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.
In accordance the lectures that have been full integrated for studens in 6Th semester, period of 2012, one of there is The Emergency Medicine Block.
There are many topics will be 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
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
PLANNERS / LECTURES TEAM
NO. NAME DEPARTMENT
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
8. dr. Putu Andrika, SpPDKIC HP 08123989192
Pulmonology
9. Dr.dr.Dyah Kanyawati, SpA(K) HP 081285705152
Pediatric
10. Dr.dr. Wayan Megadana, SpOG(K) HP 08123917002
Obstetric-Gynecologic
11. dr. Endang Sriwidiyanti, SpOG HP 081558314827
Obstetric-Gynecologic
12. Dr.dr. Gede Megaputra, SpOG(K) HP 08123636172
22.
dr. Ida Bagus Krisna Jaya Sutawan,SpAn.M.Kes HP 08123836470
dr. Made Agus Kresna Sucandra, SpAn KIC HP 081236214222
dr. I Made Darmajaya, SpB, SpBA, MARS HP 08123959701
dr. AA Gde Yuda Asmara, SpOT HP 081337870347
dr. Agus Roy Ruly Hariantana Hamid, SpBP-RE(K) HP 08123511673
dr. Made Agus Dwianthara Sueta, SpB KBD HP 081338648424
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
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. 4th ed. Pennysylvania: WB Saunders Co. Pp 1636-1642.
Note.
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).
Disaster
Vehicle crashes (e.g., car, plane, bus), mass casualty events, explosions, 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
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
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.
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.
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
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
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)
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).
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
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 CO2 and decrease in O2 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.
Principle of procedure is to give the Oxygen, CO2 removal either with or without ventilator, liquid restriction, clearing of breathing pathway, overcoming obstruction using bronchodilator, etc.
Learning Objective
Students are able to describe pathogenesis, to set diagnoses, propose examination, give medication and evaluate ARDS and ARF patients.
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.
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
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 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)
ALGORITME EPISTAKSIS
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
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.
• 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
• Clinical symptoms are often followed by increased contraction and persistent hypertonia. • Clinical symptoms: fetal tachycardia / IUFD, Virchow's triad of focal or common uterine pain, increased tone, and vaginal bleeding (85%), 15% in concealed type. Ultrasound: helps in concealed types which is retroplacental sonolucent areas, placental site to differentiate with placenta previa.
Management
• Management of placental abruption depends on clinical conditions, gestational age and amount of bleeding.
• Perform blood / fluid resuscitation as needed
• If the fetus dies or not mature enough to live outside the uterus, vaginal delivery may be considered.
• Cesarean section, respond time is important for perinatal outcome.
POSTPARTUM HEMMORRHAGE
COMPETENCE
1. Management of postpartum hemorrhage
Definition and classification
Postpartum hemorrhage (PPS) is generally defined as blood loss from the genital tract of > 500 ml after vaginal delivery or > 1000 ml after delivery by cesarean section. This limitation has become difficult, given the estimated loss of blood is usually not as much as it actually is, sometimes only half from the truth. The blood mixes with amnionic fluid or with urine. Blood is also absorbed by sponges, towels, and cloths, in buckets and on the floor. Therefore, an estimated loss of blood that exceeds "average" or 500 mL should be an obstetric concern for the possibility of excessive bleeding.
Postpartum hemorrhage may be minor (500-1000 ml) or major (> 1000 ml). Major bleeding can be divided into moderate (1000-2000 ml) or heavy (> 2000 ml). Postpartum hemorrhage may be caused by four factors: weakness of uterine tone to stop bleeding from placental insertion (tone), rupture of the perineum, vagina, to uterine lining (trauma), placental remains or blood clots that block adequate uterine contractions (tissue), and clotting factor disorders (thrombin).
Postpartum hemorrhage is divided into 2, namely:
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
- Trauma of the birth canal • Episiotomy
• Obstetric surgery • Sectio cesarea • Hysterectomy • uterine rupture
- Obstetric factors • Obesity
• Previous post-natal bleeding • Sepsis syndrome
• preeclampsia
- Atonia uteri • Overdistention • Labor induction • Abnormal labor
- Concomitant coagulopathy • Placental Solution
• IUFD
• Massive transfusion
Etiology
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 patient's condition is worse than the amount of blood coming out.
When placental retention occurs after vaginal delivery, uterine tamponade may be conducted while waiting for surgery / laparotomy
- Massage the uterus
Massive bleeding that occurs after the birth of placenta should be treated promptly with uterine massage and uterotonic drug delivery. If the uterus remains soft, internal bimanual compression should be performed using the fist inside to suppress the anterior fornix so that it is pushed upward and the outer palm presses on the back of the fundus so that the uterus is compressed.
- Oxytocin infusion / prostaglandins - IV / per rectal / IM / intramyometrial
40 units of Oxytocin in 500 cc of normal saline can be administered with the speed of 125 cc / hour. Avoid excess fluid because it can cause pulmonary edema to cerebral edema which can eventually cause seizures due to hyponatremia.
Administration of ergometrine as a second line of oxytocin may be given intramuscularly or intravenously. Initial dose is 0.2 mg (slowly), additional dose of 0.2 mg can be given after 15 minutes if still needed. The dosage may be repeated every 2-4 hours if necessary.
- Shift to theater - exclude retained products and trauma / bimanual
If massive bleeding persists, immediately evacuate the patient to the operating room. Ensure examination to exclude any residual placenta or amniotic membrane. If there is suspicion of remaining tissue, do the curettage action immediately. Bimanual compression can be done as long as the mother is taken to the operating room
- Tamponade balloon / uterine packing (conservative, non-surgical)
If bleeding persists, consider the possibility of coagulopathy accompanying refractory atony. Uterine tamponade may help reduce bleeding. This action can also allow for freezing factor correction. Tamponade test can be done by using Tube Sengstaken which has a positive predictive value of 87% to assess the success of management Postpartum hemmorrhage. - Apply compression sutures - B-Lynch / modified (conservative surgery)
- 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
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NEONATAL RESUSCITATION and ARDS (PEDIATRIC) Diah Kanyawati
Abstract
Ninety percent of asphyxia insults occur in the antepartum or intrapartum periods a a result of placental insufficiency. After delivery, the baby’s ineffective respiratory effort and decrease cardiac output. Hypoxic tissues begin anaerobic metabolism, producing metabolic acids that are initially buffered by bicarbonate.
The incidence of perinatal asphyxia usually related to gestational age and birth weight. The basic goal of resuscitation are : to expend the lungs and maintain adequate ventilation and oxygenation, to maintain adequate cardiac output and tissue perfusion. Neonatal resuscitation equipment and emergency medications should be immediately available.
Lecture 6 SHOCK IN ADULT IGAG Utara Hartawan
OBJECTIVE
1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patient's approach to shock through symptoms, physical examination and special technique examination.
3. Able to perform assessment, differential diagnosis, provide early treatment and refer patients with shock
4. Knowing the patient's prognosis with shock
INTRODUCTION
indicate abnormal cellular oxygen metabolism (> 1.5 mmol per liter). Shocks are classified as: hypovolemic, cardiogenic, obstructive and distributive.
PATHOPHYSIOLOGY
Shock may originate from four conditions of pathophysiological mechanisms: hypovolemia (from internal or external fluid loss), cardiogenic factors (eg, acute myocardial infarction, end-stage cardiomyopathy, advanced heart valve disease, myocarditis, or cardiac arrhythmias), obstructive (eg embolism Lung, cardiac tamponade, or tension pneumothorax), and distributive factors (such as severe sepsis or anaphylaxis with the release of inflammatory mediators). The first three mechanisms are characterized by low cardiac output and, therefore, inadequate oxygen transport. In distributive shocks, the major deficits are located on the peripheral, accompanied by decreased systemic vascular resistance and oxygen extraction disorders. Usually, in such cases cardiac output increases, although it may be low due to associated myocardial depression. Patients with acute circulatory failure often have this combination. For example, patients with distributive shock from severe pancreatitis, anaphylaxis, or sepsis also experience hypovolemia and cardiogenic shock in the form of myocardial depression.
The three main factors that determine the delivery of oxygen to the tissues are
cardiac output, defined as the stroke volume of heart rate; oxygen saturation bound to Hgb / O2 X100 capacity and the amount of dissolved oxygen in the blood, defined as O2 content (ml/dl blood) = ( Hgb x 1.39 X% sat O2 + (0.003 x PaO2).
Any or all of these factors may be disrupted resulting in a decrease in the release of oxygen to tissue levels in the vital organs. The result of a disturbance in these vital organs is called shock. Shock begins with a simple state, to the very severe state of the imbalance between the supply and the need for oxygen.
Hypovolaemia leads to increased activity of baroreceptor of the aortic arch and carotid. There is also an increase in baroreceptor activity in the right atrium. The activity of the sympathetic nervous system increases and results in stimulation of the heart and peripheral vasoconstriction. The pituitary gland releases ACTH and ADH, resulting in increased cortisol levels in the blood and sodium and water retention. Increased adreno-cortical activity was soon followed by epinephrine and norepinephrine release. Increased plasma renin-angiotensin-aldosterone results in greater water and sodium retention and peripheral vasoconstriction occurs more severely. As the hypovolemia weighs up, the compensation mechanism becomes lost and the organ functional disorder becomes more severe.
In addition, the vasoactive hormone is released during shock syndrome, such as prostaglandin, histamine, bradykinin, serotonin, β-endorphin, MDF (myocardial depressant factor) and cachectin. All of these substances will affect the perfusion of internal organs and may increase the permeability of blood vessels and myocardium and platelet function.
SYMPTOMPS
in chronic hypertension. In hypotension that accompanies shock occurs mental status changes ranging from agitation, anxiety accompanied by feelings of hovering, then going into a coma. This occurs due to the decrease of cerebral perfusion below the critical value. Of course the patient's response will be clear and appropriate after resuscitation action to improve the hemodynamic state in shock.
Table 1. Early symptoms on shock
Organ System Clinical signs / symptoms Cause
CNS Decrease of consciousness Decrease in CPP
CVS Tachycardia The Adrenergic Stimulus
Dysrhythmias Ischemic Coronary
Hypotension Decreased contractility,
MDF ischaemia, or RVF, also decreased SVR or preload
Murmurs Valvular dysfunction
JVP increase / decrease Decrease in volume / preload or RV failure
Respiration Takipneu Pulmonary edema,
respiratory muscle failure, sepsis, acidosis, hypoxemia
Renal Oliguria Decreased perfusion,
constriction of afferent arterioles
Skin Cold, pale, sweat Vasoconstriction,
sympathetic stimulation
Other Lactic acidosis Anaerobic metabolism
Fever Infection of hepatic
dysfunction
CNS=central nervous system; CVS=cardiovascular system; CPP=cerebral perfusion pressure; MDF=myocardial depressant factor; RVF=right ventricular failure; SVR=systemic vascular resistance.
The state of shock will affect the heart. Coronary perfusion pressure (pressure difference between diastolic pressure and left ventricular diastolic end pressure) will decrease due to hypotension and shock. Tachycardia or bradycardia reflex will also decrease diastolic filling of the coronary arteries. A decrease in mean arterial pressure is an important sign due to decreased systolic blood pressure; Peripheral vascular pressure increases and cardiac output decreases.
pulmonary edema and respiratory failure that may occur along with hypoxemia. If diastolic pressure decreases, coupled with increased LVEDP (left ventricle end-diastolic pressure) indicates coronary hypo perfusion and myocardial ischemia. Diastolic blood pressure is directly related to arterial vasoconstriction, whereas pulse (systolic-diastolic) is associated with large stroke volume and number of aortic branches and aortic stiffness. Systolic blood pressure reflects all combinations of these factors. In cardiogenic shock that may be due to chronic heart failure (CHF), shortness, tachypnea, pulmonary edema with a decrease in PaO2 and the sound gallop or the third heart sounds (S3 gallop).
The renal auto regulation system is also maintained, but with decreased perfusion due to hypotension, decreased glomerular filtration, which is clinically known as oliguria (<25-30 ml / hr / 70 kg). In this situation there will be redistribution of cortical renal blood flow to the medulla and urine becomes more concentrated. Sodium urine decreased <10 mEq / L. The presence of oliguria is one sign of shock, and urine repair is an important key in successful resuscitation in shock patients. Sometimes a lot of urine production occurs in renal failure and is confusing at the start of the diagnosis, especially in kidneys with normal or increased urine production.
Integumentary systems are also affected by decreased perfusion and vasoconstriction reflected from cold skin, changing from pale to grayish to cyanosis. The activity of the sympathetic nervous system results in increased production of sweat (a cholinergic sympathetic response).
Metabolic acidosis almost always accompanies shock with the accumulation of lactic acid into hypoxemia. Anaerobic metabolism as a complication due to decreased liver function that can produce lactic acid.
Thus, shock indicates a perfusion disorder characterized by decreased cardiac output or distribution disturbance. It may also be the inability of the tissue to utilize a substrate, thereby resembling a state of hypo perfusion. Blood flow to various organs is seen from the relationship between perfusion pressure and blood vessel resistance in these organs. In shock, this relationship is influenced by many factors.
PRIORITY AND TARGET THERAPY
Shock Hipovolemik/Hemoragik
In hypovolemic shock indicates the occurrence of bleeding. It is important to know the percentage of blood volume lost as a basis in providing appropriate therapy. In general, physical examination alone is not enough, but by following the scheme this can be helped. As an assumption that the perceived normal blood volume is 7.5 ml / kgbb, the hypovolemic shock is divided into four groups based on the estimated number of bleeds:
I. 10-15% blood loss from Estimate Blood Volume (EBV) causes mild tachycardia and shock has not occurred.
II. Blood loss of 15-25% of EBV (1000-1250ml / 70kg) arises moderate shock, with tachycardia, systolic pressure and pulse pressure drop, slightly increased diastolic pressure, slow capillary refill. Urine production is still within normal limits.
III. Blood loss 25-35% EBV (1250-1750 ml / 70kg) causes severe shock, with prominent symptoms: the skin is cold, wrinkled, and pale. Blood pressure decreased between 30-40% (systolic pressure and pulse pressure) and an increase in diastolic pressure of about 15-20%. Vasoconstriction stands out and oliguria develops. Prominent CNS disorder is confusion, which is severe until stupor occurs. Tachypnea results from secondary metabolic acidosis to hypoxemia, tissue hypo perfusion and anaerobic metabolism. The pulse rate is greater than or equal to 120x / min.
IV. Blood loss of 35-45% of EBV (1750-2250 ml / 70 kg) causes very severe shock, usually a preterminal condition. Unmeasured blood pressure, peripheral pulses are not palpable and carotid pulse is also may not palpable.
Hemorrhagic shock is accompanied by hemodilution and widespread plasma volume expansion at any given time and therefore, the hematocrit does not change for 3 to 4 hours in acute bleeding.
SHOCK CARDIOGENIC
Cardiogenic shock (CGS) is a shock characterized by many factors that interfere with the normal functioning of the heart, or (in particular) adverse factors to preload, afterload, contractility, heart rate or heart rhythm. For example right or left ventricular myocardial infarction, and in situations where cardiac pump failure, or ventricular filling or impaired cardiac discharge.
SEPTIC SHOCK
Incident and Etiology
One of the most common forms of distributive shock is septic shock. The complication of this shock is about 40% of cases by bacteremia gram negative, with a mortality rate of around 40-90%. Septic shock may be caused by bacteria, both negative and gram-positive (gram - endotoxin and gram + endotoxin); For example, staphylococci, S. pneumonia, N.meningitidis, H.gonorrhea or Clostridia, sepsis; Fungi, rickettsia or viruses. Lipopolysaccharides from endotoxin released from gram-negative cell wall bacteria may be a major part of this syndrome. Septic shock is caused by sequester or misdistribution of normal or high cardiac output in different parts of the body. Tumor necrosis factor (cachectin) is known to be a very important mediator of clinical and humoral manifestations in shock caused by endotoxins (A- and -O lipid chains) or by all gram-negative bacteria. Vasoactive mediators such as histamine, complement activation, quinine activation (especially precancerrein), prostaglandins and possibly other substances that give rise to vasodilation without compensation to maintain cardiac output. Leucocyte aggregation may cause capillary blockage with inadequate blood flow results in capillaries. Micro vascular thrombosis is determined by the amount of platelets and clotting factors and manifestations of stimuli of fibrinolysis systems such as DIC and resulting bleeding. DIC is caused by sepsis associated with a decrease of factor XII, but endotoxin is triggered by intrinsic and extrinsic blood clotting systems.
One theory says that hemorrhagic shock can develop into septic shock as a result of increased permeability of mucous membranes that facilitate enteric bacteria entering the bloodstream. In this model, severe cellular damage increases the permeability of cell membranes and extracellular fluid displacement into cells associated with impaired cell barrier function and disrupts the entry of gram negative or gram-positive bacteria into the bloodstream. This cellular damage can be overcome if resuscitation is successful, secondary phase bacteremia can be delayed. Survival may be improved if pre shock therapy is anticipated with broad-spectrum antibiotics. Both positive and gram-negative bacteria appear to cause both cardiovascular abnormalities.
Clinical Manifestations
normal cardiac output with low cardiac filling pressure and decreased systemic vascular resistance. The oxygen saturation of the mixed-vein may be normal or low. In high cardiac output, where abnormal systolic function (decreased stroke volume and decreased ejection of left ventricular fraction) and ventricular compliance. The relationship between pulmonary capillary pressure (PCWP) and left ventricular diastolic end (LVEDV) volume is not normal. At the next stage, there is a decrease in dynamic state and the picture resembles a cardiogenic shock. Regarding respiration, where respiratory frequency increases, hyperpnoea, tachypnea and respiratory alkalosis. The antigen-antibody complex activates the complement system. Septicemia is often followed by ARDS as a complication. Patients with manifest dyspnea, hypoxemia, bilateral diffuse pulmonary infiltrate, reduction of lung compliance and have usually unchanged pulmonary capillary pressure from the baseline (especially if lung function before shock is normal).
Therapy
The primary goal of treating patients with septic shock is eradication / removal of causal factors, such as infection, the harmful effects of bacterial toxins or endogenous toxins from the host and attempts to improve the cardiovascular system and other systems. Many ongoing research experiments to study drugs to counteract the effects of toxins on septic shock. For the practical use of anesthesia, most of these are clinically unimportant and are mentioned only for the completeness of the data. Currently, monoclonal antibodies as part of gram-negative bacteria, naloxone, prostaglandin inhibitors, lipid X, tumor necrosis factor antibodies (TNF), genetically engineered protease inhibitors and other recombinants or synthetic protease inhibitors. Cardiovascular support for septic shock patients consists of fluids and vasopressors required.
Fluid is required for optimization of preload and cardiac output above normal values so that MAP returns to the baseline if possible or at least initially 60 mmHg. Pulmonary capillary pressure (PCWP) is optimally 12-15 mmHg and should be monitored by invasive techniques with pulmonary artery catheter. The selected fluid type did not seem to provide much benefit with respect to the expected results, although experimental experiments in experimental animals with septic shock resulted in a significant improvement in cardiac output, Lung Water Extravascular Extension (PVR) and Venous Admixture (VR) vascular cavity when given Dextran 70 compared to Ringer's Lactate. Fluid resuscitation has shown effective results for increasing oxygen delivery (DO2) and oxygen consumption (VO2) in septic shock.
OBSTRUCTIVE SHOCK
Obstructive shock is a form of shock associated with physical obstruction of the great vessels or the heart itself. Pulmonary embolism and cardiac tamponade are considered forms of obstructive shock. Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped together. It was described as involving obstruction to flow in the cardiovascular circuit and characterized by impairment of diastolic filling or excessive afterload. The consequent obstruction of blood flow into or out of the heart causes a decrease in cardiac output, and hence inadequate oxygen delivery, which is manifest by the classic signs and symptoms of the shock state. Obstructive shock is rare in pediatrics, though the most common causes generally include tension pneumothorax, cardiac tamponade, and pulmonary embolism. Also included in this category physiologically, and more specific to pediatrics, are congenital heart lesions characterized by left ventricular outflow tract obstruction, including critical aortic stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart syndrome. Herein, we will briefly review the major causes of obstructive shock found in children.
Tension Pneumothorax
A pneumothorax is defined as the accumulation of air in the pleural space, a cavity that is normally filled with a small amount of pleural fluid. It can be spontaneous (more common in adolescent males) or secondary to underlying lung pathology, such as trauma (both penetrating and blunt trauma), asthma, cystic fibrosis, and pneumonia. Also included in this subcategory are iatrogenic causes such as barotrauma during positive pressure ventilation or during placement of central venous catheters in the chest vessels.
The incidence of secondary pneumothorax in pediatric patients is not well described, however, in critically ill children requiring mechanical ventilation it is reported to be 4-15%. Notably, the incidence of secondary pneumothorax in mechanically ventilated pediatric patients has declined markedly since the introduction of protective lung strategies. Pneumothoraces can be well tolerated in some patients, though signs and symptoms of obstructive shock can develop if the pneumothorax is under tension. In this
scenario, the air
Cardiac Tamponade
The pericardial sac around the heart is relatively noncompliant, and the accumulation of even small amounts of fluid can be sufficient to produce cardiac tamponade physiology. While acute pericardial fluid changes are usually symptomatic, the chronic accumulation of fluid may occur with little to no hemodynamic derangements, as the pericardium slowly stretches to accommodate the excess volume over time. Pericardial effusions can develop as a result of any type of pericardial inflammation (i.e., pericarditis), causing a range of physiologic perturbations along the spectrum of minor flu-like symptoms (i.e., manifestations of the pericarditis itself) to a life-threatening state characterized by cardiac tamponade and obstructive shock. Historically, the most common
cause of
pericardial effusions was infectious pericarditis, though a recent review suggests that idiopathic and neoplastic causes are much more frequent due to the success of childhood vaccinations. Other common causes include postpericardiotomy syndrome (following cardiac surgery for congenital heart disease) and trauma, most often causing hemopericardium. Effusions may also develop as a result of a central line that erodes through the thin wall of the right atrium, a phenomenon that appears primarily limited to neonates and young infants. The pathophysiology of cardiac tamponade is welldescribed. Briefly, increased intrapericardial pressure limits venous return to the heart and causes right ventricular compression. There is a progressive decline in right ventricular end-diastolic volume as end-diastolic filling lessens, worsening cardiac output. In severe
tamponade, venous
return during inspiration into the compressed right ventricle bows the interventricular septum into the left ventricle, further diminishing systemic cardiac output. As pericardial pressure increases and surpasses ventricular end-diastolic pressure, the ventricular volumes grow smaller and smaller and cardiac output worsens. Tamponade is a clinical diagnosis and classically, patients with critical cardiac tamponade present with Beck’s triad of symptoms including hypotension, quiet (“muffled”) heart sounds, and raised jugular venous pressure. Patients may present with dyspnea, compensatory tachycardia, and poor perfusion. On auscultation, a friction rub and distant heart sounds may be
present. Pulsus
paradoxus, defined as a decline in systolic blood pressure greater than or equal to 10 mm Hg during inspiration, results from the inspiratory reduction in pleural pressure that produces a fall in left ventricular output and arterial systolic pressure. An electrocardiogram may show electrical alternans due to the heart swinging within the large effusion. Formal evaluation with an urgent echocardiogram should be performed in those patients with symptoms suspicious for cardiac tamponade. However, emergent management should not wait for echocardiography and is frequently based upon the recognition of tamponade physiology in the appropriate clinical context. Pericardiocentesis is the lifesaving procedure of choice for children with cardiac tamponade and can safely be done with bedside echocardiographic guidance. Medical stabilization with fluid resuscitation and inotropic support is temporary at best and
somewhat controversial as fluid
resuscitation may worsen tamponade physiology, especially in children who are either normovolemic or hypervolemic. In the latter scenario, fluid administration will increase intracardiac pressures further, hence increasing intrapericardial pressures and worsening tamponade.
Pulmonary embolism (PE) is uncommonly diagnosed in children, making its true incidence difficult to determine. However, the incidence of PE does appear to be on the rise, though this may be due to a heightened index of clinical suspicion and better recognition by pediatric providers. Alternatively, it may be due to the fact that more
children are
surviving from previously fatal conditions that place them at an increased risk for developing PE, such as congenital heart disease and malignancy. In addition, more children are requiring central venous catheterization for vascular access, a major risk factor for venous thromboembolism (VTE), which can lead to a PE. PE is frequently fatal and difficult to diagnose. In a recent literature review comparing pediatric PE with adult PE, pediatric cases were more often diagnosed at autopsy and were associated with a higher mortality rate than adults. The clinical presentation often is confusing, perhaps compounded by the fact that very few pediatricians have much experience with this
disorder. Results of screening
tests, such as oxygen saturation, electrocardiography, and chest radiography, may be normal. Thus, a high index of clinical suspicion is necessary. Evaluation should be performed with spiral computed tomography (CT) venography, which is now widely considered the study of choice due to its >90% sensitivity and specificity in adults. Ventilation/ Perfusion (V/Q) scans are also available but are more difficult to obtain and to interpret in pediatrics. As a cause of cardiogenic shock, a massive PE has a profound impact upon gas exchange and hemodynamics. Obstruction to flow through the pulmonary artery results in increased dead space ventilation where affected lung segments are ventilated but not perfused, observed clinically as a substantial decrease in the end-tidal CO2 (ETCO2) that no longer reflects arterial PCO2. A widened alveolar-arterialgradient (A-a) is present as well. The mechanism for hypoxemia likely involves several mechanisms. In some pediatric patients, an intracardiac right-to-left shunt through a patent foramen ovale may be present and as right atrial pressure increases and eventually exceeds the left atrial pressure, deoxygenated blood can shunt directly into the systemic circulation. In addition, V/Q mismatching is compounded by the accompanying fall in cardiac output that results from massive PE, leading to mixed venous desaturation. PE increases the right ventricular (RV) afterload, resulting in an increase in the RV end-diastolic volume (EDV). The increase in RVEDV adversely affects left ventricular hemodynamics through ventricular interdependence. Specifically, the interventricular septum bows into the left ventricle (LV) and impairs diastolic filling, resulting in decreased LV preload and subsequently diminished cardiac output and hypotension. These physiologic phenomenon are manifested by respiratory distress, hypoxia, and decreased cardiac output with signs of shock.
Treatment of an acute pulmonary embolus in children should begin with initiation of a heparin infusion with or without fibrinolytic agents such as tPA, depending on the child and the extent of the clot. In the resolution period, the child will then warrant at least 3-6 months of anticoagulation with low molecular weight heparin (LMWH) or warfarin.
MONITORING SHOCK Hemodynamic Monitoring
