Wed, Thu, study guide tayang blok emergency 2017

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 16 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 Medical Education Unit Faculty of Medicine Udayana University 17 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 Medical Education Unit Faculty of Medicine Udayana University 18 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 Medical Education Unit Faculty of Medicine Udayana University 19 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 Medical Education Unit Faculty of Medicine Udayana University 20 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 Medical Education Unit Faculty of Medicine Udayana University 21 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. Medical Education Unit Faculty of Medicine Udayana University 22 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 Medical Education Unit Faculty of Medicine Udayana University 23 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 Medical Education Unit Faculty of Medicine Udayana University 24 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 Medical Education Unit Faculty of Medicine Udayana University 25 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. Medical Education Unit Faculty of Medicine Udayana University 26 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. Medical Education Unit Faculty of Medicine Udayana University 27 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: Medical Education Unit Faculty of Medicine Udayana University 28 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. Medical Education Unit Faculty of Medicine Udayana University 29 • 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 Medical Education Unit Faculty of Medicine Udayana University 30 • 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 Medical Education Unit Faculty of Medicine Udayana University 31 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 Medical Education Unit Faculty of Medicine Udayana University 32 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 Medical Education Unit Faculty of Medicine Udayana University 33 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 Medical Education Unit Faculty of Medicine Udayana University 34 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 Medical Education Unit Faculty of Medicine Udayana University 35 Medical Education Unit Faculty of Medicine Udayana University 36 ALGORITME EPISTAKSIS Medical Education Unit Faculty of Medicine Udayana University 37 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,