کاهش سطح هوشیاری ALTERD LEVEL OF CONSCIOUSNESS ALOC A SIGN NOT A DISEASE COMA THE LAST STATE OF DEPRESSED CONSCIOUSNESS

Transcription

1 بنام خدا

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3 کاهش سطح هوشیاری ALTERD LEVEL OF CONSCIOUSNESS ALOC A SIGN NOT A DISEASE COMA THE LAST STATE OF DEPRESSED CONSCIOUSNESS

4 PATHOPHYSIOLOGY 1) ARAS 2) CEREBRAL HEMISHERERS

5 Stages of depressed consciousness Stage Manifestations Lethargy Sleepy,poor attention,fully arousable Confusion Poor orientation Delirium Agitated confusion, hallucinations, autonomic abnormalities(sweating,hr,htn) Obtundation Arousable to noxious stimulation Stupor Arousable momentarily with noxious stimulation,localizes pain Coma Unarousable,does not localize pain

6 encephalopathy The term encephalopathy describes a diffuse disorder of the brain in which at least two of the following symptoms are present 1) altered states of consciousness 2) altered cognition or personality 3) Seizures Encephalitis is an encephalopathy accompanied by cerebrospinal fluid (CSF) pleocytosis.

7 ETIOLOGY

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15 EVALUATION Coma is a medical emergency whose evaluation requires a rapid, comprehensive, and systematic approach. Early identification of the underlying cause of coma can be crucial for patient management and prognosis.

16 History The etiology may be apparent from the history, when coma results from the expected progression or complication of a known illness or injury

17 General examination Assessing vital signs and the ABCs: airway patency, breathing (ventilation and oxygenation), and circulation, are important for initial stabilization, but may also inform the etiology dehydration, unusual odors, needle tracts, trauma, or signs of organ system failure Breathing patterns :Cheyne-Stokes (Cerebral, thalamic, or hypothalamic modulation of respiration has been lost), central neurogenic hyperventilation(midbrain lesion ), Gasping (dysfunction of the low brainstem-medulla)

18 Neurological examination The neurologic examination in this situation is necessarily brief and is directed at determining whether the pathology is structural or due to metabolic dysfunction (including drug effects and infection). The examiner assesses: Level of consciousness Motor responses Brainstem reflexes(ras): pupillary light, extraocular, and corneal reflexes

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21 DIAGNOSTIC STUDIES Laboratory Testing Neuroimaging Lumbar puncture Electroencephalogram

22 Laboratory Testing All patients presenting with altered consciousness should undergo a rapid bedside test for blood glucose and basic laboratory testing including: Serum electrolytes, calcium, magnesium, glucose Arterial blood gas, Liver function tests, ammonia Complete blood count Blood urea nitrogen, creatinine,urine drug screen,blood culture

23 Neuroimaging Computed tomography (CT) is the initial neuroimaging test of choice to evaluate a child in coma.. CT should be performed immediately when the examination suggests increased intracranial pressure (papilledema, bulging fontanelle in infants, or bradycardia with hypertension) or a transtentorial herniation syndrom

24 Falx cerebri and tentorium

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29 Lumbar puncture Urgent evaluation of cerebrospinal fluid (CSF) is required when there is suspected infection of the central nervous system. In a patient with altered level of consciousness, neuroimaging to exclude an intracranial mass lesion is required prior to lumbar puncture (LP) in order to avoid precipitating transtentorial herniation. Coagulation test results should also be obtained beforehand. Empiric antimicrobial treatment is recommended when the diagnosis of bacterial meningitis or herpes encephalitis is strongly suspected,

30 Encephalogram EEG should be performed in children with coma of unknown etiology. It is often the only means of recognizing nonconvulsive status epilepticus (NCSE), especially in patients who are paralyzed. Periodic epileptiform discharges may occur in NCSE but also in underlying brain injury without seizures. Periodic lateralized epileptiform discharges suggest herpes encephalitis or infarction. Multifocal or generalized periodic discharges can also be seen with metabolic and infectious etiologies and are characteristic of subacute sclerosing panencephalitis.

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34 TREATMENT Early treatment of coma is generally supportive until a definitive diagnosis is made. An important goal of early treatment is to limit brain injury. Treatments for dangerous etiologies (eg, hypoglycemia, increased intracranial pressure, bacterial meningitis,opioid intoxication) are often initiated empirically, especially if there are suggestive clinical features.

35 Airway Establishing a secure airway and providing adequate ventilation may be lifesaving and also may limit neurologic injury. Establishing a secure airway in a patient with coma may be attained by repositioning the child to open the airway,. Patients with GCS <8 are usually unable to adequately protect their airway and should be intubated.

36 Breathing Oxygen saturation should be measured and supplemental oxygen provided. Moderate hyperventilation (target PaCO2 30 to 35 mm Hg) to produce arterial constriction and lower intracranial pressure (ICP) should only be initiated for patients with increased ICP. Extreme hyperventilation has been associated with brain ischemia; the risks of aggressive hyperventilation (PaCO2 <30 mmhg) are only justified in patients with transtentorial herniation

37 Circulation Depressed level of consciousness may be an early indicator of poor end-organ perfusion in a patient with shock. Hypotension has been associated with poor neurologic outcome following traumatic brain injury (TBI) and meningitis in children Effective circulation through intravenous fluid administration and inotropes, For patients with hypertensive encephalopathy, the blood pressure should be lowered slowly to avoid superimposing an ischemic insult. The goal of therapy is to lower the diastolic blood pressure to 100 to 110 mmhg (or by a maximum of 25 percent) within two to six hours

38 Glucose Fingerstick blood sugar and a serum glucose should be checked immediately in the evaluation of a comatose child. Glucose (2.5 ml/kg of 10 percent dextrose solution) should be administered even before test results are known. If hypoglycemia is revealed, then ongoing monitoring and treatment will be needed.

39 Intracranial pressure When increased intracranial pressure (ICP) is suspected based on CT findings, papilledema, split sutures, or a herniation syndrome, emergent treatment is recommended. Increased ICP is assumed when there is coma after head injury. Early interventions to reduce intracranial pressure include treating fever, elevating the head of the bed to 30 degrees above horizontal, moderate hyperventilation (target PaCO2 30 to 35 mmhg) and administering mannitol (0.25 to 1 g/kg IV). Neurosurgery should be consulted.

40 Seizures If seizures have occurred diazepam( mg/kg), phenytoin (15 to 20 mg/kg phenytoin equivalent IV) should be administered. Recurrent seizures or status epilepticus may increase ICP and may be associated with secondary brain injury and worse neurologic outcome. (don t forget hypoglycemia&hypocalcemia) Nonconvulsive status epilepticus should be considered as a diagnosis even when there are no obvious seizure movements.

41 Infection Empiric antibiotic and antiviral therapy are recommended if bacterial meningitis (eg, ceftriaxone 100 mg/kg plus vancomycin 60 mg/kg) or viral encephalitis (acyclovir 30 to 60 mg/kg per day,) are among the suspected entities.blood cultures should be obtained prior to starting antibiotics but initiation of therapy should NOT await lumbar puncture. Therapy should be continued until these conditions have been excluded

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43 Hyperthermia Hyperthermia (>38.5 degrees C) can contribute to brain damage in cases of ischemia. Fever also increases cerebral metabolism and blood flow, thereby contributing to elevated ICP.Fever should be lowered with antipyretics and/or cooling blankets immediately. Shivering, which can contribute to elevated ICP, should be avoided.

44 Acid-base and electrolyte imbalance Electrolyte imbalance may cause or be a complication of coma, and may increase the risk of neurologic injury. Iatrogenic causes of electrolyte derangement may result from resuscitation of patients with hypotonic or large volumes of hypertonic solutions. Resuscitation of patients with cardiovascular compromise should use isotonic solutions only (normal saline or lactated Ringers). Any electrolyte abnormalities should be corrected and monitored.

45 Antidotes Antidote use is recommended only in the setting of known or strongly suspected drug overdose Naloxone (.01 to 0.1mg/kg up to 2 mg) is a relatively safe and effective treatment and should be considered when the history suggests possible opiate ingestion. Flumazenil is an antidote for benzodiazepine overdose, but will render benzodiazepines ineffective in the event of a seizure, so it should also be used with caution. Gastric lavage and activated charcoal may be recommended for very recent ingestions.

46 Agitation Agitation may increase ICP, interfere with respiratory support, and increase the risk of injury. Significant sedation, however, may obscure the neurologic exam, may contribute to hypotension and hypoventilation, and should be administered only when the benefits of relieving agitation outweigh the need for close neurologic monitoring by exam.

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49 Seizures represent the abnormal and excessive discharging of the neuralglial network. A diverse group of disturbances of cerebral function or homeostasis can lead to seizures

50 Epilepsy is defined as recurrent, unprovoked seizures. Epileptic seizures are generally separated on the basis of the mechanism of the electrical phenomena into seizures that arise from one region of the cortex (focal, partial, or localization related) and seizures that arise from both hemispheres simultaneously (generalized)

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52 Status epilepticus Status epilepticus is defined as ongoing seizure activity for greater than 30 minutes or repetitive seizures without return of consciousness for greater than 30 minutes impending status epilepticus for seizures between 5 and 30 min. The measures used to treat status epilepticus need to be started in any patient with acute seizures that do not stop within a few minutes

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55 ICU ADMISSION EEG MONITORING MIDAZOLAM DRIP ASSISTED VENTILATION FLUID THERAPY (judiciously) HEMODYNAMIC STATE SUPPORTIVE CARE TREATMENT OF ETIOLOGY

56 A complete laboratory evaluation of a child with the new onset of seizures includes a complete blood count; measurement of blood chemistries, including glucose, calcium, sodium, potassium, chloride, bicarbonate, urea nitrogen, creatinine, magnesium, and phosphorus; blood or urine toxicology screening; analysis of CSF; and EEG and brain imaging (MRI).

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58 عالیم و نشانه های نیاز قریب الوقوع به احیا

59 عالئم و نشانه های مربوط به CNS Obtundation Agitation لتارژیLethargy گیدیConfusion آژیتاطی ى دلیزی م

60 عالئم و نشانه های تنفسی آپ گزا تی گ) Grunting ( پزع پز ای بی ی) flaring )Nasal ت گی فض رتزکظی ى) Retracting ( ت فض ت ذ) Tachypnea ( خابدایی ظؼیف ا درری ا movement( )Poor air اطتزیذ ر )Stridor( خض خض طی ) Wheezing (

61 عالئم و نشانه های قلبی عروقی آریتوی) Arrhythmia ( بزادی کاردی تاکی بزگؼت آ ظت ه یزگی) Refill )Poor Capillary کاردی بط ای فؼار خ ى پاییي ظؼیف

62 عالئم و نشانه های مربوط به پوست و مخاطها هؼبک ػذى پ طت) Mottling ( ر گ پزیذگی) Pallor ( طیا س تؼزیك سیاد) Diaphoresis ( ت رگ ر ظؼیف Turgor( )Poor Membrane خؼکی طط ذ هخاطی) membranes )Dry mucous

63 فیلم ها

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65 آسپیراسیون جسم خارجی

66 Foreign Body Airway Obstruction chocking

67 FBAO (Choking) Epidemiology & Recognition More than 90% of deaths occur in children < 5 y/o. Signs: a sudden onset of respiratory distress with coughing, gagging, stridor, or wheezing

68 FBAO (Choking) Severe airway obstruction The victim cannot cough or make any sound. Mild airway obstruction The child can cough & make some sounds.

69 Heimlich maneuver Conscious Child Standing Conscious or Unconscious Child, Lying

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71 Back Blow & Chest Thrust in an Infant

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73 Unresponsive Victim Perform CPR but should look into the mouth before giving breaths. If you see a foreign body, remove it. Do not perform blind finger sweeps because it may push obstructing objects further into the pharynx & may damage the oropharynx. Attempt to remove an object only if you can see it in the pharynx. Then attempt ventilation & follow with chest compressions.

74 Finger Sweep Maneuver Administered to an Unconscious Victim of FBAO

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76 Emergency Department Management of Asthma Exacerbations

77 Severity of Asthma Exacerbations

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80 Management of Asthma Exacerbations in Acute Care Setting

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96 Definition of shock Shock is an acute, complex state of circulatory dysfunction result in failure to deliver sufficient amount of oxygen and other nutrients to meet tissue metabolic demand.

97 Classification of the cause of shock Hypovolemic Cardiogenic Distributive Obstructive Septic Dissociative

98 hypovolemic Blood loss: hemorrhage Plasma loss: burns, nephrotic syndrome Water/electrolyte loss: vomiting, diarrhea ( the most common shock in pediatrics )

99 CARDIOGENIC Congenital heart disease Cardiomyopathies: infectious or acquired, dilated or restrictive Ischemia Arrhythmias

100 DISTRIBUTIVE Anaphylaxis Neurologic: loss of sympathetic vascular tone secondary to spinal cord or brainstem injury Drugs

101 SEPTIC Hypovolemic: third spacing of fluids into the extracellular, interstitial space Distributive: early shock with afterload Cardiogenic: myocardial function by endotoxins

102 OBSTRUCTIVE Tension pneumothorax Pericardial tamponade Pulmonary embolism Anterior mediastinal masses Critical coarctation of the aorta

103 DISSOCIATIVE SHOCK Oxygen not released from hemoglobin(co poisoning) Methemoglobinemia

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106 Stages of shock Compensated shock :presence of normal blood pressure by compensatory mechanism (Hypoperfusion state) Decompensate shock: fail of compensatory mechanism. Hypotension and organ dysfunction Irreversible shock :progression of organ dysfunction

107 Hypotension definition Neonate (0-28 days): < 60 mmhg Infant (1-12 months): < 70 mmhg Children (1-10 years): < 70 + [2 age (y)] mmhg >10 years: <90 mmhg

108 compensation Increasing cardiac output( HR, stroke volume, systemic vascular resistance) increasing oxygen extraction Redistributing blood flow to the brain, heart, liver & kidneys at the expense of the skin and GI tract & muscles Increased respiratory rate renin-angiotensin-aldosterone, ADH, cortisol and catecholamine,anf, Renal excretion of H + and retention of HCO 3 to maintain normal body ph

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110 Multisystem Organ Dysfunction

111 Cardiovascular Despite administration of isotonic intravenous fluid bolus 60 ml/kg in 1 hour: Decrease in BP (hypotension) <5th or systolic BP <2 SD below normal for age OR Need for vasoactive drug to maintain BP in normal range (dopamine >5 µg/kg/min or dobutamine, epinephrine, or norepinephrine at any dose) OR Two of the following: Unexplained metabolic acidosis: base deficit > 5.0 meq/l Increased arterial lactate: >2? upper limit of normal Oliguria: urine output <0.5 ml/kg/hr Prolonged capillary refill: >5 sec Core to peripheral temperature gap >3?C

112 Respiratory Pao 2 /Fio 2 ratio <300 in absence of cyanotic heart disease or pre-existing lung disease OR Paco 2 >65 torr or 20 mm Hg over baseline Paco 2 OR Proven need for >50% Fio 2 to maintain saturation 92% OR Need for nonelective invasive or noninvasive mechanical ventilation

113 Neurologic GCS score 11 OR Acute change in mental status with a decrease in GCS score 3 points from abnormal baseline

114 Hematologic Platelet count <80,000/mm 3 or a decline of 50% in the platelet count from the highest value recorded over the last 3 days (for patients with chronic hematologic or oncologic disorders) OR INR >2

115 Renal Serum creatinine 2? upper limit of normal for age or 2-fold increase in baseline creatinine value

116 Hepatic Total bilirubin 4 mg/dl (not applicable for newborn) Alanine transaminase level 2? upper limit of normal for age

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118 Systemic inflammatory response syndrome The presence of at least two of the following four criteria, one of which must be abnormal temperature or leukocyte count: - Core temperature of > C or < 360 c - Tachycardia - High respiratory rate - Lukocyte count elevated or depressed for age

119 Infection Suspected or proven infection or a clinical syndrome associated with high probability of infection

120 Sepsis SIRS plus a suspected or proven infection

121 Severe sepsis Sepsis plus one of the following : cardiovascular organ dysfunction OR acute respiratory distress syndrome OR two or more other organ dysfunctions

122 Septic shock Sepsis and cardiovascular organ dysfunction

123 Clinical Manifestations depends in part on the underlying etiology If unrecognized and untreated, all forms of shock follow a common and untoward progression of clinical signs and irreversible shock and death

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125 Tachycardia Each 1 0 Core temperature rises HR 12 beat/min

126 Tachypnea Each 1 0 Core temperature rises RR 5-10 /min

127 Poor Perfusion Mottled or cool extremities Mental status change Decreased urine output Capillary filling > 3 sec Decreased peripheral (dorsalis pedis or radial )pulses compared to central pulses Increase in central to peripheral temperature gradient(gap>3 c)

128 Diagnosis Shock is diagnosed clinically on the basis of a thorough history and physical exam

129 Laboratory Findings Leukocytosis Identifying an infectious etiology(cultures,analyses of body fluids, imaging, ) Organ dysfunction detection(renal,hepatic, ) hematologic abnormalities and electrolyte disturbances(plt,pt,ptt,fsp,anemia, PMN, Ca, or BS, Alb,metabolic acidosis, Svo2 & serum lactate (marker for the adequacy of oxygen delivery and the effectiveness of therapeutic interventions)

130 SvO2 or Svco 2 & Serum lactate marker for the adequacy of oxygen delivery and the effectiveness of therapeutic interventions

131 Oxygen delivery normally exceeds oxygen consumption by threefold. The oxygen extraction ratio is approximately 25%, thus producing a normal of 75-80%. A falling value, as measured by co-oximetry, reflects an increasing oxygen extraction ratio and documents a decrease in oxygen delivery relative to consumption. Serum lactate measurements

132 Management Early recognition and prompt intervention

133 for each unrecognizedand untreated hour of shock, the mortality rate is estimated to increase twofold.

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135 Fluid administration isotonic crystalloid solution(ns) increments of 20 ml/kg Max ml/kg sometimes require as much as 200 ml/kg

136 Within the bolus fluid dose Rales Gallop rhythm Hepatomegaly Increased work of breathing Increased oxygen need,

137 Titration of Fluid resuscitation Untill normalization of: heart rate (according to age-based heart rates) urine output (to 1 ml/kg/hr) capillary refill time (to <2 sec) mental status

138 Antibiotics After cultures provided this does not significantly delay antibiotic administration (2 or more B/C ) Within 1 hour of recognition of sepsis Broad spectrum Cover likely organism High infected tissues penetration Hospital acquired: know local resistance pattern 3rd-generation cephalosporin or.

139 Early sepsis: When intubate? Respiratory alkalosis from central mediated hyperventilation Late sepsis: Hypoxemia Metabolic acidosis The decision to intubate and ventilate is based on clinical assessment of: Increased work of breathing Hypoventilation Decreased level of consciousness Patient in fluid refractory shock should be intubated and ventilated

140 If no clinical improvement (fluid refractory) Add vasoactive infusions : Low dose dopamine (2 to 5 mcg/kg/min) for children who are normotensive Beta adrenergic dose of dopamine (5 to 10 mcg/kg/min) or norepinephrine for those who are hypotensive and vasodilated Epinephrine for children who are hypotensive and vasoconstricted despite maximum beta adrenergic doses of dopamine and/or norepinephrine

141 If catecholamine resistant after sample for baseline cortisol levels Patients at risk for adrenal insufficiency: congenial adrenal hypoplasia abnormalities of the hypothalamic-pituitary axis recent therapy with corticosteroids (asthma, rheumatic dis., malignancies,& IBD Septic shock with Purpura fulminant

142 Corticosteroid dose Recommended dose is a wide range from 2mg/kg /day for stress coverage to 50 mg/kg /day titrated to reversal of shock Dexamethasone (0.1 mg/kg, maximum 10 mg) may be given as the initial steroid dose in the emergency department since (unlike hydrocortisone) it will not interfere with subsequent testing of adrenal function

143 Therapeutic goal in emergency room: Capillary refill 2 secs, Normal pulses with no differential between the quality of peripheral and central pulses, Warm extremities, Urine output >1 ml/kg/h Normal mental status Normal blood pressure for age Normal glucose concentration Normal ionized calcium concentration.

144 Transfer to PICU

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146 Monitor CVP in PICU Attain normal MAP-CVP & SvO2> 70%

147 What is MAP-CVP CO= (MAP CVP) / SVR Q= dp/r, (Q= Blood flow, dp= perfusion pressure, R=resistance) MAP CVP = PP (PP= Perfusion pressure) For example: Renal perfusion pressure Mean renal arterial pressure mean renal venous pressure Renal vascular resistant One goal of shock treatment is to maintain perfusion pressure above the critical point below which blood flow can not effectively maintain in individual organ.

148 The value of CVP monitoring is doubted. CVP has a very poor correlation with intravascular volume CVP is influenced not only by intravascular volume and venous return, but by Venous tone (hypotensive patient can exhibit normal BP due to vasoconstriction) Intrathoracic pressure Rt heart function Myocardial compliance However low CVP can guide fluid resuscitation CVP = cm H2O Perfusion pressure (MAP CVP) > 65 mmhg

149 Cold shock with normal blood pressure (High SVR) Cold shock with low blood pressure (High SVR) Warm shock with low blood pressure (Low SVR)

150 Cold shock with normal blood pressure (High SVR) 1. Titrate fluid and epinephrine ScvO2 > 70%, Hb> 10 g/dl 2. If ScvO2 < 70% Add vasodilator with volume loading (milrinone, Sodium Nitroprusside)

151 Cold shock with low blood pressure (High SVR) 1. Titrate fluid and epinephrine ScvO2 > 70%, Hb> 10 g/dl 2. If still hypotensive consider norepinephrine 3. If ScvO2 still < 70% consider Dobutamine, milrinone

152 Warm shock with low blood pressure(low SVR) 1. Titrate fluid and norepinephrine ScvO2 > 70%, Hb > 10 gr/dl 2. If still hypotensive add vasopressin 3. If ScvO2 still < 70% consider low dose epinephrine shock not reversed

153 Shock not reversed? Persistant catecholamine resistant shock Rout and correct pericardial effusion pneumothorax, intra-abdominal pressure > 12 mmhg Goal C.I > 3.3 and < 6.0 L/min/m2 Shock not reversed Refractory shock : ECMO

154 successful treatment of septic shock cannot begin in the ICU for patients who present to the ED in shock; it must begin at the time of triage in the ED

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156 نویساتاردیهد ا اگ اب ی اراویب خا ه نی ػ یه ک لاػ زب غیاه ذ راذ گ جایتحا ب ىازبخ د بوک غیاه سا تطد تفر ب تر ص زیغ یؼیبط ار نیراد لثه غفد دایس غیاه رد لا طا ؽازفتطا ا یشیز خ ای رد يیا درا ه لاػ زب غیاه ذ راذ گ ذیاب ى یطاتارذی د ای نک یبآ ار ن ىازبخ.نی ک يیا نک یبآ یه ذ ا ت سا كیزط یکار خ اب یا ل لحه یکار خ یتیل زتکلا لثه ORS ای یذیر تر ص رد مذػ لوحت یکار خ یذغت.د ػ ماد ا

157 د یذراتاطی ى خفیف:ک دک ػیار اطت فمط هختصزا تؼ گی دارد ت رگ ر پ طتی طبیؼی ب د گ دافتادگی چؼو ا ذارد. د یذراتاطی ى هت طط:ػذیذا بی لزار اطت لغ ػذیذ ب هایؼات دارد ت رگ رپ طتی کا غ یافت چؼو اگ د افتاد اطت. د یذراتاطی ى ػذیذ: بی حال اطت ت ا ائی ػیذى ذارد ت رگ ر پ طتی اظحا کا غ یافت چؼو ا خیلی گ د افتاد اطت.

158 در ص رتی ک ک دک بز اطاص طبم ب ذی در دطت ػذیذ طبم ب ذی ػ د بایذ طزیؼا هایغ درها ی را با طزػت سیادتز خ ت خل گیزی اس ػ ارض ػز ع ػ د با ت خ ب ایک در ایي ه ارد بایذ در سهاى کن هیشاى سیادی هایغ )حذالل 20cc/kg حذ د یک ط م حدن خ ى( ب فزد بذ ین بایذ هایغ ا تخابی اس ظز اطو الرتی طذین شدیک ب خ ى باػذ در ایي ه ارد ط ع طزم را اطتفاد هی ک ین ػاهل زهال طالیي-ری گز ری گزالکتات ز 15 تا 30 دلیم تا بز طزف ػذى حالت د یذرتاطی ى ػذیذ یا ػ ک یا ای ک تا ط بار ایي کار را ا دام د ین اداه هی د ین

159 در ه اردی ک بیوار در ػ ک وی باػذ یا با درهاى ا لی اس ػ ک خارج ػذ اطت بز اطاص ع طذین بیواراى ب 3 دطت ایپز اتزهیک ایپ اتزهیک ایش اتزهیک تمظین ب ذی هی ػ د

160 دهیدراتاسیون ایزو ناترمیک در ایي حالت هیشاى هایغ کلی ک ک دک بایذ طی 24 طاػت دریافت ک ذ ػاهل هایغ گ ذار ذ + د یذراتاطی ى اطت. ک در 8 طاػت ا ل 1/2 deficit+1/3 maintance را هی د ین اگز د یذراتا طی ى اس لبل هؼل م ػذ هیشاى کلی هایغ هحاطب ػذ هایؼی را ک ب ص رت طزیغ بزای درهاى ػ ک داد این اس هایغ 8 طاػت ا ل کن هی ک ین. در ایي ع د یذراتاطی ى ب ص رت تیپیک اس هایغsaline Dw5%1/2 normal اطتفاد هی ک ین.گا ا هی ت ا ین خ ت ط لت کار اس طزم 3/2-3/1 وزا پتاطین اطتفاد ک ین

161 دهیدراتاسیون هایپو ناترمیک حتوا هایغ تد یش ػذ طذین 75meq/lit ب باالداػت باػذ ب ویي ػلت حذالل اس طزمDw5 1/2 Normal Salin اطتفاد ک ین ک حدن کلی ػاهلMaintance+Deficit اطت

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163 کیموتانرپیه نویساتاردیهد ىاشیه صذح ى یطاتارذی د رد يیا ىاکد ک لکؼه تطا ازیس اب خ ت ب نیذط لااب ى خ رد اد یا تیرلا وطا ى خ رد ا یا تطلااب ب يیو تلػ غیاه ىایه یتفاب یل لط لخاد لیاوت ب يتفر ب لخاد ق زػ دراد ب يیو تلػ رد يیا ندح ىاکد ک لخاد یل زػ زتزید غ اک یه ذبای راویب نئلاػ زتزید ذیذػ ى یطاترذی د ار ىاؼ یه.ذ د

164 دهیدراتاسیون هیپرناتومیک در ایي ک دکاى احتوال ایداد ػالئن هغشی ب خاطز اطو الرتی باال کؼیذ ػذى هایغ داخل طل ی هغشی د یذراتاطی ى بیؼتز طل ل ای هغشی اتفاق هی افتذ ػاهل تزهب س خ زیشی طکت هغشی اس ایي دطت ا ذ

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166 دهیدراتاسیون هیپرناتومیک در طی درهاى ایي ک دکاى ػال بز ک تزل د یذراتاطی ى بایذ طزػت اصالذ طذین طزیؼتز اس 12 meq/lil در ر س با طزیؼتز اس 0 /5mEq/kg/h باػذ چ ى فزد دچار ادم هغشی هی ػ د ن ادم هغشی ن ػ ارض هغشی دیگز هی ت ا ذ باػث تؼ ح طکل ایداد ک ذ

167 دهیدراتاسیون هیپرناتومیک ایي ػولیات ویؼ هایغ کل ب دطت آهذ ػاهل 1/25 بزابز 1/5 هایغ گ ذار ذ کل هایغ ه رد یاس 24 طاػت ک دک هی ػ د دیگز یاسی ب تؼییي هایغ گ ذار ذ د یذراتاطی ى یظت.

168 . اس ظز هیشاى طذین در ک دکاى کوتز اس 10-20kg ب تز اس طزم NS DW5% 1/4 وزا 20 هیلی اکی االى پتاطین ػز ع ػ د طپض ز 4 تا 6 طاػت طذین چک ػ د در ص رتی هیشاى طذین طزیؼتز اس 0/5 meq/kg/h پائیي افتاد یا هیشاى طذین هایغ را تبذیل ب DW5% 1/2 NS هی ک ین یا حدن هایغ را کظز هی ک ین ک ػول ا ل ب تز اطت. حال اگز هیشاى طذین کوتز اس 0/5 meq/kg/h پائیي افتاد یا طذین هحل ل را کوتز هی ک ین یا حدن هایغ را %10-%20 افشایغ هی د ین

169 در ایي ه ارد اگز بیوار د بار ػالئن د یذراتاطی ى ػذیذ را ؼاى داد دیگز طزػت هایغ را سیاد وی ک ین بلک د بار یک د س 20cc/kg اس هایغ زهال طالیي اظاف هی د ین

170

171 lower respiratory tract infection Bronchitis Bronchiolitis Pneumonia Any combination of these

172 Pneumonitis

173

174

175

176 Risk factors Gastroesophageal reflux Neurologic impairment (aspiration) Immunocompromised states Anatomic abnormalities of R. tract Residence in residential care facilities for handicapped children Hospitalization,(ICU) or requiring invasive procedures.

177 CLINICAL MANIFESTATIONS MOSTLY AGE DEPENDENT Neonate fever(may be with subtle sym & sign) Older infants and children Fever, chills, tachypnea, cough, malaise, pleuritic chest pain, retractions, apprehension,

178 CLINICAL MANIFESTATIONS Viral pneumonias are associated more often with cough, wheezing, or stridor & fever is less prominent than with bacterial pneumonia Bacterial pneumonias typically are associated with higher fever, chills, cough, dyspnea, and auscultatory findings of lung consolidation

179 CLINICAL MANIFESTATIONS flaring of the alae of the nose, intercostal and subcostal retractions, and grunting If significant pneumonias : localized crackles and decreased breath sounds Pleural effusion may cause dullness to percussion

180 LABORATORY AND IMAGING STUDIES Sputum study CBC(white blood cell) Viral Or Bacterial B/C Rapid viral antigen detection of upper respiratory secretions Cold agglutinins, may be confirmed by Mycoplasma IgM or more specifically (PCR)

181 SPECIAL PATIENTS Patients who are ill and hospitalized Immunocompromised patients Patients with recurrent pneumonia Patients with pneumonia unresponsive to empirical therapy

182 Bronchoscopy with bronchoalveolar lavage and brush mucosal biopsy Needle aspiration of the lung Open lung biopsy

183 Effusion or empyema, performing a thoracentesis to obtain pleural fluid can be diagnostic and therapeutic

184 Acute lobar pneumonia of the lingula in a 6-year-old child with high fever, cough, and chest pain

185 Diffuse viral bronchopneumonia in a 12-year-old boy with cough, fever, and wheezing. Frontal chest radiograph shows bilateral, perihilar, peribronchial thickening and shaggy infiltrate. Focal airspace disease representing consolidation or atelectasis is present in

186

187 Factors Suggesting Need for Hospitalization of Children with Pneumonia

188 Clinical Manifestations fever, anorexia, poor feeding, headache, symptoms of upper respiratory tract infection, myalgias, arthralgias, tachycardia, hypotension, and various cutaneous signs, such as petechiae, purpura, or an erythematous macular rash. Meningeal irritation is manifested as nuchal rigidity, back pain, Kernig sign, and Brudzinski sign. Increased ICP is suggested by headache, emesis, bulging fontanel or diastasis (widening) of the sutures, oculomotor (anisocoria, ptosis) or abducens nerve paralysis, hypertension with bradycardia, apnea or hyperventilation, decorticate or decerebrate posturing, stupor, coma, or signs of herniation. focal neurologic signs.

189 Papilledema is uncommon in uncomplicated meningitis and should suggest a more chronic process, such as the presence of an intracranial abscess, subdural empyema, or occlusion of a dural venous sinus. Focal neurologic signs usually are due to vascular occlusion. Cranial neuropathies of the ocular, oculomotor, abducens, facial, and auditory nerves may also be due to focal inflammation. Overall, about

190 Seizures (focal or generalized) due to cerebritis, infarction, or electrolyte disturbances. Alterations of mental status are common among patients with meningitis and may be due to increased ICP, cerebritis, or hypotension; manifestations include irritability, lethargy, stupor, obtundation, and coma Additional manifestations of meningitis include photophobia and tache c?r?brale, which is elicited by stroking the skin with a blunt object and observing a raised red streak within sec.