Meaning of the Terms Class of Recommendation (COR) Class of recommendation (COR) is also called strength of recommendation # COR 1 isa Strong recommendation (benefit is more and Risk is less)-also calleda Recommended guideline, * COR 2ais Moderate (the benefitis more than the Risk)-itis a Reasonablerecommendation + COR 2b is Weak (Benefit is more than Risk but not so robust as the above two) -can be considered sodteeKCOR 3 is No benefit (Benefit is equal to risk); Hence Not recommended, also writtenas 3NB * COR 3is Harm (Risk is more than the benefit)-Should not be performed, also called 3H Level of Evidence (LOE) © Level Ais High-quality Evidence, © Level B-R: is Moderate from randomized ® trials, (Randomised data is always better than non -randomized data) * Level B- NR: is Moderate from non-randomized (NR) data Evidence, * Level C- LD: Data wit execution Evidence. + Level C- EO: Consensus of expert opinion (EO) Evidence. ooors limitation of design (LD) or Pediatrie Chains of Survival oootos ay recoriion Aathaton ot Heh Quay evar Postcard {CA (In hospital eardiae arrest)-6 periodic changes ean occur: Barly recognition and prevention of cardiac arrest © Activation of emergency response © High-Quality CPR # Advanced Resuscitation means initial CPR isnot working, © Post-Cardiac Arrest care when the child is successfully resuscitated © Recovery includes rehabilitation and long-term neurological format Aawatonat Hg Quaty Prvaron Abend PEDIATRIC ADVANCED LIFE SUPPORT OHCA (Out of hospital cardiac arrest) ‘* Activation of Emergeney Response © High-Quality CPR © Advanced Resuscitation ‘© Post-Cardiac Arrest care = Recovery (Except prevention) Key Points and Recommendations in Pals wo«r7 Initiation of CPR ‘© Lay rescuers - the person who first attains the patient is a lay rescuer, not a medical professional. It should begin CPR for any unresponsive victim, not breathing normally, does not have signs of life, and does not check their pulse. ‘© Healthcare providers - check fora pulse for up to 10 sas soon as definite pulses feel and begin compression unless a definite plusiis felt. This is regarding the initiation of CPR. ‘© Initiate CPR with C-A-B (Compression - airway - breathing) rather than A-B-C Components of High-Quality CPR ‘In CPR, start chest compressions along with rescue breaths in cardiac ares. If unable o give rescue breaths, compressions aloneare tobe given. + Thechest compression rate should be 100-120/min. ‘© Allow adequate chest recoil between 2 compressions The compression depth should be at least 1/3rd the AP diameter of the chest. In infants, approximately 1.5 inches (4om), andin children, 2 inches (Sem). ‘Adult compression depth of 5-6 em post-puberty should not exceed 6em © Arhythm checks every 2 min every rhythm check should last for 10sec. When giving CPR without anadvanced airway ©. Single rescuer: Compression to Ventilation rate of 30:2 © Compression to Ventilation ratio of 15:2 ‘© The child Should be given ventilation with 100% Oxygen. ‘© When giving CPR with an advanced airway, give one breath every 2-3 sec, Le, target a 20- 30 /min RR. Rates exceeding these may compromise hemodynamics. aoa,CPR Technique 2 Finger 2 Thumb encircling For Infants ‘© Single rescuer: Two fingers technique or 2 thumbs placed just below the intermammary line. * ‘Two rescuers: Use the 2 thumb and encircling hands technique, © Forinfants, ifthe rescu sannol achieve an adequate depth, itmay be reasonable to use the heel of I hand, Children # Forchildren, it may be reasonable to use eithera I or 2-hand technique to perform chest compressions. Support Surfaces for CPR’ During IHCA, activate the bed's “CPR MODE” to increase mattress stiffness on soft surfaces when available, CPR isnot, that effective. * Useabackboard ora firm surface to give c ifunavailable. st compressions ‘Opening the Airway - special manoeuvre to use which depends ‘on whether the cervical injury is suspected or not If no cervical injury is suspected, the manoeuvre of choice ‘would be the Head tilt-chin lift manoeuvre. In case of Suspected cervical spine injury choice would be jaw thrust without head tlt, [fit fails, use a head till-chin lift Advanced Airway Intervention in CPR © Bag and mask ventilation is reasonable compared with advanced airway interventions during cardiac arrestin OHCA. Drug Administration During CPR ‘+ For paediatric patients in any setting, itis reasonable to administer epinephrine. IV/1O is preferable to endotracheal tube (ETT) administration ‘+ The initial dose of epinephrine should be given within $ ‘minutes of starting chest compressions. ‘+ IL is reasonable for pediatric patients in any setting, itis, reasonable to administer epinephrine every 3-5 min until ROSC (retum of spontaneous circulation isachieved. ‘+ Either amiodarone or lidocaine may be used for shock- reffactory VFipVT (p- pulseless) ‘© Routine administration of sodium bicarbonate is not recommended in pediatric cardiac arrest without hyperkalaemia or sodium blockers ike tricyclic antidepressants toxicity, ‘© Routine calcium administration is not recommended. For paediatric eardiac arrest without documented hypocalcaemia, calcium channel blocker overdose, hypermagnesemia, or hyperkalemia + Using the child's body weight to calculate resuscitation drug doses while not exceeding the recommended dose for adults, isrecommended for resuscitation medication dosing, Management of VF/PVT. Energy Dose for Defibrillation ‘© Initial dose should be 2-4 J/kg and usually itis 20/kg ‘* Forrefractory VF (ventricular fibrillation):4 J/kg ‘* Subsequently, doses 4J/kg and even higher can be used, but they should not exceed 10 J/kg or the maximum adult dose. Coordination of Shock Therapy and CPR ‘© Perform CPR till the device is ready. veasingle shock, then immediately start CPR. ‘© Minimise interruptions of chest compressions. © Onceread ‘Type of Defibrillator ‘© When using an AED on infants and children, preferably using synchronizeris available. ‘© For infants under the care of a trained healthcare provider, a manual defibrillator is recommended when a shockable rhythms identified. ‘© Use the largest paddles or self-adhering electrodes that will fit on the child's chest. Place them Antero-Lateral or Antero- Posteriorly ‘+ Both paddlesand electrodes are equally effective. Assessment of Resuscitation Quality ‘© If continuous invasive BP monitoring is available during cardia arrest, use Diastolic BP toassess CPR Quality. ‘+ ETCO2 (end-tidal) monitoring may be considered to assess chest compression quality, but exact values in children are not yet determined.© Ifavailable, Use CPR feedback devices © ECG may be considered to identify potentially treatable arrest eauses, such as pericardial tamponade and inadequate ventricular filling. Still, the potential benefit should be ‘weighed against the risks ofinterrupting chest compressions. ‘diac Arrest Care and Monitoring 02056 ‘Targeted Temperature Monitoring (ITM) © For infants and children between 24hr and 18 yrs who remain comatose after OHCA or IHCA, use either TTM 32- 34C followed by TTM 36-37.5C or only TTM 36 -37.5C. © Continuous core temperature monitoring is needed during TT™. wring and Ventilation # Ifavailable Continuous atrial pressure monitoring is given. # After ROSC, use fluids /drugs to maintain SBP above the Sth percentile for age © Wean 02 to target saturation 02 10 94-99%, © If it is off ©2, Target normoxemia and avoid hypo and hypercapnia as both are associated with advanced neurological outcomes. Neuromonitoring and Seizure Treatment © ifavailable, Continuous EEG monitoring for detecting non~ convulsive Seizures following cardiae arrestin patients with persistent encephalopathy need to identify «Recommended to treat clinical seizures after cardiac arrest ‘Inthe case of non-convulsive status epileptic to reat following cardiac arrest in consultation with experts. s,itis reasonable Prognostication Following Cardiac Arrest © Performingan EEG 1 week after the post-arrestis 1 factor for prognostication. © Consider multiple factors when predicting outcomes in infants and children who survive cardiac arrests. Recovery «Survivors need evaluation for rehabilitation needs. «Refer survivors forging neurological evaluation for at leastthe Ist yearaftercardiae arrest Family Presence During Resuscitation ‘© Whenever possible, provide family members with the option of begin present during the resuscitation of the infant or child (if the presence of family interrupts, they can be asked politely toleave). Evaluation of Sudden Unexplained Cardiac Arrest # Consider autopsy and appropriate preservation of biological ‘material for genetic analysis if the child does not survive. ee ’ ‘© If no causes are found on autopsy, refer to @ healtheare provider or centre with expertise in inherited cardiac diseases and cardiac genetic counselling. ‘© For infants, children, and adolescents who survive, obtain a complete past medical and family history, review previous BCGs,and refer toa cardiologist Resuscitation in Shock Septie Shock ‘© Inpatients with septic shock, itis reasonable to administer uid in 10 mbkg or 20 mbkkg aliquots with frequent reassessment, ‘© Either isotonic crystalloids or colloids can be initial fluids. ‘© Either balanced or unbalanced solutions can be effective ‘© Providers should reassess after every fluid bolus for responsiveness anda sign of volume overloaded. ‘© Using either epinephrine or norepinephrine as an initial vasoactive infusion is reasonable for infants and children with fuid-refractory septic shocks. ‘If epinephrine and norepinephrine are not available, then dopamine may be considered. Cardiogenie Shock + Early expert consultation sneeded, preferably cardiologist + Use epinephrine, dopamine, dobutamine (alone, eannot be used) ormilrinoneasan inotropic infusion. Acute Traumatic Hemorrhagie Shock ‘* To administer blood products (PRBC prefers whole blood transfusion when available) instead of crystalloid for “ongoing volume resuscitation. Treatment of Respiratory Failure naa Treatment of Inadequate Breathing with a Pulse Present ‘© Provide rescue breaths, 1 breath every 2 to 3s (20-30 breaths! min) Foreign Body Airway Obstruction (FBAO) ‘If mild FBAO, allow the child to remove it by coughing, monitor, ‘© If severe FBAO is given Abdominal thrusts till either itis expelled or the child becomes unresponsive ‘For infants with server FBAO, deliver repeated eycles of 5 back blows (slaps) followed by 5 chest compression until the ‘objectis expelled or the victim becomes unresponsive ‘© Once unresponsive, start CPR, Remove any visible FB while ‘opening the airway, but no blind finger sweeps must be performed, Opioid-Related Respiratory and Cardiac Arrest ‘© For patients in respiratory arrest, rescue breathing or bag- ‘mask ventilation should be maintained until spontaneous breathing returns f ———-For a patient with suspected opioid overdose who has definite pulse but no normal breathing or only gasping (ie... respiratory arrest), give life support and administer intramuscular orintranasal naloxone For patients in cardiac arrest related to opioid intake, standard resuscitative measures should take priority over naloxone administration, tubation Cricoid pressure during BMV (bag and mask ventilation) to prevent gastric insufflation, Not recommended routine use of cricoid pressure during intubation, Ifused, discontinue crieoid pressure if it interferes with ease of intubation or ventilation, Choose cuffed over uncuffed ETTs for intubating infants and children ‘* When a cuffed ETT is used, attention should be paid to ETT size, position, and cuff inflation pressure, usually <20-25 em H20 (inpractice, itkept 1S to 18.as the max) ‘© Use atropine 0.02 mg/kg as a premedication to prevent bradycardia during an emergency for intubation with a high risk of bradycardia, ¢.g., uccinylcholine use. ‘© In all settings, for infants and children with a perfusing rhythm, use exhaled CO? detection (colorimetric detector or ccapnography) to confirm ETT placement.MANAGEMENT GUIDELINES [2 | SHOCK IN CHILDREN: SUMMARY AND + Shock 38 * An acute process in which the body is unable to deliver adequate oxygen to meet the metabolic demands of vital ‘organs and tissues. # Itisadelivery failure of oxygen and nutrients, ‘Types of Shock in Children Hypovolemie Shock © Mechanism: Extrinsic or intrinsic blood/ECF losses produce reduction in preload, © Examples: Blood loss: Haemorrhage, © Plasma loss: Burns, Nephrotic syndrome Water/ electrolyte loss: Vomiting, Diarrhoea Cardiogenic Shock ‘© Myocardial dysfunction produces pump failure. © Examples: © Congenital heart diseases ‘© Cardiomyopathies (© Ischemia © Amhythmia Distributive Shock # Abnormalities of vasomotor tone from loss of venous and arterial capacitance. © Examples: (© Anaphylaxis Drug-induced © Neurological shock: Loss of sympathetic vascular tone due to brainstem of spinal cord injury. Obstructive Shock © There is an obstruction to the left ventricle or right ventricle outflow producing low cardiac output © Examples: ~ ‘© Severe/Critical CoA Hypoplastic left heart syndrome Severe aortic stenosis Interrupted aortic arch syndrome © Tension Pneumothorax * Pericardial Tamponade Anterior Mediastinal Masses Septic Shock ‘© Multiple mechanisms are there, septic/infection-related process I. Hypovolemic element: 3” space losses. Il. Distributive element: Early shock with reduced afterload i.e., reduction in systemic vascular resistance that produces vasodilation and warm shock. Inthe early stages there is warm shock (in hypovolemic element) and late stages cold shock. ee ’ Il.Cardiogenic element: Due to myocardial depression by toxin/LRS ‘© Examples: Bacterial, viral, and fungal sepsis Septic Shocksin Children coos Systemic Inflammatory Response Syndrome (SIRS) Any 2 out of criteria (Lor I should be there) L. Abnormal core temperature (rectaV/oral/ catheter/ bladder) greater than 38.5°C (101.3°F)orlessthan 36°C IL, Abnormal Leukocyte count: Either elevated or depressed for age (not secondary to chemotherapy) or 10% immature neutrophils IIL, Abnormal heart rate: Tachycardia with mean HR greater than +2 standard division above mean. Unexplained persistent elevation of hear rate over 0.5 to 4 hr or persistent bradycardia, over0.5hrin the infant. IV. Abnormal respiratory rate: More than plus two standard 10 © High PEEP upto 10-15 cmH20 may beneeded. hoke/min + Givea tial of prone positioning during ventilation. FEE eT ES + Routine us of inaled NO should beavoided but can be used treardiae perfusion at high asa rescue therapy if oxygenation is not improving despite contractility _kg/min doses high PEEP due o pulmonary hypertension. aaa oaneRLars + Neuromuscular blockade may be useful inpatients requiring a ir ventilation fasynehony happens. H, Enteral feeds to be preferred over TPN cere + Whereverpossible use enteral feeds. at high doses + Orogastic feeds canbe given, Dobutamine 1 Cardiac 1-10 yg/ky/min * Simply the use of catecholamines is not enough to stop contractility enteral feeds Peripheral 1. Avoid any blood transfusion ifthe childisstableand His vasodilator more than orequalto7 gid. Norepinepvie Potent 1 Blood pressure J. Avoid regular use of levothyroxine, zine, plasma vasoconstriction 1.5 secondary 1 f exchange, and high-volume hemofiltration. pkg’ systemic vascular K. Early renal replacement ean be done. Haemodlalyss or min resi peritoneal dialysis can be used for the treatment or Nose aS prevention of fluid overload in children with renal Lecenen a dysfunction, contractility 7 ‘and refractory hypoxia. ‘vasoconstriction jig/kg/ hypertension M.There is no routine use of IVIG, stress ulcer prophylaxis orDVT prophylaxis. min 10, consumption Prognosisin Septic Shock co'ssos +# Insepticshock, mortality rates areas low as 3% in previously between oxygen delivery (DO2) and oxygen consumption _ealthy children and 6.9% in children with chronic illness (Vo2. (compared with 25-30% in adult). ‘© With early recognition, the mortality rate for paediatric shock continues to improve, but shock and MODS are the leading, ‘cause of death in infants and children. Key Points from Nelson 21" Ed osto3 © Hallmark of an uncompensated shock is an imbalance © DV imbalance is an imbalance between oxygen delivery and consumption. © The gold standard measurement of $vO2 is from a pulmonary artificial catheter, but measurements from this location are often clinically feasible Sites such as right ventricle, right atrium, superior vena cava (SvCO2) or inferior vena cava can be surrogate measures of mixed venous blood to follow the accuracy of oxygen delivery and effectiveness ofthe therapeutic intervensions, ———_.._ —#Table 2.1 Omin Recognize decreased mental status and perfusion. Begin high flow O, and establish IO/IV access according to PALS. Smin Ifno hepatomegaly or rales / crackles then push 20 mL/kg isotonic saline boluses and reassess after each bolus up to 60 mL/kg until improved perfusion. Stop for rales, crackles ‘or hepatomegaly. Correct hypoglycemia and hypocalcemia, Begin antibiotics. 15min Fluid refractory shock? peripheral IV/10 inotrope infusion, preferably Epinephrine 0.05-0.3 yg/kg/min Use Atropine / ketamine IV/IO/IM if needed for Central Vein or Airway Access Titrate Epinephrine 0.05-0.3 .g/kg/min for Cold Shock. (Titrate central Dopamine 5-9 igikg/min if Epinephrine not available) Titrate central Norepinephrine from 0.05 ug/kg/min and upward to reverse Warm Shock. (Titrate Central Dopamine > 10 yigikg/min if Norepinephrine not available) 60 min Catecholamine-resistant shock? fat risk for Absolute Adrenal Insufficiency consider Hydrocortisone. Use Doppler US, PICO, FATD or PAC to Direct Fluid, Inotrope, Vasopressor, Vasodilators Goal is normal MAP-CVP, SevO, > 70% and C13.3-6.0 L/min’ Normal Blood Pressure Low Blood Pressure Low Blood Pressure Cold Shock Cold Shock Warm Shock SovO, < 70%" /Hgb > I0gidL on SevO, < 70%" / Hb > 10g/dL on Epinephrine? Epinephrine? SevO,> 7 norepinephrine? Begin Milrinone infusion, ‘Add Norepinephrine to Epinephrine to attain normal If euvolemic, add Vasopressin, ‘Add Nitroso-vasodilator if CI<3.3 diastolic blood pressure. If C1<3.3 Limin/m' add Terlipressin, or Angiotensin. But Limin/m’ with High SVRI and/or Dobutamine, Enoximone, Levosimendan, or if Cl decreases below 3.3 poor skin perfusion. Consider Milrinone. Liminim’ add Epinephrine, Levosimendan iff unsuccessful. dobutamine, Enoximone, Levosimendan, Persistent Catecholami resistant shock? Refractory Shock? Evaluate pericardial Effusion or Pneumothorax, Maintain IAP et < 1mmHgAcute Respiratory Distress Syndrome (ARDS) © ARDS stands for acute respiratory distress syndrome. ‘It is defined asa syndrome with non-cardiogenic pulmonary oedema, is characterized by hypoxemia, Itischaracterized by radiologically visible infiltrate. Decrease in functional residual capacity. Decrease in lung compliance. ‘The mortality ate of ARDS in children (0-18 years) is 18-22%. ARDS is responsible for 30% mortality rate in ICU. ooar7 Definition of ARDS-an evolving concept #11994, twoentities were given: ALI and ARDS. # In 2012, the Berlin classification simplified it, giving three categories: mild, moderate, and severe. * In 2015, paediatric ARDS classification came as PARDs criteria, ‘Terminology used © PIF ratio stands for PaO2/Fi02 if it is low (S 300); the hypoxemia indicatoris associated with ARDS. # The SF ratio, stands for SPO2/FiO2, is « marker/congener ‘ailo used for oxygenation ifP/F ratiois unavailable « W’sfbvis the accurate value in children only if the SPO2 is between 80-97%. + Nelson says the P/F ratio of 200mm Hg and 300 mm Hg correlate approximately with the S/F ratio of 235 and 315, respectively. * PaO2/PAO2 ratio is the partial pressure of oxygen in the arterial blood PO2/ alveolar blood PO2. © Itisthe alveolar ventilation marker that indicates alveolar epithelial injury ifderanged # The oxygenation index (Ol) used to access the degree of ‘ventilatory support needed to maintain oxygenation «Illustrate the need for MAP and Fi02 needed during ventilation The formula for oxygenation index (OD-MAPx Fi02 (°%4) P02. # If Fi02 is in decimal, then the formula of (Ol) is = MAPxFi02x100/Pa02. + Oxygen saturation index (OSI): when SpO2 is used instead of Pa02 # The ventilation index (VI) measures CO2 elimination, suggesting alveolar ventilation ¢ The formula of VIis=R x (PIP-PEEP) xPaCO2/1000. # Fullface mask bilevel ventilation is non-invasive, and BiPAPis the kind of ventilation used # In CPAP, the same pressure is given in inspiration and expiration. ee ’ PEDIATRICS ARDS: A BRIEF REVIEW © In BiPAP, different pressure is given in inspiration and expiration, In BiPAP, higher pressure is given in inspiration, and slightly Jower pressure is used in expiration, © Lower pressure in expiration allows the clearance of CO2 better Definition of Pediatric ARDS ‘© Pediatric acute lung injury consensus conference (PALICC) group. meas Age Excludes patients with perinatal-related lung disease, Timing Within 7 days of known clinical insult, Origin of Respiratory failure not fully explained by edema cardiac failure or fluid overload. ‘© Chest imaging finding of new infiltrates consistent with the ‘acute pulmonary parenchymal disease. ‘© Patient with abnormal oxygenation, ‘© Non-invasive ventilation (© Full-face mask bilevel ventilation or CPAP>Sem H20 © PFratio<300 ©. SFratio<264, ‘© Ininvasive mechanical ventilation: 4< O18 8<01<16 olzi6 SS emH20), (© Moderate- PF 100 t0<200 onat least PEEP>Sem H20), (©. Severe- PF <100(onat least PEEP=Sem H20). Causes of pediatric ARDS, They canbe divided into two parts: 260 © The single most common cause of ARDS ‘© Adults Severe sepsis/systemic sepsis ‘© Children-pneumonia (viral pneumonia with secondary bacterial complication), erry reer reo ag (Alveolar-Capillary) ‘© Pneumonia ‘= Sepsis/ SIRS © Aspiration ‘© Major trauma = Drowning ‘= Acutepancreatitis ‘ Inhalationalinjury — * Burns * PulmonaryContusion © Shock © TRALI/Massive Transfusion ‘© Headinjury + Cardiopulmonary bypass + Drug Overdose Pathophysiology ‘To understand the pathophysiology, understanding a normal alveolar's microscopic structure prevents fluid accumulation inthe alveolus, * A single layer of epithelial cells lines the inside of the alveolus. ‘# Thereare 2 types ofepithelial cells © (0) Flattened epithelial cells or type 1 alveolar epithelial cellsand ‘© (U) Cuboidal epithelial cells or type 2 alveolar epithelial cells. Referimage3.1 What happens in ARDS? * There are two types of injury, ie., direct, and indirect. * Clot formation leads to fibrin degradation, and plasmin will be formed. plasmin again will eause multiple injuries to the further alveolar epithetium, biury Damage o Aveo ela Vascular eo Bair ot Sige of neal Hail & “pe tepals Type 2eptetatcols” cco Rit Vtech as . seme xchange | fui? Scant yokines —etane t Me imacrobagss Mente noe 8 foOS Ala Avot io ‘iene : ReferImage3.2 ‘© Loft half of the normal alveolus and the right half of the injured alveolus during the acute phage ‘Ventilation abnormalitiesin ARDS coarse ‘© In the dependent parts of the lung regions, there will be collapse/consolidation. And some areas will be functional, while other show the tendency of hyperinflation, Consoidation Over distension & mportant Information * Injury to the alveolar epithelial-vascular endothelial interface, © Flooding of interstitium and alveoli with edema fluid. ‘© Damage to type | alveolar epithelial cells- impaired gas exchange and hypoxemia. © Damage to type 2 alveolar epithelial cells- surfactant deficiency and reduced Na*/H20 transport. ‘© Inflammatory damage- activation of macrophages and migration of neutrophils into the alveolar lumen. * Cytokines worsen the damage and cause MODS. © Healing by fibrosis, © Mechanical ventilation can worsen/sustain damage if improperly used.‘Stages/phases of PARDS, CDT Pediatrics 2020 © Phase I: Early changes Radiology] Symptoms | Lab findings [Pathophysiol Normal Dyspnea, Hypoxemia: Neutrophil tachypnea, absent or mild sequestration normal Hypercapnia examination mild pulmonary HTN * Phase2: Onset of parenchymal changes non Patchy Dyspnea, Hypoxemia: Neutrophil alveolar —_tachypnea, moderate to infiltration, infiltrates cyanosis, severe vascular No tachycardia, decreased congestion, cardiomegaly coarse rales lung pulmonary compliance edema, platelet pulmonary clumps, type 1 HTN epithelial cell damage ‘© Phase 3: Acute respiratory failure with progression; 2-10 days," a Diffase Tachypnea, Worsened Alveolar and alveolar tachycardia, hypoxemia _ interstitial infiltrate, air signs of and shunt inflamma bronchogram pneumoniacon faction low exudate with reduced lung solidation, compliance, macrophages, volume, diffuse rhonchi increased type 2 cells No sepsis signs minute and fibroblasts cardiomegaly ventilation may impaired proliferate, 02 thromboemboli ‘extraction ‘Phase 4: Pulmonary fibrosis, pneumonia with progression; >10 days | ass [en] ain ra Persistent Phase3_—-Phase3—— Type 2 cell diffase symptoms changes + hyperplasia alveolar +MODS progressive interstitial infiltrates, features Jung failure, thickening. superimposed may appear MODS —_loculated new features pneumonia pneumonic fibrosis medial infiltrates air thickening of leak cor arterioles pulmonale and lymphocytes cardiomegaly infiltration a 7 Management of PARDS waeas Principles of Therapy ‘© The ventilation strategies (© Manage hypoxemia, © Alsoprevent ventilator-associated lung injury. ‘© Fluidmanagement ‘* Managing the complications ‘© Nutritional supplements and ‘© Managing the underlying cause ‘© Adjunctive therapies Ventilation in ARDS ‘© The high-flow nasal cannula and NIV role is limited and not recommended in pediatrie ARDS. ‘ Ininvasivemechanical ventilation, © Aim is to balance the management of hypoxemia with preventing ventilator-associated lung injury. Invasive mechanical ventilation in PARDS. + Lung-protective ventilation is used PCV mode vs VCV mode: Anarea of conficting opinions. + Relative lack of pediatric data, and most data is still extrapolated from adult studies ‘Guidelines given by PALICC in 2015 and regularly updated. + Tidal volume-3-6mbkg (predieted/deal body weight) in poor compliance ‘© Tidal volume-5-Smlkg (predietedideal body weight) in better compliance. + Inspiratory plateau pressure~<28emH20. + In those with increased chest wall elastance, pressure up to 29-32.emH20 canbe allowed. ‘+ PEEP must bekept between 10-15 em H20 and titrated + Inthose with severe PARDS, >15 em H20 PEEP can be used but watch forplateau pressure + Recruitment manoeuvres, PALICC recommended that careful recruitment of manocuvres by slow incremental and decremental PEEP steps be formed to improve severe oxygenation failure. ‘© However, sustained inflation was notrecommended. # Gasexchange goals, ©. Mild PARDS with PEEP <10 em H20: target Sp? is 92- 97%. (© More severe PARDS with PEEP >10cm H20: target Sp0288-92%, ©. Permissive hypercapnia is allowed with a target blood pH. of 7.15-7.30, HFOV in PARDS. ‘© An alternative ventilatory mode in those with elevated plateau pressure>28em H20 despite the absence of reduced compliance.# Use is controversial since no pediatric studies are there. # Adults studies like the OSCILLATE and the OSCAR showed no significant difference between the use of HFOV and conventional controlled ventilation. ‘Use in pediatric ARDS is institution/clinician-dependent and Is agrey area, Fluids managementin PARDS © Current PALICC guidelines su, resuscitation goal-directed fluid management should be used. to maintain adequate volume while aiming to prevent a positive fluid balance. © Evidence in adults ARDS shows that a conservative fluid strategy targeting lower cardiac filling pressures, with CVP <4mm Hg, is associated with better oxygenation and a short duration of mechanical ventilation (CDT paediatries, 2020), rest that, after initial fluid Nutrition in PARDS * PALICC stresses the importance of nutrition, preferably enteral, in maintaining growth, meeting metabolic needs, and facilitating recovery. ‘In general, critically ill children have reduced mortality when enteral nutrition is started within 48 hours of admission. ‘Research on the potential benefits of Omega -3 FA-enriched lipid emulsion for PARDS but not yet recommended, Adjunct approaches to PARDS © InhaledNO © Acts as a pulmonary vasodilator and can improve mismatch and reduce dead space ventilation, © Although PALICC does not recommend the routine use of iNO in PARDS, they recommend use in severe cases or cases complicated by pulmonary hypertension or severe right heart strain © RCTshave shown transient benefits in oxygenation but no overall improvement in survival © Limited to use as a stop-gap therapy in severe hypoxemia and/or pulmonary HTN in clinical practice, 1Q ‘© Pronepositioning ©. Improve oxygenation in ARDS, through a combination of improved V/Q matching, recruitment of lower-lobe atelectasis, reduced ventilator-induced lung injury, improved secretion clearance, and improved right ventricular dysfunction ‘© Studies in children demonstrate no improved outcome and survival despite short-term improvement in oxygenation ‘© PALICC currently recommends consideration of prone positioning in severe cases of PARDS, © Corticosteroids © Even though used in 20-60% of patients of PARDS, the {guidelines by PALICC do not recommend corticosteroids as routine therapy for PARDS, ©. May benefit PARDS in children with co-morbidities like reactive airway disease, BPD, and PCP, although no standard recommendations exist ‘© Exogenous surfactant with no benefits and not recommended ‘© Deep sedation and neuromuscular blockage © No routine use recommended by PALICC; no major RCTsavailable, (©. Helpful theoretically to prevent asynchrony and reduce VLI ECLSin PARDS © ECLS-extracorporeal life suppor. © PALICC recommends consideration of ECLS in severe PARDS, where the cause is likely reversible, or the child is suitable for lung transplantation, uns ‘© Veno-venous ECMO is most commonly applied strategy of ECLS. ‘© Survival rates of>70% have been reported when venovenous ECMO isused in viral infection-associated severe ARDS. ‘© Beneficial if used within the Ist 7 days of mechanical Ventilation with high levels of support ‘Area o focus on PARDS for SS entrance exams ‘Definitions of PARDS and how itdfers from Bertin criteria, Phases of PARDS. + Ventilation strategies for PARDS. + Satus ofadjunct therapies for PARDS.Image 3.1 Epithelial basement membrane Venule Type | alveolar epithelial cell Claudin ’ Fibroblast > Epithelial sodium channel Alveolar wall liquid Alveolar macrophage ‘Type Il alveolar epithelial cell Sodium-Potassium ATPase Capillary Red blood cellImage 3.2 Normal alveolus Injured alveolus during the acute phase Alveolar air space ‘Sloughing of bronchial epithelium Protein rich edema fluid Necrotic or apoptotictype | cell Epithelial basement Red cell membrane Type Il coll Intact type tI cell Aveolar macrophage Denuded ‘basement membrane Hyaline membrane Migrating neutrophil teases Widened edematous interstitium Surfactant layer! Endothelial basement membrane ij, Swollen, injured Fibroblast 1 Gap NeUrmPhl erotneial cals formation