dewasa.
Diagnosis, Manajemen, Penanganan dan Prognosis kedaruratan bedah pada pasien

anak-anak
Secara garis besar kasus-kasus emergency pada bedah anak dapat disebabkan oleh
beberapa hal diantaranya:
 Perdarahan
 Obstruksi usus
 Kasus-kasus infeksi
 Strangulasi usus
 Kombinasi hal tersebut diatas.
Berdasarkan usia anak kasus–kasus emergency pada bedah anak dapat digolongkan
menjadi kasus emergensi pada neonatus dan kasus emergensi pada anak.
Kasus emergensi pada neonatus diantaranya:
 Stenosis pylorus
 Hernia diafragmatika
 Trakeo esophageal fistula (TEF)
 Defek dinding abdomen (Gastroschisis dan ophlalokel)
 Necrotizing Enterokolitis yang mengalami perforasi.
Adapun kasus kasus emergensi pada anak yang lebih besar diantaranya:
 Intussusepsi.
 Appendicitis akut
 Hernia inguinalis inkarsetara
 Hirschsprung's dengan entererokolitis
 Malrotasi dengan Volvulus
 Torsio Testis
Pada tulisan ini akan dibahas dengan ringkas beberapa kelainan yang paling sering
didapatkan dan biasanya datang pertama kali ke dokter umum maupun dokter anak.
1. Stenosis Pylorus .
Hypertropic Pyloric Stenosis (HPS) adalah suatu kondisi yang menyerang bayi dimana
bagian serat otot sirkuler pylorus lambung mengalami hipertrofi sehingga terjadi
penyempitan kanal pylorus oleh kompresi lipatan-lipatan longitudinal dari mukosa dan
perpanjangan pylorus yang menyebabkan hambatan dalam pengosongan lambung.
Penyebab HPS masih belum diketahui. HPS bisa merupakan kejadian congenital maupun
di dapat.
Manifestasi Klinis HPS adalah Obstruksi yang menyebabkan muntah proyektil non bilious
(tanpa empedu) yang progresif sesudah pemberian minuman formula atau ASI. Keadaan
Jaundice terjadi pada kira-kira 2% bayi dengan HPS sekunder. Tujuh persen berhubungan
dengan malformasi. Tiga malformasi utama yaitu malformasi intestinal, obstruksi uropati
dan atresia esophagus.
Untuk menegakkan diagnosis HPS diperlukan pemeriksaan fisik, pemeriksaan

laboraatorium dan pemeriksaan penunjang. Pemeriksaan penunjang meliputi pemeriksaan
foto abdomen, pemeriksaan USG dan pemeriksaan gastrointestinal dengan kontras.
Penderta HPS sering datang ke rumah sakit dalam keadaan emergensi medis dan bukan
emergensi untuk pembedahan. Penanganan awal meliputi tata laksana cairan berfokus
untuk mengkoreksi dehidrasi termasuk gangguan elektrolit dan keseimbangan asam-basa.
Kemudian setelah keadaan pasien stabil, dilakukan tindakan pembedahan. Standar
operasi pasien pada pasien HPS adalah Ramstedt Pyloromyotomy. Sebagian besar
bayi membaik setelah operasi dan tidak memerlukan tambahan intervensi medis lebih
jauh.
2. Hernia Diafragmatika
Hernia diafragmatika adalah kelainan yang terjadi akibat adanya penonjolan organ perut ke
dalam rongga thoraks melalui suatu defek (lubang) pada diafragma. Diafragma adalah
sekat yang membatasi rongga dada dan rongga perut. Lubang Hernia dapat terjadi di
peritoneal (tipe Bochdalek) yang sering di temukan, anterolateral (tipe morgagni) atau di
esophageal hiatus hernia. Penyebab pasti hernia masih belum diketahui.
Gejala dapat berupa:
- Gangguan pernafasan berat
- Sianosis
- Takipneu
- Bentuk dinding dada kiri dan kanan tidak sama (asimetris)
- Takikardia.
Pemeriksaan fisik didapatkan gerakan pernafasan yang tertinggal, perkusi pekak, fremitus
menghilang, suara pernafasan menghilang dan mungkin terdengar bising usus pada
hemitoraks yang mengalami gangguan.
Kesulitan untuk menegakkan diagnosis hernia diafragmatika preoperative menyebabkan

sering terjadinya kesalahan diagnosis dan untuk itu diperlukan pemeriksaan penunjang
untuk memastikan diagnosisi hernia diafragmatika.
Pemeriksaan penunjang yang penting adalah dilakukannya pemeriksaan radiologi yaitu

pemeriksaan foto thoraks. Adanya defek pada diafragma bila dilihat dari thoraks foto dapat
ditemukan gambaran abnormal seperti adanya isi abdomen pada rongga thoraks, terlihat
selang NGT di dalam rongga thoraks, peninggian hemia diafragma (kiri lebih tinggi dari
kanan), dan batas diafragma yang tidak jelas. Pemasangan sonde langsung dapat di
gunakan untuk memastikan diagnosis sebab sonde dapat membelok kembali ke atas
diafragma. Foto zat kontras kadang diperlukan jika kolon tersangkut di dalamnya. Bila di
dapatkan abnormalitas pada pemeriksaan foto thoraks, selanjutnya dilakukan pemeriksaan
CT-scan atau USG FAST untuk memastikan diagnosis rupture diafragma dan hernia
diafragma. Kadang-kadang diperlukan fluoroskopi untuk membedakan antara paralisis

diafragmatika dengan eventerasi (usus menonjol ke depan dari dalam abdomen).
Pada hernia diafragmatika dapat terjadi penyulit berupa perdarahan dan obstruksi. Bila
defek hernia besar kemungkinan terjadi insufisiensi kardiovaskular yang dapat mengancam
jiwa. Komplikasi yang paling membahayakan adalah strangulasi isi hernia. Lambung,
usus, hati dan limfa dapat menonjol melalui hernia. Jika hernia yang besar, biasanya paru-
paru pada sisi hernia tidak berkembang secara sempurna. Setelah lahir, bayi akan
menangis dan bernafas sehingga usus akan segera terisi oleh udara. Terbentuk massa
yang mendorong jantung sehingga menekan paru-paru dan terjadilah sindroma gawat
pernafasan.
Konseling prenatal dilakukan segera setelah diagnosis dibuat berdasarkan USG. Setelah
melalui berbagai pemeriksaan tersebut, tim medis harus menjelaskan segala kemungkinan
pilihan tatalaksana kepada orangtua seperti terminasi kehamilan, meneruskan kehamilan
dan melahirkan bayi tersebutdi pusat pelayanan medis yang memadai termasuk prognosis
dari kasus ini. Tatalaksana hernia diafragmatika yang optimal harus memperhatikan
berbagai hal yang terkait antara lain:
1. Proses persalinan dan unit perawatan intensif neonatus
2. Stabiliasai preoperative
3. Ventilasi mekanik konvensional
4. Extracorporeal Membrane Oxygenation (ECMO)
5. Pemberian Surfaktan
6. Terapi Antenatal
7. Terapi Pembedahan Perinatal
8. Transplantasi Paru
9. Perawatan Pasca Bedah
Perawatan pasca bedah meliputi perawatan jangka pendek (segera setelah pembedahan)
dan perawatan jangka panjang. Perawatan bedah jangka pendek meliputi deteksi dan
tatalaksana komplikasi yang dapat terjadi setelah pembedahan. Komplikasi yang mungkin
timbul dapat berupa perdarahan, distress pernafasan, hipotermia, produksi urin yang
menurun, infeksi dan obstruksi usus. Pengawasan yang dilakukan saat pasien masih
dirawat di rumah sakit meliputi monitoring pernafasan, evaluasi neurologis, dan masalah
pemberian makanan. Perawatan jangka panjang meliputi pemantauan tumbuh kembang
pasien. Pertumbuhan kasus dipantau karena risiko terjadi gagal tumbuh besar akibat
adanya penurunan asupan kalori sebagai akibat penyakit paru khronis, gastroesophageal
refluks dan feeding yang buruk terutama pada pasien dengan defek neurologis yang berat.
3. TEF (Tracheo Esofageal Fistula)

TEF merupakan suatu kelainan kongenital dimana terdapat saluran abnormal yang
menghubungkan trakea dengan esofagus . Di dunia, angka insiden TEF adalah satu dalam
3.000-4.500 kelahiran hidup. Sebagian kelahiran dengan TEF terjadi bersamaan dengan
kelainan lainnya dimana yang tersering ialah kelainan jantung (cardiac). Keadaan ini
merupakan bagian dari sindrom VACTERL, yaitu vertebral (17%), anorektal (12%), cardiac
(20%), tracheo, esophageal, renal (16%), dan limb (10%). TEF dapat pula terjadi hanya
sendiri tanpa kelainan penyerta (nonsyndromic oesophageal atresia).
Sampai saat ini penyebab TEF belum diketahui secara pasti, namun dikatakan terjadi akibat
multifaktorial, termasuk faktor genetik sebesar 6-10%. Faktor genetik tersebut antara lain
kelainan kromosom [trisomi 13 (Patau syndrome), 18 (Edwards syndrome), 21 (Down
syndrome)] dan gangguan single gene (CHARGE syndrome, Feingold syndrome, Opitz
syndrome, Fanconi anemia). Faktor lingkungan diduga juga ikut berpengaruh terhadap
kelahiran bayi dengan TEF. Faktor tersebut antara lain ibu terpapar zat methimazole atau
diethylstilbestrol (DES), pengguna hormon sex eksogen, perokok atau peminum alkohol,
dan pekerja di pertanian atau perkebunan, penggunaan insulin pada diabetes mellitus, usia
terlalu tua, dan defisiensi vitamin A.
Bayi dengan AE/TEF dapat mengalami gangguan proses menelan karena tidak normalnya
peristaltik esofagus. Selain itu dapat terjadi trakeomalasia yang disebabkan oleh dilatasi
segmen proksimal akibat menumpuknya cairan amnion sehingga terjadi penekanan pada
perkembangan trakea dan mengakibatkan gangguan perkembangan cincin tulang rawan
trakea.
Janin dengan AE tidak dapat menelan cairan amnion dengan efektif. Pada janin dengan AE
dan TEF distal, cairan amnion akan mengalir menuju trakea ke fistula kemudian ke usus
yang dapat mengakibatkan terjadinya polihidramnion. Polihidramnion sendiri dapat
menyebabkan kelahiran prematur. Trakea dapat mengalami kolaps secara parsial ketika
makan, setelah manipulasi atau terjadi GERD yang dapat mengakibatkan kegagalan nafas,
hipoksia, bahkan apnea.
Beberapa keadaan yang merupakan gejala dan tanda TEF antara lain:
a. Gangguan menelan saliva sehingga terjadi penumpukan saliva dan sekret.
b. Mulut berbuih karena adanya gelembung udara dari hidung dan mulut.
c. Tersedak atau batuk saat menyusui.
d. Sesak nafas, hipoksia, bahkan apnea.
e. Sianosis.
f. Gejala pneumonia akibat regurgitasi saliva dari esogafus yang buntu dan regurgitasi
cairan lambung melalui fistula ke dalam jalan nafas.
g. Perut kembung karena udara melalui fistula masuk ke dalam lambung dan usus.
h. Oligouria karena tidak ada cairan yang masuk.
i. Sering disertai dengan kelainan bawaan lainnya yang disingkat dengan VACTERL
yaitu Vertebra, Anorektal, Cardiac, Tracheal, Esophageal, Renal, dan Limb.
Diagnosis prenatal sering sulit diketahui sebab skrining hanya dapat dilakukan saat wanita
hamil melakukan USG kandungan. TEF dan kelainan lainnya biasanya tidak tampak jelas
hingga umur kehamilan 24 minggu. Terjadinya polihidramnion (33-66%) berhubungan
dengan obstruksi aliran cairan amnion melalui janin. Pada USG juga tidak ditemukan
gambaran cairan dalam gaster (10-40%) dengan tampak gaster berukuran kecil, perkiraan
berat badan janin rendah (40%), dan ditemukan kantong esofagus yang melebar.
Diagnosis Postnatal: Bayi akan terlihat sangat lapar dan apabila diberikan susu akan
terlihat rakus, tetapi pada saat menelan, maka susu tersebut akan keluar melalui mulut dan
hidung yang mengakibatkan terjadinya gangguan pada pernafasannya. Bayi akan
mengeluarkan saliva putih berbuih yang sangat banyak pada mulut dan terkadang pula
lewat hidung. Sekret tersebut dapat dibersihkan dengan pengisapan secara agresif tetapi
dengan cepat berulang. Pernafasan bayi dapat terdengar berderak dengan episode batuk,
tersedak, dan sianosis. Episode ini akan meningkat selama pemberian makanan. Apabila
terdapat fistula antara trakea dan esofagus akan terlihat abdomen semakin distensi.
Kelainan lain seperti pada anus, tulang atau jantung dapat terdeteksi dalam pemeriksaan
fisik tetapi dapat pula tidak sehingga memerlukan perhatian dan pemeriksaan yang teliti.
Apabila timbul kecurigaan adanya AE/TEF segera dilakukan pemasangan selang

nasogastrik yang radioopaque dengan ukuran 8 F (untuk bayi prematur) atau 10 F (untuk
bayi yang matur) melalui hidung menuju lambung. Pada penderita AE/TEF, selang tersebut
akan berhenti setelah masuk 10-12 cm.
Pemeriksaan Penunjang : foto polos thoraks AP/lateral dan abdomen dapat menunjukkan
selang nasogastrik yang melingkar di kantong atas esofagus. Jika AE dengan TEF akan
tampak gaster dan usus yang terisi udara di bagian bawah diafragma. Terkadang selang
nasogastrik dapat menggulung di dalam esophagus proksimal. Foto toraks juga
memberikan informasi mengenai bayangan jantung, lokasi arkus aorta, anomali dari
vertebra atau tulang kosta serta adanya infiltrat pada paru-paru.
CT scan beresolusi tinggi merupakan modalitas non-invasif alternatif. Diagnosis AE dengan

CT-scan 3D sangatlah berguna, dengan tingkat sensitivitas dan spesifitas sebesar 100%.
MRI prenatal memungkinkan visualisasi seluruh lesi dan hubungan anatominya. MRI fetus
terbukti akurat menetapkan diagnosis prenatal AE dengan atau tanpa TEF pada bayi
berisiko tinggi berdasarkan temuan USG. Namun, MRI fetus tidak akurat pada kasus
polihidramnion.
Berdasarkan klasifikasi Waterston, evaluasi faktor risiko akan mampu memprediksi hasil
dan menentukan waktu yang tepat untuk pembedahan. Tiga faktor utama yang
dipertimbangkan antara lain berat badan lahir, adanya kelainan kongenital, dan pneumonia.
Bayi dengan berat lahir kurang dari 1.500 gram dan disertai penyakit jantung bawaan
diprediksikan akan meningkatkan tingkat morbiditas dan mortalitas secara signifikan.
Klasifikasi Waterston
Category Weight/Comorbidities Surgical Timing
A > 2.500 gram Can undergo surgery
B 1.800-2.500 gram or pneumonia or Short-term delay, needs stabilizing

congenital anomaly treatment before surgery
C < 1.800 gram or Requires staged repair
severe pneumonia or congenital
anomaly
Penanganan Awal
Sebagai penatalaksanaan preoperasi, daerah faring dan mulut harus dibersihkan dan
selang nasogastrik 8 F dipasang agar dapat dilakukan pengisapan secara teratur. Kepala
bayi harus dievaluasikan dengan posisi setengah duduk sebab aspirasi cairan lambung
lebih berbahaya dibandingkan dengan saliva sedangkan bayi dengan AE murni diletakkan
dengan kepala lebih rendah (posisi Trendelenberg). Pemasangan akses vena harus
dilakukan untuk memberikan nutrisi, cairan dan elektrolit. Terapi oksigen diberikan untuk
menjaga agar saturasi oksigen tetap normal. Apabila bayi mengalami distress pernafasan
perlu diberikan perhatian khusus, seperti intubasi endotrakeal atau ventilasi mekanik.
Ventilasi dengan bag dan masker tidak dianjurkan karena dapat menyebabkan distensi
lambung akut yang membutuhkan gastrostomi segera. Pemantauan tekanan
intraabdomen yang meningkat akibat udara juga perlu dilakukan. Apabila dicurigai adanya
sepsis atau infeksi paru, perlu diberikan antibiotika spektrum luas (ampisilin dan gentamisin)
yang telah terbukti secara empiris sebagai profilaksis karena tingginya risiko terjadinya
aspirasi. Bayi harus dirujuk ke pusat kesehatan yang mempunyai unit perawatan intensif
untuk neonatus dan diletakkan pada inkubator dan terus dipantau tanda vitalnya.
Sebelum koreksi bedah, bayi harus dievaluasi dengan teliti terhadap adanya kelainan lain
misalnya dengan pemeriksaan foto thorak untuk mengevaluasi kelainan pada tulang,
jantung, atau pneumonia serta EKG untuk mencari kelainan jantung. Pemberian terapi
untuk kelainan lain yang ada, seperti hipoglikemi, hiperbilirubinemia dan pnemonia harus
diberikan. Bila terjadi atelektasis yang persisten yang umumnya terjadi di lobus kanan atas,
perlu dilakukan penghisapan dengan laringoskopik direk. Gastrostomi untuk dekompresi
dari lambung dilakukan untuk penderita dengan pneumonia dan atelektasis untuk
mencegah refluks isi lambung melalui fistula ke dalam trakea.
Tindakan Pembedahan
Tindakan pembedahan merupakan terapi definitif untuk atresia esofagus. Pada umumnya
tindakan pembedahan dilakukan dalam jangka waktu 24-72 jam pada neonatus yang
sehat. Hal ini termasuk tindakan penyelamatan hidup (life threatening) yang memerlukan
penanganan segera karena bahaya masuknya saliva dan sekresi gaster ke paru-paru
melalui fistula serta ketidakmampuan untuk makan dan minum per oral.
Tindakan pembedahan primer meliputi isolasi dan ligasi fistula yang diikuti oleh
anastomosis primer esofagus yang dilakukan dengan pembiusan umum. Pada kondisi
yang berbeda dimana esofagus bagian atas terlalu pendek dan terdapat jarak yang cukup
jauh antara ujung esofagus bagian atas dan bawah, tindakan pembedahan rekonstruksi
tidak dapat dilakukan segera, namun asupan nutrisi harus tetap diberikan untuk
pertumbuhan bayi. Untuk kasus ini, pilihannya adalah dilakukan gastrostomi, yaitu saluran
yang langsung menuju lambung untuk pemberian nutrisi.
Prognosis
Prognosis menjadi lebih buruk apabila diagnosis terlambat ditegakkan akibat penyulit pada
paru. Keberhasilan pembedahan tergantung pada beberapa faktor risiko antara lain berat
badan bayi lahir, ada atau tidaknya komplikasi pneumonia dan kelainan kongenital lainnya
yang menyertai. Prognosis jangka panjang lainnya tergantung pada ada tidaknya kelainan
bawaan lain yang mungkin multipel.
Kriteria menurut Spitz dipakai untuk menentukan prognosis bayi dengan TEF berdasarkan
berat badan lahir dan keberadaan penyakit jantung kongenital.
Klasifikasi Spitz
Group Features Survival,
%
I Birth weight >1,500 gram; no major cardiac 98,5
anomaly
II Birth weight <1,500 gram or major cardiac anomaly 82
III Birth weight <1,500 gram and major cardiac 50
anomaly
4. PENYAKIT HIRSCHSPRUNG’S
Penyakit Hirschsprung’s (Megakolon Kongenital) adalah suatu kelainan kongenital dengan
karakteristik tidak terdapatnya sel ganglion pada pleksus myenterik Auerbach, submukosa
dalam pleksus Henle dan submukosa pleksus Meissner pada kolon distal. Sehingga
menyebabkan terakumulasinya feses dan dilatasi kolon yang masif.
Penyakit Hirschsprung’s terjadi akibat tidak adanya sel ganglion di dinding usus (dari anus
sampai ke proximal dengan derajat yang bervariasi). Segmen Aganglion yang ada di recto
sigmoid terjadi pada 75 % pasien, 10 % pada seluruh colon. Total Aganglion bowel disease
sangatlah jarang terjadi.
Penyakit Hirschsprung’s dikategorikan berdasarkan seberapa banyak kolon yang terkena.

Tipe penyakit Hirschsprung’s meliputi:
 Ultra short segment: Ganglion tidak ada pada bagian yang sangat kecil dari rectum.
 Short segment: Ganglion tidak ada pada rectum dan sebagian kecil dari colon.
 Long segment: Ganglion tidak ada pada rectum dan sebagian besar colon.
 Very long segment: Ganglion tidak ada pada seluruh colon dan rectum dan kadang
sampai sebagian usus kecil.
Diagnosis
Diagnosis penyakit ini dapat dibuat berdasarkan adanya konstipasi pada neonatus. Gejala
konstipasi yang sering ditemukan adalah terlambatnya mekonium untuk dikeluarkan dalam
waktu 48 jam setelah lahir. Tetapi gejala ini biasanya ditemukan pada 6% atau 42% pasien.
Gejala lain yang biasanya terjadi adalah distensi abdomen, gangguan pasase usus, poor
feeding, vomiting. Apabila penyakit ini terjadi pada neonatus yang berusia lebih tua maka
akan didapatkan kegagalan pertumbuhan.
Hal lain yang harus diperhatikan adalah jika didapatkan periode konstipasi pada neonatus
yang diikuti periode diare yang massif kita harus mencurigai adanya enterokolitis. Pada bayi
yang lebih tua penyakit hirschsprung’s akan sulit dibedakan dengan kronik konstipasi dan
enkoperesis. Faktor genetik adalah faktor yang harus diperhatikan pada semua kasus.
Pemeriksaan barium enema akan sangat membantu dalam menegakkan diagnosis. Akan
tetapi apabila barium enema dilakukan pada hari atau minggu awal kelahiran maka zone
transisi akan sulit ditemukan. Penyakit hirschsprung’s klasik ditandai dengan adanya
gambaran spastik pada segmen distal intestinal dan dilatasi pada bagian proksimal
intestinal.
Gambaran klinis
Gambaran klinis penyakit Hirschsprung’s dapat dibedakan berdasarkan usia . Pada
neonatus ada trias gejala klinis yang sering dijumpai, yakni pengeluaran mekonium yang
terlambat, muntah hijau dan distensi abdomen. Pengeluaran mekonium yang terlambat
(lebih dari 24 jam pertama) merupakan tanda klinis yang signifikan. Muntah hijau dan
distensi abdomen biasanya dapat berkurang apabila mekonium dapat dikeluarkan segera.
Sedangkan enterokolitis merupakan ancaman komplikasi yang serius bagi penderita
penyakit Hirschsprung’s . Gejalanya berupa diare, distensi abdomen, feces berbau busuk
dan disertai demam.
Pada anak yang lebih besar, gejala klinis yang menonjol adalah konstipasi kronis dan gizi
buruk (failure to thrive). Dapat pula terlihat gerakan peristaltik usus di dinding abdomen.
Jika dilakukan pemeriksaan colok dubur, maka feces biasanya keluar menyemprot,
konsistensi semi-liquid dan berbau tidak sedap. Penderita biasanya buang air besar tidak
teratur, sekali dalam beberapa hari dan biasanya sulit untuk defekasi.
Diagnosis Banding
1. Meconium plug syndrome
2. Mekonium ileus
3. Atresia ani
4. Neuronal intestinal dysplasia
5. Konstipasi fungsional
Pemeriksaan Penunjang
Pemeriksaan radiologi merupakan pemeriksaan yang penting pada penyakit
Hirschsprung’s. Pada foto polos abdomen dapat dijumpai gambaran obstruksi usus letak
rendah, meski pada bayi sulit untuk membedakan usus halus dan usus besar. Pemeriksaan
yang merupakan standar dalam menegakkan diagnosis Hirschsprung’s adalah barium
enema, yakni akan dijumpai 3 tanda khas.
1. Tampak daerah penyempitan di bagian rektum ke proksimal yang panjangnya
bervariasi.
2. Terdapat daerah transisi, terlihat di proksimal daerah penyempitan ke arah daerah
dilatasi
3. Terdapat daerah pelebaran lumen di proksimal daerah transisi.
Apabila dari foto barium enema tidak terlihat tanda-tanda khas penyakit Hirschsprung’s,
maka dapat dilanjutkan dengan foto retensi barium, yakni foto setelah 24-48 jam barium
dibiarkan membaur dengan feces.
Biopsi rektal merupakan "gold standard" untuk mendiagnosis penyakit hirschsprung’s

Pada bayi baru lahir metode ini dapat dilakukan dengan morbiditas minimal karena
menggunakan suction khusus untuk biopsy rektum.
Pemeriksaan manometri anorektal adalah suatu pemeriksaan objektif mempelajari fungsi

fisiologi defekasi pada penyakit yang melibatkan spinkter anorektal. Dalam prakteknya,
manometri anorektal dilaksanakan apabila hasil pemeriksaan klinis, radiologis dan
histologis meragukan.
Penatalaksanaan
Terapi terbaik pada bayi dan anak dengan penyakit Hirschsprung’s tergantung dari
diagnosis yang tepat dan penanganan yang cepat. Keputusan untuk melakukan
pulltrough ketika diagnosis ditegakkan tergantung dari kondisi anak dan respon dari
terapi awal. Dekompresi kolon dengan pipa besar, diikuti dengan washout serial, dan
meninggalkan kateter pada rektum harus dilakukan. Antibiotik spektrum luas diberikan,
dan mengkoreksi hemodinamik dengan cairan intravena.
Tindakan bedah sementara pada penderita penyakit Hirschsprung’s adalah berupa

kolostomi pada usus yang memiliki ganglion normal paling distal. Tindakan ini bertujuan
menghilangkan obstruksi usus dan mencegah enterokolitis sebagai salah satu
komplikasi yang berbahaya.
Dalam beberapa tahun terakhir sudah terbukti bahwa prosedur pull-through primer dapat
dilakukan secara aman bahkan pada periode neonatus. Pendekatan ini mengikuti prinsip
terapi yang sama seperti pada prosedur bertingkat melindungi pasien dari prosedur
pembedahan tambahan. Banyak dokter bedah melakukan diseksi intra abdominal
menggunakan laparoskopi. Terapi definitif yang umum dilakukan pada penyakit
Hirschsprung’s meliputi:
1. Prosedur Swenson
2. Prosedur Duhamel
3. Prosedur Soave
4. Prosedur Rehbein
5. Prosedur Trans Anal Endorectal Pull-Through ( TEPT)
Komplikasi
Secara garis besar, komplikasi pasca tindakan bedah penyakit Hirschsprung’s dapat
digolongkan atas kebocoran anastomose, stenosis, enterokolitis dan gangguan fungsi
spinkter. Sedangkan tujuan utama dari setiap operasi definitif pull-through adalah
menyelesaikan secara tuntas penyakit Hirschsprung’s, dimana penderita mampu
menguasai dengan baik fungsi spinkter ani dan kontinen.
4. INTUSSUSEPSI
Intusssusepsi adalah masuknya segmen usus proksimal ke segmen usus bagian distal
terutama ileum terminalis ke kolon, tanpa menyingkirkan kemungkinan masuknya
segmen usus halus ke usus halus atau kolon ke kolon dengan manifestasi klinis
gambaran obstruksi dan strangulasi intestinalis.
Berdasarkan penyebab terjadinya intussusepsi maka patofisiologinya terdiri atas:

 Intussusepsi idiopatik
 Intussusepsi dengan “lead point”
 Intussusepsi pasca bedah abdomen dan torak terjadi sebagai akibat gangguan
motilitas saluran pencernaan walaupun tidak ditemukan adanya lead point.
Gejala klinis :
Intussusepsi idiopatis merupakan kelainan paling sering ditemukan pada bayi usia 6-8 bulan
(sekitar 50-85% kasus). Sedangkan intussusepsi dengan lead point dapat terjadi pada
semua usia. Intussusepsi khas didapatkan pada bayi sehat dengan gizi baik, terdapat
riwayat gastroenteritis dan atau infeksi saluran nafas sebelumnya. Nyeri sistemik intermitten
merupakan gejala paling sering menyebabkan bayi dibawa ke dokter. Dapat terlihat pada
saat serangan bayi menangis sambil kakinya ditarik, wajahnya pucat seperti dalam keadaan
sakit berat dan keadaan ini dapat berlangsung sekitar 20 detik selanjutnya bayi terlihat
normal kembali. Serangan dan gambaran seperti ini dapat terulang lagi dengan interval
waktu 1 sampai 2 jam. Muntah ditemukan pada 90% bayi dengan intussusepsi dan
kadangkala juga terlihat dehidrasi. Distensi abdomen kadangkala terlihat pada kasus
intussusepsi lanjut atau telah terdapat komplikasi seperti perforasi usus. Keluhan defekasi
berdarah yang khas “ Current jelly stool” didapat kan pada 50% kasus intussusepsi. Pada
perabaan dinding abdomen yang masih lembut umumnya dapat diraba massa berbentuk
sosis pada kwadran kanan atas dan ditemukan pada hampir sebagian besar pasien
intussusepsi yang datang lebih awal. Pemeriksaan rektum kadang-kadang dapat diraba
pseudoportio dari ujung distal intussuseptum dan pada sarung tangan terdapat darah dan
atau lendir. Intussusepsi lanjut dapat juga terlihat prolaps intussuseptum melalui anus
sehingga seringkali sulit dibedakan dengan prolaps mukosa rektum.
Intussusepsi pada anak lebih besar sulit dibedakan secara klinis dengan obstruksi usus
mekanis oleh penyebab lainnya sehingga dibutuhkan pemeriksaan penunjang medis seperti
radiologi, laboratorium. Intussusepsi pasca bedah abdomen dan toraks umumnya terjadi
pada hari ke 2 sampai ke 5 setelah pembedahan. Umumnya tanpa keluhan nyeri, yang
terlihat adanya peningkatan produksi cairan lambung yang berwarna seperti empedu.
Kondisi pasien secara umum lebih memburuk.
Pemeriksaan Penunjang :
1. Pemeriksaan laboratorium akan didapatkan gambaran leukositosis (>20.000
mm3) dan pergeseran sel ke kiri (shift to the left).
2. Pemeriksaan radiologis dengan foto polos abdomen posisi AP tegak dianjurkan
jika gejala klinis belum mendukung karena fase awal akan terlihat gambaran
distribusi udara dalam usus lebih banyak pada sisi kiri abdomen sedangkan
gambaran udara usus sisi abdomen kanan menghilang.
3. Pemeriksaan dengan kontras enema barium dapat dilakukan pada kasus tanpa
komplikasi atau gejala klinis belum jelas. Gambaran kontras akan memperlihatkan
adanya “cupping” seperti gambaran huruf “U” terbalik didaerah intussusepsi dan
intussuseptum dari kolon.
Diagnosis intussusepsi ditegakkan secara klinis dengan riwayat adanya currant jelly’s stool
dan teraba massa berbentuk sosis pada abdomen dan perabaan melalui pemeriksaan
rectum teraba massa seperti pseudo portio.
Pengelolaan intususepsi dapat non operatif dan operatif. Penanganan non operatif dengan
reposisi intussusepsi dengan tekanan hidrostatis (enema barium) umumnya berhasil pada
intussusepsi idiopatik jika dikerjakan pada tahap awal terjadinya intussusepsi sedangkan
intussusepsi dengan lead point tidak akan memberikan hasil bahkan membahayakan akan
terjadinya perforasi.
5. HERNIA INGUINALIS LATERALIS INKARSERATA
Hernia inguinalis lateralis inkarserata adalah masuknya isi abdomen kedalam kantong
peritoneum melalui processus vaginalis persisten kemudian terjepit pada annulus internus
kanalis inguinalis sehingga isi kantong tersebut tidak dapat kembali ke dalam rongga
abdomen.
Diagnosis hernia inguinalis lateralis inkarserata ditegakkan bila terdapat riwayat adanya
benjolan yang timbul hilang didaerah inguinal, secara tiba-tiba benjolan didaerah inguinal
menetap dan memberikan gejala / keluhan nyeri hebat atau menyebabkan anak/bayi rewel
dan menangis terus menerus disertai dengan muntah-muntah. Pemeriksaan fisik didaerah
inguinal ditemukan benjolan yang keras dan menetap serta didapatkan tanda-tanda
obstruksi intestinalis pada pemeriksaan abdomen.
Penanganan Hernia Inguinalis Lateralis yang mengalami inkarserata adalah dengan

melakukan intestinal dekompresi, pemberian cairan intra vena dan pemberian sedative dan
analgetika. Reposisi manual dapat dilakukan dengan cara menekan benjolan hernia secara
perlahan-lahan pada saat pasien telah tertidur nyenyak. Jika reposisi berhasil pasien
dirawat dengan pengawasan ketat untuk pembedahan berencana 48 jam berikutnya. Jika
reposisi gagal pembedahan dilakukan untuk melepaskan jepitan pada isi kantong hernia.
6. APPENDISITIS AKUT PADA ANAK

Apendisitis akut adalah peradangan pada apendiks vermiformis. Peradangan yang progresif
dari apendiks vermiformis diawali dengan terjadinya obstruksi lumen dan kemudian
mengalami gangrene dan perforasi. Obstruksi lumen apendiks vermiformis sebagai awal
dari proses peradangan (imflamasi) dapat terjadi karena adanya fekolit (feses yang
mengeras) dan atau hiperflasi jaringan limfoid dinding apendiks vermiformis akibat infeksi
virus.
Sekresi yang terus menerus mukosa apendiks menyebabkan terjadinya timbunan cairan
dalam lumen sehingga dinding apendik menipis menyebabkan gangguan vaskularisasi
dengan segala konsekwensinya. Peradangan apendik tanpa obstruksi dapat juga terjadi
namun dapat menghilang secara spontan tanpa perlu terapi.
Invasi bakteri aeorob dan anaeorob yang normal ada dalam lumen apendiks akan
memperberat proses peradangan dan terbentuknya pus. Escheria coli dan bacteriodes
merupakan kuman yang didapatkan dalam biakan. Selanjutnya mukosa apendik mengalami
ulserasi sehingga pus masuk ke lapisan serosa membentuk fibrinofuluren exudat. Akibat
gangguan vaskularisasi, apendik mengalami gangrene sampai perforasi.
Mikro perforasi apendik menimbulkan iritasi lokal peritoneum sekitarnya sehingga terjadi
peritonitis lokal dan atau pengumpulan pus disekitar apendik (peri apendiks abses). Pada
anak-anak kemampuan omentum dan usus dalam melokalisir exudat yang keluar dari
perforasi dinding apendik, kurang sehingga mempermudah terjadinya peritonitis umum
dengan segala manifestasi klinisnya.
Apendisitis akut memberikan gejala yang khas berupa nyeri perut daerah periumbilikus
akibat distensi apendiks vermiformis selanjutnya nyeri perut berpindah kedaerah kwadran
kanan bawah abdomen ( Mc Burney) sebagai manifestasi adanya iritasi lokal peritoneum
oleh exudat yang ada pada lapisan serosa dinding apendik atau karena mikroperforasi
yang terjadi. Mual dan muntah terjadi setelah timbul gejala nyeri perut, seringkali sulit
dibedakan dengan gejala gastroenteritis, kadang-kadang anak lebih besar terdapat gejala
anoreksia sehingga semakin menyulitkan diagnosis.
Pemeriksaan fisik akan mendapatkan anak yang tiba-tiba mengalami sakit, wajah nampak
pucat, agak sulit berjalan dan tungkai kanan terlihat fleksi pada saat tiduran, bibir terlihat
kering, pipi kemerahan, anak mengalami demam dengan suhu axilla diatas 38 derajat
celcius, tetapi jika suhu tinggi perlu dibedakan antara apendisitis perforasi dengan
kemungkinan penyebab lain. Pemeriksaan palpasi abdomen ditemukan titik nyeri daerah
“Mc Burney’s” terutama pada apendisitis akut. Spasme otot-otot abdomen kwadran kanan
bawah terjadi karena iritasi peritoneum dibawahnya, kadang-kadang disertai dengan tanda-
tanda “rebound tenderness regiditas” dinding abdomen muncul jika telah terjadi perforasi
apendiks. Obturator dan psoas sign sebagai petunjuk lain terdapat proses keradangan
didaerah posterior lokasi apendiks namun jarang ditemukan pada anak-anak. Pemeriksaan
rektum dilakukan jika penemuan gejala seperti diatas masih belum dapat membantu
diagnosis apendisitis, pada pemeriksaan ini akan ditemukan tenderness kearah kanan
dinding rectum, kadangkala dapat diraba adanya massa atau pembentukan abses.
Gejala klinis seperti tersebut diatas hanya ditemukan pada setengah kasus apendisitis akut
anak-anak. Beberapa kasus memberikan gejala nyeri perut ringan kemudian menjadi
progresif secara lambat, namun seringkali kasus tidak sampai menimbulkan perforasi. Nyeri
perut kanan bawah seringkali tanpa didahului nyeri periumbilikus sehingga agak sulit
menentukan secara pasti kelainan di apendik. Tidak jarang anak tanpa memperlihatkan
gejala demam, demikian pula apendisitis retrorektal atau pelvinal gejala abdomen minimal
sekali dan hanya dengan pemeriksaan rectum dapat ditemukan adanya tanda-tanda iritasi
peritoneum dan pembentukan abses.
Beberapa kasus memperlihatkan gejala peritonitis umum yang lebih menonjol akibat
terjadinya perforasi dan pembentukan abses. Anak terlihat sakit berat, demam tinggi
abdomen distensi dan tegang. Pada pemeriksaan abdomen terdapat nyeri perut yang
menyeluruh dan seluruh dinding abdomen mengalami rigiditas, jika abses terlokalisir dalam
rongga peritoneum maka gejala klinis yang terlihat dan ditemukan minimal hanya teraba
massa dengan palpasi bimanual dari dinding abdomen dan pemeriksaan rectum.
Pemeriksaan laboratorium umumnya ditemukan leukolsitosis (11.000-15.000 mm3) dengan

pergeseran sel kekiri namun demikian hasil pemeriksaan leukosit normal dapat ditemukan
pada anak dengan apendisitis, sedangkan jika hasil pemeriksaan leukosit mencapai
20.000mm3 dengan gejala klinis minimal untuk apendisitis kemungkinan disebabkan
keadaan lain. Perlu diperiksa jika terdapat gejala klinis yang sulit dibedakan dengan infeksi
saluran kencing. Umumnya hasil pemeriksaan urine normal pada apendisitis pada
beberapa kasus apendisitis dapat ditemukan sel darah merah dan atau sel darah putih
pada sedimen urine.
Untuk gejala apendisitis tertentu membutuhkan pemeriksaan radiologi dan atau ultrasound
(USG). Foto polos abdomen akan memperlihatkan gambaran mass effect akibat hilangnya
gambaran gas di daerah abdomen kanan bawah, ditemukan pada 10% kasus dapat terlihat
gambaran fekolit (feses yang mengeras sebagai penyebab sumbatan obstruksi lumen
apendiks). Ultrasound/USG dapat terlihat ukuran apendiks lebih besar dari normal disertai
gambaran abses periapendikuler atau tumpukan abses di daerah rongga pelvis.
Pemeriksaan ini dapat dikerjakan rutin pada anak dengan gejala klinis minimal atau anak
yang gemuk. Enema barium perlu dikerjakan pada anak dengan nyeri perut berulang tanpa
gejala penyerta yang jelas. Tanda-tanda apendisitis akut akan terlihat gambaran barium
yang menunjukkan penyempitan lumen apendiks dan tiba-tiba terhenti (cut off) akibat
adanya obstruksi.
Apendisitis akut dapat ditegakkan diagnosisnya dengan gejala klinis saja terutama yang
memperlihatkan gejala klinis klasik. Pemeriksaan penunjang laboratorium untuk
menemukan adanya tanda-tanda infeksi akut dalam darah (leukosit dan pergeseran sel ke
kiri). Apendisitis dan gejala klinis yang tidak jelas atau minimal membutuhkan pemeriksaan
penunjang radiology dan ultrasound (USG) bahkan CT-Scann abdomen. Setelah diagnosis
ditegakkan pembedahan untuk apendiktomi harus segera dilakukan.
7. Omphalocele pecah dan Gastroschisis

Omphalocele :
Defek dinding abdomen di daerah tali pusar karena gangguan penutupan secara kongenital
pada janin usia 8 minggu di dalam kandungan, sehingga isi rongga abdomen seperti hepar
dan usus halus berada diluar rongga abdomen, hanya di tutupi lapisan peritoneum, dengan
besar defek berkisar antara 2-15 cm.
Gastroschisis :
Kegagalan penutupan dinding abdomen secara kongenital di sekitar umbilicus (umumnya di

sebelah kanan umbilicus), sehingga usus halus dan atau sebagian kolon berada di luar
rongga abdomen (jarang ditemukan hepar atau lien) tanpa ditutupi oleh peritoneum atau
lapisan dinding abdomen lainnya, dengan lebar defek umumnya kurang dari 5 cm.
Secara bersamaan omphalocele dan gastoschisis dapat disertai kelainan lain seperti :
1. Exstrophy cloaca :
Omphalocele disertai agenesis hindgut, imperforasi anus, exstrophy vesika urinaria,
dan vesikointestinal fistula.
2. Pentalogy Cantrell :
Omphalocele epigastrium, celah sternum, kelainan jantung kongenital, tidak
terbentuknya diafragma sentral dan pericardium.
Pengelolaan penderita dengan gastrosciziz dan omphalokel pecah meliputi pemberian

cairan intravena sesuai kebutuhan, pemasangan nasogastric tube 10-12, pemberian
antibiotik spectrum luas sesuai kebutuhan, bungkus isi rongga abdomen yang berada di
luar dengan kasa atau bahan steril dan dibasuhi dengan NaCl hangat (cairan fasiologis)
dan tempatkan bayi dalam inkubator untuk mempertahankan suhu bayi optimal.
Terapi pembedahan pada penderita gastrosciziz dan omphalokel bisa melalui prosedur satu
tahap (one stage) maupun bertahap (multistage repair) tergantung kondisi penderita dan
kondisi usus saat pertama kali datang ke rumah sakit.
Daftar Pustaka
1. Chirdan LB, Ameh EA, Thomas AH. Infantile Hypertropic Pyloric Stenosis. J Pediatric
Surgeon; 2008: 43: 1227-29
2. Gilchrist BF, Lessin MS,2010. chapter 29 : Lesion of the stomach, In Ashcraft Pediatric
Surgery 5th edition. Saunders Company. Philadelphia, p: 405- 414.
3. Holschneider A., Ure B.M., 2010. Chapter 35: Hirschsprung's Disease in: Ashcraft
Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 456-67.
4. Hackam D.J., Newman K., Ford H.R. 2005. Chapter 38: Pediatric Surgery in: Schwartz's
Principles of Surgery. 8th edition. McGraw-Hill. New York, p: 1496-8.
5. Ziegler M.M., Azizkhan R.G., Weber T.R. 2003. Chapter 56: Hirschsprung Disease In:
Operative Pediatric Surgery. McGraw-Hill. New York, p: 617-40.
6. Puri P. 2009. Chapter 26: Hirschsprung's Disease in: Springer Pediatric Surgery 3rd
edition. Saunders Company. Philadelphia, p: 275-83.
7. Leonidas J.C., Singh S.P., Slovis T.L. 2004. Chapter 4 Congenital Anomalies of The
Gastrointestinal Tract In: Caffey's Pediatric Diagnostic Imaging 10l edition. Elsevier-
Mosby. Philadelphia, p: 148-53.
8. Kartono D. Penyakit Hirschsprung. Sagung Seto. Jakarta. 2004.
9. Aresman R.M, Bambini D.A, 2010 . Congenital Diafragmatic Hernia and Eventeration.
In: Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 304-319..
10. ElisabethM, Janine f, Annelies K, Dick T. Etiology of Esophageal Atresia and Tracheo
esophageal fistula, Curr Gastroenterology Rep. 12 , 2010 : 215-222
11. Spitz L, 2010. Esophageal Atresia and tracheoesophageal Malformation, In Ashcraft
12. Morrow SE, Newman KD, 2010. Appendicitis, In Ashcraft Pediatric Surgery 5th edition.
Saunders Company. Philadelphia, p: 577-584.
13. Weber TR, Tracy TF, Keller MS,2010. Groin Hernia and Hydroceles, In Ashcraft
14. Fallat ME, 2010. Intussusception, In Ashcraft Pediatric Surgery 5th edition. Saunders
Company. Philadelphia, p: 533-542.
15. Klein MD,2010. Congenital Abdominal Wall Defects, In Ashcraft Pediatric Surgery 5th
edition. Saunders Company. Philadelphia, p: 659-668.
Lecture 21
Traumatic Brain Injury Resuscitation
I Pt Pramana Suarjaya/ IB Krisna Jaya Sutawan
Learning Obyektif
1. To describe Traumatic Brain Injury (TBI)
2. To implement Glasgow Coma Scale to classiflying severity of TBI
3. To implement initial brain recucitation
a. Primary survey
i. Airway
ii. Breathing/Ventilation
iii. Circulation
iv. Disability
v. Exposure
b. Secondary survey
4. To describe management of elevated ICP
Abstract
Traumatic Brain Injury (TBI)
TBI is a nondegenerative, noncongenital insults to the brain from external mechanical force,
possibly leading to permanent or temporary impairment of cognitive, physical, and
psychosocial functions, with an associated diminished or altered state of consciousness.
TBI from trauma results from two distinct processes: primary injury and secondary injury.
Primary injury is the damage produced by the direct mechanical impact and the
acceleration-deceleration stress onto the skull and the brain tissue, which results in skull
fractures and intracranial lesions. The intracranial lesions are further classified into two
types: diffuse injury and focal injury.
1. Diffuse brain injury
a. Brain concussion : loss of consciousness lasting < 6 hours
b. Diffuse axonal injury : traumatic coma lasting > 6 hours
2. Focal brain injury
a. Brain contusion
b. Epidural hematoma (EDH)
c. Subdural hematoma (SDH)
d. Intracerebral hematoma (ICH)
Secondary injury develop within minutes, hours or days of the initial injury and cause further
damage to nervous tissue. The common denominators of secondary injury are cerebral
hypoxia and ischemia. Secondary injuries are caused by the following disorders:
1. Respiratory dysfunction: hypoxemia, hypercapnia
2. Cardiovascular instability: hypotension, low cardiac output (CO)
3. Elevation of ICP
4. Metabolic derangements
Glasgow Coma Scale (GCS) to classifying severity of TBI

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

4 years to Adult Child < 4 years Infant
Eye Opening
4 Spontaneous Spontaneous Spontaneous
3 To speech To speech To speech
2 To pain To Pain To Pain
1 No respon No respon No respon
Verbal
response
5 Alert and oriented Oriented, social, coos, babbles
speaks, interacts
4 Disoriented Confused speech, Irritable cry
disoriented,
consolable, aware
3 speaking but Inappropriate cries to pain
nonsensical words,inconsolable,
unaware
2 Moan or unintelligible Incomprehensible, Moans to pain
sounds agitated, restless,
unaware
1 No response No response No response
Motor response
6 Follows commands Normal, spontaneous Normal, spontaneous
movements movements
5 Localizes pain Localizes pain withdraws to touch
4 Moves or withdraws to Withdraws to pain withdraws to pain
pain
3 Decorticate flexion Decoritcate flexion Decorticate flexion
2 Decerebrate extension Decerebrate decerbrate extension
extension
1 No response No response No response
Initial Brain Resuscitation

Patients who have TBI should be either treated at a designated trauma center that has
neurosurgical coverage or transferred to such a center after initial stabilization. The prompt
assessment and management of TBI begin with the treatment of associated injuries that
may cause hypoxia, hypoventilation and shock. This is best accomplished using a
systematic approach such as the Advanced Trauma Life Support (ATLS) Algorithm, which
consists of primary and secondary surveys.
1. Primary Survey
A brief history is obatained according to the AMPLE mnemonic (Allergies, Medications, Past
medical history, Last meal, Event). Examination and immediate resuscitation are performed
according to ABCDE mnemonic (Airway, Breathing, Circulation, Disability, Exposure). Plans
for initial operative or non-operativemanagements are based on the results of the
primary and the secondary surveys.
a. Airway: in the setting of TBI, airway management is performed with
particular attention to changes in mean arterial pressure (MAP), ICP, arterial
oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2) and cervical
stability.
i. Indications for intubation include inability to protect the airway,
difficulty with oxygenation or ventilation, shock, a GCS score < 9, and
rapid neurologic deterioritation
ii. Manual inline stabilization (MILS)
iii. Rapid squence induction (RSI)
iv. Induction agent that can be used are propofol, thiopental and
etomidate.
v. Several neuromuscular blocking drugs are appropriate for TBI such
as succinylcholine, rocuronium and mivacurium.
vi. As with all intubations, airway manager should consider awake-
topical intubation if they are uncertain about their ability to establish
an airway quickly and safely.
vii. Lidocaine IV
viii. Laryngeal mask airway (LMA) devices are useful backup tools for
ventilation and intubation. Surgical airway techniques, such as
cricothyroidotomy and tracheostomy are also backup methods for
intubation.
ix. Endotracheal intubation must be confirmed by physical examinaton
plus a method for CO2 detection such as colorimetric or continous
capnography.
x. Chest x-ray are useful for verification of endotracheal tube positionas
well as identificationof associated chest pathology such as
pneumothorax, lung contusion, and pulmonary edema.
b. Breathing/ventilation
i. High-flow oxygen is provided as supplement to all patients before
intubation to prevent hypoxia and provide sufficient apneic time in
case further RSI is needed.
ii. Oxygen saturation should be maintained above level now concidered
acceptable for patients who have acute respiratory distress syndome.
iii. Positive-pressure ventilation is provided as needed to maintain
adequate ventilation and oxygenation.
iv. The PaCO2 should be kept at normocarbia
v. Sedation : The ideal sedative drug in TBI should have rapid onset and
offset, anticonvulsant properties, and favorable effects on CPP.
vi. Analgesia and blunting of stimulation associated with the
endotracheal tube can be achieved with opioids
c. Circulation: Systemic hypotension is one of the major contributor to poor
outcome after TBI. When necessary, fluid resuscitation is initiated
immediately, inotropic and vasopressor drugs are administered as required to
stabilize the blood pressure (BP) at or above 90 mmHg.
i. Life-threatening cardiogenic shock as from tension pneumothorax and
cardiac tamponade is identified and either controlled or treated
definitively.
ii. Hypovolemic shock should be resuscitated.
iii. Total osmolality is the most important factor in determining brain
edema formation.
iv. Patient who have a low hematocrit may require a tranfusion.
v. Glucose-containing solutions are avoided.
vi. Inotropes and vasopressors. If the BP and cardiac output (CO) cannot
be restored through fluid resuscitation, the administration of
intravenous inotropic and vasopressor drugs may be necessary. An
infusion of either phenylephrine or dopamine is recommended to
maintain the CPP above 60 mmHg.
d. Disability : When not absolutely contraindicated by the need for immediate
endotracheal intubation, the initial neurological assessment should be
performed before the administration of sedative or neuromuscular-blocking
drugs. Neurological status is assessed by using GCS with attention to the
signs and symptoms of increased ICP and brain herniation. In addition, the
examiner notes the pupillary response and diameter, presence of lateral
deficits, and level of spinal motor and sensory deficits. Emergency therapy
for brain herniation includes reassessment and treatment of extracranial
insults such as hypoxia and shock, head elevation to 30 o, mannitol infusion,

brief hyperventilation, and surgical decompression.
e. Exposure : The patient is fully undressed and examination for any
associated
injuries while precautions are taken to avoid hypothermia.
2. Secondary survey
a. The secondary survey includes a more complete history and physical
examination as well as laboratory and ancillary testing to diagnose the extent
of TBI and associated injuries.
b. Commonly requested investigation include x-ray examination of the chest
and pelvis, complete metabolic panel, complete blood count, clotting
parameters, serum osmolarity, urinalysis, ethanol blood level.
c. Unless contraindicated by need for immediate laparotomy or other procedure
to prevent death from shock, all TBI patients should have a non-contrast
computed tomographic (CT) scan of the head and cervical spine as soon as
possible.
Management of elevated ICP

The reduction of elevated ICP and the maintenance of BP are crucial in the management of
intracranial hypertension because CPP is directly related to both MAP and ICP. ICP
monitoring is recommended in patient who have CT evidence of elevated ICP including
midline shift, effaced ventricles, compressed basal cisterns, or the presence of an
intracranial space-occupying lesion.
1. Hyperventilation: when evidence of transtentorial herniation in patients who have
severe TBI exist, hyperventilation should be instituted because hyperventilation can
reduce ICP rapidly and effectively.
2. Diuretic therapy: manitol is administered to patients in whom transtentorial herniation
is suspected. The serum osmolality is monitor frequently.
3. Posture: a head-up tilt to 10o to 30o facilitates cerebral venous and CSF drainage
and lower ICP.
4. Barbiturate: are known to exert cerebral protective and ICP-lowering effects. High
dose barbiturate therapy may considered in severely head injuries patients whose
intracranial hypertension is refractory to maximal medical and surgical ICP-lowering
therapy. However the prophylactic use of barbiturate come is not indicated.
5. Decompressive craniectomy: is an surgical advanced treatment option for ICP
control in severe TBI.
Lecture 22
Enviromental injury
Agus Roy Rusly Hariantana Hamid
A. Definisi Luka bakar

Suatu trauma panas yang disebabkan oleh air / uap panas, arus listrik, bahan kimia, radiasi
dan petir yang terutama mengenai jaringan permukaan yang menyebabkan kerusakan atau
kehilangan jaringan.
Fase Luka Bakar Fase Akut / Fase Syok Saat di tempat kejadian sampai saat penanganan
di Instalasi Gawat Darurat. Masalah yang ada pada fase ini adalah masalah penyelamatan
hidup terutama untuk pernafasan dan cairan. Disamping itu masalah perawatan luka juga
penting karena sangat mempengaruhi kondisi umum pasien dan juga penyembuhan luka.
B. Penilaian Luka Bakar. Berdasarkan:

1. Kedalaman luka bakar
a. Derajat I : epidermis
b. Derajat II : dermis, superfisial/ permukaan, dalam
c. Derajat III : seluruh tebal kulit/ lebih dalam sampai otot, tulang
Kedalaman luka bakar tergantung:
a. Tingginya panas
b. Penyebab
c. Lamanya kontak
d. Ketebalan kulit
e. Suplai darah
Derajat Kedalaman Klinis Rasa nyeri

Derajat I Hyperemis Hyper estesia
Derajat II A Bulla, merah Hyper estesia
Derajat II B Bulla, pucat Hypo estesia
Derajat III Hitam, kering An estesia
2. Luas luka bakar. Berdasarkan Rule of Nine dari Wallace
10 14 18
9 9 9 9 9 9
18 18 18 18 18 18
18 18
16 16
14 14
15 tahun 5 tahun 0 –1 tahun
Untuk luka bakar yang tersebar dalam bentuk pulau-pulau dapat dihitung dengan telapak
tangan penderita dianggap 1%.
3. Keparahan Luka Bakar

a. Luka bakar ringan
1) Luka bakar derajat II < 15%
2) Luka bakar derajat II < 10% pada anak-anak
3) Luka bakar derajat III < 1%
b. Luka bakar sedang
1) Luka bakar derajat II 15-25% pada orang dewasa
2) Luka bakar derajat II 10-20% pada anak-anak
3) Luka bakar derajat III < 10%
c. Luka bakar berat
1) Luka bakar derajat II 25% atau lebih pada orang dewasa
2) Luka bakar derajat II 20% atau lebih pada anak-anak
3) Luka bakar derajat III 10% atau lebih
4) Luka bakar mengenai tangan, wajah, telinga, mata, kaki dan genetalia/
perineum.
5) Luka bakar dengan cedera inhalasi, listrik, disertai trauma lain
4. Indikasi Rawat
a. Luka bakar sedang
b. Luka bakar Grade II
1) Dewasa >20%
2) Anak / Orang tua > 15%
c. Luka Bakar Grade III
d. Luka Bakar dengan komplikasi jantung, otak dll
5. Komplikasi
a. Gagal pernafasan
b. Syok hipovolemik
c. Gagal ginjal
Lecture 23
UROLOGYC CONCERN IN CRITICAL CARE FOR NON TRAUMA CASE
Gede Wirya Kusuma Duarsa
Objectives
1. To understand the basic principles of non trauma urologic emergency
2. Comprehend the definition, etiology, special investigation and basic management the
acute urinary retention, acute scrotum, penile emergencies, priapism, external genital
trauma, anuria, urosepsis, Fournier’s gangrene, colic, hematurisa, etc.
Abstract
The primary care physician plays a key role in the diagnosis and initial management of most
urologic emergencies. It is critical to stratify patients into those who require urgent care (eg,
phimosis, epididymitis) and those who require emergent care (eg, Fournier's gangrene,
testis torsion, anuria, ureteral or renal colic, hematuria, acute urinary retention, priapism,
external genital trauma, urosepsis, acute scrotum, etc.), because the time to therapy may
significantly impact on outcome between these two groups. Mismanagement of these
conditions may result in significant sequelae, which are preventable in most cases.
Fortunately, most urologic emergencies are precisely diagnosed with a combination of
clinical acumen and appropriate radiologic or adjunctive studies. This article reviews the
diagnosis and management of the most common urologic emergencies, and highlights
pragmatic information of use to the general practitioner
Acute urinary retention is defined as the sudden inability to void despite a distended bladder
(urine volume in the bladder more than its capacity). It is usually preceded by a history of
progressively decreasing force of stream. The most common obstructive cause of acute
urinary retention is benign prostatic hyperplasia. Prostate cancer, urethral strictures, bladder
stones or bladder tumors may also cause obstructive urinary retention, hematuria and clots
should be suspected of harboring an underlying bladder tumor. Less common obstructive
etiologies include urethral foreign bodies, penile constricting bands, and meatal stenosis.
The most common infectious cause for acute retention is acute prostatitis. Other infectious
causes of retention include urethral herpes, periurethral abscesses, and tuberculous cystitis.
There are many pharmacologic agents that may contribute to urinary retention. Neurogenic
causes of urinary retention may be broadly categorized into upper motor neuron lesions,
lower motor neuron lesions, and peripheral nerve lesions.
The initial diagnosis of the patient who presents with acute scrotal pain may be challenging.
Although testis torsion is the least common cause of the acute scrotum, it should be high in
the differential diagnosis because testicular salvage rates correlate inversely with time to
exploration. Most patients suffer from epididymitis, torsion of a testicular appendage. The
availability of more accurate radiologic imaging studies has helped to reduce the incidence
of negative scrotal explorations, but the importance of the initial evaluation and clinical
findings still remains the most powerful tool in correctly treating the acute scrotum.
Testis torsion may occur in the neonatal period secondary to lack of fixation of the tunica
vaginalis to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion has a
low salvage rate. If the tunica vaginalis inserts in an abnormally high position on the
spermatic cord (the “bell clapper deformity”), the testis may freely rotate on the cord. Testis
torsion may occur in the neonatal period secondary to lack of fixation of the tunica vaginalis
to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion has a low salvage
rate. If the tunica vaginalis inserts in an abnormally high position on the spermatic cord (the
“bell clapper deformity”), the testis may freely rotate on the cord. This is known as
“intravaginal torsion,” and testis ischemia is dependent on the number of rotations of the
cord. The spermatogenic cells are the most sensitive to ischemia, whereas the testosterone-
producing Leydig's cells are more resistant. Salvage of testicular function is close to 100% if
detorsion occurs within 6 hours of pain onset, but this drops to less than 20% beyond 12
hours. Successful treatment is time dependent in this case
Epididymitis arises from pain and swelling of the epididymis. It usually arises secondary to
infection or inflammation from the urethra or bladder. If the process remains untreated, it
may involve the adjacent testis and scrotum, and eventually result in abscess formation.
Fever and leukocytosis are present in between 30% and 50% of cases. Antibiotic treatment
for epididymitis depends on patient age and probable underlying pathogen. Neisseria
gonorrhoeae and Chlamydia trachomatis account for most cases in men under 35, and
these may be treated with intramuscular ceftriaxone plus a course of doxycycline. In men
over 35, urine culture usually reveals Escherichia coli, and treatment consists of an oral
fluoroquinolone for 21 days.
Necrotizing fasciitis of the scrotum and perineum (Fournier's gangrene) is a rare but life-
threatening cause of acute scrotal pain. It is typically found in debilitated or
immunocompromised patients with significant medical comorbidities, particularly diabetes
and alcoholism. The infection usually originates from a perianal or periurethral source, and
includes multiple pathogens, including E coli, Bacteroides, and Streptococci. Patients
present with early systemic toxicity, and genital examination typically reveals erythema,
tenderness, induration, and crepitus. The perineum may appear frankly necrotic and foul
smelling.
Phimosis results from stenosis of the distal aspect of the foreskin, preventing it from being
successfully retracted over the glans. It is a physiologic finding in uncircumcised infants, and
physiologic adhesions typically prevent complete retraction of the foreskin in this age group.
Forcible retraction of the foreskin should not be attempted because it may actually tear the
adhesions and create pathologic phimosis. Phimosis is rarely an emergent condition, but it
may rarely cause urinary retention if the foreskin has sealed off. In this case, the preputial
sac balloons out with each void. Temporary or emergent management of this condition
includes hemostat dilation of the stenotic foreskin. Topical steroids have been successful in
progressively reducing phimosis, but circumcision should be considered in chronic or
refractory cases.
Paraphimosis arises when the foreskin has been retracted proximal to the glans, and cannot
be returned to its normal position secondary to a tight, constricting ring of skin. With time,
the retracted prepuce becomes edematous because of impaired venous and lymphatic
drainage. Treatment of paraphimosis is urgent reduction of the foreskin.
Priapism is defined as a prolonged, painful erection that is unrelated to sexual arousal.

Although the corpora cavernosa are typically rigid and filled with stagnant blood, the glans
and corpus spongiosum remain flaccid. Stuttering priapism refers to recurrent painful
erections with intervening detumescence, whereas malignant priapism implies a locally
invasive malignant condition in the corpora, and is frequently a preterminal event.
Penile fracture (or rupture) implies disruption of the tunica albuginea surrounding the
corpora cavernosa. This injury typically occurs during vigorous intercourse, when the rigid
penis is misdirected against the partner's pubic bone, and results in buckling trauma. This
injury may also be self-inflicted by abrupt bending of the erect penis during masturbation.
The classic history involves the scenario described previously, with patients usually
reporting a popping sound as the tunica tears, followed by pain, swelling, and rapid
detumescence.
Blood in urine is a common symptoms in urology. There are many causes of Haematuria
including medical bleeding and surgical bleeding. Prompt diagnosis and good management
will prevent further damage or complication.
Lecture 24
UROLOGYC CONCERN IN CRITICAL CARE FOR TRAUMA CASE
Wayan Yudiana
Objectives
1. To understand the basic principle and pathophysiology of genitourinary injuries
2. To describes the clinical features and investigations of genitourinary trauma
3. To provide an appropriate management of genitourinary trauma
Abstract
Traumatic injuries to the genitourinary system are commonly divided into injuries to the
kidney, ureter, bladder, urethra and the external genitalia.
The kidneys are the most commonly injured genitourinary organs from external trauma.
Advances in radiographic staging, improvements in hemodynamic monitoring, and wider
use of angioembolization have improved the rates of renal preservation and decreased
unnecessary surgery.
Iatrogenic ureteral injury most commonly occurs during hysterectomy. An unrecognized or

mismanaged ureteral injury can lead to significant complications.
Most bladder injuries occur in association with blunt trauma. Eighty-five percent of these
injuries occur with pelvic fractures, with the remaining 15% occurring with penetrating
trauma and blunt mechanism not associated with a pelvic fracture.
Urethral injury is predominantly a male problem. Injuries to the posterior urethra are mostly
secondary to pelvic fractures, while injuries to the anterior urethra are caused by straddle-
type or penetrating injuries. Urethral injuries from trauma constitute only 10% of all GU
injuries.
Injuries to the external genitalia (ie, the penis and the scrotum) are usually secondary to
injuries caused by penetration, blunt trauma, sexual pleasure enhancing devices, and
mutilation (self-inflicted or otherwise).
The primary goal in the management of the genitourinary injuries is to preserve the maximal
amount of functional tissue while minimizing the complication. Complications can occur
because of missed urologic injury at the time of initial presentation, the nature and severity
of the injury itself, and/or inadequate or inappropriate initial management. Minimizing
delayed complication occurrence can be achieved by appropriately staging the injuries,
followed by the proper selection of surgery of expectant therapy.
LEARNING TASK FOR SGD
LEARNING TASK
HIGHLIGHT EMERGENCY MEDICINE
Case 1
There is an earthquake report in village with estimately 500 people. From the report, 12
people have been found dead, 50 people have either minor or major injury, and 120 people
have not been found. You are a head of emergency department in nearby hospital.
1. Is this a disaster? If true, what kind of disaster is it from the source of disaster?
2. How do you prepare to treat the victims of this event?
3. If you make a support area, what components should be there?
4. Specify the components that must exist in triage team
Case 2
From 50 people with injuries was found,
- 12 people complaining pain, hungry, and cold. They asked for the food
- 5 people shout loudly in pain
- 10 people are not making any sound, still breath irregulerly
- 10 people are not breathing
How do u clasify these victims? After u clasify, how do u treat them?
LEARNING TASK
PHLEGMON
1. Patient female, 28 years old, with complaints of pain in the lower chin, up to the front of
the neck feel hard when touched, fever, difficulty swallowing and difficulty breathing, the
patient appears weak. Intra-oral examination is difficult because patients with difficulty
opening the mouth, tongue looks lifted and swelling of the gums behind that cover most
of the right mandibular M3. Pain in the gums behind the perceived than 4 days ago, the
patient just gargling with warm salt water when not withstand the pain.
a. As a doctor what would you do?
b. What examinations will you do for this case?
c.What is the diagnosis?
d. What does your planning for management in this case?
2. Patient male, 38 years old, come to RSPTN with dread because of the pain that is felt in
mandibulla left with swelling to the left cheek, intra oral condition appears to exist in the
dental caries with mobillity o2 M2 residual roots on the left, buccal fold appears elevated,
palpation there is fluctuation exudate. Dental pain is felt starting from 3 days ago but
have not had time to check to the dentist, just buy painkillers to reduce the pain.
a. What you should ask to complete the anamnesis?
b. What is the diagnosis?
c. What does your planning for management in this case?
3. Patient woman, 38 years old, with complaints mandibulla swollen and hard when
touched on the lower jaw side since a few months ago, seemed teeth no complaints.
There is no pain and illness but the patient had never examined the situation to the
doctor or dentist.
a. What you should ask to complete the anamnesis?
b. What is the diagnosis?
c. What does your planning for management in this case?
Self Assassment:
1. Explain the difference between mandibulla with phlegmon abscess?
2. In addition to any abscess mandibulla differential diagnosis of phlegmon?
3. Discuss with your group the most important management of phlegmon?
LEARNING TASK
STATUS EPILEPTICUS AND OTHER SEIZURE DISORDERS
SELF ASSESSMENT
1. Able to explain the causes of “status epileptikus”
2. Able to give first aid for “status epileptikus”
3. Able to identify patient with refractory epilepsy
LEARNING TASK
COMA AND DECREASE OF CONSCIOUSNESS
SCENARIO
A 59 years old man admitted to emergency room unconsciously. From general exam there
was no history of head trauma, no fever or head stiffness. Hemodynamic with BP 110/70
mmHg, HR:100 bpm, and respiratory distress (RR:28 times/minute, Kussmaul’s type). From
neurologic exam, he came with GCS 5, bilateral fixed dilated pupil, and no sign of
lateralization. Blood serum showed high glucose value. Blood gas showed compensated
metabolic acidosis, with keton found in urine test. Head scan revealed mild cerebral edema.
SELF ASSESSMENT
1. How is pathophysiology mechanism to develop coma in this case?
2. How is “structural coma” distinguished from “metabolic coma”?
3. What could be the differential and possible diagnosis to this case?
4. How to manage and provide initial management and when do you refer the
patient?
Learning 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.
LEARNING TASK
ACUTE PSYCHIARTIC EPISODE
1. The Presence of medical illness should be strongly considered when psychiatric

symptoms appear suddenly in a previously well-functioning person. An old patient
with psychotic symptoms appearing for the first time, an awareness or conviction
that the symptoms are foreign, and especially with concomitant symptoms of
cognitive dysfunction should be considered to have a possible organic illness.
a) A patient with delirious condition usually have personality disorders
b) Increase of temperature, pulse and respiratory rate is common in psychiatric
patient, especially paranoid schizophrenia.
c) Suicide attempted are an easily manage, because they are only seeking
attention
d) Cognitive dysfunction should be considered to have a possible organic
illness.
e) A patient under the age 30 with psychotic symptoms appearing for the first
time should be considered to have an organic brain disorder.
2. The patient was a 25-year old female graduate student in physical chemistry who
was brought to the emergency room by her roommates, who found her sitting in her
car with the motor running and the garage door closed at 1.00 AM. She was crying,
looked tiredness, and difficulty in falling a sleep. What is the considerable of the
patient treatment?
SELF ASSESSMENT
1. Mampu menegakkan diagnosis Gangguan Mental Organik, membedakannya
dengan Gangguan Psikosis fungsional lainnya.
2. Mampu melakukan wawancara singkat untuk menggali data dan merencanakan
pemeriksaan penunjang yang diperlukan untuk kasus-kasus Accute Psychiatry.
3. Mampu membuat perencanaan awal untuk menangani kasus-kasus Accute
Psychiatry.
4. Mengerti etio-patogenesis, pato-fisiologis dan psikodinamika terjadinya kasus-kasus
Accute Psychiatry.
5. Mampu membuat prediksi/prognosis suatu kasus AccutePsychiatry serta tahu kapan
harus merujuk pasien tersebut.
LEARNING RESOURCES
1. Kaplan & Saddock’s Synopsis of Psychiatry, 10th ed
2. Kaplan & Saddock’s Study Guide and Self Examination Review in Psychiatry, 7th ed.
LEARNING TASK
RADIOLOGY IMAGING
1. Describe the radiology imaging of thorax which is specific for :

a. IRDS
b. Bronchopneumonia
c. Congenital Heart Disease
d. Lung Edema
e. Pneumothorax
f. Pleural Effusion
g. Vena Cava Superior Syndrome.
SELF ASSESMENT :
1. Female, 20 years old patient complaining fever, nausea, vomitting and abdominal pain
that localized to right lower quadrant, patient is difficult to walk because of pain.
a. What radiological examination should be performed to make sure the diagnose?
b. Describe the posible radiological examination finding!
c. Mention the other Differential Diagnoses!
2. Male, 35 years old complaining right back pain the radiating to front lower abdomen,
nausea, and difficult to defecation, there is no fever.
a. What is the radiological examination should be performed?
b. What is the posible finding from radiological examination?
LEARNING TASK
ACUTE UPPER AIRWAY OBSTRUCTION ENT
LEARNING TASK :
Male, 9 month years old complained by his parent with dyspneu, stidor and cough,
immediately after choking peanut without history of upper respiratory infection.
QUESTION
1. What you should ask to complete the anamnesis?
2. What will you find from the physical examination?
3. What kind of other examination to support the diagnosis?
4. What possibility diagnosis of this patient?

5. How to manage and provide initial management and when do tou refer the patient?
LEARNING TASK
Case:
A mother of 6 years old child complained about difficult breathing with her child after eating
grape. There is no fiver. ENT condition with normal limited.
Task:
1. What are other helpful informations you should get from his mother for complete
management of this case?
2. Considering the onset of manifestation: please describe other clues you should find
during physical examination on this child!
3. Do you need laboratory investigation?
4. What are your suggestions for the mother?
5. What are your planning for manage this case?
Self assessment:
1. What causes acute upper airway obstruction?
2. Describe the etiopathogenesis of foreign body airway obstruction.
3. Describe the risk factor of foreign body airway obstruction.
4. Describe symptom and sign of foreign body airway obstruction.
5. Describe the imaging studies of acute upper airway obstruction.
6. Describe the management of acute upper airway obstruction.
LEARNING TASK
BLEEDING DISORDERS (ENT)
Epistaxis
Learning task
1. Female, 22 yo, pregnant 20 week gestation, comes to fast track because of bleeding
of the nose.
a. What kind of information that we need more?
b. Describe the pathophisiology, why is this happened?
c. What kind of complication that can be occurred in this patient? How to avoid it?
2. A boy, 6 yo, company by the parents complaining about habitual bleeding
a. What question we sould asked in order to recover the caused?
b. Explained the pathophisiology in this boy!
c. How to avoid bleeding int the future?
3. Male, 17 yo, comes to fast track because of bleeding of the nose and from the
mouth.
a. What do you think is happening to him? Why?
b. Describe the pathophisiology, why is this happened?
c. What exam that he need more?
LEARNING TASK
BLEEDING DISORDER IN PREGNANCY
CASE 1 :
A 25 years old G3 woman presents to the maternity unit with vaginal bleeding. Fetal heart
rate is 140 per minute and her blood pressure is 110/60 and her HR is 85/minute. Fundal
height is 28 cm. she has been given nothing. What are the possible diagnosis?
CASE 2 :
You have just delivered a 37 weeks twins pregnancy pervaginam. The third stage is
complicated by postpartum hemorrhage unresponsive to uterine massage and use of
oxytocin. What would your next management steps be ?
LEARNING TASK
NEONATAL RESUSCITATION & ARDS (PEDIATRIC)
LEARNING TASK :
Case 1 :
A baby born at 33 weeks gestation following a caesarean section present with respiratory
distress soon after birth with bradypnoea (RR : 18 times/minutes). Heart rate 80
times/minutes regulary. The baby is requiring oxygen, an intravenous line inserted to
provide maintenance fluids. The mother had a temperature of 380 C.
TASK :
1. What is the diagnosis?
2. What investigation should be carried out?
3. What treatment would you institute of this condition?
4. Despite your effort above the baby has a cardio – respiratory arrest with the ECG
monitor, what is the immediate management?
5. what is the prognosis?
SELF ASSESSMENT :
1. To describe definition of perinatal asphyxia
2. To describe pathophysiology and etiology of asphyxia
3. To describe :
 Perinatal management
 Delivery room management
 Postnatal management
4. To describe prognosis of perinatal asphyxia
LEARNING TASK
SHOCK IN ADULT
Essay
1. 22 year old male presents following a motorcycle crash. He complains of the inability to
move or feel his legs. His blood pressure is 80/50 mm Hg, heart rate is 100, respiratory
rate is 20. GCS is 15. Temp 37 Oxygen is 99%on 2L nasal prongs. Chest X-ray, pelvic
X-ray, FAST are normal. Extremities are normal.
a. What the diagnose
b. Describe the emergency problem of the patient
c. How the management
2. Male 56 years admitted to the ICU for 1 week initially treated patients with symptoms of
urinary tract infections. Patient suddenly loss of consciousness followed by shortness
followed decreased urine output. On Physical examination are BP 90/50 pulse 120 RR
30 temp 40
a. Diagnose for ths patient
b. Decribe the management
3. A 67 year man unconcious felt down from 5 meters of tree, there are stab wound in
posteror of head. The backbone are fuly pain and can’t move legs. On Physical
examination are BP 80/50 pulse 88RR 20 temp 37. Paraparese found in lower
extremitas
a. what is the diagnose
b. what the supporting examination do you need?
c. describe the management this patient
4. A 24 year woman arrives in ER with dyspneau and skin rash on her chest and
abdominal, the woman unconsious and her lip was thiked and numbness, history of
allergic was denied. On Physical examination are BP 100/90 Pulse 100x/menit RR
37x/mnt temp 37, wheezing +/+ on right and left pulmo, rhonki -/- angioodema was
found.
a. Diagnose the patient
b. The different diagnose are
c. can describe the algorithm of management
d. Describe the Hypersensitivity Reaction
5. 22-year-old man sustains a shotgun wound to the left shoulder. His blood pressure
is initially 80/40. After two liters of Ringer's lactate solution his blood pressure
increases to 122/84. His pulse rate is now 100 beats per minute and his
respiratory rate is 28 breaths per minute. His breath sounds are decreased in the
left hemithorax,
a. Diagnose and the differential diagnosis
b. Describe the management
LEARNING TASK
SHOCK IN PEDIATRIC
Learning Task
Case 1
A 5 years old boy with body weight 20 kg, came with chief complain cold in palms and soles
since 24 hours before admitted to the hospital. History of fever occurred 5 days before
admitted to the hospital, but 1 day before admitted, the fever being decreased. The patient
had been urinated 10 hours before admitted to the hospital.
Physical examination
Patient with decreased of consiousness, pulse 140 x/minute regular smooth pulsation,
capillary refill time > 2 seconds.
Complete blood count
WBC: 2.000/uL, Hb: 15 g/dL, HCT: 45%, Plt: 20.000/uL
Self Assesment
1. Discuss about the assessment
2. Discuss about the therapy
3. Discuss about the monitoring
LEARNING TASK
CARDIAC ARREST AND CPR
Case Scenario 1
As on duty doctor at hospital, you are received emergency call from 2 nd floor hospital.
The nurse said that there is a 70 yo male patient, diagnose as stable angina, suddenly
suffered SOB after eating, getting worse shortly, but still concious. After 10 minute, the
patient became unconcious.
1. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy?
2. What happen to her?
3. Can we prevent this patient became unconcious?
Case Scenario 2
A 30 year old woman attends your clinic with asthma attack. She has a long history of
asthma, with severe attacks requiring hospitalisation. Despite continuous nebulised
salbutamol, she rapidly gets worse over about ten minutes with severe respiratory
distress, she is unable to talk and is becoming increasingly confused and unconcious.
From the monitor you already attach, the ECG shown takikardi and became bradikardia
and continue to asystole.
1. Based on immediate observation, what is the patient going through and what
actions should be done ?
2. Based on your analysis what would have caused this emergency and explain
its pathogenesis and pathophysiology.
3. Can you prevent this patient from asystole? Explain it.
4. Explain the management of asystole.
Case Scenario 3
85 year old man is delivered by car to your clinic. He was found collapsed 10 minute ago
by his family in the garden. At Physical examination, no pulse at a.jugularis, no heart
sound. A monitor is attached and the rhytm is VF.
1. What are you going to do?
2. How long we need to do CPR at this patient?
3. Explain the algorithm of Shockable cardiac arrest
Case Scenario 4
As doctor on duty at emergency room, you received a 50 years old man with history of
chest pain and suddenly unconscious in front of you. After doing fast examination, you
diagnose the patient as cardiac arrest with VT pulseless
1. Explain about the resuscitation team to perform good CPR on this patient.
2. How would you build a good resuscitation team?
3. Explain how would you doing defibrillation on this patient.
SELF ASSESSMENT
1. Explain the etiopathogenesis and pathophysiology of cardiac arrest
2. Explain the Guideline of BLS and ALS
3. Explain about “shockable” and “non shockable” cardiac arrest.
4. Explain the complication and prognosis of cardiac arrest.
LEARNING TASK
PAIN MANAGEMENT
1. A 55-year-old man has severe pain on gentle touching of the arm. Six months ago,
the median nerve was damaged during creation of an arteriovenous fistula for
dialysis.
a. What is the best terms to describes this phenomenon, explain about it?
b. What is pain and chronic pain?
c. Explain about three different types of chronic pain and give the examples!
2. A 21-year-old female softball pitcher had a surgical ulnar nerve transposition/release

for pain in her pitching arm three months ago. Now she still complains of severe pain
daily. She can barely bend her elbow and has decreased function of her hand. She
notes increased sensitivity to cold temperatures and generalized swelling, which is
more pronounced on the ulnar side of her hand. She is in your office for pain
management.
a. What is her diagnosis?
b. How will you confirm the diagnosis?
c. How will you treat the patient’s pain?
3. A 47-year-old female presents for a total knee arthroplasty. Her medical history is
positive for hypertension, rheumatoid arthritis, and a previous history of drug abuse.
Her current medications include hydrochlorothiazide (HCTZ), lisinopril, and
buprenorphine hydrochloride (Subutex).
a. What is the definition of opiod addiction and tolerance?
b. Mention opioid receptor types!
c. Mention side effects of oipioid!
LEARNING TASK
EMERGENCY TOXICOLOGY AND POISONING
Case 1
Male 25 years, came to the ER carried by his family in a state of unconsciousness. After
approximately 24 hours ago attend the party. Previous patients with mild drunk and sleepy,
then complained of blurred vision and blind
Learning task 1
1. Describe the symptoms and clinical signs in these cases?
2. What are the other anamnesis and the other physical examination that needed
3. What the laboratory examination is needed to confirm the diagnosis
4. What the differential diagnosis above case
5. What the diagnosis above case
6. How to manage the above case
Case 2
Male 20 years, student, came to the ER Sanglah, was brought by his parents in a state of
unconsciousness. On physical examination found coma, blood pressure 80/60 mm Hg,
pulse 48 beats per minute, frequency of breathing 12 times per minute. The pupils: miosis.
Abdominal examination: decreased bowel sounds. At the forearm found needle track marks.
Learning task 2
Case 3
Male, 20 years old, a builder, came to the ER escorted by his friend, the pain after
accidentally ingesting drinking colored floor cleaning liquid is clear and odorless. On
physical examination lip until pharing area look red and swollen.
Learning task 3
1.Describe the symptoms and clinical signs in these cases?
Case 4
Male 30 years old come to the ER, in between by his girlfriend, complained of fatigue and
vomiting - vomiting after drinking Baygon (insecticide), approximately 6 hours ago. Patients
also complain of frequent urination and defecation. On physical examination found the pulse
of 48 beats per minute, miosis, lacrimation, salivation.
Learning task 4
LEARNING TASK
ACUTE BLISTERING AND EXFOLIATIVE SKIN
Case 1
A 22 years old male come to emergency unit sanglah hospital with blistering skin rash. He
had fever and seizure since 8 days before and get medication such us phenytoin,
parasetamol, and vitamine B tablets from general practitioner. Three days later, he
developed blister and erythematous lesions over his extremities, face and trunk. Patient with
weak condition, BP 100/80 mmHg, temp 39°C, RR 22x/minutes. From eye examination
there is redness and secret on conjungtiva, from mouth and genetalia examination we find
multiple erosion with hemmoragic crust. From his extremities, face and trunk we find
multiple purpuric lesion and some part of rash with bullous and erotion that involve 25%
BSA.
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What other information do you need to support the diagnosis?
3. What other examination you should do to this patient?
4. What monitoring should you do to this patient?
5. How do you manage this patient?
6. What is the complication of this condition?
7. What information you should give to patient and his family?
SELF ASSESSMENT
1. Describe the principle clinical features of SJS, SJS overlapping TEN, TEN.
2. Describe the pathogenesis of SJS, SJS overlapping TEN, TEN.
3. Explain more detail the basic principle of management of SJS, SJS overlapping
TEN, TEN.
4. Describe the prognosis and complication of SJS, SJS overlapping TEN, TEN.
Case 2
A 60 years old woman come to dermatology polyclinic Sanglah hospital with skin rash all
over the body. She had a fever, cough and rhinitis 4 days before. Two days later, she
developed erythematous rash around the nose and the rash widespread all over her body
with the skin peel easyly. She have history of acute renal failure. She takes paracetamol
tablet and Actifed ® syrup but there is no improvement. Patient with weak condition, temp
40°C, HR 90X/minutes, RR 28x/minutes. Skin effloresence from face, trunk, back, and
extremities, we find erythematous macule, some part of the lesion with multiple vesicle and
desquamation skin.
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What is the other differential diagnosis for this case?
3. What other information do you need to support the diagnosis?
4. What other examination you should do to this patient?
5. What monitoring should you do to this patient?
6. How do you manage this patient?
7. What is the complication of this condition?
8. What information you should give to patient and her family?
SELF ASSESSMENT
1. Describe the principle clinical features of SSSS.
2. Describe the pathogenesis of SSSS.
3. Explain more detail the basic principle of management of SSSS.
4. Describe the prognosis and complication of SSSS.
LEARNING TASK
PREGNANCY INDUCED HYPERTENSION
1. A Woman 38 y.o aged, and she is in third pregnancy with twice obstetric history were
term pregnancy, spontaneous delivery and also both child still alive today. There was no
past medical history. Estimated due date in next 15 days. She was complained
headache and epigastric pain. Fetal movement was good and no labor pain. Physical
examination found composmentis consciousness, BP 170/110 mmHg, pulse 90
x/minute, respiration rate 24 x/minute. General examination: there were no cardiac and
pulmonary abnormality. Obstetric examination: head presentation, FHB 11.11.12 and no
uterine contraction.
a. As a doctor on duty, what is additional examination to confirm diagnosis and what
next management will perform firstly?
b. What is suitable diagnosis for above case?
c. What is possible complication to this patient?
2. A woman 31 y.o aged, and she is in second pregnancy, with history of preterm
pregnancy (her first child delivered by cesarean section cause by impending eclamptic
status), body weight 88 kg, height 147 cm, 26 weeks of pregnancy. Visited outpatient
clinic with history of high blood pressure (BP 150/90 mmHg). History of hypertension,
known since 21 y.o and took irregular antihypertensive drug.
a. What are additional physical examination and laboratory testing will perform to
confirm the diagnosis?
b. What is suitable diagnosis for above case?
c. Appropriate management for this case is?
d. Possible complication for the mother and fetus are?
3. A woman 40 y.o aged, and she is in forth pregnancy (gravid 4, para 3), 36-37 weeks of
pregnancy, admitted to the emergency department by her family with history of seizure
(3 times) and then unconscious after the seizure. Brief examination: patient
unconscious, BP 190/110 mmHg.
a. As emergency Doctor on duty, appropriate initial management for this patient is?
b. What is additional history taking and physical examination will perform to build
diagnosis?
c. What is the diagnosis for above case?
d. Correct management for this case is?
LEARNING TASK
SHOULDER DYSTOCIA
You are urgently called to the delivery room of a 26-year-old woman to help deliver the
baby. The mother is 41 weeks into her second pregnancy, having had a normal term
delivery of a 3.97 kg female infant 2 years ago. Nuchal and anomaly scans were normal
and antenatal care was unremarkable. The baby was moving normally prior to labour.
When she arrived on labour ward contracting, the symphysio-fundal height was noted to be
41 cm. At first assessment the cervix was 3 cm dilated and she was advised to continue
mobilizing. Spontaneous rupture of membranes occurred and she was examined again after
4h and the cervix was still 3 cm. A oxytocine infusion was commenced to augment labour
and an epidural sited, with cardiotocograph monitoring also commenced. After 4h, the cervix
was 7cm and then 10cm after a further 4h. The woman was encouraged to start active
pushing and 35 min later the head had crowned in a direct occipito-anterior position.
The midwife noticed that the head did not extend normally on the perineum and that the
chin appeared to be wedged against the perineum. She had attempted delivery of the
shoulders with the next two contractions but this had not been achieved.
Questions
1.What is the diagnosis?
2. What are the risk factors in this case?
3. How would you manage this scenario?
4. What kind of complications that possibly happened in this case?
SELF ASSESSMENT
6. Discuss the diagnosis of shoulder dystocia

7. Discuss the incidence of shoulder dystocia
8. Discuss the risk factors of shoulder dystocia
9. Discuss the complications of shoulder dystocia
10. Discuss appropriate management of shoulder dystocia
LEARNING TASK
TRAUMA WHICH POTENTIALLY DISABLING AND LIFE THREATENING CONDITIONS
SELF DIRECTING LEARNING
Basic knowledge that must be known:

1. Airway management
2. Breathing Management
3. Circulatory management
4. Disability Management
SCENARIO
A trauma call went out after 30 years old man was brought to the emenrgency Department
Sanglah hospital following an assault. He was set upon by a gang of youths reportedly
wielding baseball bats and knives. He came to our hospital Unconcious, On Primary
survey : airway clear, Breathing : Repiratory rate 30 x/minute, Circulatory : Blood pressure
80/60 mmhg and Heart rate 120 x/minute. Disability Pain Response.
1. What are the patient problem?
2. What are the symptom and sign of Tension Pneumothorax, Massive Hematothorax
and Cardiac Tamponade?
3. How you manage the patient ?
A 33 year old woman is involved in a head-on motor vehicle crash. It took 30 minutes to
extricate her from the car. Upon arrival in the emergency department, her heart rate is 120
beats per minute, BP is 90/70 mmHg, respiratory rate is 16 breaths per minute, and her
GCS score is 15. Examination reveals bilaterally equal breath sounds, anterior chest wall
ecchymosis, and distended neck veins. Her abdomen is flat, soft, and not tender. Her pelvis
is stable. Palpable distal pulses are found in all 4 extremities.
1. What are the patient diagnosis?
2. How you manage the patient ?
Learning Task
1. Hematothorax & Massive Hemathotorax?
2. Simple Pneumothorax, Open Pneumothorax and Tension Pneumothorax?
3. Cardiac Tamponade?
Self Assessment
Describe about Life threathening condition in breathing ?
LEARNING OBJECTIVE
Establish tentative diagnosis, provide initial assessment in circulatory
Scenario
A 45-year-old male arrived at the ER, a large tree having fallen across his pelvis. The
patient was hypotensive at the scene. He received over 1500 ml of crystalloid in route to the
emergency room. Upon arrival to Sanglah Hospital , the patient had a systolic pressure of
70. His heart rate was in the 130 s. The patient was awake and alert. 2 Intravenous line
were placed and he was transfused with two units of O-blood. The patient’s abdomen was
soft and nontender. The patient had blood at his meatus. The patient’s pelvis was tender to
palpation.
 What are the patient problem?
 What are the symptom and sign of abdominal trauma and pelvic trauma ?
 How you manage the patient ?
Learning Task
 Abdominal Trauma?
 Pelvic Trauma ?
Self Assessment
Describe about Life threathening condition in circulation ?
Reference
ATLS ; Advance Trauma Life Support for Doctor (Student Course Manual),8th Edition.
LEARNING TASK
EMERGENCY IN PEDIATRIC (NON TRAUMA)
1. Anak laki-laki 2 tahun , dibawa orang tuanya dengan keluhan benjolan di scrotum
kanan yang baru diketahui sejak 6 jam lalu, benjolan tidah bisa keluar masuk, anaknya
juga rewel, tiap diberi minum muntah.
 Apa diagnosis pasien ini
 Apa masalah kegawat daruratan pasien iniBagaimana manajemen awal dan
prognosisnya
2. Bayi baru lahir 4 jam lalu dibawa dengan usus terburai, bayi lahir di klinik ditolong
bidan ,penderita langsung menangis, BB 2,3 kg. Ibu pasien ANC di bidan.
 Ada diagnosis dan diagnosis banding pasien ini
 Bagaimana manajemen awal penderita ini
 Bagaiman prognosis pasien ini.
3. Anak laki laki 6 tahun dikeluhkan nyeri perut sejak sehari sebelumnya, nyeri terutama
diperut bagian bawah. Pasien juga dengan keluhan muntah dan demam. Penderita juga
tidak mau makan sejak kemarin. Saat datang pasien sadar baik, temp axial 38°C, Nadi
100 x/mnt.
 Apa diagnosis saudara
 Apa problem pada pasien ini
 Bagaimana manajemen dan prognosis pasien ini.
LEARNING TASK
BRAIN RESUSSCITATION
Case disscusion
Uncooperative, agitated 28 years old male is brought to emergency room after motorcycle
accident. The examination show that the patient is gurgling, and when he was given pain
stimulation, he was opening his eyes, speaking nonsensical and withdrawing from pain.
Blood pressure 85/45 mmHg, pulse 115 x/sec, respiratory rate 25 x/sec, and saturation
oxygen 90-92 %
1. How do you classified the patient according to severity of the TBI? What is your plan
for this patient?
2. Will you intubate the patients? Why?
3. Will you give this patients fluids resuscitation? Why? And what kind of fluid will you
choose for this patients?
4. When do you suspect this patients have an elevated ICP or brain herniation?
5. What do you know about first and second tier therapy?
LEARNING TASK
ENVIROMENTAL INJURY
1. Pasien laki laki, 28 tahun datang ke UGD dengan keluhan luka bakar pada wajah, leher,
dada dan kedua lengan setelah terkena ledakan gas elpiji di ruang tertutup. Luas luka
bakar 30 % TBSA, Berat badan 60 kg
a. Sebutkan tanda tanda trauma inhalasi ?
b. Sebutkan pembagian luas luka bakar berdasarkan Role of Nine ?
c. Bagaimana cara pemberian cairan resusitasi pasien ini?
d. Menggunakan rumus apa untuk resusitasi cairan ?
LEARNING TASK
UROLOGIC CONCERN IN CRITICAL CARE FOR NON TRAUMA CASE
Case 1 An old man that unable to void
A 70-year-old man with multiple medical problems presented with complaints that he could
not void and had pain in the lower abdomen since yesterday. He had a mild dementia, so
much of the history was from his wife, who accompanied him to the clinic. She stated that
he had neither ifever, nausea, nor vomiting, and he had not had any recent acute illnesses.
The patient had not had any recent change in medications, doses, or frequency of dosing of
his pain medication. He had similar problems in the past, but the symptoms had resolved
after he underwent a transurethral resection of the prostate (TURP) 10 years ago. His wife
also stated that he had been complained of frequently in mictie, incontinence, small caliber
urination for last 1 month. Unwell treated of type 2 diabetes melittus and hypertension since
4 years ago also reported.
His medications included an extended-release morphine tablet for pain, insuline for his
diabetes, and recently discontinued ramipril and hydrochlorothiazide, which he had taken in
the past for his hypertension. On examination, he was mildly tender over the bladder, which
was palpably distended. He attempted to void for a urinalysis specimen and was unable to
do so. A 16 fr Foley catheter was placed, and 1350 mL of urine was collected. The urinalysis
showed a trace of protein, and laboratory results were otherwise negative.
Question Learning Task
1. What are some possible causes of acute urinary retention?

2. What tests would be helpful in determining the cause of this patient's urinary retention?
3. What treatments would be useful in relieving the symptoms?
4. What is the definitive treatment for this case?
4. What are some complications of untreated acute urinary retention?
LEARNING TASK
UROLOGIC CONCERN IN CRITICAL CARE FOR TRAUMA CASE
LEARNING TASK TRAUMA UROLOGI
1. Seorang laki2 50 thn datang ke UGD setelah tertembak di bagian perut kanan atas 1
jam sebelumnya. Kencing berwarna merah. vital sign stabil.
Jelaskan;
Informasi anamnesa dan pemeriksaan fisik yang anda perlukan?
Pemeriksaan penunjang yang anda sarankan?
Manajemen kasus diatas?
2. Seorang laki2 25 thn datang ke UGD dengan keluhan keluar darah menetes dari ujung
kemaluan setelah jatuh dari tangga dalam posisi terduduk.
Jelaskan
Informasi anamnesa dan pemeriksaan klinis yang anda butuhkan?
3. Seorang laki -laki datang ke ugd dengan nyeri perut bawah dan kencing tersendat
bercampur darah, setelah kecelakaan lalu lintas. Perut bawah terbentur stir saat
mengendarai mobil 2 jam sblm ke ugd. Pemeriksaan fisik vital sign stabil, ditemukan
jejas supra symphisis dan nyeri tekan. Di UGD dilakukan pemasangan kateter urine tapi
tidak keluar urine. pasien kesakitan mengeluh tidak bisa kencing.
Jelaskan
Diagnosa yang paling mungkin?
4. Seorang anak laki2 12 thn mengeluh luka pada scrotum setelah terjatuh dari sepeda.
kencing tersendat dan pemeriksaan fisik tampak luka terbuka pada scrotum kiri
sepanjang 4 cm.
Jelaskan
pemeriksaan penunjang yang anda sarankan
5. Seorang wanita datang ke UGD dengan keluhan nyeri pinggang kanan dan kencing
bercampur darah setelah kecelakaan lalu lintas. Vital sign saat datang stabil, tapi 30 mnt
kemudian tekanan darah 90/60 dan nadi 102x/mnt, tidak membaik dengan pemberian
cairan kristaloid.
Jelaskan
DAFTAR DOSEN PENGAJAR BLOK EMERGENCY MEDICINE 2019
No. Nama Dosen No HP Departemen Topik

1 Dr.dr.Tjok Gde 08133771 Anestesiologi Penanggung jawab Blok dan
Agung Senapathi, 1220 dan Terapi dosen pengajar topik :
SpAn (KAR) Intensif Highlight Emergency Disaster
Preparedness
2 Drg. Lestari 08155764 PS Pendidikan Dosen pengajar topik :
Sudirman 446 Dokter Gigi Phlegmon
3 dr. IGN Budiarsa, 08113996 Ilmu Penyakit Dosen pengajar topik : seizure
SpS 73 Saraf and mental changes disorder
status epilepticus dan
pengelola dan fasilitator BCS
4 dr. IA Sriwijayanti, 08133766 Ilmu Penyakit Dosen pengajar topik : coma
MBioMed, SpS 7939 Saraf and decrease consciousness ,
pembimbing dan penguji
student project topik malaria
serebral, dan pengelola dan
fasilitator BCS kegawatan
neurologi dan psikiatri
5 Dr.dr.Tjokorda Bagus 08162957 Psikiatri Dosen pengajar topik acute
Jayalesmana,SpKJ. 79 psychiatric episode ,
MARS pembimbing dan penguji
student project topik post
traumatic disorder, dan
kegawatan neurologi dan
psikiatri
6 dr. Sri 08164745 Radiologi Dosen pengajar topik radiology
Laksminingsih, SpR 561 imaging
(K)
7 dr. Wayan Sucipta, 08125318 THT Dosen pengajar topik upper
SpTHT KL 941 airway obstruction
8 dr. Sari Wulan, 08123787 THT Dosen pengajar epistaksis dan
SpTHT KL 4447 pembimbing dan penguji
student project topik carcinoma
nasofaring
9 Dr.dr. Wayan 08123917 Obstetri dan Dosen pengajar topik bleeding
Megadana, SpOG(K) 002 Ginekologi disorder, haemorrhage in
pregnancy: antepartum and
post partum dan dosen
student project topik abrupsio
plasenta
10 Dr.dr.Dyah 08128570 Ilmu Penyakit Dosen pengajar topik neonatal
Kanyawati, SpA(K) 5152 Anak resuscitation and ARDS
(pediatric) dan dosen
student project topik febris and
seizures in pediatric patient
11 dr. IGAG Utara 08113891 Anestesiologi Dosen pengajar topik shock in
Hartawan, SpAn. 490 dan Terapi adult dan pembimbing dan
MARS Intensif penguji student project topik
septic shock
12 dr. Nyoman 08123633 Ilmu Penyakit Dosen pengajar topik shock in

Budihartawan, MSc, 3221 Anak pediatric patient dan dosen
SpA pembimbing dan penguji
student project topik dengue
shock siyndrome in pediatric
patient
13 dr. Pontisomaya 08113800 Anestesiologi Dosen pengajar topik cardiac
Parami, SpAn. 107 dan Terapi arrest and CPR
MARS Intensif
14 dr. Made Agus 08189547 Anestesiologi Dosen pengajar topik pain
Kresna Sucandra, 0888 dan Terapi management
SpAn KIC Intensif
15 Dr.dr. Agus Somya, 08123989 Ilmu Penyakit Dosen pengajar emergency
SpPD. KPTI 353 Dalam toxicology and poisoning dan
student project topik intoksikasi
organoposfat
16 dr. Nyoman 08174472 Ilmu Penyalit Dosen pengajar topik dermato-
Suryawati, SpKK 79 Kulit dan emergencies dan pembimbing
Kelamin dan penguji student project
topik steven johnson syndrome
17 Dr.dr. Gede 08123636 Obstetri dan Dosen pengajar topik
Megaputra, SpOG(K) 172 Ginekologi pregnancy induced
hypertension dan pembimbing
dan penguji student project
topik hipertensi dalam
kehamilan
18 dr. Endang 08155831 Obstetri dan Dosen pengajar topik shoulder
Sriwidiyanti, SpOG 4827 Ginekologi dystocia dan pembimbing dan
penguji student project topik
distosia
19 Dr.dr. Ketut Suyasa, 08155872 Bedah Dosen pengajar topik trauma
SpB. SpOT(K)Spine 4088 Ortopedi dan which potentially disabling and
Traumatologi life threatening conditions dan
student project topik spine :
fraktur dan dislokasi
20 dr. IGN. Wien 08113852 Bedah Dosen pembimbing dan
Aryana, SpOT 63 Ortopedi dan penguji student project topik
Traumatologi trauma sendi
21 dr. I Made 08123959 Bedah Anak Dosen pengajar topik
Darmajaya, SpB, 701 emergency in pediatric (non
SpBA, MARS trauma)
22 Dr. dr. I Putu 08113948 Anestesiologi Dosen pengajar topik traumatic
Pramana Suarjaya, 11 dan Terapi brain injury dan dosen
SpAn. MKes. KMN. Intensif pembimbing dan penguji
KNA student project topik
subarachnoid hemorrhage
23 dr. Ida Bagus Krisna 08123836 Anestesiologi Dosen pembimbing dan
Jaya Sutawan, 470 dan Terapi penguji student project topik
SpAn. MKes. KNA Intensif resuscitation in pregnancy
24 dr. Agus Roy Ruly 08123511 Bedah Plastik Dosen pengajar topik
Hariantana Hamid, 673 environmental injury dan
SpBP-RE(K) pembimbing dan penguji
student project topik blust
injury dan pengelola dan
fasilitator BCS Kegawatan
Trauma
25 Dr. dr. Gd Wirya 08155753 Bedah Urologi Dosen pengajar topik urology
Kesuma Duarsa, 377 concerning in critical care for
SpU (K), MKes non trauma case dan
student project topik retention
urine in emergency setting
26 dr. Wayan Yudiana, 08133870 Bedah Urologi Dosen pengajar topik urology
SpU 8195 concern in critical care for
trauma case dan pembimbing
dan penguji student project
topik pelvic injury dan
Kegawatan Urology
27 dr. Made Agus 08133864 Bedah Digestif Dosen pembimbing dan
Dwianthara Sueta, 8424 penguji student project topik
SpB KBD angina ludwig
28 dr. AA Gde Yuda 08133787 Bedah Dosen pembimbing dan
Asmara, SpOT 0347 Ortopedi dan penguji student project topik
Traumatologi hematothorak dan pengelola
dan fasilitator BCS Kegawatan
Trauma
29 dr. IB Putra 08180543 Bedah Urologi Pengelola dan fasilitator BCS
Pramana, SpU 0537 Kegawatan Urology
30 dr. I Gde Sastra 08133871 Obstetri dan Pengelola dan fasilitator BCS
Winata, MBiomed. 3951 Ginekologi Kegawatan Obstetri
SpOG K
31 dr. Ryan Saktika 08214708 Obstetri dan Pengelola dan fasilitator BCS
Mulyana, SpOG 7905 Ginekologi Kegawatan Obstetri
32 dr. FX Adinda Putra 08113601 Anestesiologi Pengelola dan fasilitator BCS
Pradhana, SpAn 619 dan Terapi Shock dan CPR
Intensif
33 dr. Christoper 08214422 Anestesiologi Pengelola dan fasilitator BCS
Ryalino, SpAn 4466 dan Terapi Shock dan CPR
Intensif
34 dr. I Putu Santhi 08133876 THT Pengelola dan fasilitator BCS
Dewantara, SpTHT 9908 Kegawatan THT
KL
35 dr. Ni Putu Oktaviani 08133894 THT Pengelola dan fasilitator BCS
Rinika P, SpTHT KL 0957 Kegawatan THT
36 dr. IA Pramahamsa, 08214591 Bedah Umum Pengelola dan fasilitator BCS
MBiomed, SpB 1378 Kegawatan Urology
37 dr. IA Sri Indrayani, Ilmu Penyakit Pengelola dan Fasilitator BCS
SpS Saraf Kegawatan Neurologi dan
Psikiatri
38 dr. Sri Yenni Ilmu Penyakit Pengelola dan Fasilitator BCS
Trisnawati, Saraf Kegawatan Neurologi dan
M.Biomed, SpS Psikiatri
39 dr. Ketut Widyastuti, Ilmu Penyakit Pengelola dan Fasilitator BCS

SpS (K) Saraf Kegawatan Neurologi dan
Psikiatri
40 dr. Putu Witari, SpS Ilmu Penyakit Pengelola dan Fasilitator BCS
Saraf Kegawatan Neurologi dan
Psikiatri
41 dr. Agus Eka 08993933 Mikrobiologi Penanggung Jawab BCS Blok
Darwinata, S.Ked, 144 Emergency Medicine
PhD
JADWAL BCS
1. BCS Kegawatan Neurologi dan Psikiatri; penanggung jawab : dr. dr. IA Sri Wijayanthi, M Biomed, SpS (HP 081337667939) dan Dr.dr.
Tjokorda Bagus Jayalesmana,SpKJ. MARS (HP 0816295779)
2. BCS Kegawatan THT; penanggung jawab : dr. I Putu Santhi Dewantara, SpTHT KL (HP 081338769908) dan dr. Ni Putu Oktaviani
Rinika P, SpTHT KL (HP 081338940957)
3. BCS Kegawatan Shock dan CPR; penanggung jawab : dr. FX Adinda Putra Pradhana, SpAn (HP 08113601619) dan dr. Christoper
Ryalino, SpAn (HP 082144224466)
4. BCS Kegawatan Obstetri (Bleeding Disorder dan Shoulder Distosia), penanggung jawab : dr. I Gde Sastra Winata, MBiomed. SpOG K
(HP 081338713951) dan dr. Ryan Saktika Mulyana, SpOG (HP 082147087905)
5. BCS Kegawatan Trauma (Trauma dan Enviromental Injury); penanggung jawab : dr. AA Gde Yuda Asmara, SpOT (HP 081337870347)
dan dr. Agus Roy Ruly Hariantana Hamid, SpBP-RE(K) (HP 08123511673)
6. BCS Kegawatan Urology; penanggung jawab : dr. IB Putra Pramana, SpU (HP 081805430537) dan dr. Wayan Yudiana, SpU (HP
081338708195)

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Study Guide Emergency Medicine

STUDY GUIDE THE EMERGENCY MEDICINE

First Edition March 2019

Mastering of basic knowledge with its clinical and practical implication.

Personal Development/ Attitude

PLANNERS/ LECTURES TEAM

NO. NAME DEPARTMENT

Regular Class (Class A)

English Class (Class B)

Student Project (SP) Emergency Medicine

 Pembimbing dan penguji SP disesuaikan dengan tabel di bawah ini.

FORM BIMBINGAN STUDENT PROJECT

Topik Student Project :

Bimbingan/tanggal Pembahasan Tanda tangan pembimbing

III tanggal …..

FORM PENILAIAN STUDEN PROJECT

No. Penilaian Nilai maksimal Nilai

Tjokorda Gde Agung Senapathi

Table 1 Types of Disarter

Table 2 Factors That May Hinder ED Response to Disasters

DISASTER PREPAREDNESS AND PLANNING

There are various types of status epilepticus and a classification:

Status epilepticus confined to early childhood

Status epilepticus confined to later childhood

Status epilepticus occurring in childhood and adult life

In clinical practice status epilepticus classified :

Principle of management of status epilepticus

Consciousness can be defined by two components: arousal and awareness. Disorders of

cause unconsciousness or delirium must be identified quickly followed by rapid clinical

Emergency occur in psychiatric just as we do in every field of medicine. However,

Gambar 1. Vaskularisasi septum nasi

Penyebab lokal Penyebab sistemik

-Anamnesis riwayat penyakit, tentang perdarahan,

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

-Evaluasi dan terapi kausa

Tampon hidung ulang Angkat tampon

Perdarahan tidak berhenti

Konsultas-rawat bersama Hematologis-onkologis:

- Tocolytic therapy is administered up to 48 hours after admission.

Solusio Placenta (placenta abruption)

Postpartum hemorrhage is divided into 2, namely:

Trauma of the birth canal

General prevention and treatment

Management is done with the principle of "HAEMOSTASIS", namely:

eventually cause seizures due to hyponatremia. Administration of ergometrine as a

In addition, the vasoactive hormone is released during shock syndrome, such as

Table 1. Early symptoms on shock

CNS Decrease of consciousness Decrease in CPP

CVS Tachycardia The Adrenergic Stimulus

Dysrhythmias Ischemic Coronary

Hypotension Decreased contractility, MDF ischaemia, or RVF,

Murmurs Valvular dysfunction

JVP increase / decrease Decrease in volume / preload or RV failure

Respiration Takipneu Pulmonary edema, respiratory muscle failure,

Renal Oliguria Decreased perfusion, constriction of afferent

Skin Cold, pale, sweat Vasoconstriction, sympathetic stimulation

Other Lactic acidosis Anaerobic metabolism

Fever Infection of hepatic dysfunction

CNS=central nervous system; CVS=cardiovascular system; CPP=cerebral perfusion pressure;

Integumentary systems are also affected by decreased perfusion and vasoconstriction

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

PRIORITY AND TARGET THERAPY

Incident and Etiology