11. Tue,
26 Sept 2016
09.00-10.00 Lecture 11.
Shoulder Dystocia
Class room dr. Endang
Sriwidiyanti,SpOG
10.00-11.30 Student Project
- 11.30-12.00 Break
Disc room Facilitators
12.00-13.30 Individual Learning 13.30-15.00 SGD
15.00-16.00 Plenary Class room
dr. Endang Sriwidiyanti,SpOG
12. Wed,
27 Sept 2016
09.00-10.00 Lecture 12.
Acute Blistering and Exfoliative Skin
dr. Nyoman Suryawati Sp.KK
10.00-11.30 Student Project
- 11.30-12.00 Break
Fasilitator 12.00-13.30 Individual Learning
13.30-15.00 SGD 15.00-16.00 Plenary
dr. Nyoman Suryawati Sp.KK
13. Thu,
28 Sept 2017
09.00-10.00 Lecture 13.
Trauma Which Potentially Disabling
and life Threatening Conditions
Dr.dr. Ketut Suyasa, SpB SpOTK Spine
dr. IGN Wien Aryana, SpOT
10.00-11.30 Student Project
- 11.30-12.00 Break
Disc room Fasilitators
12.00-13.30 Individual Learning 13.30-15.00 SGD
15.00-16.00 Plenary
Dr.dr. Ketut Suyasa, SpB SpOTK Spine
dr. IGN Wien Aryana, SpOT
DAYDATE TIME
LEARNING ACTIVITY
VENUE CONVEYER
14 Mon,
2 Oct 2017
09.00-10.00 Lecture 14.
Phlegmon Brain Resuscitation
Class room drg. Lestari Sudirman
Dr.dr. I Pt Pramana Suarjaya, SpAn
MKes.KMN.KNAdr. IB Krisna Jaya
Sutawan, SpAn MKes
10.00-11.30 Student Project
- -
11.30-12.00 Break
Disc room Facilitators
12.00-13.30 Individual Learning
13.30-15.00 SGD
Medical Education Unit Faculty of Medicine Udayana University
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15.00-16.00 Plenary
Class room drg. Lestari Sudirman
Dr.dr. I Pt Pramana Suarjaya, SpAn
MKes.KMN.KNAdr. IB Krisna Jaya
Sutawan, SpAn MKes
15 Tue,
3 Oct 2017
09.00-10.00 Lecture 15.
Urologic Concern in Critical Care for
NonTrauma Case
Class room Dr.dr. Gede Wirya
Kusuma Duarsa, M.Kes, SpUK
10.00-11.30 Student Project
- 11.30-12.00
Break Disc room
Facilitators 12.00-13.30
Individual Learning 13.30-15.00
SGD 15.00-16.00
Plenary Class room
Dr.dr. Gede Wirya Kusuma Duarsa,
M.Kes, SpUK
16 Wed,
4 Oct 2017
09.00-10.00 Lecture 16.
Urologic Concern in Critical Care for
Trauma Case
Class room
dr. Wayan Yudiana, SpU
10.00-11.30 Student Project
- -
11.30-12.00 Break
Disc room Facilitators
12.00-13.30 Individual Learning
13.30-15.00 SGD
15.00-16.00 Plenary
Class room dr. Wayan Yudiana,
SpU
1 Thu,
5 Oct 2017
08.00-selesai Basic clinical skill
12 Basic Trauma Care
English Class jam 08.00-11.30 WITA;
Regular class jam : 12.30-15.00 WITA
Clinical skill lab
Dr.dr. Ketut Suyasa, SpB. SpOTKSpine
dr. IGN. Wien Aryana, SpOT
dr. AA Gde Yuda Asmara, SpOT K
dr. Made Agus Dwianthara Sueta,
SpB KBD
2 Fri,
6 Oct 2017
08.00-selesai Basic clinical skill
12 CPR
Regular Class jam 08.00-11.30 WITA;
English Class jam 12.30-15.00
SMF Anestesiologi
dan Terapi Intensif
Dr.dr.Tjok Gde Agung
Senapathi,Sp.AnKA R
Dr.dr. I Putu Pramana
Suarjaya,SpAn.M.K es.KMN.KNA
dr. IGN. Mahaalit
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Aribawa,SpAn.KA R
dr. Ida Bagus Krisna Jaya
Sutawan,SpAn.M.K es dr. IGAG Utara
Hartawan,SpAn.M ARS
dr. IGAG Utara Hartawan,SpAn.M
ARS
3 Mon,
9 Oct 2017
08.00-Finish
Student Project
Team
4 Tue,
10 Oct 2017
Prepare For Examination
Thu, 12 Oct
2017 EXAMINATION
NB Tanggal 20 September 2017 kuliah dr. IGN. Mahaalit Aribawa, SpAn KAR pindah
ke tanggal 26 September 2017
Tanggal 22 September 2017 kuliah Dr.dr. Agus Somya, SpPD KPTI pindah ke
tanggal 20 September 2017
Tanggal 26 September 2017 kuliah dr. Endang Sriwidiyanti,SpOG pindah ke
tanggal 22 September 2017
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ASSESSMENT METHOD
Assessment will be carried out onthe day written according to class calendar. There will be 100 questions consisting mostly of Multiple Choice Questions MCQ and some other types
of questions. The minimal passing score for the assessment is 70.Other than the examinations score, your performance and attitude during group discussions will be consider in the
calculation of your average final score.Final score will be sum up of student performance in small group discussion 5 of total score and score in final assessment 95 of total score.
Clinical skill will be assessed in form of Objective structured clinical examination OSCE at the end of semester as part of Basic Clinical Skill Block’s examination.
STUDENT PROJECT
Students have to write a paperwork with topic given by the lecturer. The topic will be chosen randomly on the first day. Each small group discussion must work on one paperwork
with different tittle. The paperwork will be written based on the direction of respective lecturer. The paperwork is assigned as student project and will be presented in class. The
paper and the presentation will be evaluated by respective facilitator and lecturer.
Format of the paper :
1. Cover Title TNR 16
Name Green coloured cover Student Registration Number
Faculty of Medicine, Udayana University 2017 2. Introduction
3. Journal critismliterature review 4. Conclusion
5. References
Example :
Journal
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Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA Protection from Oxidative Damage is Increased in Woman. Am J Clin Nutr 111:79-
84.
Textbook
Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 4
th
ed. Pennysylvania: WB Saunders Co. Pp 1636-1642. Note.
Minimum 10 pages; line spacing 1.5; Times new roman 12
LEARNING PROGRAMS
Abstracts of Lectures
Lecture 1 : HIGHLIGHT EMERGENCY DISASTER PREPAREDNESS
Tjokorda Gde Agung Senapathi Disasters have claimed millions of lives and cost billions of dollars world-wide in the past
few decades. Examples of large-scale disasters include the terrorist attacks of September 11, 2001; the 2004 Pacific Ocean tsunami; the 2010 earthquake in Haiti; the 2011 earthquake
and tsunami in Japan; and Superstorm Sandy of 2012. Emergency physicians frequently have extensive responsibilities for community and hospital-level disaster preparedness and
response.
DISASTER DEFINITION
The World Health Organization defines a disaster as a sudden ecologic phenomenon of sufficient magnitude to require external assistance. A disaster is an event that overwhelms
the resources of the region or location in which it occurs. Furthermore, a hospital disaster may similarly be defined as an event that overwhelms the resources of the receiving hospital.
A hospital disaster may be of any size and is not limited to mass casualty incidents. A single patient who ingested an organic phosphorous pesticide may overwhelm the resources of a
hospital if that hospital is not prepared to decontaminate external to the ED. A single patient with suspected small-pox or a single influential patient e.g., world leader or a celebrity may
use so many ED resources that it affects the care of other patients.
Whether an event is a disaster further depends on the time of day, nature of the injuries, type of event, and the amount of preparation time before the arrival of patients. The
ED “surge capacity” ability of the ED to care for more patients than is typical may be severely limited by hospital overcrowding.
When it appears that the normal procedures of an ED may be interrupted by an event, there must be policies and procedures in place to activate a disaster response, direct the
mobilization of personnel and equipment, and permit the rapid triage, assessment, stabilization, and definitive care of victims.
TYPES OF DISASTERS
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Disasters are subdivided into several categories Table 1. External disasters occur at locations that are physically separate from the hospital e.g., transportation accident,
industrial accident. An internal disaster is an event that occurs within the confines of the hospital e.g., bomb scare, laboratory accident involving radiologic agents, power failure.
Disasters can be both internal and external e.g., earthquake with mass casualties as well as damage to the internal hospital.
Table 1 Types of Disarter
Disaster Type
Definition Examples
Natural disaster
Disaster caused by a naturally occurring event
Earthquakes, tsunamis, tornadoes, hurricanestyphoons, volcanic
eruption, pandemic influenza
Manmade disaster
Nonnatural events that are not purposefully produced
Vehicle crashes e.g., car, plane, bus, mass casualty events, explosions,
fires, industrial accidentchemical release
Terrorist related
disaster Events that are purposefully
produced in an effort to cause terror
Events of September 11, 2001, as well as intentional chemical, biological,
radiologic, or toxin releases
Internal disaster
An event that occurs within the hospital
Hazardous materials spill in hospital laboratory, fire or explosion within
hospital, power failure External
disaster An event that occurs external to
the hospital Transportation accident, industrial
accident Acute
disaster Disaster that occurs in a narrow
and welldefined time frame Explosion, industrial release,
earthquake
Nonacute disaster
Disaster with no well defined start point or continuous
production of casualties over a broad time frame
Pandemic infectious disease, incremental release of a biological or
toxin e.g., anthrax sent through mail
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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.
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Lecture 2 : SEIZURE AND MENTAL CHANGES DISORDER STATUS EPILEPTICUS
IGN Budiarsa
Status epilepticus is defined as a continuous or intermittent seizure activity for more than 5 minutes without regaining consciousness. It means the seizure can take the form of
prolonged seizure or repetitive attack without recovery in between. The etiology of status epilepticus approximately 30 of all cases is caused by withdrawal of anticonvulsant,
cerebrovascular diseases and alcohol withdrawal. There are various types of status epilepticus and a classification :
Table below Status epilepticus confined to early childhood
1. Neonatal status epilepticus 2. Status epilepticus in specific neonatal epilepsy syndrome
3. Infantil spasms
Status epilepticus confined to later childhood 1. Febrile status epilepticus
2. Status in childhood partial epilepsy syndrome 3. Status epilepticus in myoclonic – static epilepsy
4. Electrical status epilepticus during slow wave sleep 5. Landau – Kleffer syndrome
Status epilepticus occurring in childhood and adult life 1. Tonic – clonic status epilepticus
2. Absence status epilepticus 3. Epilepsia partialis continua
4. Status epilepticus in coma 5. Specific form of status epilepticus in mental retardation
6. Syndrome of myoclonic status epilepticus 7. Simple partial status epilepticus
8. Complex partial status epilepticus
In clinical practice status epilepticus classified : A. Convulsive status epilepticus
B. Non convulsive status epilepticus
Principle of management of status epilepticus 1. Lifesaving ABC
2. Stop seizures immediately 3. Manage in ICU
Lecture 3 : COMA AND DECREASE OF CONCIOUSNESS IA Sriwijayanti
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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
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breathing, the size and reactivity of pupils and ocular movements, the motor response, the airway clearance, the pattern of breathing and circulation integrity, etc.
Coma may result from a variety of conditions including intoxication, metabolic abnormalities, central nervous system diseases, acute neurologic injuries such as stroke,
hypoxia or traumatic injuries including head trauma caused by falls or vehicle collisions. Looking for the pathogenesis of coma, two important neurological components must
function perfectly that maintain consciousness. The first is the gray matter covering the outer layer of the brain and the other is a structure located in the brainstem called the reticular
activating system RAS or ARAS, a more primitive structure that is in close connection with the reticular formation RF, a critical anatomical structure needed for maintenance of
arousal. It is necessary to investigate the integrity of the bilateral cerebral cortices and the reticular activating system RAS, as a rule. Unilateral hemispheric lesions do not produce
stupor and coma unless they are of a mass sufficient to compress either the contralateral hemisphere or the brain stem Bateman 2001. Metabolic disorders impair consciousness by
diffuse effects on both the reticular formation and the cerebral cortex. Coma is rarely a permanent state although less than 10 of patients survive coma without significant
disability Bateman 2001; for ICU patients with persistent coma, the outcome is grim. Maneuvers to be established with an unconscious patient include cardiopulmonary
resuscitation, laboratory investigations, a radiological examination to recognize brain edema, as well as any skull, cervical, spinal, chest, and multiple traumas. Intracranial pressure and
neurophysiological monitoring are important new areas for investigation in the unconscious patient.
Lecture 4 : ACUTE PSYCHIATRIC EPISODE Tjokorda Bagus Jayalesmana
Objective: 1. To describe etio-pathogenesis and pathophysiology of acute psychiatric episodes
2. To implement a general strategy in the approach to patients with acute psychiatric episodes through history and special technique investigations
3. To manage by assessing, provide initial management and refer patient with acute psychiatric episodes
4. To describe prognosis patient with acute psychiatric episodes Emergency occur in psychiatric just as we do in every field of medicine. However,
psychiatric emergencies are often particularly disturbing because we do not just involve the body’s reactions to an acute disease state, as must as actions directed against the self or
others. These emergencies, such as suicidal acts, homicidal delusions, or a serve in ability to care for oneself, are more likely than medical ones to be sensationalized when they are
particularly dramatic or bizarre. Frequently identified medical causes of abnormal behavior include hypoglycemia, hypoxia, seizures, head trauma, and thyroid abnormalities. Patients
should also be assessed for the presence of delirium or dementia, as both have potentially treatable causes.
Psychosis is difficult term to define and is frequently misused, not only in the newspaper, movies, and on television, but unfortunately among mental health professionals
as well. Stigma and fear surround the concept of psychosis and the average citizens’ worries about long-standing myths of mental illness, including psychotic killers, psychotic rage, and
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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.
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LECTURE 5 : ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE Putu Andrika
ARDS is an emergency in the lung area due to disturbance in alveolocapiler membrane permeability by a number of thing causing liquid accumulationbuild up inside
alveoli or bronchus oedema. While ARF is a kind of ARDS complication which is a distability of lung to do respiration function causing accumulation of CO
2
and decrease in O
2
inside the artery. Incident of ARDS is high. In the USA, 150.000 cases were found per year and 50 of them died due to breathing failure.
Diagnosed based on : complaint, sudden breathing difficulties, coughing, tiredness and decrease in consciousness and usually preceded by basic illness and triggering factors.
On the thorax photo it was found infiltrate diffuse in the two lungs region, while in ARF depend on basic illness. The important thing is examination of blood gas analyses where
there is a decrease on PaO
2
until below 50 and PaO
2
above 50 or refer to as rule of fifty. Principle of procedure is to give the Oxygen, CO
2
removal either with or without ventilator, liquid restriction, clearing of breathing pathway, overcoming obstruction using
bronchodilator, etc.
Learning Objective Students are able to describe pathogenesis, to set diagnoses, propose examination, give
medication and evaluate ARDS and ARF patients.
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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:
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NEONATAL RESUSCITATION and ELECTROLITE IMBALANCE Diah Kanyawati
Abstract Ninety percent of asphyxia insults occur in the antepartum or intrapartum periods a a result
of placental insufficiency. After delivery, the baby’s ineffective respiratory effort and decrease cardiac output. Hypoxic tissues begin anaerobic metabolism, producing metabolic
acids that are initially buffered by bicarbonate. The incidence of perinatal asphyxia usually related to gestational age and birth weight. The
basic goal of resuscitation are : to expend the lungs and maintain adequate ventilation and oxygenation, to maintain adequate cardiac output and tissue perfusion. Neonatal resuscitation
equipment and emergency medications should be immediately available.
RADIOLOGY Srie Laksminingsih
Learning Objective At the end of meeting, the student will be able to :
1. Describe the radiology imaging of thorax photo for IRDS Idiopathic Respiratory Distress Syndrome case, Bronchopneumonia, CHD, Pericardial Effusion, Lung
Edema, Pneumothorax, Pleural Effusion, Vena Cava Superior Syndrome. 2. Describe the imaging of abdominal plain photo in : Illeus Obstruction, Paralytic
Illeus, Stone in the Urinary Bladder, Peritonitis, NEC, Cholelithiasis Acute Cholecystitis.
Lecture 6 : BLEEDING DISORDER HEMORRHAGE IN PREGNANCY : ANTEPARTUM AND POST PARTUM
Wayan Megadhana ANTEPARTUM HEMMORRHAGE
COMPETENCE Manage pregnancy with Placenta previa and abruption placenta
Placenta Previa Definition
A condition where the placenta intrudes the lower uterine segment, which resulted in it covering the internal uterine os partialy or completely during the 20th week of pregnancy or
further.
Classification • Classification:
• Placenta previa: the placenta covers the internal oral ostium partially or completely.
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• 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
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• 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, Virchows 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
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Postpartum hemorrhage PPS is generally defined as blood loss from the genital tract of 500 ml after vaginal delivery or 1000 ml after delivery by cesarean section. This limitation
has become difficult, given the estimated loss of blood is usually not as much as it actually is, sometimes only half from the truth. The blood mixes with amnionic fluid or with urine.
Blood is also absorbed by sponges, towels, and cloths, in buckets and on the floor. Therefore, an estimated loss of blood that exceeds average or 500 mL should be an obstetric concern
for the possibility of excessive bleeding. Postpartum hemorrhage may be minor 500-1000 ml or major 1000 ml. Major bleeding
can be divided into moderate 1000-2000 ml or heavy 2000 ml. Postpartum hemorrhage may be caused by four factors: weakness of uterine tone to stop bleeding from placental
insertion tone, rupture of the perineum, vagina, to uterine lining trauma, placental remains or blood clots that block adequate uterine contractions tissue, and clotting factor disorders
thrombin.
Postpartum hemorrhage is divided into 2, namely: 1. Primary postpartum haemorrhage: postpartum haemorrhage occurring within the first 24
hours of labor. 2. Secondary postpartum haemorrhage: postpartum haemorrhage occurring after the first 24
hours of labor Predisposing factors
- Placental abnormalities • Placenta previa
• Placental Solution • Placenta adhesiva
• Ectopic pregnancy • Hydatidiform mole
- Trauma of the birth canal • Episiotomy
• Obstetric surgery • Sectio cesarea
• Hysterectomy • uterine rupture
- Obstetric factors • Obesity
• Previous post-natal bleeding • Sepsis syndrome
• preeclampsia
- Atonia uteri • Overdistention
• Labor induction • Abnormal labor
- Concomitant coagulopathy • Placental Solution
• IUFD • Massive transfusion
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Etiology 1. Primary postpartum hemorrhage is often caused by placental retention, laceration of birth
canal, rest placenta, uterine atony, uterine inversion, uterine rupture, clotting disorders. 2. Secondary postpartum bleeding is often caused by rest placenta, from a former cesarean
section, infection endometritis. General prevention and treatment
Although efforts have been made to prevent postpartum bleeding, eventually some women still require therapy for excessive bleeding. Multiple interventions medical, mechanical,
invasive surgery, and non-surgical that require different techniques and skills may be needed to control the bleeding. Effective postpartum bleeding therapy often requires simultaneous
multidisciplinary interventions. Health workers should start resuscitation efforts as soon as possible, establish the cause of the bleeding, seek other departments’ healthcare workers,
such as obstetrics, anesthesia and radiology. Avoiding delays in diagnosis and therapy will have a significant impact on sequelae and prognosis life expectancy.
If postpartum hemorrhage occurs, the first cause of bleeding should be determined first, then the management is performed simultaneously, including the repair of uterine tone, evacuation
of residual tissue, and open wound suture accompanied by preparation of clotting factor correction. The following stages of PSS management can be abbreviated as
HAEMOSTASIS. Bleeding is usually caused by tone, tissue, trauma or thrombin. If uterine atony develops,
repair the uterine tone. If the cause of bleeding comes from the tissue, do evacuate the remaining tissue of the placenta. Conduct an open wound suture in case of trauma and
clotting factor correction if there is interference with the thrombin.
Management is done with the principle of HAEMOSTASIS, namely: - Ask for HELP
Immediately request help or be referred to the hospital if the birth is midwife public health. The presence of obstetricians, midwives, anesthesiologists, and hematologists is very
important. - Assess vital parameters, blood loss and Resuscitate
It is important to immediately assess the amount of blood that comes out as accurately as possible and determine the degree of hemodynamic change. The value of the level of
consciousness, pulse, blood pressure, and when facility permits, oxygen saturation should be monitored.
When installing an intravenous line with a 14G-16G albocath, immediate blood samples should be taken to check for hemoglobin, clotting profiles, electrolytes, blood type
determination, and crossmatch - Establish Etiology, Ensure Availability of Blood, Ecbolics Oxytocin, Ergometrin or
Syntometrine bolus IV IM While resuscitation is ongoing, attempts are made to determine the etiology. Evaluate uterine
contractions, look for free fluid in the abdomen, if there is a risk of trauma former cesarean section, difficult artificial delivery or when the patients 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
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compression should be performed using the fist inside to suppress the anterior fornix so that it is pushed upward and the outer palm presses on the back of the fundus so that the uterus is
compressed. - Oxytocin infusion prostaglandins - IV per rectal IM intramyometrial
40 units of Oxytocin in 500 cc of normal saline can be administered with the speed of 125 cc hour. Avoid excess fluid because it can cause pulmonary edema to cerebral edema which
can eventually cause seizures due to hyponatremia. Administration of ergometrine as a second line of oxytocin may be given intramuscularly or
intravenously. Initial dose is 0.2 mg slowly, additional dose of 0.2 mg can be given after 15 minutes if still needed. The dosage may be repeated every 2-4 hours if necessary.
- Shift to theater - exclude retained products and trauma bimanual If massive bleeding persists, immediately evacuate the patient to the operating room. Ensure
examination to exclude any residual placenta or amniotic membrane. If there is suspicion of remaining tissue, do the curettage action immediately. Bimanual compression can be done as
long as the mother is taken to the operating room - Tamponade balloon uterine packing conservative, non-surgical
If bleeding persists, consider the possibility of coagulopathy accompanying refractory atony. Uterine tamponade may help reduce bleeding. This action can also allow for freezing factor
correction. Tamponade test can be done by using Tube Sengstaken which has a positive predictive value of 87 to assess the success of management Postpartum hemmorrhage.
- Apply compression sutures - B-Lynch modified conservative surgery In making decisions, consideration between sustaining life and the desire to maintain fertility
should always be made. Before attempting any conservative surgical procedure, the patient should be reassessed based on the estimation of the amount of blood coming out, ongoing
bleeding, hemodynamic state, and parity.
- Systematic pelvic devascularization - uterine ovarian quadruple internal iliac Ligation a. Uterine and ligation a. Hypogastrics
- Interventional radiologist, if appropriate, uterine artery embolization - Subtotal total abdominal hysterectomy
.
EPISTAXIS SARI WULAN
ENT TEAM Objective
Able : 1. To explained anatomi, histologi and phisiology of the nose
2. To explained etiology that cause epistaksis 3. To explained patophisiology the simtomp of epistaksis
4. To explained and choose the adding examination lab, x-ray, nasoendoscopi 5. To make diagnosis base on phisical diagnostic
6. To explained the therapy of epistaksis 7. To do work-up to epistaksis
Abstract
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Epistaksis is one of emergency case in ENT field, that can be fatal if not threaten well. The bleeding comes from the nose n mouth, because epistaksis caused by an alteration of normal
hemostasis whitin the nose. Hemostasis is compromised by mucosal abnormalities, vessel pathology or disorders of coagulation. Etiology of epistaxis may be local or systemic. The
local epistaxis commonly causes by mild trauma, climate changing, infection. The systemic can be caused by systemic ds, ex. hypertension, malignancy, dengue fever, hemophilia.
Epistaksis mostly can stopped spontaneously, only 1-2 patient must be refered to hospital. Management of epistaxis is stop the bleeding, avoid complication treatment of initial
disorders.
Gambar 1. Vaskularisasi septum nasi
Tabel 1. Etiologi epistaksis
Penyebab lokal Penyebab sistemik
Sering Jarang
Sering Jarang
Trauma wajah Mengorek hidung
Benda asing Perforasi septum
Deviasi atau spina septum Polip hidung
Tumor sinonasal Tumor nasofaring
Hemangioma hidung Mukosa kering
Inhalasi kimiawi Barotrauma
Sinusitis Rinitis
Lesi metastatik Angiofibroma juvenil
Iritasi lingkungan Hereditary Hemorrhagic
Telangiectasia HHT Leukemia
Trombositopenia Anti platelet aspirin,
clopidogrel Polisitemia vera
Anemia aplastik Hemofilia
Obat antikoagulan
heparin, warfarin Defisiensi vitamin K
Penyakit Von Willebrand Tuberkulosis
Mononukleosi s
Demam scarlet
Demam reumatik
Sifilis Penyakit
hepar Uremia
ISPA
Penanganan : Penekanan pada cuping hidung selama 15 menit, disertai kompres es di bagisn
pangkal hidung. Bila perdarahan berlanjut, dapat dipasang tampon anterior. Persiapan alat meliputi lampu kepala, speculum hidung, pinset, alat penghisap suction hidung, alat kauter
dan tampon hidung kassa pita
Gambar 2. Pemasangan tampon pita pada epistaksis
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ALGORITME EPISTAKSIS
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EPISTAKSIS
-Anamnesis riwayat penyakit, tentang perdarahan, riwayat trauma, penggunaan obat2an, kebiasaan
merokok alkohol -Pemeriksaan klinis Laboratorium
Identifikasi lokasi perdarahan rinoskopi anterior, nasoendoskopi rigid fleksible: -Anterior
-Posterior -Lokasi perdarahan tidak jelas
Tindakan lokal menghentikan perdarahan: -kauter kimiawi elektrik
-tampon hidung anterior posterior
Berhasil
-Evaluasi dan terapi kausa untuk mencegah kekambuhan
-Edukasi self care penderita untuk mencegah kekambuhan
Tidak berhasil
Tampon hidung ulang
Berhasil
Tidak ada perdarahan lagi
Angkat tampon 48-72 jam
Perdarahan tidak berhenti Perdarahan
berulang
Intervensi pembedahan: -Septum koreksi
-Ligasi arteri karotis eksterna -Ligasi arteri maksillarisinterna
-Ligasi arteri sfenopalatina -Ligasi arteri etmoidalis
Embolisasi arteri maksilaris cabangnya Radiasi kasus-kasus malignansi
Kasus HHT Laser, fibrin glue, nasal obliterasi
Berhasil
Konsultas-rawat bersama Hematologis-onkologis: Koreksi gangguan koagulopati:
-FFP - vit K
-cryprecipitate -trombosit
Penatalaksanaan dengan fibrin glue Syok hipovolemik, penderita
tua, risiko perdarahan profus Resusitasi cairan
Identifikasi kausa
Gangguan faal perdarahan
LECTURE 7 : SHOCK IN ADULT IGAG Utara Hartawan
OBJECTIVE 1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patients approach to shock through symptoms,