2018 Study Guide Emergency Medicine Block

  

INTRODUCTION

  Emergency Medicine has long been established especially in Australasia, Canada, Ireland, the United Kingdom and the United States, in Asiaothe emergency medicine officially inauguration of Asian Society of Emergency Medicine in Singapore on the 24th of October 1998 at the first Asian Conference on Emergency Medicine which as Prof.DR.dr. Eddy Rahardjo,SpAnKIC and dr. Tri Wahyu Murni sat as member of Board Director. It is thus sometimes seen to be synonymous with emergency medical careand within the province and expertise of almost all medical practitioners. However, theEmergency Medicine incorporates the resuscitation and management of allundifferentiated urgent and emergency cases until discharge or transfer to the care ofanother physician. Emergency Medicine is an inter-disciplinary specialty, one which isinterdependent with all other clinical disciplines. It thus complements and does not seekto compete with other medical specialties. Basic science concepts to help in the understanding of the phatophysiology and treatment of disease.The medical curriculum has become increasingly vertically integrated, with a much greater use of clinical examples and cases to help in the understanding of the relevance of the underlying basic science, The Emergency Medicine block has been written to take account of this trend, and to integrate core aspects of basic science, pathophysiology and treatment into a single, easy to use revision aid.

  Th

  In accordance the lectures that have been full integrated for studens in 6 semester, period of 2012, one of there is The Emergency Medicine Block. There are many topics will be discuss as below: Seizure and mental status changes, acute Psychiatric episode, Acute respiratory distress syndrome and failure, Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding) ,Shock, Cardiac critical care (Cardiac arrest and CPR), Emergency toxicology and poisoning, Pregnancy induce Hypertension, Shoulder dystocia, Urologic concern in critical care, Phlegmon, Acute Blistering and Expoliative skin, Trauma which potentially disabling and Life threatening condition and Basic Clinical Skill Beside those topics, also describes the learning outcome, learning objective, learning task, self assessment and references. The learning process will be carried out for 4 weeks (20 days). Due to this theme has been prepared for the second time, so many locking mill is available on it. Perhaps it will better in the future

  Thank you. Planner

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CURRICULUM CONTENTS

Mastery of basic knowledge with its clinical and practical implication.

  Establish tentative diagnosis, provide initial management and refer patient with :

• Seizure and mental status changes
• 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

  Medical Education Unit Faculty of Medicine Udayana University

  Medical Education Unit Faculty of Medicine Udayana University

PLANNERS / LECTURES TEAM

NO. NAME

  Psychiatric

  Obstetric-Gynecologic

  12. Dr.dr. Gede Megaputra, SpOG(K) HP 08123636172

  Obstetric-Gynecologic

  13. dr. Wayan Yudiana, SpU HP 081338708195

  Urologic Surgery

  14. Dr.dr.Tjokorda Bagus Jayalesmana,SpKJ HP 0816295779

  15. dr. Nyoman Suryawati, SpKK 0817447279

  Obstetric-Gynecologic

  Dermatology 16.

  17.

  18.

  19.

  20.

  21. dr. Sri Laksminingsih SpR (K) HP 08164745561 dr. IA Sriwijayanti,MBioMed,SpS HP 081337667939 dr. IGAG Utara Hartawan,SpAn.MARS dr. Nyoman Budihartawan,M.Sc,SpA HP 081236333221 dr. Pontisomaya Parami, SpAn MARS HP 08113800107 Dr.dr. Ketut Suyasa, SpB. SpOT(K)Spine

  11. dr. Endang Sriwidiyanti, SpOG HP 081558314827

  10. Dr.dr. Wayan Megadana, SpOG(K) HP 08123917002

  DEPARTMENT

  4. dr. Sari Wulan,SpTHT KL HP 081237874447

  1. Dr.dr.Tjok Gde Agung Senapathi,Sp.AnKAR (Coordinator) HP 081337711220

  Anesthesiology and Intensif Terapy

  2. Dr.dr. Gd Wirya Kesuma Duarsa, SpU,MKes HP 08155753377

  Urologic Surgery

  3. dr. IGN Budiarsa,SpS HP 0811399673

  Neurology

  ENT 5.

  Pediatric

  6. Drg. Lestari Sudirman HP 08155764446 Dr.dr. I Putu Pramana Suarjaya,SpAn.M.Kes.KMN.KNA HP 0811394811

  Dentistry Anesthesiology and Intensif Terapy

  7. Dr.dr. Agus Somya, SpPD. KPTI HP 08123989353

  Internal Medicine

  8. dr. Putu Andrika, SpPDKIC HP 08123989192

  Pulmonology

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

  Radiology Neurology Anesthesiology and Intensif Terapy Pediatrician Anesthesiology and Intensif Terapy Ortophedic Surgery HP 081558724088 22. dr. IGN. Wien Aryana,SpOT Ortophedic Surgery

  HP 0811385263 23. dr. Wayan Sucipta,SpTHT KL ENT

  HP 08125318941 24. dr. Ida Bagus Krisna Jaya Sutawan,SpAn.M.Kes Anesthesiology and

  HP 08123836470 Intensif Terapy 25. dr. Made Agus Kresna Sucandra, SpAn KIC Anesthesiology and

  HP 081236214222 Intensif Terapy 26. dr. I Made Darmajaya, SpB, SpBA, MARS Pediatric Surgery

  HP 08123959701 27. dr. AA Gde Yuda Asmara, SpOT Orthopedic Surgery

  HP 081337870347 28. dr. Agus Roy Ruly Hariantana Hamid, SpBP-RE(K) Plastic Surgery

  HP 08123511673 29. dr. Made Agus Dwianthara Sueta, SpB KBD Digestive Surgery

  HP 081338648424

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.

  Medical Education Unit Faculty of Medicine Udayana University

  Medical Education Unit Faculty of Medicine Udayana University Format of the paper :

  1. Cover  Title (TNR 16) Name Green coloured cover Student Registration Number

  Faculty of Medicine, Udayana University 2017

  2. Introduction

  3. Journal critism/literature review

  4. Conclusion

  5. References Example :

  Journal

  Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA Protection from Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79- 84.

  Textbook

  Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 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

  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

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  Medical Education Unit Faculty of Medicine Udayana University Disaster Type

  Definition Examples Natural disaster

  Disaster caused by a naturally occurring event Earthquakes, tsunamis, tornadoes, hurricanes/typhoons, volcanic eruption, pandemic influenza Man-made disaster Nonnatural events that are not purposefully produced Vehicle crashes (e.g., car, plane, bus), mass casualty events, explosions, fires, industrial accident/chemical release Terrorist- related disaster

  Events that are purposefully produced in an effort to cause terror Events of September 11, 2001, as well as intentional chemical, biological, radiologic, or toxin releases

  Internal disaster An event that occurs within the hospital

  Hazardous materials spill in hospital laboratory, fire or explosion within hospital, power failure External disaster An event that occurs external to the hospital Transportation accident, industrial accident Acute disaster Disaster that occurs in a narrow and well-defined time frame Explosion, industrial release, earthquake Nonacute disaster Disaster with no well- defined start point or continuous production of casualties over a broad time frame Pandemic infectious disease, incremental release of a biological or toxin (e.g., anthrax sent through mail)

DISASTER CHARACTERISTICS

  Regardless of the cause, most disasters have common characteristics that are important for disaster preparedness and planning. In an acute disaster, or a disaster with an identifiable time of onset that produces casualties (e.g., explosion, chemical release, fire,

  

earthquake), the event is followed by a large number of minimally injured patients presenting

to the nearest hospitals, usually without prehospital triage or evaluation. This is typically

followed by prehospital transport of the most affected patients to the same hospitals. Initial

patients can be expected within minutes, and peak volumes can be expected at 2 to 3 hours

after the event. The vast majority (~80%) of patients are not transported by prehospital

agencies, but instead self-transport by car, van, police vehicle, cabs, foot, or any means

available to the nearest ED. Even in acute events, ED volumes tend to remain elevated for

days to weeks after events. In nonacute events, such as a pandemic of an infectious disease,

ED volumes have a slower onset of surge, but ED and hospital volumes remain elevated for

extended periods.

  Based on previous events, common factors that may hinder ED response are listed in

  

Table 2. A large amount of federal funding has been supplied to address these issues, but

they likely remain as the major common limitations to effective ED disaster response. Table 2 Factors That May Hinder ED Response to Disasters Poor communication between ED and disaster scene Poor communication within the hospital (e.g., ED to emergency operations center, emer- gency operations center to patient care areas)
 Inability to control volunteer healthcare personnel who are unfamiliar with the ED function and their roles in disaster response Inability to engage and control convergence of media to the ED Inability to engage, control, and direct visitors who are searching for loved ones Inability to control large numbers of patients (i.e., crowd control)
 Difficulty maintaining high staffing needs for extended periods

  DISASTER PREPAREDNESS AND PLANNING

  Planning for any type of disaster consists of common elements. A hospital disaster planning group is responsible for generating the hospi tal’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.

  

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.

  Medical Education Unit Faculty of Medicine Udayana University

  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).

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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

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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

  Medical Education Unit Faculty of Medicine Udayana University 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 3

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

  Medical Education Unit Faculty of Medicine Udayana University 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.

  

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 4

ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE

Putu Andrika

  ARDS is an emergency in the lung area due to disturbance in alveolocapiler membrane permeability by a number of thing causing liquid accumulation/build up inside alveoli or bronchus oedema. While ARF is a kind of ARDS complication which is a distability of lung to do respiration function causing accumulation of 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

  2

  2 there is a decrease on PaO until below 50 and PaO above 50 or refer to as rule of fifty.

  Medical Education Unit Faculty of Medicine Udayana University

  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.

  

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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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

  Medical Education Unit Faculty of Medicine Udayana University

  Medical Education Unit Faculty of Medicine Udayana University 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 Mononukleos is 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

• 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 perdara
• Evaluasi dan terapi kausa untuk mencegah kekambuhan
• Edukasi &self care penderita untuk mencegah kekambuhan
• kauter (kimiawi/ elektrik)
• tampon hidung ( anterior & posterior)
• 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)
• FFP - vit K -cryprecipitate -trombosit Penatalaksanaan dengan fibrin glue Syok hipovolemik, penderita tua, risiko perdarahan profus Resusitasi cairan

  Medical Education Unit Faculty of Medicine Udayana University

ALGORITME EPISTAKSIS

EPISTAKSIS

  Berhasil

  Tidak berhasil Tampon hidung ulang

  Berhasi l Tidak ada perdarahan lagi Angkat tampon 48-72 jam

  Perdarahan tidak berhenti Perdarahan berulang Intervensi pembedahan:

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

  Identifikasi kausa Gangguan faal perdarahan

  

Lecture 5

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.
• 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)

  Medical Education Unit Faculty of Medicine Udayana University

• 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.

  Medical Education Unit Faculty of Medicine Udayana University