Laporan Diskusi Kelompok Blok Emergency Medicine System Semester 6

Nama Nim Kelas Tutorial Fasilitator

: Lim Ru Xian : 060100226 : B-14 : dr. Zukesti Effendi, Histologi

Fakultas Kedokteran Universitas Sumatra Utara 2009

BLOCK TEAM : Septic Shock (Pediatric) FASILITATOR TUTOR : dr. Zukesti Effendi, Histologi DATA : A. Date of tutorial: 13 APRIL 2009 dan 16 APRIL 2009 B. Case no-2 C. Time : 10.00-12.30 WIB D. Venue : Tutorial room-14 CASE : Andi, seorang anak laki-laki berusia 1 tahun, datang di bawa ibunya ke RS karena mengalami penurunan kesadaran. Setibanya di RS, didapati Andi mengalami kejang pada seluruh tubuh. Dari anamnesis dijumpai riwayAt mencret dan demam sejak 1 minggu sebelumnya. Buang air kecil tidak dijupai 1 hari yang lalu. Dari pemeriksaan fisik dari pemeriksan fisik dijumpai sianosis, fekuensi napas 80x/menit (tampak pernapasan cuping hidung, rektraksi di suprasteral, intercostal dan epigastrial) frekuensi jantung 16-0x/menit, akral dingin dan pols tidak teraba. Tindakan apa yang harus segera dilakukan pada Andi? MORE INFO I: Setelah pemberian cairan sebanyak 60cc/ kbBB, pols masih belum teraba pemeriksan fisik lain yang didapat sat ini adalah : -Frekuensi nadi menjadi 150x/menit, reguler, teraba halus -Akral : teraba dingin, CRT > 3 detik -Tekanan darah : 60/40 mmHg -SKG : 6 -Urine : sedikit (5 cc), berwarna kuning pekat Kegawatan apa yang terjadi pada Andi dari awal hingga jatuh pada kondisinya sekarang, dan tindakan apa yang harus dilakukan selanjutnya? MORE INFO II: Hasil pemeriksaan laboratorium adalah : -Hb 14 gr/dL -Lekosit 20.000/mm3 -Hematokrit 42% -Trombosit 115.000/mm3 -Natrium : 130 mEq/dL, Kalium : 2,1 mEq/dL, Chloride : 110 mEqq/dL Dari hasil di atas, bagaimana pendapat anda sekarang mengenai keadaan bayi ini ?

LEARNING ISSUES: 1) Pediatric Assessment Triangle ( PAT) 2) Pediatric Basic Life Support (PBLS) and Pediatric Advanced Life Support (PALS) 3) Etiology for pediatric shock 4) Pediatric diarrhea 5) Pathophysiology of shock and diarrhea 6) Fluids resusitation 7) Fever 8) Septic shock 9) Management of elektrolyte 10) Etiology of loss of conciousness and febrile seizures 11) Pathophysiology of loss of conciousness and febrile seizures 12) Workup and interpretation the results of this emergency medicine case 13) Monitoring and reevaluation patient in this emergency medicine case 14) Definitive Care 15) Pediatric Intensive Care Unit (PICU) WE DONT KNOW: 1) Seizures- Defination? etiology? Treatment? 2) What is loss of consciousness? 3) Electrolyte disturbances- Defination? Causes? Classification? Pathophysiology? Diagnosis? Treatment? 4) What is shock? 5) What is PAT? 6) What is PBLS? 7) Whar is Septic shock? 8) Why cyanosis? 9) Interpretation of case,more info 1 and 2? 10) The management of pediatric emergency medicine case? ANSWER : 1) Pediatric Assessment Triangle ( PAT) PEDIATRIC ASSESSMENT General Impression (First view of patient) Airway & Appearance (Open/Clear Muscle Tone /Body Position) Abnormal: Abnormal or absent cry or speech. Decreased response to parents or environmental stimuli. Floppy or rigid muscle tone or not moving. A Normal: Normal cry or speech. Responds to parents or to environmental stimuli such as lights, keys, or toys. Good muscle tone. Moves extremities well.

Work of Breathing (Visible movement / Respiratory Effort) Abnormal: Increased/excessive (nasal flaring, retractions or abdominal muscle use) or decreased/absent respiratory effort or noisy breathing. Normal: Breathing appears regular without excessive respiratory muscle effort or audible respiratory sounds. Circulation to Skin (Color / Obvious Bleeding) Abnormal: Cyanosis, mottling, paleness/pallor or obvious significant bleeding. Normal: Color appears normal for racial group of child. No significant bleeding. Decision/Action Points: Any abnormal findings or life-threatening chief complaint such as major trauma/burns, seizures, diabetes, asthma attack, airway obstruction, etc (urgent) proceed to Initial Assessment. Contact ALS if ALS not already on scene/enroute. All findings normal (non-urgent) proceed to Initial Assessment. Initial Assessment (Primary Survey) Airway & Appearance (Open/Clear Mental Status) Abnormal: Obstruction to airflow. Gurgling, stridor or noisy breathing. Verbal, Pain, or Unresponsive on AVPU scale. Normal: Clear and maintainable. Alert on AVPU scale. Breathing (Effort / Sounds / Rate / Central Color) Abnormal: Presence of retractions, nasal flaring, stridor, wheezes, grunting, gasping or gurgling. Respiratory rate outside normal range. Central cyanosis. Normal: Easy, quiet respirations. Respiratory rate within normal range. No central cyanosis. Circulation (Pulse Rate & Strength / Extremity Color & Temperature / Capillary Refill / Blood Pressure) Continue assessment throughout transport Abnormal: Cyanosis, mottling, or pallor. Absent or weak peripheral or central pulses; Pulse or systolic BP outside normal range; Capillary refill > 2 sec with other abnormal findings. Normal: Color normal. Capillary refill at palms, soles, forehead or central body 2 sec. Strong peripheral and central pulses with regular rhythm.

Decision/ Action Points: Any abnormal finding (C, U, or P) Immediate transport with ALS. If ALS is not immediately available, meet ALS intercept enroute to hospital or proceed to hospital if closer. Open airway & provide O2. Assist ventilations, start CPR, suction, or control bleeding as appropriate. Check for causes such as diabetes, poisoning, trauma, seizure, etc. Assist patient with prescribed bronchodilators or epinephrine auto-injector, if appropriate. All findings on assessment of child normal (S) Continue assessment, detailed history & treatment at scene or enroute. Normal Respiratory Rate: Normal Pulse Rate: BP: Infant (<1yr): 30- 60 Toddler (1-3yr): 24 -40 Preschooler(4-5yr): 22- 34 School-age(6-12yr): 18 -30 Adolescent(13-18yr): 12 -20
yr)

Lower Limit of Normal Systolic Infant: >60 (or strong pulses) Toddler: >70 (or strong pulses) Preschooler: >75 School-age: >80 Adolescent: >90 Estimated min.SBP >70 +(2x age in

Infant: 100-160 Toddler: 90-150 Preschooler: 80-140 School-age: 70-120 Adolescent: 60-100 . Pulses slower in sleeping Children/athlete

Pediatric CUPS (with examples) 1) Critical- Absent airway, breathing or circulation (cardiac or respiratory arrest or severe traumatic injury) 2) Unstable- Compromised airway, breathing or circulation (unresponsive, respiratory distress, active bleeding, shock, active seizure, significant injury, shock, near-drowning, etc.) 3) Potentially Unstable- Normal airway, breathing & circulation but significant mechanism of injury or illness (post-seizure, minor fractures, infant < 3mo with fever, etc.) 4) Stable- Normal airway, breathing & circulation No significant mechanism of injury or illness (small lacerations or abrasions, infant 3mo with fever) \ Glasgow Coma Score Infants Children /Adults Eye Opening Spontaneous 4 Spontaneous To speech/sound 3 To speech To pain 2 To pain No response 1 No response Verbal Response Coos or babbles 5 Oriented Irritable crying 4 Confused Cries to pain 3 Inappropriate words Moans to pain 2 Incomprehensible None 1 None

Motor Response Spontaneous . Withdraws touch Withdraws pain . Abnormal flexion Abnormal extension No response

5 4 3 2 1

Localizes pain Withdraws pain Abnormal flexion Abnormal extension No response

Neonatal Resuscitation 1) Dry, Warm, Position, Tactile Stimulation.Suction Mouth then Nose. 2) Call for ALS back-up. 3) Administer O2 as needed. 4) Apnea/Gasping, HR <100 or central cyanosis Ventilate with BVM @ 40-60/min 5) HR<60 after 30 sec BVM Chest Compressions @ 120/min - 3:1, 1/3 to 1/2 chest depth, 2 thumb encircle chest or 2 fingers 6) ALS available & HR <60 Intubate Epinephrine 0.01-0.03mg/kg IV/IO/ET 1:10,000 q 3-5 min APGAR Score 0 pts Pulse Absent Resp Absent Tone Limp Reflex None Color Blue 1 pt <100 Slow Irregular Some flexion Grimace sneeze Pink Body, Blue Limbs 2 pts 100 Good Active motion Cough All Pink

Respiratory / Cardiac Arrest Treatment Infant Child Teen <1yr 1-8yr 9-18yr Ventilation only 20/min 20/min 12/min CPR method 2 fingers 1 hand 2 hand Chest Depth 1/3-1/2 1/3-1/2 1/3-1/2 Compression Rate 100/min 100/min 100/min Ratio 5:1 5:1 5:1 CPR should be started for HR<60. Only AEDs with pediatric capabilities should be used on patients < 8 yrs. of age (approx. 25kg or 55lb). ALS Guidelines Asystole or PEA Assess airway & start CPR Intubate & ventilate with oxygen Epinephrine: 0.01 mg/kg 1:10,000 IV/ IO 0.1 mg/kg 1:1000 ET

Continue Epinephrine q 3-5 min, same dose Consider hi dose 0.1 mg/kg 1:1000 IV/IO/ET Consider possibility of hypoxia, hypovolemia, hypothermia, hyper/hypokalemia, tamponade, tension pneumothorax, toxins/poisons/drugs or thromboembolism & treat if present.

Bradycardia Assess airway & give oxygen Intubate if decreased consciousness Start CPR if HR<60. Epinephrine: 0.01 mg/kg 1:10,000 IV/ IO 0.1 mg/kg 1:1000 ET Continue Epinephrine q 3-5 min, same dose Atropine 0.02 mg/kg IV/ IO / ET, minimum dose 0.1 mg, maximum dose 0.5 mg child; 1.0 mg teen VF or pulseless VT Defibrillate up to 3 times as needed 2j /kg 4j /kg 4j /kg Start CPR, intubate, ventilate with O2 Epinephrine: 0.01 mg/kg 1:10,000 IV/ IO 0.1 mg/kg 1:1000 ET Defibrillate 4j / kg Amiodarone 5mg/kg IV/IO or Lidocaine 1mg / kg IV/ IO/ ET or Magnesium 25-50mg/kg IV/ IO (for torsades de pointes or hypomagnesemia) Defibrillate 4j / kg ( Source : NEW YORK STATES Emergency Medical Services) 2) Pediatric Basic Life Support (PBLS) and Pediatric Advanced Life Support (PALS) Pediatric Basic Life Support Changes in the pediatric section of the International Guidelines 2000 generally represent qualifications and refinements rather than major paradigm shifts from the 1992 Guidelines.1 The new guidelines continue to emphasize prevention of cardiac arrest. Pediatric BLS guidelines detail specific modifications of adult techniques necessary to address anatomic, physiological, etiologic, and psychosocial issues for infants and children. The initial sequence of BLS interventions in the pediatric Chain of Survival continues to be based on the most common etiology of arrest for a given age group, with modifications encouraged for special resuscitation circumstances. Multiple studies have documented poor skills retention by participants of traditional BLS courses and improved skills retention when course information is simplified. As a result, all potential

science changes were evaluated with respect to their effect on the complexity of teaching. Changes expected to simplify CPR teaching were encouraged. Highlights of the pediatric resuscitation section of the International Guidelines 2000 are as follows: Chain of Survival

An etiology-based sequence for resuscitation was considered, but the age-based sequence ("phone fast" for infants and children, "phone first" for children >8 years old and adults) was retained (Class Indeterminate). Lay rescuers should be taught exceptions to the age-based sequence of resuscitation, which may include the following: Lone rescuers should "phone fast" (provide immediate rescue breathing and other steps of CPR before phoning the EMS system) when submersion victims of any age are rescued from the water. Lone rescuers should "phone first" (phone EMS before beginning CPR) after the sudden collapse of a child with a known history of heart disease. There is a need for more and better data regarding the epidemiology, treatment, and outcome of pediatric cardiopulmonary arrest.2 There is insufficient data to guide recommendations for pediatric resuscitation. Data collection efforts should use consistent terminology and record important time intervals. Critical elements for data collection have been described by an international consensus process, the Pediatric Utstein Guidelines for Reporting Outcome of Pediatric Cardiopulmonary Arrest.3 Teaching of cardiopulmonary resuscitation skills must be simplified, and courses must be skill-based and outcome driven.

Basic Life Support Sequence Pulse Check

All rescuers are instructed to assess for signs of circulation before beginning chest compressions: Lay rescuers are instructed to assess for signs of circulation rather than attempt to check a pulse (Class IIa). Healthcare providers are instructed to assess for signs of circulation, including a pulse check.

Rescue Breathing and Bag-Mask Ventilation Education in bag-mask ventilation should be included in all BLS curricula for the healthcare provider (Class IIa). Bag-mask ventilation can provide lifesaving support for infants and children in both the out-ofhospital and in-hospital settings and is a skill that BLS providers should master (Class IIa). Chest Compressions and Use of Automated External Defibrillators

If 2 or more suitably trained healthcare providers are present, the 2 thumbencircling hands chest compression technique is preferred over the 2-finger compression technique for infants when technically feasible. This technique is not taught to lay rescuers.

If the victim of out-of-hospital cardiac arrest is 8 years old (approximately >25 kg body weight), use of automated external defibrillators (AEDs) is encouraged (Class IIb), although data regarding the use of AEDs in this age group is limited.

Relief of Foreign-Body Airway Obstruction

The extremely complex skills sequence for lay rescuer relief of foreign-body airway obstruction (FBAO) in the unconscious victim has been simplified. The sequence for healthcare provider relief of FBAO in the unconscious victim remains unchanged (Class IIb).

Pediatric Advanced Life Support International Terminology In the preparation of these guidelines, we recognized that certain terms that are commonplace in the United States are uncommon internationally and vice versa. Because these are international guidelines, efforts were made to use terms consistently throughout. To avoid confusion, the reader should note the use of the following terms:

Tracheal tubecommonly called an endotracheal tube. Note that a tracheal tube may be incorrectly placed in the esophagus, so the term does not mean a correctly positioned tube in the trachea. Moreover, a tracheostomy tube is not the same as a tracheal tube as used in these guidelines, even though both tubes are placed in the trachea. The procedure of placing a tracheal tube is still called endotracheal intubation. Manual resuscitatorrefers to a bag-valve device used to provide mask, tracheal tube, or tracheostomy tube ventilation to a victim. A manual resuscitator may be self-inflating or flow-inflating (ie, an anesthesia manual resuscitator). Exhaled CO2detectionrefers to detection of carbon dioxide in exhaled gas. End-tidal CO2 monitors are a subset of exhaled CO2 detectors, but they specifically detect and measure the quantity of CO2 at the end of exhalation. Capnography graphically displays the change in exhaled CO2 over time, whereas exhaled CO2 detectors often are colorimetric systems designed to detect any CO2 during exhalation and not just at the end of expiration. Defibrillationalthough commonly used interchangeably with "shocks," defibrillation is the untimed (asynchronous) depolarization of the myocardium that successfully terminates ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). Thus, shocks are administered to victims in an attempt to achieve defibrillation.

Epidemiology and Recognition of Shock and Respiratory Failure

We emphasize the need for better data regarding the epidemiology and treatment of pediatric cardiopulmonary arrest. There is a critical need for identification, tracking, and reporting of key resuscitation interventions and their relationship to various outcome measures, such as return of spontaneous circulation, survival, and neurological outcome. Published reports of resuscitation outcome are essential to provide data in future guideline

reviews. Data collection efforts should use consistent terminology and record important time intervals. Critical elements for data collection have been described by an international consensus process called the Pediatric Utstein Guidelines for Reporting Outcome of Pediatric Cardiopulmonary Arrest.1 An age-defined sequence of "phone fast" resuscitation is still appropriate for treatment of out-of-hospital arrest in infants and children, but a "phone first" approach to resuscitation from sudden collapse should be used for children at high risk for arrhythmias.

Support of Ventilation

The method of advanced airway support (endotracheal intubation versus laryngeal mask versus bag-mask) provided to the patient should be selected on the basis of the training and skill level of providers in a given advanced life support (ALS) system and on the arrest characteristics and circumstances (eg, transport time and perhaps the cause of the arrest). Proficiency in the skill of bag-mask ventilation is mandatory for anyone providing ALS in prehospital and in-hospital settings (Class IIa). Secondary confirmation of proper tracheal tube placement is required for patients with a perfusing rhythm by capnography or exhaled CO2 detection immediately after intubation and during transport (Class IIa). We strongly encourage the use of exhaled or end-tidal CO2 detection. It is extremely reliable in a spontaneously perfusing victim (Class IIa), although it has lower specificity in the cardiac arrest victim (Class IIb). Adequate oxygenation should also be confirmed in a victim with a perfusing rhythm using pulse oximetry.

Fluid Therapy

Rescuers should increase attention to early vascular access, including immediate intraosseous access for victims of cardiac arrest, and extend the use of intraosseous techniques to victims >6 years old.

Medications

There is renewed emphasis on the need to identify and treat reversible causes of cardiac arrest and symptomatic arrhythmias, such as toxic drug overdose or electrolyte abnormalities. For cardiac arrest victims, we provide specific drug selection and dose recommendations but acknowledge the lack of adequate data to make such recommendations on the basis of firm evidence. For example, data supporting the use of high-dose epinephrine and the use of vasopressin in cardiac arrest is inadequate to allow firm recommendations (for further details, see the following section, "Drugs Used for Cardiac Arrest and Resuscitation").

Treatment of Arrhythmias

We introduce vagal maneuvers into the treatment algorithm for supraventricular tachycardia.

We introduce the drug amiodarone into the treatment algorithms for pediatric VT and shock-refractory VF. Automated external defibrillators (AEDs) may be used in the treatment of children 8 years of age (approximately >25 kg body weight) in cardiac arrest in the prehospital setting.

Postarrest Stabilization

We place increased emphasis on postresuscitation interventions that may influence neurological survival, which include maintenance of normal ventilation rather than hyperventilation (Class IIa) in most victims, control of temperature (avoid hyperthermia), management of post-ischemic myocardial dysfunction, and glucose control.

Education and Training

Simplification of education and reinforcement of skill acquisition and core competencies are essential in all American Heart Association courses. See also, in "Part 9: Pediatric Basic Life Support," Education and Training and Introduction. (Source: American Heart Association- Learn and Life)

3) Etiology for Pediatric Shock Several etiologic classifications of shock are recognized. In each of these classifications, one or more of the physiologic principles defined above are disturbed. The major categories are as follows:

Hypovolemic Distributive Cardiogenic Septic Obstructive Miscellaneous

Hypovolemic Shock Hypovolemic shock results from an absolute deficiency of intravascular blood volume. It is a leading cause of pediatric mortality in the United States and worldwide, although the specific causative agents may be different around the world. Gastroenteritis results in 6-20 million deaths in infants and children annually worldwide. Children with gastroenteritis may lose 10-20% of their circulating volume within 1-2 hours.1 Rehydration is often impeded by concurrent vomiting, and deterioration may be rapid. Common infectious etiologies include bacterial causes of gastroenteritis, such as Salmonella, Shigella, and Campylobacter species and Escherichia coli, and viral causes, such as rotaviruses, adenoviruses, norovirus, and enteroviruses. Worldwide, infectious amebiasis and cholera are also important causes.

Physiologically, rapid loss of intravascular volume reduces ventricular preload, resulting in decreased stroke volume and CO and, thus, decreased DO 2 . In addition, a hemorrhagic component or dysentery may reduce Hb content, resulting in decreased CaO2. In the United States, the leading cause of death in children older than 1 year is trauma. Trauma kills more children than all other causes of death combined.2 A major component of traumatic death is hemorrhage. Hemorrhagic shock reduces both CaO2 and preload, resulting in decreased DO2 to the tissues. Other causes of hypovolemia include capillary leak and tissue third spacing, which results in leakage of fluid out of the intravascular space into the interstitial tissues. Etiologies include burns, sepsis, and other systemic inflammatory diseases. Patients with such etiologies may appear "puffy" and total-body fluid overloaded; however, they are actually significantly intravascularly depleted, with inadequate preload, and are in significant shock. By understanding the physiologic disturbance affecting intravascular volume and preload, such patients need even more fluid administration, despite their overall edematous appearance, in order to improve DO2 and prevent or correct a state of shock. Therapy is discussed more in detail below (see Treatment of Shock and Pharmacologic Therapy). Causes of hypovolemic shock

Intravascular volume loss o Gastroenteritis o Burns o Diabetes insipidus o Heat stroke Hemorrhage o Trauma o Surgery o GI bleeding Interstitial loss o Burns o Sepsis o Nephrotic syndrome o Intestinal obstruction o Ascites

Distributive Shock In certain clinical states, normal peripheral vascular tone becomes inappropriately relaxed. Common causes include anaphylaxis, neurologic injury, sepsis, and drug-related causes. Vasodilation results in increased venous capacitance, causing a relative hypovolemia even if the patient has not actually lost any net fluid. However, the common physiologic disturbance that affects DO2 in all forms of distributive shock is a decrease in preload that results from inadequate effective intravascular volume as a result of massive vasodilation.

Reference range blood pressure in children In neonates, the 10th to 90th percentile ranges are used.3 In children, the 50th to 90th percentile ranges are indicated.4 The following is modified from Hazinski's 1992 discussion in Nursing Care of the Critically Ill Child.5

Birth (12 h, <1000 g) - Systolic pressure, 39-59 mm Hg; diastolic pressure, 16-36 mm Hg Birth (12 h, 3 kg) - Systolic pressure, 50-70 mm Hg; diastolic pressure, 25-45 mm Hg Neonate (9 h) - Systolic pressure, 60-90 mm Hg; diastolic pressure, 20-60 mm Hg Infant (6 mo) - Systolic pressure, 87-105 mm Hg; diastolic pressure, 53-66 mm Hg Toddler (2 y) - Systolic pressure, 95-105 mm Hg; diastolic pressure, 53-66 mm Hg School aged child (7 y) - Systolic pressure, 97-112 mm Hg; diastolic pressure, 57-71 mm Hg Adolescent (15 y) - Systolic pressure, 112-128 mm Hg; diastolic pressure, 66-80 mm Hg

Common causes of distributive shock

Anaphylaxis o Medications (eg, antibiotics, vaccines, other drugs) o Blood products o Envenomation o Foods o Latex Neurologic causes o Head injury o Spinal shock Drugs Sepsis

Anaphylaxis results in mast cell degranulation with resultant histamine release and vasodilation. Neurologic injury can interrupt sympathetic input to vasomotor neurons, resulting in vasodilation. Spinal shock may result from cervical cord injuries above T-1, which interrupt the sympathetic chain, allowing for unopposed parasympathetic stimulation. Such patients may present with the clinical picture of hemodynamic instability and hypotension accompanied by bradycardia because they may lose sympathetic vascular tone (resulting in vasodilation) while unable to mount an appropriate sympathetic-mediated tachycardic response. Drugs may also cause vasodilation. Finally, sepsis results in the release of many vasoactive mediators that may cause profound vasodilation resulting in an aspect of distributive shock. Sepsis is discussed more in detail below (see Sepsis). Cardiogenic Shock Impairment of cardiac contractility defines cardiogenic shock. A decreased contractile state results in decreased SV and CO and, therefore, in decreased DO2. Causes include congestive

heart failure, ischemic heart disease (common in adults, rare in children), cardiomyopathy, cardiac tamponade, sepsis, and drugs. Obstructive Shock Certain physical causes of shock must be considered in pediatric patients, especially in neonates within the first few weeks of life, who may be born with obstructive congenital heart disease. Examples include coarctation of the aorta, interrupted aortic arch, and severe aortic valvular stenosis. In addition, acquired heart disease from diseases such as rheumatic fever or subacute bacterial endocarditis, as well as hypertrophic cardiomyopathy, can lead to direct obstruction of CO. Although ultimate treatment of such obstructive causes of CO that result in clinical shock clearly depends on surgical correction or palliation of the physical obstruction, temporizing measures in neonates may require maintaining patency of the ductus arteriosus in order to bypass the obstruction until more definitive surgery can be performed. The discussion of surgical correction of obstructive congenital heart lesions is beyond the scope of this article. Sepsis Sepsis may be defined as a systemic inflammatory response triggered by the presence of infectious agents or their toxins. The presence of infectious agents such as endotoxin or grampositive bacterial cell wall components together with the resultant release of inflammatory mediators and cytokines such as tumor necrosis factor (TNF)alpha; interleukins (IL) such as IL1, IL-2, and IL-6; products of the coagulation cascade; complement activation; and bradykinins may lead to disturbances of virtually every variable in the DO2 equation. Sepsis can induce activity of the enzyme nitric oxide synthase, resulting in production of the potent direct vasodilator nitric oxide, leading to inappropriate and often massive regional and systemic vasodilation. This distributive effect reduces effective preload and impairs CO and DO2. Sepsis may disrupt capillary integrity, resulting in intravascular fluid leak into tissue third spaces, causing hypovolemia. Many different circulating toxins and inflammatory mediators can depress myocardial function and reduce cardiac contractility, adding a cardiogenic component to impaired CO. Overactivation of the clotting cascade can result in DIC, which can directly plug and block critical tissue capillary beds, resulting in microvascular obstructive shock, as well as hemorrhage further depleting intravascular volume and decreasing critical oxygen carrying capacity by reducing Hb. Finally, multiple system organ failure, including respiratory failure, may result in hypoxia, complicating efforts at optimizing systemic DO2. Septic shock may disturb many, if not all, of the physiologic variables that determine systemic DO2. ( Source: http://emedicine.medscape.com/article/908930-overview)

4) Pediatric Diarrhea Introduction Background Acute diarrhea is defined as the abrupt onset of abnormally high fluid content in the stool (more than the normal value of approximately 10 mL/kg/d). This situation typically implies an increased frequency of bowel movements, which can range from 4-5 to more than 20 times per day. The augmented water content in the stools is due to an imbalance in the physiology of the small and large intestinal processes involved in the absorption of ions, organic substrates, and thus water. A common disorder in its acute form, diarrhea has many causes and may be mild to severe. Childhood acute diarrhea is usually caused by infection; however, numerous disorders may cause this condition, including a malabsorption syndrome and various enteropathies. Acuteonset diarrhea is usually self-limited; however, an acute infection can have a protracted course. By far, the most common complication of acute diarrhea is dehydration. Although the term "acute gastroenteritis" is commonly used synonymously with "acute diarrhea," the former term is a misnomer. The term gastroenteritis implies inflammation of both the stomach and the small intestine, whereas, in reality, gastric involvement is rarely if ever seen in acute diarrhea (including diarrhea with an infectious origin); enteritis is also not consistently present. Examples of infectious acute diarrhea syndromes that do not cause enteritis include Vibrio cholerae induced diarrhea and Shigella -induced diarrhea. Thus, the term acute diarrhea is preferable to acute gastroenteritis. Diarrheal episodes are classically distinguished into acute and chronic (or persistent) based on their duration. Acute diarrhea is thus defined as an episode that has an acute onset and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days. The distinction, supported by the World Health Organization (WHO), has implications not only for classification and epidemiological studies but also from a practical standpoint because protracted diarrhea often has a different set of causes, poses different problems of management, and has a different prognosis. Causes Although infectious agents are by far the most common cause for sporadic or endemic episodes of acute diarrhea, one should not dismiss other causes that can lead to the same presentation.

Causes of acute diarrhea include the following: o Infections Enteric infections (including food poisoning Extraintestinal infections o Drug-induced Antibiotic-associated Laxatives Antacids that contain magnesium

Opiate withdrawal Other drugs o Food allergies or intolerances Cow's milk protein allergy Soy protein allergy Multiple food allergies Olestra Methylxanthines (caffeine, theobromine, theophylline) o Disorders of digestive/absorptive processes Sucrase-isomaltase deficiency Late-onset (adult-type) hypolactasia, resulting in lactose intolerance o Chemotherapy or radiation-induced enteritis o Surgical conditions Acute appendicitis Intussusception o Vitamin deficiencies Niacin deficiency Folate deficiency o Vitamin toxicity Vitamin C Niacin, vitamin B3 o Ingestion of heavy metals or toxins (eg, copper, tin, zinc) o Ingestion of plants (eg, hyacinths, daffodils, azalea, mistletoe, Amanita species mushrooms Infectious causes of acute diarrhea in developed countries o Viruses Rotavirus - 25-40% of cases Calicivirus - 1-20% of cases Norovirus - 10% of cases Astrovirus - 4-9% of cases Enteric-type adenovirus - 2-4% of cases o Bacteria Campylobacter jejuni - 6-8% of cases Salmonella - 3-7% of cases E Coli - 3-5% of cases Shigella - 0-3% of cases Y enterocolitica - 1-2% of cases C difficile - 0-2% of cases Vibrio parahaemolyticus - 0-1% of cases V cholerae - Unknown Aeromonas hydrophila - 0-2% of cases o Parasites Cryptosporidium - 1-3% of cases G lamblia - 1-3% of cases

Common Bacteria and Optimum Culture Mediums Organism Aeromonas species Microbiologic Characteristics Oxidase-positive flagellated gramBlood agar negative bacillus (GNB) Rapidly motile curved gramCampylobacter negative rod (GNR); Campylobacter Skirrow agar species jejuni 90% and Campylobacter coli 5% of infections Anaerobic spore-forming gramCycloserine-cefoxitin-fructose-egg (CCFE) positive rod (GPR); toxin-mediated C difficile agar; enzyme immunoassay (EIA) for diarrhea; produces toxin; latex agglutination (LA) for protein pseudomembranous colitis Anaerobic spore-forming GPR; C perfringens None available toxin-mediated diarrhea MacConkey eosin-methylene blue (EMB) E coli Lactose-producing GNR or Sorbitol-MacConkey (SM) agar Plesiomonas Blood agar Oxidase-positive GNR species Blood, MacConkey EMB, xylose-lysineSalmonella Nonlactose nonH2S-producing deoxycholate (XLD), or Hektoen enteric species GNR (HE) agar Oxidase-positive Aeromonas flagellated gramBlood agar species negative bacillus (GNB) Rapidly motile curved gram-negative rod Campylobacter (GNR); Campylobacter Skirrow agar species jejuni 90% and Campylobacter coli 5% of infections Anaerobic sporeCycloserine-cefoxitinforming gram-positive fructose-egg (CCFE) agar; rod (GPR); toxinC difficile enzyme immunoassay (EIA) mediated diarrhea; for toxin; latex agglutination produces (LA) for protein pseudomembranous colitis Anaerobic sporeC perfringens None available forming GPR; toxinmediated diarrhea MacConkey Lactose-producing GNR E coli eosinmethylene Detection Method

blue (EMB) or SorbitolMacConkey (SM) agar Plesiomonas species Blood agar Blood, MacConkey EMB, xyloselysinedeoxycholate (XLD), or Hektoen enteric (HE) agar Oxidase-positive GNR

Salmonella species

Nonlactose nonH2Sproducing GNR

Culture mediums used to isolate bacteria include the following:

o o o o o o o o

Blood agar - All aerobic bacteria and yeast; detects cytochrome oxidase production MacConkey EMB agar - Inhibits gram-positive organisms; permits lactose fermentation XLD agar; HE agar - Inhibits gram-positive organisms and nonpathogenic GNB; permits lactose fermentation H2S production Skirrow agar - Selective for Campylobacter species SM agar - Selective for enterohemorrhagic E coli CIN agar - Selective for Y enterocolitica TCBS agar - Selective for Vibrio species CCFE agar - Selective for C difficile

5) Pathophysiology of Shock and Diarrhea Pathophysiology Diarrhea Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. Such a derangement can be the result of either an osmotic force that acts in the lumen to drive water into the gut or the result of an active secretory state induced in the enterocytes. In the former case, diarrhea is osmolar in nature, as is observed after the ingestion of nonabsorbable sugars such as lactulose or lactose in lactose malabsorbers. Instead, in the typical active secretory state, enhanced anion secretion (mostly by the crypt cell compartment) is best exemplified by enterotoxin-induced diarrhea. In osmotic diarrhea, stool output is proportional to the intake of the unabsorbable substrate and is usually not massive; diarrheal stools promptly regress with discontinuation of the offending

nutrient, and the stool ion gap is high, exceeding 100 mOsm/kg. In fact, the fecal osmolality in this circumstance is accounted for not only by the electrolytes but also by the unabsorbed nutrient(s) and their degradation products. The ion gap is obtained by subtracting the concentration of the electrolytes from total osmolality, according to the formula: ion gap = osmolality [(Na + K) 2]. In secretory diarrhea, the epithelial cells ion transport processes are turned into a state of active secretion. The most common cause of acute-onset secretory diarrhea is a bacterial infection of the gut. Several mechanisms may be at work. After colonization, enteric pathogens may adhere to or invade the epithelium; they may produce enterotoxins (exotoxins that elicit secretion by increasing an intracellular second messenger) or cytotoxins. They may also trigger release of cytokines attracting inflammatory cells, which, in turn, contribute to the activated secretion by inducing the release of agents such as prostaglandins or platelet-activating factor. Features of secretory diarrhea include a high purging rate, a lack of response to fasting, and a normal stool ion gap (ie, 100 mOsm/kg or less), indicating that nutrient absorption is intact.

6) Fluids Resusitation

Shock requires immediate interventions to preserve life. Therefore, the early recognition and treatment is essential even before a specific diagnosis is made. Most forms of shock seen in trauma or sepsis respond initially to aggressive intravenous fluids ( ie. 1 l normal saline bolus over 10 minutes ). Therefore this treatment is usually instituted as the person is being further evaluated. Re-establishing perfusion to the organs is the primary goal through restoring and maintaining the blood circulating volume ensuring oxygenation and blood pressure are adequate, achieving and maintaining effective cardiac function, and preventing complications. Patients attending with the symptoms of shock will have, regardless of the type of shock, their airway managed and oxygen therapy initiated. In case of respiratory insufficiency (i.e. diminished levels of consciousness, hyperventilation due to acid-base disturbances or pneumonia) intubation and mechanical ventilation may be necessary. A paramedic may intubate in emergencies outside the hospital, whereas a patient with respiratory insufficiency in-hospital will be intubated usually by a respiratory therapist, paramedic, or physician. In hypovolemic shock, caused by bleeding, it is necessary to immediately control the bleeding and restore the casualty's blood volume by giving infusions of isotonic crystalloid

solutions. Blood transfusions, packed red blood cells (RBCs), Albumin (or other colloid solutions), or fresh-frozen plasma are necessary for loss of large amounts of blood (e.g. greater than 20% of blood volume), but can be avoided in smaller and slower losses. Hypovolemia due to burns, diarrhea, vomiting, etc. is treated with infusions of electrolyte solutions that balance the nature of the fluid lost. Sodium is essential to keep the fluid infused in the extracellular and intravascular space whilst preventing water intoxication and brain swelling. Metabolic acidosis (mainly due to lactic acid) accumulates as a result of poor delivery of oxygen to the tissues, and mirrors the severity of the shock. It is best treated by rapidly restoring intravascular volume and perfusion as above. Inotropic and vasoconstrictive drugs should be avoided, as they may interfere in knowing blood volume has returned to normal.

Table 1: Shock and Fluid Resuscitation: Hypovolemic Shock Caused by Body Fluid Loss

Regardless of the cause, the restoration of the circulating volume is priority. As soon as the airway is maintained and oxygen administered the next step is to commence replacement of fluids via the intravenous route. Opinion varies on the type of fluid used in shock. The most common are:

Crystalloids - Such as sodium chloride (0.9%), or Lactated Ringer's. Dextrose solutions

which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia.

Colloids - For example, polysaccharide (Dextran), polygeline (Haemaccel), succunylated

gelatin (Gelofusine) and hetastarch (Hespan). Colloids are, in general, much more expensive than crystalloid solutions and have not conclusively been shown to be of any benefit in the initial treatment of shock.

Combination - Some clinicians argue that individually, colloids and crystalloids can

further exacerbate the problem and suggest the combination of crystalloid and colloid solutions.

Blood - Essential in severe hemorrhagic shock, often pre-warmed and rapidly infused.

It is to be noted that NO plain water should be given to the patient at any point, as the patient's low electrolyte levels would easily cause water intoxication, leading to premature death. An isotonic or solution high in electrolytes should be administered if intravenous delivery of recommended fluids is unavailable. Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to their relative inefficacy in the setting of acidosis, and because the body, in the setting of hemorrhagic shock, is in an endogenously catecholaminergic state. Definitive care and control of the hemorrhage is absolutely necessary, and should not be delayed.

7) Fever Introduction Background Pediatric patients presenting in the ED with fever are sometimes the more challenging patients emergency physicians face. Patients with fever can be present in a wide variety of clinical presentations ranging from mild clinical conditions to the most serious of bacterial illnesses. Fever is both a high-impact and a high-frequency chief complaint. The clinician should be knowledgeable about febrile conditions that occur in pediatric patients. Although clinical guidelines have been reported and scrutinized in major journals in the past few years, definitive conclusions are sometimes elusive.1 Fever phobia is well described as existing with both caregivers as well as medical providers.2 Inconsistent treatment approaches exist even in the most experienced pediatric EDs.3 For related information, see Medscape's Pediatrics Resource Center. Pathophysiology A child's core temperature may normally vary by as much as 1-1.5F throughout the day. This variation occurs with or without pathology being present. An elevated temperature above the normal range is defined as a fever. The standard definition of fever is a rectal temperature of 100.4F (38.0C) or higher. In the face of pathology, pyrogens release prostaglandin E1 and D2. Pyrogens are lowmolecular-weight proteins produced by leukocytes. Prostaglandins mediate the set point for heat regulation in the human body. Their effects act on the hypothalamus and affect the body's response to heat by altering vascular constriction and other heat production and/or release mechanisms. Causes Causes of elevated temperature include the following:12

Infectious etiologies (SBI is the concern in the evaluation of the child with fever) o Meningitis, or encephalitis o Upper respiratory tract infection (URI) o Bacterial or viral pneumonia o Otitis media o Local skin infections, such as cellulitis o Oral infections, including pharyngitis due to Streptococcus pyogenes (group A Streptococcus species) and viral herpetic gingivostomatitis

Urinary tract infection (UTI) Generalized viral illness Parents may be overly concerned about possible outcomes of prolonged high temperature, or they may believe that every fever requires antibiotic therapy.13 The emergency physician may spend time educating parents on these subjects. In fact, not all temperature elevations are caused by bacterial infections. Temperature elevations may occur without infectious etiology. o Noninfectious causes of fever include environmental factors, such as the following: High external temperature (especially in the warmer weather months) Over bundling of children in colder weather months Malignancy Rheumatoid diseases Recent immunization administration Complications of routine administration of childhood vaccinations carry the risk of temperature elevation as a common adverse effect. o Administration of the diphtheria, tetanus, and pertussis (DTP) vaccine may cause fever within a few hours after administration and may persist up to 48 hours. o Administration of live-virus vaccinations, such as the measles, mumps, and rubella (MMR) vaccine, may result in temperature elevations up to 7-10 days after its administration.
o o

Complications Dehydration is common in children with untreated fevers. Specific attention on the hydration should be addressed in febrile children. Occult bacteremia in the unimmunized child may progress to secondary sites of infection such as meningitis or osteomyelitis. Localized infections may lead to hematogenous seeding and sepsis. Morbidity and mortality are related to untreated sepsis syndromes and meningitis. Prognosis The prognosis for routine febrile children treated as described is generally good but ultimately depends on the etiology of the fever. ( Source: http://emedicine.medscape.com/article/) 8) Septic Shock Alternative Names Bacteremic shock; Endotoxic shock; Septicemic shock; Warm shock Definition Septic shock is a serious condition that occurs when an overwhelming infection leads to lifethreatening low blood pressure.

Causes Septic shock occurs most often in the very old and the very young. It also occurs in people who have other illnesses. Any type of bacteria can cause septic shock. Fungi and (rarely) viruses may also cause the condition. Toxins released by the bacteria or fungi may cause tissue damage, and may lead to low blood pressure and poor organ function. Some researchers think that blood clots in small arteries cause the lack of blood flow and poor organ function. The body also produces a strong inflammatory response to the toxins. This inflammation may contribute to organ damage. Risk factors for septic shock include:

Diabetes Diseases of the genitourinary system, biliary system, or intestinal system Diseases that weaken the immune system such as AIDS Indwelling catheters (those that remain in place for extended periods, especially intravenous lines and urinary catheters) Leukemia Long-term use of antibiotics Lymphoma Recent infection Recent surgery or medical procedure Recent use of steroid medicines

Symptoms Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and intestines. Symptoms may include:

Cool, pale extremities High or very low temperature, chills Lightheadedness Low blood pressure, especially when standing Low urine output Palpitations Rapid heart rate Restlessness, agitation, lethargy, or confusion Shortness of breath

Exams and Tests

The inflammatory triad of fever, tachycardia, and vasodilation is common in children with benign infections. Septic shock is suspected when children with this triad have a change in mental status manifested as inconsolable irritability, lack of interaction with parents, or inability to be aroused. The clinical diagnosis of septic shock is made in children who have a suspected infection manifested by hypothermia or hyperthermia and have clinical signs of decreased perfusion, including decreased mental status, prolonged capillary refill of >2 secs (cold shock) or flash capillary refill (warm shock), diminished (cold shock) or bounding (warm shock) peripheral pulses, mottled cool extremities (cold shock), or decreased urine output of >1 mL/kg/hr. Hypotension is not necessary for the clinical diagnosis of septic shock; however, its presence in a child with clinical suspicion of infection is confirmatory. Blood tests may be done to check for infection, low blood oxygen level, disturbances in the body's acid-base balance, or poor organ function or organ failure. A chest x-ray may show pneumonia or pulmonary edema. Treatment Septic shock is a medical emergency. Patients are usually admitted to the intensive care unit of the hospital. Treatment may include:

Breathing machine (mechanical ventilation) Drugs to treat low blood pressure, infection, or blood clotting Fluids given directly into a vein (intravenously) Oxygen Surgery

There are new drugs that act against the extreme inflammatory response seen in septic shock. These may help limit organ damage. Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be required. This can only be done with special equipment and intensive care nursing. Outlook (Prognosis) Septic shock has a high death rate. The death rate depends on the cause of the infection, how many organs have failed, and how quickly and aggressively medical therapy is started. Possible Complications

Respiratory failure, cardiac failure, or any other organ failure can occur. When to Contact a Medical Professional Go directly to an emergency department if you develop symptoms of septic shock. Prevention Prompt treatment of bacterial infections is helpful. However, many cases of septic shock cannot be prevented. (Source: http://www.nlm.nih.gov/medlineplus/ency/article/000668.htm) 9) Management of Elektrolyte Prehospital Care

Address emergent airway, breathing, and circulatory problems first. Obtain intravenous access, and give an isotonic fluid bolus (Ringer lactate or isotonic sodium chloride solution) to children with severe volume depletion. This should not delay transport to the appropriate facility.

Emergency Department Care Mild dehydration Patients with minimal-to-mild dehydration should be encouraged to continue an age-appropriate diet and adequate intake of oral fluids. Oral rehydration solution (ORS) should be used. Children should be given sips of ORS (5 mL or one teaspoon) every 5 minutes. As an estimate for the amount of fluid to replace, the goal should be to drink 10 mL/kg body weight for each watery stool and 2 mL/kg body weight for each episode of vomiting.1 If commercially prepared ORS is not available, the following recipe may be followed:

In 1 liter of water, add 2 level tablespoons of sugar or honey, one-fourth teaspoon of table salt (NaCl), and one-fourth teaspoon of baking soda (bicarbonate of soda). If baking soda is not available, use another quarter teaspoon of salt instead. If available, add one half cup of orange juice, coconut water, or a mashed ripe banana to the drink. The water is safer if boiled, but do not lose time doing this if the child is very ill. Before giving the drink, taste it to be sure it is no saltier than tears.

Moderate dehydration

The literature supports use of oral rehydration for the moderately dehydrated child. Similar outcomes have been achieved in randomized studies comparing ORS with intravenous fluid therapy (IVF) with fewer complications and higher parent satisfaction in the ORS groups. Moreover, ORS can typically be initiated sooner than IVF. However, children must be cooperative and have caregivers available to instruct and administer the oral fluids.2 With ORS, patients should receive approximately 50-100 mL/kg body weight over 2-4 hours, again starting with 5 mL every 5 minutes.1 If the child can tolerate this amount and asks for more fluids, the amount given can gradually be increased. Once the fluid deficit has been corrected, parents should be instructed on how to replace volume losses at home if the child continues to have vomiting or diarrhea. Children who fail ORS should be given a 20-mL/kg bolus of isotonic fluid intravenously. This may be followed by 1.5-2 times maintenance therapy as described below. Over the next few hours, the patient may be transitioned to oral rehydration as tolerated, at which point, the intravenous therapy may be discontinued. Severe dehydration Patients with severe dehydration should receive intravenous isotonic fluids in 20- to 60-mL/kg fluid boluses.1 In children with difficult peripheral access, perform intraosseous or central access promptly. Fluid boluses should be repeated until vital signs, perfusion, and capillary refill have normalized. If a patient reaches 60-80 mL/kg in isotonic crystalloid boluses and is not significantly improved, consider other causes of shock (eg, sepsis, hemorrhage, cardiac disease) and consider vasopressors and advanced monitoring such as with a bladder catheter, central venous pressure, and measuring mixed venous oxygen saturation. Although physicians typically give normal saline for these initial boluses, it is important to remember to check a bedside glucose level for patients who appear lethargic or altered. Treat hypoglycemia promptly. The appropriate dose is 0.25 g/kg (2.5 mL/kg of 10% dextrose or 1 mL/kg of 25% dextrose) IV. Once vital sign abnormalities are corrected, initiate maintenance fluid therapy plus additional fluid to make up for any continued losses. For the early phase of rehydration, 1.5-2 times maintenance therapy should be adequate. Daily requirements for maintenance fluids can be approximated as follows:

If the patient weighs less than 10 kg, give 100 mL/kg/d. If the patient weighs less than 20 kg, give 1000 mL/d plus 50 mL/kg/d for each kilogram between 10-20 kg. If the patient weighs more than 20 kg, give 1500 mL/d, plus 20 mL/kg/d for each kilogram over 20 kg. Divide the total by 24 to obtain the hourly rate.

Daily fluid requirements may be met using dextrose 5% in half-normal saline solution. For those with significant hyponatremia or hypernatremia, it is preferable to use dextrose 5% in normal saline. Dextrose is important to include because these patients generally have a notable ketosis.

The emergency physician also should consider daily sodium and potassium requirements as follows:

Sodium 2-3 mEq/kg/d Potassium 2-3 mEq/kg/d

Isonatremic and hyponatremic volume depletion states may be treated with normal saline or other isotonic solutions. Hypernatremic volume depletion should be corrected more slowly because of the possibility of CNS complications resulting from rapid correction of the osmolar gradients. Full correction of severe sodium abnormalities usually should be staged over 24 hours or longer. Although a potassium deficit is present in all cases of volume depletion, it is not usually clinically significant; few patients with moderate dehydration require supplemental potassium. However, failure to correct for hypokalemia during volume repletion may result in clinically significant hypokalemia. Add potassium to fluids when the patient has documented hypokalemia. For all other patients, avoid adding potassium to fluids until the patient has received several hours of resuscitation and the patient has demonstrated adequate urine output. Consultations Infants and children who present to the ED with mild-to-moderate dehydration may respond to fluid boluses and be discharged home with close follow-up with their primary care provider. Patients who are severely volume depleted or who are unable to tolerate oral fluids must be admitted, with a pediatric consultation if appropriate.

If the child is in shock, unable to drink fluids, or does not respond to intravenous bolused therapy, significant abnormalities requiring correction may exist. In such patients, obtain pediatric consultation for admission and further therapy. If renal tubular acidosis (RTA) or other primary renal or endocrine disorder is suspected, specialty consultation may be indicated.

Medication Acute gastroenteritis is typically a self-limited condition that does not require antibiotics. Chronic infectious cases of diarrhea may require antimicrobial agents after appropriate stool studies have indicated the etiology. Antidiarrheal agents are not recommended. When dehydration is caused by other disease processes, such as diabetic ketoacidosis or sepsis, appropriate pharmacologic therapy should be initiated as soon as possible. The emergency medicine literature now supports the use of a single dose of oral ondansetron in combination with oral rehydration for patients with dehydration, nausea, and vomiting.3 However, the use an antiemetic should not shift the focus away from adequate fluid resuscitation. (Source: http://emedicine.medscape.com/article/801012-treatment)

Etiology of Loss of Conciousness and Febrile Seizures Causes of loss of consciousness

Neuroregulatory causes o Three forms of neurally mediated syncope have been described, as follows: The vasodepressor form, characterized by severe hypotension with minimal drop in cardiac frequency The cardioinhibitory form, characterized by marked bradycardia that produces hypotension The mixed form, which shares features of both o These distinctions may be helpful in guiding treatment. For example, most patients with the vasodepressor form of neurally mediated syncope benefit from increased water and salt intake. If these measures fail, a mineralocorticoid is also prescribed, in which case initial periodic measurements of blood pressure and serum electrolyte levels are recommended). o Beta-blockers may be most effective in patients with the cardioinhibitory form of neurally mediated syncope. However, if recurrent syncopal episodes persist, a pacemaker (to pace the heart during extreme bradycardia) may be indicated. Recognize that pacemaker efficacy is less when the vasodepressor component of the neurally mediated syncope is important, such as in the mixed type of neurally mediated syncope. Heat exposure: Heat syncope is characterized by dizziness or fainting while standing still in the heat for an extended period. It may also occur immediately following vigorous exercise. This results from cutaneous vasodilation, in which blood pools in the skin and lower extremities, and from volume depletion due to water loss, which results in decreased blood flow to the brain. Treatment consists of rest in a cooler environment. Prevention is based on acclimatization and avoidance of long periods of immobility or vigorous exercise in the heat. Micturition: This form of syncope represents 2.4-8.4% of cases of syncope in adult or combined series but is a less frequent cause of syncope in children. In the older patient, an association with orthostatic hypotension has been demonstrated. Cough: This form of syncope (ie, tussive syncope) occurs particularly in adolescents with asthma or cystic fibrosis. It accounts for 2-5% of syncope presentations in children. Swallowing: Similar to most neuroregulatory types of syncope, swallowing (ie, deglutition) syncope appears to be caused by vasovagal nervous modulation (of a GI stimulus) rather than by pre-existing intrinsic heart disease. However, tachycardias and bradycardias other than sinus bradycardia are occasionally induced by swallowing. Stretch: Syncope may be induced in adolescents who stretch with the neck hyperextended. Studies indicate that the mechanism is not simply the Valsalva maneuver but also involves a combination of vertebral and posterior cerebral artery compression (despite an intrinsically normal vessel) and a familial tendency to faint. Exercise: Exercise-related syncope may be related to multiple causes or pathophysiologies, not all of which are benign. Vasovagally mediated hypotension and bradycardia are believed to be a common but difficult-to-prove cause of this form of

syncope. Exercise-related syncope from a neurally mediated mechanism is typically thought to occur immediately following the activity (rather than at the peak of exercise). Orthostatic cardiac isolated decrease in cardiac ejection: Orthostatic hypotension is defined as a drop in blood pressure related to a change to a more upright posture and may be the end result of different pathophysiologies. Dysautonomia may result in failure of peripheral vasoconstriction in response to hypotension or shifts in blood volume. In this setting, additional signs of dysautonomia are usually present (eg, sweating, GI distress with diarrhea or constipation), with abnormal cold pressor test results, handgrip response, and response to Valsalva maneuver. Aortic stenosis: In patients with severe aortic stenosis, ventricular baroreceptor reflex bradycardia and peripheral vasodilatation have been implicated as a mechanism for syncope. The occurrence of symptoms correlates well with end-systolic wall stress. The presence of syncope in patients with aortic valve stenosis is a serious symptom associated with a mean projected survival time of only 27 months after its occurrence if the stenosis is left untreated. Unrepaired tetralogy of Fallot o In infants and young children with unrepaired tetralogy of Fallot, symptomatic periods are characterized by episodes of markedly increased cyanosis that frequently culminate in syncope. They are considered to result from increasing stenosis of the muscular subpulmonary infundibulum. This is usually a progressive abnormality and can be exacerbated by increased heart rate and contractility, presumably through the initiation of pulmonary infundibular spasm. For this reason, digoxin and other inotropic medications, as well as chronotropic medications, are relatively contraindicated in these patients before repair of tetralogy of Fallot. o Beta-blockade can relieve these symptomatic periods. Additional immediate therapies of tetralogy symptoms include placement of the patient in a knee-chest position (to increase systemic venous return and elevate systemic vascular resistance), morphine infusion (to prevent agitation and resultant tachycardia), and, if necessary, phenylephrine administration (to elevate systemic vascular resistance). Patients with tetralogy symptoms may be transiently treated successfully with oral beta-blockade, but this should be a temporizing measure while complete surgical repair of the tetralogy of Fallot is being arranged. Pulmonary hypertension: The diagnosis of primary pulmonary hypertension is often difficult and, for that reason, may be significantly delayed following the onset of symptoms. The presence of syncope in either primary or secondary pulmonary hypertension is a poor prognostic sign. Hypertrophic cardiomyopathy: Syncope may affect as many as 15-25% of patients with hypertrophic cardiomyopathy. It may be secondary to atrial arrhythmias, ventricular arrhythmias, obstructed blood flow through the left ventricular outflow tract (especially during exercise), or diastolic dysfunction that causes impaired filling of the ventricles. All of these factors decrease blood flow to the brain by decreasing stroke volume. In this setting, syncope is an ominous sign, and such patients should receive a defibrillator. Dilated cardiomyopathy: Patients with dilated cardiomyopathy may have syncope secondary to atrial arrhythmias, ventricular arrhythmias, atrioventricular conduction defects, or poor cardiac output due to myocardial dysfunction. A history of syncope in

this setting is associated with a high risk of sudden death. These patients should also receive a defibrillator. Intracardiac tumors: Atrial myxoma is the most common primary tumor of the heart and arises from the endocardium as a pedunculated mass. Approximately 80% of myxomas occur in the left atrium, and 20% occur in the right atrium. Atrial myxomas can cause syncope by decreasing atrial filling, thus decreasing ventricular filling with consequent decreased stroke volume. In this setting, syncope usually occurs during exercise. Myxomas may cause syncope when embolization occurs, either to the brain (causing decreased blood flow with decreased oxygenation) or to the coronary arteries. In this setting, syncope may be secondary to arrhythmias or myocardial infarction, both of which cause decreased stroke volume. Congenital coronary anomalies o Anomalous origin of coronary arteries is a congenital disease found in approximately 0.3% of all autopsies and in 0.5% of coronary angiograms. o Congenital coronary anomalies described in the literature include the following: Anomalous left coronary artery originating from the pulmonary artery Left main coronary artery takeoff from the right coronary sinus, with a course between the aorta and the right ventricular outflow tract Anomalous origin of the right coronary artery from the left sinus of Valsalva, coursing between the aortic root and the right ventricular outflow tract Single origin from the right sinus of Valsalva for both right and left coronary arteries in which the left coronary artery is compressed between the aorta and the pulmonary trunk Anomalous circumflex artery originating from the right sinus of Valsalva and passing behind the aortic root o Most of these studies involved young athletes with a history of syncope who experienced sudden cardiac death. Pathological findings included myocardial fibrosis, necrosis, or both. Therefore, exertional syncope should be thoroughly evaluated, and surgery should be performed when coronary anomalies are present because of the high risk of sudden cardiac death. In these cases, syncope may be secondary to ischemia-induced tachyarrhythmias or bradyarrhythmias or myocardial dysfunction. Acquired coronary anomalies: Acquired coronary artery disease in childhood may be caused by inflammatory processes (eg, Kawasaki disease), atherosclerosis (eg, postorthotopic heart transplant), or, rarely, primary hypercholesterolemia. In patients with acquired coronary artery disease, syncope may also be related to ischemia-induced bradyarrhythmias or tachyarrhythmias or myocardial dysfunction, which is an ominous sign. Right ventricular outflow tract obstruction: Syncope has been described in patients with right ventricular outflow tract obstruction that results from a double-chambered right ventricle. A case report of an intracardiac tumor that caused third-degree heart block secondary to infiltration and right ventricular outflow tract obstruction was recently reported in a child who presented with syncope. Carditis

Transient myocarditis may be due to viral infections, such as coxsackievirus, adenovirus, and echovirus. The most frequent histological pattern is lymphocytic infiltration of the myocardium, followed by mixed inflammatory infiltration and a granulomatous infiltration. The clinical presentation of myocarditis may be asymptomatic or may involve heart failure, cardiac arrest, or, less frequently, syncope and chest pain. o Individuals with Lyme carditis may develop syncope secondary to transient complete atrioventricular block. o Rheumatic fever is uncommon in Western countries but is prevalent in nonindustrialized countries. It may be seen in immigrants from these poorer areas. When carditis is present, it is usually manifested by first-degree atrioventricular block. However, complete atrioventricular block may occur with syncope as its presenting symptom. o According to one study, patients with Brugada syndrome who presented with syncope were found to have carditis based on endomyocardial biopsy.4 Histology revealed prevalent or localized right ventricular myocarditis in most patients, with detectable viral genomes in some. o Giant cell myocarditis is a rare condition that usually affects young, previously healthy people. In these patients, syncope may be due to rapid development of complete atrioventricular block, ventricular arrhythmias, or heart failure. They often require cardiac transplantation. o Chagas myocarditis is one of the manifestations of a parasitic disease secondary to Trypanosoma cruzi infection, which is prevalent in Latin America. Syncope occurs secondary to varying degrees of atrioventricular and bundle block. Psychiatric conversion: Dizziness and syncope may be symptoms of depression, anxiety, panic disorder, somatization, and substance abuse. Unexplained syncope is likely to have a psychiatric etiology. These individuals tend to have multiple somatic symptoms and report frequent syncope. Treatment of these psychiatric illnesses results in lower rates of syncope recurrence. Hyperventilation syncope: Syncope is attributed to respiratory alkalosis, which induces cerebral vasoconstriction and, thus, hypoperfusion. Breath-holding spells (BHSs): These refer to involuntary episodes that occur in otherwise healthy children. After a few cries, the child becomes silent and apneic; this is quickly followed by pallor or cyanosis. Simple BHSs resolve with no associated syncope or postural change. However, severe BHSs are characterized by a loss of consciousness and a change in postural tone with occasional myoclonic jerks. The episodes last from seconds to a minute and end with a deep inspiration. In children with pallid BHSs, noxious stimuli may lead to cardiac inhibition through the vagus nerve, inducing bradycardia or brief asystole. In children with the cyanotic type of BHS, central inhibition of respiratory movements mediated through the vagus nerve is thought to occur. In both types of spells, cerebral hypoxia is the end result. Inappropriate pacemaker function: Patients who have pacemakers may develop syncope secondary to inappropriate pacemaker settings. For example, the ventricular lead may oversense atrial depolarizations and misinterpret them as ventricular depolarizations, which causes failure to pace the ventricle when needed. Other causes include inadequate device functioning (ie, when the battery is depleted due to the pacemaker reaching "end
o

of life" or due to insulation defects in the lead with rapid current drain) and lead fracture, which causes failure to capture or make the ventricle contract when paced. Patients who have ventricular pacing may develop pacemaker syndrome in which presyncope or syncope are secondary to ventriculoatrial conduction of the paced beat, with consequent atrial distension, reflex vasodilation, and decreased stroke volume. Bradycardia: When the heart rate is slower than is required to maintain an adequate cardiac output, the brain becomes underperfused and the individual develops syncope. Examples include the following: o Sinus node disease: In these patients, syncope is generally due to marked sinus bradycardia, which causes inadequate cardiac output with cerebral hypoperfusion. Sinus node disease is frequently encountered in older individuals with congenital heart disease who have undergone Mustard or Senning surgery for Dtransposition of the great arteries, which have been largely replaced by the arterial switch operation. Sinus node disease is also encountered in patients who had undergone the classic Fontan surgery for palliation of single ventricle and in some patients who have undergone other types of cardiac surgery, such as secundum and sinus venosus atrial septal defect repair. Sinus node disease may also be encountered in individuals with unrepaired atrial septal defects, polysplenia syndromes, and Ebstein anomaly of the tricuspid valve. o Congenital and acquired heart block: Syncope may develop in individuals with complete heart block, when the escape rhythm is too slow to maintain adequate cardiac output and, therefore, adequate cerebral perfusion. Tachycardia: Syncope may develop secondary to a rapid heart rate that decreases diastolic filling time enough to induce decreased stroke volume, myocardial ischemia, or both. This leads to cerebral hypoperfusion. Syncope secondary to tachycardia may occur during the following: o Atrial tachycardia: Syncope may occur secondary to decreased atrial filling because of loss of the "atrial kick," such as in atrial fibrillation or flutter, with subsequent decreased ventricular filling and cerebral hypoperfusion. o Supraventricular tachycardia (SVT): Syncope may be secondary to rapid conduction through the atrioventricular node and up through an accessory pathway. If the SVT is prolonged, syncope may be due to myocardial dysfunction, with a consequent inadequate cardiac output to maintain a normal cerebral perfusion. o Ventricular tachycardia (VT): VT is defined as 5 or more consecutive beats that arise below the atrioventricular node at a rate of more than 100 beats per minute. Syncope occurs because of ineffective stroke volume and myocardial ischemia, which aggravates the picture, with consequent cerebral hypoperfusion. o Ventricular fibrillation: This occurs when VT degenerates into chaotic electrical activity and the myocardium is rendered without synchronization and without effective myocardial contractions. Ventricular fibrillation leads to sudden cardiac death in minutes if it is not cardioverted or if it is unable to be cardioverted to a more stable rhythm. o Polymorphic VT: This type of VT is irregular in rate and rhythm and has varying shapes or morphologies on ECG. Ventricular fibrillation may occur. Long QT syndromes (LQTSs) are typically associated with a polymorphic VT often called

torsades de pointes because of the original French description of the QRS complexes as twisting about its axis. LQTS LQTSs develop in young individuals with generally structurally normal hearts who carry certain mutations in the cardiac ionic channels that predispose them to ventricular fibrillation under emotional or physical stress, thereby putting the person at risk for sudden death. In these patients, a prior history of syncope is a serious event compatible with an aborted episode of sudden death secondary to polymorphic VT or torsade de pointes, which may degenerate into ventricular fibrillation. Mutations in certain genes that encode for certain ion channels produce a derangement in ionic flows across the cytoplasmic membranes of cardiac cells. This produces prolongation of the cardiac action potential and lengthening of the QT interval on the surface ECG. These genes encode for potassium channels, with the exception of SCN5A, which encodes for the sodium channel. KCNQ1 mutations (in the LQT1 gene) are the most frequent, followed by HERG (in the LQT2 gene) and SCN5A (in the LQT3 gene) mutations. KCNE1 mutations (in the LQT4 and LQT5 genes) and KCNE2 mutations (in the LQT6 gene) are less frequent. Because KCNQ1 mutations are the most frequent, homozygous mutations in the KCNQ1 gene are generally associated with Jervell and LangeNielsen syndrome. Heterozygous mutations of this gene cause RomanoWard syndrome. Jervell and Lange-Nielsen syndrome is the autosomal recessive inherited variant associated with sensorineural deafness and is mostly caused by mutations in the KCNQ1 gene or, less frequently, in the KCNE1 gene. These genes encode for the I(Ks) current. One study showed that this variant is the most severe variant of LQTS; most patients are symptomatic by age 3 years.5 In patients with Jervell and Lange-Nielsen syndrome, the QTc is markedly prolonged (557 65 ms) and beta-blockers have limited efficacy. Most arrhythmic events are triggered by emotions or exercise. Females are at lower risk for cardiac arrest and sudden death. Mutations in the KCNE1 gene have a more benign course. A QTc of more than 550 milliseconds and occurrence of syncope during the first year of life are independent predictors of subsequent cardiac arrest and sudden death. In these patients, early therapy with defibrillators must be considered. Romano-Ward syndrome is the autosomal dominant inherited variant of LQTS and is the most frequent variant of inherited LQTS. When syncope occurs in these patients, ventricular fibrillation should be suspected as the cause and a defibrillator should be implanted. Acquired LQTS may be caused by various drugs, such as quinidine, sotalol, and dofetilide, and numerous antihistamines, antibiotics, antipsychotics, and others. In addition, prolongation of the QTc may be

o o

secondary to electrolyte abnormalities such as hypokalemia and hypomagnesemia, CNS lesions, and significant bradyarrhythmias. Short QT syndrome: This is a newly recognized congenital inherited channelopathy associated with familial atrial fibrillation and/or sudden death or syncope. Three different mutations in 3 genes (KCNH2, KCNQ1, KCNJ2) that encode for cardiac potassium channels have been identified. These mutations cause an increase in the net outward potassium current, leading to shortening of repolarization, a shorter QTc of less than 300-320 milliseconds, a lack of adaptation during increasing heart rates, and shorter atrial and ventricular refractory periods, with increased susceptibility to ventricular and atrial fibrillation. Brugada syndrome: This is an inherited channelopathy caused by mutations in the SCN5A gene, which can cause idiopathic ventricular fibrillation. Quinidine syncope: This refers to development of ventricular fibrillation with the use of quinidine. According to the Vaughan-Williams classification, quinidine is a class IA antiarrhythmic agent. Quinidine depresses the rapid inward depolarizing sodium current, with resulting prolongation of refractory periods in the atria, ventricles, and Purkinje tissues. It is used for treatment of reentrant SVTs, atrial fibrillation, and ventricular arrhythmias. Quinidine syncope is estimated to occur in 0.5-4.4% of treated patients. Quinidine syncope is dose-independent and occurs most frequently when elimination of atrial fibrillation or flutter is attempted. The ECG reveals a prolonged QTc and large U waves. It is thought to represent a reentry tachycardia caused by unequal recovery times in different parts of the ventricular myocardium. Arrhythmogenic right ventricular dysplasia: This is an autosomal dominant type of cardiomyopathy seen primarily in children and young adults and is characterized by fibrofatty replacement of the right ventricular myocardium, with associated arrhythmias originating in the right ventricle. As many as 80% of individuals present with syncope or sudden cardiac death secondary to VT. Catecholamine-sensitive monomorphic VT This is an arrhythmogenic disease characterized by myocardial electrical instability that is exacerbated by activation of the adrenergic nervous system by acute emotions or during exercise. VT may self-terminate or degenerate into ventricular fibrillation, causing syncope and sudden death. Syncope occurs in 60-70% of individuals, and most events occur during childhood. An alternating, 180-degree QRS axis on a beat-to-beat basis (also known as bidirectional VT) and irregular polymorphic VT without a QRS vector alternans may be seen on ECG. RYR2 and CASQ2 are the 2 genes associated with this entity. Beta-blockers have proven efficacy for approximately 60% of individuals, and the remaining 40% of individuals in whom exercise stress testing does not demonstrate adequate control of arrhythmias with the highest tolerated dose of beta-blockers may benefit from an ICD.

Repaired tetralogy of Fallot: Ventricular arrhythmias in patients after total surgical repair of tetralogy of Fallot have been associated with late sudden death. In a large study, spontaneous premature ventricular contractions and induced VT were related to delayed age at repair, longer follow-up interval, symptoms of syncope or presyncope, and right ventricular systolic pressure of more than 60 mm Hg.6 A large study in Japan showed that the risk factors for ventricular arrhythmias (in patients who developed syncope) included longer postoperative survival duration and QRS duration of longer than 120 milliseconds, whereas the risk factor for atrial fibrillation and flutter was older age at operation.7 Isolated Wolff-Parkinson-White syndrome: During atrial fibrillation, syncope may be secondary to rapid conduction through the accessory pathway, which becomes ventricular fibrillation because of ventricular pre-excitation. Mixed or unclear hypertrophic cardiomyopathy: Syncope results from left ventricular outflow tract obstruction, mostly during exercise, or from the development of ventricular arrhythmias. See Hypertrophic cardiomyopathy. Mitral valve prolapse: Patients with mitral valve prolapse are thought to be prone to endocardial ischemia and, thus, prone to development of ventricular arrhythmias. A study concluded that, in patients with mitral valve prolapse syncope, inferolateral repolarization changes, complex ventricular ectopy, and a markedly myxomatous valve are consistent with higher risk of sudden death, and, unfortunately, mitral valve surgery may not provide control of ventricular arrhythmias.8

(Source: http://www.google.co.id/search?hl=id&q=etiology+of+pediatric+loss+of+consciousemedicine&meta=) Causes of febrile seizures

Risk factors for developing febrile seizures o Family history of febrile seizures o High temperature o Parental report of developmental delay o Neonatal discharge at an age greater than 28 days (suggesting perinatal illness requiring hospitalization) o Daycare attendance o Presence of 2 of these risk factors increases the probability of a first febrile seizure to about 30%. o Maternal alcohol intake and smoking during pregnancy has a 2-fold increased risk. o Interestingly, no data support the theory that a rapid rise in temperature is a cause of febrile seizures. About one third of all children with a first febrile seizure experience recurrent seizures. o Risk factors for recurrent febrile seizures include the following: Young age at time of first febrile seizure Relatively low fever at time of first seizure Family history of a febrile seizure in a first degree relative Brief duration between fever onset and initial seizure

Patients with all 4 risk factors have greater than 70% chance of recurrence. Patients with no risk factors have less than a 20% chance of recurrence.

(Source: http://emedicine.medscape.com/article/801500-overview) 10) Pathophysiology of Loss of Conciousness and Febrile Seizures Pathophysiology of loss of consciousness Neuroregulatory syncope Common faint was previously termed vasovagal syncope but is now usually known as neuroregulatory or neurogenic syncope. Syncope is caused by a sudden decrease in blood pressure, which deprives the brain of sufficient oxygen, temporarily causing dizziness (presyncope) or a brief loss of consciousness (syncope). The Bezold-Jarisch reflex, which is an extreme or overshoot of a normal response to hypotension, is the postulated cause. Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is accentuated if the individual is dehydrated, as may occur following vigorous exercise, significant sweating, or prolonged restriction of fluid intake. The resultant arterial hypotension is sensed in the carotid body baroreceptors, and afferent fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, indicating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. The relative autonomic responses are helpful in determining whether the faint is primarily hypotensive (vasodepressor), bradycardic (cardioinhibitory), or mixed (see Media file 1). Syncope due to dysrhythmias Abnormalities of cardiac rhythm that result in decreased cardiac output may cause syncope without warning. These dysrhythmias include supraventricular tachycardia (SVT), ventricular tachycardia (VT), ventricular fibrillation, and extreme forms of bradycardia (eg, heart block). An unusual etiology for syncope in pediatric patients with normal cardiac anatomy may be paroxysmal or transient advanced second-degree or third-degree atrioventricular block. In these patients, the sinus node rate does not decrease and even increases during syncopal episodes. These patients may benefit from permanent pacemaker implantation.1 SVT usually produces some type of warning, such as palpitations, dizziness, or both, before causing syncope. Syncope in the patient with documented pre-excitation (ie, Wolff-ParkinsonWhite syndrome), with or without previously documented SVT, can be serious, suggesting a risk of sudden death. This can occur if the patient develops atrial fibrillation with resultant rapid conduction over an accessory pathway with a short refractory period. These patients should be

treated with a pathway-specific medication (eg, Vaughan-Williams class IC or III antiarrhythmics) until curative radiofrequency catheter ablation therapy can be arranged. Patients with VT may present with palpitations, dizziness, or both if the VT is monomorphic or nonsustained. Patients may also present with complete loss of consciousness if the VT is rapid or polymorphic. Polymorphic VT or ventricular fibrillation may be secondary to catecholaminesensitive VT or the congenital long QT syndromes (LQTSs). Intermittent heart block with a slow escape rate can cause sudden syncope, termed Stokes-Adams attack. Treatment of these patients in the absence of irreversible VT consists of permanent pacing. Hemodynamic causes of syncope The presence of structural heart disease (subtle or otherwise) may initiate or influence syncopal episodes.

Hypertrophic obstructive cardiomyopathy may reduce cardiac output because of subaortic muscular obstruction, intermittent coronary artery compression, or diastolic dysfunction (ie, poor ventricular filling) and predisposes patients to dysrhythmias (eg, atrial fibrillation, SVT, VT, heart block). Aortic stenosis may also initiate syncope because of diminished cardiac output or coronary ostial obstruction. Pulmonary hypertension may cause syncope when the right ventricle fails to pump against the high pulmonary pressure. As a result, cardiac output suddenly decreases, decreasing the blood and oxygen supply to the brain. Congenital or acquired coronary abnormalities may be susceptible to intermittent obstruction that results in sudden syncope. For example, ischemic heart disease due to anomalous coronary artery origin, hypercholesterolemia, or acute inflammatory diseases such as Kawasaki disease and myocarditis may predispose to syncope secondary to inadequate cardiac output, arrhythmias, or both. The interaction of hemodynamic residua of repaired congenital heart disease with atrial or ventricular dysrhythmias may result in syncope (eg, patients with tetralogy of Fallot or who have undergone Fontan or Mustard repair). Pericardial tamponade may cause syncope by decreasing cardial output secondary to atrial filling restriction.

Pathophysiology of febrile seizures Febrile seizures occur in young children at a time in their development when the seizure threshold is low. This is a time when young children are susceptible to frequent childhood infections such as upper respiratory infection, otitis media, viral syndrome, and they respond with comparably higher temperatures. Animal studies suggest a possible role of endogenous pyrogens, such as interleukin 1, that, by increasing neuronal excitability, may link fever and seizure activity. Preliminary studies in children appear to support the hypothesis that the cytokine network is activated and may have a role in the pathogenesis of febrile seizures, but the precise clinical and pathological significance of these observations is not yet clear. Febrile seizures are divided into 2 types: simple febrile seizures (which are generalized, last <15 min and do not recur within 24 h) and complex febrile seizures (which are prolonged,

recur more than once in 24 h, or are focal). Complex febrile seizures may indicate a more serious disease process, such as meningitis, abscess, or encephalitis. Viral illnesses are the predominant cause of febrile seizures. Recent literature documented the presence of human herpes simplex virus 6 (HHSV-6) as the etiologic agent in roseola in about 20% of a group of patients presenting with their first febrile seizures. Shigella gastroenteritis also has been associated with febrile seizures. One study suggests a relationship between recurrent febrile seizures and influenza A. Genetics: Febrile seizures tend to occur in families. In a child with febrile seizure, the risk of febrile seizure is 10% for the sibling and almost 50% for the sibling if a parent has febrile seizures as well. Although clear evidence exists for a genetic basis of febrile seizures, the mode of inheritance is unclear. (Source: http://emedicine.medscape.com/article/801500-overview) 11) Workup and Interpretation the Results of this Emergency Medicine Case Children: -Respiratory Rate: <2 yrs- tachypnea> 40x/mnt >2yrs- tachypnea> 30x/mnt - Heart rate: 75-120x/mnt. -BP: infant (6mo)- Systolic pressure. 87-105mmHg; diastolic pressure, 53-66mmHg. -Urine output: > 1-2 ml/kg/h -Lab for 1-24 mo children: Hb(g/dL)- m: 9.5-14.0 f: 9.5-14.0 Leucocyte (x10^9/L)- m: 5.0-13.0 f: 5.0-13.0 Hematocrite (%)- m:30-41 f:30-41 Trombosit (10^9/L)- m: 1.8-9.0 f: 1.8-9.0 Na (1mo- 1yr)- m: 131-140 f: 131-140 K (6mo- 1yr)- m: 3.5-6.3 f: 3.5-6.3 Cl (6mo- 1yr)- m: 97-106 f: 97-106 Diagnosis: Shock: - clinical recognition that the bodys tissues and cells are not receiving adequate delivery of oxygen and metabolic substrate. - symptoms and clinical findings are an extension of organs not getting what they need to function. - a lack of kidney perfusion results in decreased urine output. If the brains needs are not met, mental status changes occur. The lack of delivery of metabolic needs results in changes to gut and liver function. Clinical History: - a child with vomiting. profuse diarrhea, or both is at risk for hypovolemic shock.

- a child who has experienced trauma is at risk for bleeding that may result in hemorrhagic shock. - fever may herald an infection that could result in septic shock. - lethargy, weakness, a sense of malaise, decreased urine output, fussiness, and poor feeding are all nonspecific symptoms that may accompany shock. - however, the approach to any patient who present acute ill. regardless of the differential diagnosis, must begin with an initial evaluation of the patients ABCs. - If the patients circulation is compromised, that patient is said to be in shock, and therapy must be immediately initiated while further evaluation is performed. Clinical evaluation: - Compensated versus decompensated shock-first determine the central blood pressure. Pediatric advanced life support (PALS) defines infants with fifth-percentile systolic blood pressure as follows: Newborn- 60 mmHg. Infant (1mo to 1 yr) 70mmHg. Child (>1 yr)- 70+ 2x age (in yr). Children with poor perfusion and blood pressure below the parameters listed above may be said to have decompensated shock. - Tachycardia is generally a fairly early and specific finding in both compensated and decompensated shock. - Distal pulses are diminished, the skin appears cool, and capillary refill is prolonged (ie, . 5s). At normal room temperature, the distal capillary bed normally refills within 2-3 seconds. Refill time longer than 5 seconds is considered prolonged. - Renal perfusion may be reflected by absolute urine output. Typically, in the absence of renal damage, a well-perfused kidney can produce 1-2 ml urine/kg. - Mental status may reflect central perfussion to the brain. Altered mental status may coincide with profound central shock or more. Investigation 1. Diarrhea: - check for signs of dehydration. - Stool examination DURING diarrhea. 2. Dehydration: - history: fluid intake, weight loss, underlying illness, etc. - physical: clinical assessment of severity of dehydration. 3. Fever: - History: temperature changes. - Birth history - Previous diagnostic & results (e.g culture) - observation: quality of cry, attitude, etc - physical exam: dyspnea, tachypnea, flaring. retractions, etc. - lab: full sepsis workup: CBC, blood culture, urinalysis, urine culture, LP

12) Monitoring and Reevaluation Patient in this Emergency Medicine Case Monitoring the Child in Shock in the Primary Care Setting Capillary refill Documentation of mental status Pulse oximetry Continuous electrocardiogram Blood pressure (cuff) Temperature Urine output Glucose and ionized calcium level Serum hemoglobin or hematocrit Hepatomegaly is a reliable indicator of volume overload and cardiac compromise. Successful resuscitation is recognized by: Return of pulse rate to normal Improvement in mental status Return of capillary refill Improvement in acid-base status (Source: http://www.pediatriccareonline.org/pco/ub/view/AAP-Textbook-of-PediatricCare/394358/6/chapter_358:_shock) 13) Definitive Care AMERICAN COLLEGE OF CRITICAL CARE MEDICINE CLINICAL PRACTICE PARAMETERS FOR HEMODYNAMIC SUPPORT OF PEDIATRIC AND NEONATAL SHOCK Five minutes: o First, secure airway and ventilation. Children have low lung volumes and are at risk for hypoxemia. Establish venous access within 5 minutes of recognition of shock. An intraosseous device or peripheral intravenous device suffices for this purpose. (Central access is not part of the 1st response.) o Begin monitoring the child (see monitoring guidance in BOX 358-5). Fifteen minutes: In the first 15 minutes, administer intravenous fluids. Fluid needs can exceed 60 mL/kg of body weight. The volume of each fluid bolus should be 20 mL/kg. Thirty minutes (15 minutes after fluid therapy begins): o For children who do not immediately respond to fluid administration (15 minutes from beginning of fluid therapy), begin infusion of dopamine, catecholamine agent of 1st choice, at a dose of 5 to 20 mcg/kg/min. Infants younger than 6 months may not respond as well to dopamine.[9]

Children who do not respond to dopamine infusion up to 20 mcg/kg/min and fluid resuscitation have dopamine-fluid refractory shock. Institute epinephrine (for cold shock) or norepinephrine (for warm shock) infusions. Glucose, serum hemoglobin or hematocrit, acid-base homeostasis, and ionized calcium should be monitored and restored to normal values. Sixty minutes: Children who do not respond to fluid and an infusion of 2 catecholamine agents within 60 minutes have catecholamine resistant shock, and adrenal insufficiency should be considered. Refer to a tertiary care pediatric intensive care unit if children do not respond to fluid administration and to dopamine and epinephrine or norepinephrine infusions. These children require diagnostic evaluation for cardiac function and will require central venous access, echocardiography, and mixed venous oxygen saturation monitoring.

Treatment of shock, especially in primary care settings, is based on principles of restoring adequate circulating blood volume, thereby achieving adequate delivery of glucose and oxygen to all tissues. Drugs and fluids for the treatment of shock are listed in Table 358-5. Monitoring and documenting the patient's response to each intervention is essential. Patients who develop organ failure have a markedly worse prognosis in shock. Specific definitions of organ failure are listed in BOX 358-6. Early volume resuscitation and vasopressor therapy are always indicated in the treatment of shock. Hepatomegaly is a reliable clinical indicator of volume overload. In children who develop hepatomegaly but remain hemodynamically unstable, cardiac or renal failure must be considered. Clinicians should bear in mind that fluid requirements in shock may exceed 60 mL/kg, and a more common error is to give too little fluid too slowly. Rather than fearing fluid overload and thus undertreating the vast majority of patients, the clinician should gauge the patient's response to fluid administration. Patients who remain tachycardic with poor capillary refill and have inadequate urine output (<0.5 mL/kg/hr) after 60 mL/kg of fluid and the addition of 2 vasopressors are critically ill and in catecholamine-resistant shock. Placement of a central venous catheter is recommended at this point. Patients in this decompensated state will require referral to a tertiary pediatric intensive care unit for further diagnosis and treatment. No conclusive data are found in the literature proving superiority of one fluid over another.[19] [24] [25] Commonly used solutions are normal saline, lactated Ringer solution, or 5% albumin. The volume of the bolus should be 20 mL/kg of body weight. Children consume glucose at a faster rate than adolescents and adults. In infants and toddlers, glucose levels should be considered a vital sign, and blood glucose needs to be added to maintain adequate blood glucose levels. Glucose replacement is crucial, especially in very young patients. Glucose should be maintained at over 60 mg/dL. All patients in shock should immediately be given 100% oxygen; oxygenation should be monitored continuously with a pulse oximeter and the values documented in the patient's record. Because normal oxygen saturation does not reflect adequate oxygen content, the hemoglobin (the

carrying vehicle for oxygen) should be maintained at a normal level. In hypovolemic shock, occult blood loss is in the differential diagnosis. In septic shock, the outcome in children may depend on adequate oxygen delivery. Clinicians need to appreciate that normal oxygen saturation on a pulse oximeter does not imply adequate tissue delivery.[20] [26] [27] Blood transfusions may be necessary to ensure adequate oxygen delivery. If the circulation is compromised and cardiac output falls, then oxygen delivery to tissues will be compromised. In septic shock, adequate oxygen delivery is associated with improved survival.[10] Oxygen delivery is the product of oxygen content and cardiac output. Oxygen content = 1.36 the percentage of saturation hemoglobin (in grams) and is expressed as milliliters of oxygen per 100 mL of blood. In healthy children, oxygen consumption is 25% of oxygen delivery. In shock states, oxygen consumption may increase simultaneously with inadequate cardiac output, leading to inadequate tissue oxygenation. If lung disease is present or hypoventilation occurs, then hemoglobin is desaturated, and oxygen delivery is compromised further. Despite concerns over the adverse effect of transfusion, the hemoglobin or hematocrit must be monitored, and maintaining the hemoglobin at least 10-g percentage is reasonable.[23] Arterial lactic acidosis (normal is <2 mmol/L) or an increasing base deficit (>3 mEq) document inadequate perfusion. The effects of restoring the pH to over 7.25 are important: Myocardial contractility is enhanced, sensitivity to catecholamines is improved, and potassium is returned to the intracellular space. Sodium bicarbonate may be required to improve blood pH to over 7.25 and serum bicarbonate levels to more than 15 mEq/dL. Any remaining base deficit may be corrected by using the following guide: 0.3 body weight in kilograms base deficit = milliequivalents of sodium bicarbonate.[28] Hypocalcemia is common. Total calcium measurements do not correlate with measurements of the biologically important ionized calcium.[29] Restoring ionized calcium to normal levels improves myocardial contractility.[24] In general, unless bleeding is evident, platelet counts of 20,000 to 50,000 cells/mm[3] are tolerated well. Prothrombin time and partial thromboplastin time should be maintained at approximately 1.3 times the normal values. Fresh frozen plasma, administered at 10 mL/kg, is a reasonable method of both repairing volume deficit and replenishing coagulation factors. Rapid infusion of fresh frozen plasma can contribute to hypotension resulting from the presence of vasoactive kinins.[2] (Source: http://www.pediatriccareonline.org/pco/ub/view/AAP-Textbook-of-PediatricCare/394358/6/chapter_358:_shock)

14) Pediatric Intensive Care Unit (PICU) Guidelines and Levels of Care for Pediatric Intensive Care Units Guidelines and Levels of Care for Pediatric Intensive Care Units Introduction The practice of pediatric critical care has matured dramatically throughout the past 3 decades. Knowledge of the pathophysiology of life-threatening processes and the technological capacity to monitor and treat pediatric patients suffering from them has advanced rapidly during this period. Along with the scientific and technical advances has come the evolution of the pediatric intensive care unit (PICU), in which special needs of critically ill or injured children and their families can be met by pediatric specialists. All critically ill infants and children cared for in hospitals, regardless of the physical setting, are entitled to receive the same quality of care. In 1985, the American Board of Pediatrics recognized the subspecialty of pediatric critical care medicine and set criteria for subspecialty certification. The American Boards of Medicine, Surgery, and Anesthesiology gave similar recognition to the subspecialty. In 1990, the Residency Review Committee of the Accreditation Council for Graduate Medical Education completed its first accreditation of pediatric critical care medicine training programs. In 1986, the American Association of Critical Care Nurses developed a certification program for pediatric critical care, and in 1999, a certification program for clinical nurse specialists in pediatric critical care was initiated. In view of recent developments, the Pediatric Section of the Society of Critical Care Medicine and the Section on Critical Care Medicine and Committee on Hospital Care of the American Academy of Pediatrics believe that the original guidelines for levels of PICU care from 1993[1] should be updated. This report represents the consensus of the three aforementioned groups and presents those elements of hospital care that are necessary to provide high-quality pediatric critical care. The concept of level I and level II PICUs as established in the guidelines set forth in 1993 will be continued in this report. Individual states may have PICU guidelines, and it is not the intent of this report to supersede already established state rules, regulations, or guidelines; however, these guidelines represent the consensus report of critical care experts. Pediatric critical care is ideally provided by a PICU that meets level I specifications. The level I PICU must provide multidisciplinary definitive care for a wide range of complex, progressive, and rapidly changing medical, surgical, and traumatic disorders occurring in pediatric patients of all ages, excluding premature newborns. Most, although not all, level I PICUs should be located in major medical centers or within children's hospitals. It is also recognized that in the appropriate clinical setting and as a result of many forces, including but not limited to the presence of managed care, the insufficient supply of trained pediatric intensivists, and geographic and transport limitations, level II PICUs may be an appropriate alternative to the transfer of all critically ill children to a level I PICU. The level I PICU should provide care to the most severely ill patient population. Specifications for level I PICUs are discussed in detail in the text and are summarized in Table 1 . Level I PICUs will vary in size, personnel, physical characteristics, and equipment, and they may differ in the types of specialized care that are provided (e.g., transplantation or cardiac surgery). Physicians and specialized services may differ between levels, such that level I PICUs will have

a full complement of medical and surgical subspecialists, including pediatric intensivists. Each level I and level II PICU should be able to address the physical, psychosocial, emotional, and spiritual needs of patients with life-threatening conditions and their families. Some pediatric patients with moderate severity of illness can be managed in level II PICUs. Level II PICUs may be necessary to provide stabilization of critically ill children before transfer to another center or to avoid long-distance transfers for disorders of less complexity or lower acuity. It is imperative that the same standards of quality care be applied to patients managed in level II PICUs and level I PICUs. Requirements for level II PICUs differ from those for level I PICUs primarily with respect to the type and immediacy of physician presence and hospital resources. A level II PICU does not require a full spectrum of subspecialists, as outlined in the Table 1 . Level II units should be located according to documented demand or need and in concert with accepted principles of regionalization of medical care.[2] Each level II unit must have a well-established communications system with a level I unit to allow for timely referral of patients who need care that is not available in the level II PICU. Although other special care units may be appropriate for hospitals with small pediatric inpatient services, they should not be considered PICUs. Cooperation among hospitals and professionals within a given region is essential to ensure that the appropriate numbers of level I and level II units are designated. Duplication of services may lead to underutilization of resources and inadequate development of skills by clinical personnel and may be costly. Detailed discussion of the importance of regionalization of critical care services has been provided by the American College of Critical Care Medicine and the American Academy of Pediatrics.[3] This report provides the minimum acceptable guidelines for the following aspects of pediatric critical care: organization and administrative structure, personnel, hospital facilities and services, drugs and equipment, prehospital care, quality improvement, and training and continuing education ( Table 1 ). These guidelines are intended to assist hospitals, in properly determining resource allocation and equipment needs; physicians, as a reference for referral and care of critically ill infants and children; emergency medical services (EMS) personnel, for proper prehospital triage; and level I and level II PICUs, as a means of ensuring proper patient care. In preparing this report, significant efforts were made to build on previous work describing regional and national guidelines and standards that apply to these guidelines and, when possible, to incorporate those previous recommendations. The existing guidelines for PICUs established by the American Academy of Pediatrics and the Society of Critical Care Medicine were used as the major reference source.[1] In addition, this report incorporates the experience, expertise, and opinions of pediatric caregivers including pediatric critical care physicians and nurses representing diverse regions of the country and types of practice. ( Source: http://www.medscape.com/viewarticle/491710) COMMENT: All the information from the reference books and websites are the same.And our tutorial mates have had agreed with what we discuss during the second meeting of tutorial B14.

CONCLUSION : In this case, Andi, a 1 year old child came to hospital with an impaired consciousness. Once he was in hospital, he experienced a seizure attack whole bodily. He has the history of diarrhea and fever for a week ago after anamnesis being done. Diarrhea and fever from this case lead us to think that Andi had an infection a week ago. Further anamnesis found out that he had anuria since a day before. Diarrhea had cause Andi to be in dehydration states that his body finally compensated physiologically to retain water by having no urine output. From physical examination it was found that Andi was having cyanosis, with respiratory rate 80x/min, cool extremities and impalpable pulse. Cyanosis is a sign of hypoxia condition that comes together with a drop in respiration rate and cool extremities whereas impalpable pulse is a sign of hypotension. Dehydration state previously had caused a reduction of blood flow circulate through the whole body. Oxygen supply can hardly be maintained to all organs and thus body counteracted with heart pumping vigorously to maintain blood circulation in giving oxygen supplementation only to a few of vital organ such as liver and kidney. This thus decreases blood flow to extremities and hence causes cyanosis condition with cool extremities on Andi. Further examination was taken such as GSC scale, BP, pulse pressure, and urine output after fluid infusion of 60 cc/kg BW was given to Andi. The differential diagnosis of hypovolemic shock is excluded for there was no improvement after fluid therapy was given. We concluded that he was in a septic shock state with his mean arterial pressure is 47%. It is kown that septic shock is similar to hypovolemic shock except in the first stage and there is no improvement despite fluid resuscitation. For further diagnosis, it was best to do a laboratory workup. Therefore, More Info II stated that there is an increased in leucocyte in spite of the infection and imbalanced in potassium - chloride ions where Andi had a severe dehydration due to infection that caused him to diarrhea persistently one week. From the case and further check-ups for diagnosis of Andis disease, it is concluded that Andi suffering septic shock accompanied by seizure. It is found out that Andi also suffering severe dehydration from post-infection and hence lead to shock.As a general practice, i will do primary survey and resuscitation for Andi.Then I will treat his seizures with IV diazepam.To treat the septic shock that Andi suffered, I will give fluid resuscitation and broard septum antibiotic to Andi.

REFERENCES A. http://www.medscape.com/viewarticle/491710 B. http://www.pediatriccareonline.org/pco/ub/view/AAP-Textbook-of-PediatricCare/394358/6/chapter_358:_shock) C. http://emedicine.medscape.com/article/801500-overview D. http://www.google.co.id/search?hl=id&q=etiology+of+pediatric+loss+of+consciousemedicine&meta= E. http://emedicine.medscape.com/article/801012-treatment F. http://www.nlm.nih.gov/medlineplus/ency/article/000668.htm G. www.circ.ahajournals.org/cgi/content/full/102/suppl_1/I-291

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http://circ.ahajournals.org/cgi/content/full/102/suppl_1/I-253 I. http://www.health.state.ny.us/nysdoh/ems/pdf/pediatricreferencecard-04.pdf J. http://emedicine.medscape.com/article/ K. http://emedicine.medscape.com/article/908930-overview