Management of a neonate with respiratory distress

Soumyaranjanparida 7,162 views 79 slides Nov 27, 2017
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About This Presentation

Management of a neonate with respiratory distress


Slide Content

Management of a Neonate with Respiratory Distress Soumya Ranjan Parida

Defining Respiratory Distress Identifying the severity Etiology Clinical Clues for Diagnosis Investigations Monitoring Management (O2/ CPAP/NIV/HHFNC/IMV/HFOV)

Defining Respiratory Distress Presence of 2 of the following Tachypnea Retractions ( intercostal and/or Subcostal ) Grunt Ensure baby is quite, normothermic before counting Respiratory rate ( count RR for 1min)

Respiratory Distress: increase in work of breathing Respiratory Failure: ineffective ventilation or oxygenation or both. Associated worsening sensorium , slow or fast breathing Respiratory Arrest: No spontaneous breathing, cyanosis, unresponsiveness

Knowing the severity Downe’s Score Silverman-Anderson Score WHO Classification of respiratory distress

Silverman-Anderson Score

Downe’s Vidyasagar Score

WHO Classification of Respiratory Distress

WHO Classification of Respiratory Distress

Etiology Based on Gestation and Age Of Onset Preterm RDS Cong.Pneumonia TTN Pneumothorax Lung malformations Cong.Pneumonia Aspiration Syndromes PDA Shock CHD-duct Dependant Lung Malformations Pneumothorax Acquired Pneumonia Aspiration Syndromes PDA Shock CHD-Duct Dependant Lung Malformations Pneumothorax Pulmonary Haemorrhage < 6 hrs 6-24 hrs > 24 HRS

Etiology Based on Gestation and Age Of Onset Term TTN Cong.Pneumonia Asphyxial Lung Aspiration Syn Malformations Pneumothorax Rds Aspiration Syn Cong.Pneumonia CHD-duct Dep. Shock Lung Malfor . Pneumothorax Acquired Pneumonia Shock Chd -duct Dependant Lung Malformations Pneumothorax Pulmonary Haemorrhage < 6 hrs 6-24 hrs > 24 hrs

Risk factor Based Approach to Respiratory Distress Ask for risk factors Suggestive of Worsening on bag & mask ventilation CDH, Air Leak Prolonged labor, difficult labor, assisted delivery, fetal distress, MSAF Asphyxia Lung disease, MAS, Birth Injury Elective Caeserian Section TTNB Maternal Fever, Foul Liquor, prolonged labour , multiple PV examinationPPROM , PROM >12hrs, Assisted Delivery Congenital pneumonia No antenatal Steroid to mother, infant of diabetic mother, Rh Issoimmunisation , Perinatal Asphyxia RDS Polyhydramnios CDH, TEF Oligohydramnios MAS, Pulmonary Hypoplasia

Risk factor Based Approach to Respiratory Distress Ask for risk factors Suggestive of Maternal Hypertension, Preeclampsia Asphyxia, MAS Placenta Previa or abruption Shock Family h/o unexplained neonatal deaths, still births RDS, IDM, CHD, IEM Post Feed worsening GERD, Isolated Cleft Palate, TEF, IEM Relationship with Crying Crying worsens cyanosis (CHD) Crying relieves cyanosis ( Choanal atresia ) Chronic course, O2 dependency BPD, CHD (TAPVC), Atypical Infection(CMV, Fungus, Chlamydia), Recurrent aspiration (GER, Pharyngeal incordination , H shaped TOF), Osteopenia of Prematurity

Physical Assessment Sensorium Color Tone, posture Response to touch Cry Gestation Weight Vital Parameters (Temp, HR, RR, BP, SPO2) Work of Breathing ( Downe’s or silverman score) Perfusion (HR, Color, core- axillary temp, CRT, urine output, BP) Danger Signs

Systematic Evaluation SGA MAS, Asphyxia, Polycythemia LGA Birth Trauma, Asphyxia, Polycythemia , RDS, CHD, Hypoglycemia Potter Facies Hypoplastic Lungs Barrel chest MAS Large caput or bruises Difficult or prolonged Labour Frothing at Mouth TEF Meconium staining MAS Pallor Anemia, Shock Plethora Polycythemia Cyanosis CHD, Severe Luung disease, Shunt, abnormal Hb , Air Leak

Systematic Evaluation Murmur, Hepatomegaly , cardiomegaly , abnormal pulses, differential cyanosis CHD, Shunt Fever, hypothermia, Cold Stress, Umbilical sepsis, foul smell, pustules, petechiae , bleeding tendency, sclerema Sepsis, pneumonia Twins Twin to twin transfusion Inbility to pass orogastric tube TEF Isolated Cleft palate Aspiration syndrome Scaphoid abdomen, distal heart sounds, shift of heart sounds, ipsilateral decreased air entry CDH Absent femorals Coarctation of Aorta Cardiomegaly CHD, Cardiomyopathy

Identifying the Lung pathology Isolated Tachypnea : CHD, Metabolic acidosis, anemia, hypoglycemia, temp instability, renal failure Grunt: Alveolar Lung disease (RDS, Pneumonia, MAS) Stridor : Upper airway obstruction, Laryngo tracheomalacia Cyanosis: CHD, severe lung disease, abnormal Hb , CNS dysfunction

Respiratory vs Cardiac cause Resp System CVS System Breathing Retractions Tachypnea Cardiac evaluation Normal Gallop, weak pulses, hepatomegaly , absent femorals Second Heart Sound Split Single X ray Chest Parenchymal lesion Abnormal shape, size of heart Abnormal pulmonary vasculature pCO2 High Low Pulse Oxymeter Improvement with O2 Not much improvement with O2, differential cyanosis Hyperoxia Test PaO2 >300mmHg rules out cardiac disease PaO2 does not rise

Clues to congenital Heart Disease Cyanosis disproportionate to clinical status Differential cyanosis (UL > LL saturation) Single S2 Murmur Isolated Hepatomegaly Sudden deterioration Lack of response to O2 Cardiomegaly

Investigations Hb RBS Sepsis Screen Blood Culture X ray Chest ABG Imaging (USG Chest, CT Thorax, MRI Chest, 2D ECHO)

Radiological Signs & Etiology Radiological Signs Etiology Low Lung volume RDS, Pulmonary hypoplasia High Lung Volume MAS, TTNB, Hyperventilation, Air Bronchogram RDS, Pneumonia Diffuse parenchymal infiltrates MAS, Pneumonia Lobar Consolidation Pneumonia, CLE, CCAM Pleural effusion Pneumonia, pulmonary Lymphagiectasia Reticular granular pattern RDS, Pneumonia Hyperinflation MAS, Pulmonary lymphagiectasia Fluid accumulation in interlobar space TTN, pulmonary Lymphagiectasia Cystic Mass CCAM, CDH, Pulmonary sequestration Pneumothorax , pneumomediastinum Spontaneous, MAS, RDS, pneumonia

Indicators of Gas Exchange Alveolar-arterial O2 gradient(A-aDO2) PAO2-PaO2 = FIO2 (PBAR – PH2O) – PACO2/RQ-PaO2 normal range in newborn-5-15 abnormal -15-40 Definitely abnormal >40 a/A ratio (Ratio of PaO2 to PAO2) >0.8 is normal <0.6 –Needs Oxygen Therapy <0.15-severe Hypoxemia Oxygen Index (OI) =(MAP X FiO2)/PaO2 25-45-severe Respiratory Failure, mortality risk 50-60% >40-mortality risk>80%

Initial Management Of A Neonate with Respiratory Distress Administer O2,attach To Pulse Ox Maintain Airway In Sniffing Position ,Clear Secretions Examine For Features Of Respiratory Distress Assess Circulation {skin Color,perfusion,pulses,crt } PLACE VASCULAR ACESS,ABG LOCATE THE PATHOLOGY,SCORE,SEND CALL FOR CXR APPLY SUCTION TITRATE FIO2 TO SAO2 SUPPORTIVE MEASURES LIKE TEMP,SUGAR,FLUID AND ELECTROLYTE

Supportive Measures Thermal care Nursing IV Fluids Nutrition Antibiotics Inotropes Infection control Pain reducing Measures Monitoring

Preterm <34wks Near Term/Term EARLY CPAP IF RDS SUSPECTED,EARLY SURFACTANT CONSIDER SENDING BLOOD CULTURE AND START ANTIBIOTICS Poor Respiratory Efforts Worsening Shock PPHN Massive Pulmonary Haemorrhage Malformations(CDH} Collapse With Apnea And Failure To Respond To Bag And Mask Ventilation MECHANICAL VENTILATION START CPAP (5-7cm H2O) worsening resp distress metaolic acidosis{ph,7.2 with BE>-10} respiratory acidosis or worsening ABG FAILURE OF CPAP No Yes

Oxygen therapy Judicious use of O2 Administer appropriate O2 conc by using air-O2 blender or indigenous air-O2 mixing Target O2 saturations 90-95% Avoid Hypo or Hyperoxia Use O2 analyser to check FiO2 when O2 is given Set Pulse Oximeter alarms Use prewarmed & humidified Oxygen specially at flow rate >2l/min Through nasal canula , nasal prongs, nasopharyngeal prongs, O2 hoods

O2 Delivery Systems Type Landmark for depth of insertion Recommended flow rate(L/min) FiO2 at an avg RFR Complications Remarks Nasal Canula Nares to inner margin of eye brow 1-2 25-45 Crausting , nasal trauma, erosion, inadvertent PEEP Alternate between nares every 12hrs Nasopharyngeal Canula Alae nasi to Tragus 1-2 45-60 Crausting , nasal trauma, erosion, inadvertent PEEP Alternate between nares every 12hrs Nasal Prong 1-2 25-45 Crusting, erosion Short binasal prongs recommended O2 Hood 4 30-70 RFR should be at least 4 times that of minute vol. Lesser flow rate risk of CO2 retention

SpO 2 85-89% Vs 91-95 % BPD 25% ROP 50% Mortality 20%

Julius Comroe (1945) “The clinician must bear in mind that oxygen is a drug and must be used in accordance with well recognized pharmacologic principles; i.e., since it has certain toxic effects and is not completely harmless (as widely believed in clinical circles) it should be given only in the lowest dosage or concentration required by the particular patient.”

In preterm baby receiving O2, the saturation target should be 90-94% To achieve this, suggested alarm limits should be 89-95%

Respiratory Support General Principles A. The aims of respiratory support are to maintain adequate oxygenation and ventilation, to reduce respiratory work and to prevent lung injury. B. With mechanical ventilation, use small or normal tidal volumes and the lowest effective ventilator pressures. Both large tidal volumes and high pressures cause lung injury and inflammation, especially in preterm infants. C. PEEP is critical for maintenance of FRC. PEEP is the main factor that influences PAW, a major determinant of oxygenation.

Adequacy of Respiratory Support Comfortable baby Minimal retraction, no grunt Normal capillary refill, BP Normal saturations: 87% - 93% Normal ABG (PaO 2 60-80, PaCO 2 40-60, pH 7.35-7.45, BE ± 2)

Modes of Respiratory Support Non Invasive CPAP NIV HHHFNC Invasive IMV/SIMV HFOV

The Best Ventilator: Least Lung Injury

What’s the Target of Respiratory Support Optimise Oxygenation and Ventilation Correct V/Q mismatch Comfortable Baby Lung Recruitment Avoid Lung Hyperinflation & Lung Injury

Evidences of hyperinflation Lung expansion > 6 ribs anteriorly or > 8 ribs posteriorly Flattening of diaphragms Increased lucency of lungs Air under the heart or herniation of lung to other side Ribs more horizontal

Stable Alveoli

Unstable Alveoli

HFOV

Abnormal Gas Exchange Hypoxemia can be due to: hypoventilation V/Q mismatch shunt diffusion impairments Hypercarbia can be due to: hypoventilation V/Q mismatch

CO2 elimination is determined by Recruit maximal alveoli Minimize alveolar dead space No collapse / over-distension Minimize external dead space Tidal volume Reduce resistance & obstruction of airways Expiratory time and rates

High CO2 - Cerebral Vasodilation ---------------risk of IVH Low CO2 –Cerebral Vasoconstriction----------risk of PVL

Clinical assessment Appearance – color, posture, comfort Vitals – HR, RR, CRT,SaO2, NIBP, IBP, Respiratory – RDS, effort, retractions, alae nasi, breath sounds, air entry, symmetry, ABG Circulatory – HR, CFT, BP, UO Abdomen- AG, feeds, orogastric tube, bowel sounds Neurological- state, activity, tone, posture, pain relief

CPAP Application of continuous distending pressure through out the respiratory cycle in a spontaneously breathing infant

CPAP machine Bubble CPAP Ventilator CPAP Infant Flow Driver

Indications of CPAP Respiratory distress syndrome Transient tachypnoea of newborn Post Extubation Apnea of prematurity MAS Pneumonia Laryngo / Tracheo / Broncho malacia Spontaneously breathing Haemodynamically stable No upper airway anomalies Not in severe respiratory failure

CPAP from birth in all babies at risk of RDS System delivering CPAP is of little importance, however the interface should be short binasal prongs CPAP start at 5-6cm H2O and then individualise depending on clinical condition, oxygenation and perfusion

Contraindications of CPAP Progressive respiratory failure and unable to maintain oxygenation, PaCO2 >60 mm Hg and/or pH 7.25 or less Congenital malformations: congenital diaphragmatic hernia, tracheoesophageal fistula, choanal atresia , cleft palate, gastroschisis Infants with severe cardiovascular instability (hypotension, poor ventricular function) Neonates with poor or unstable respiratory drive (frequent apnea, bradycardia, and/or oxygenation desaturation ) that is not improved by CPAP

DEVICE ADVANTAGE DISADVANTAGE Ventilator CPAP No need of a separate equipment Can be easily switched over to Mechanical ventilation, if CPAP fails Expensive Standard flow of 5-8L/ min may be insufficient in the presence of high leak Difficult to know if the set flow is sufficient or not (insufficient flow can lead to increased WOB) Bubble CPAP Simple and inexpensive Oscillations produced by continuous bubbling might contribute to gas exchange (akin to HFV) Can identify large leaks at the nares (bubbling stops) Flow has to be altered to ensure proper bubbling It is difficult to detect high flow which can ead to over distension of the lungs Variable Flow Device Maintains more uniform pressure Might decrease the WOB Recruits lung volume more effectively Expensive Requires more technical expertise

Flow, PEEP and FiO2 PEEP 5 cms Chest recessions, air entry, CXR FiO 2 50% Flow 2 to 5 liters Minimum to ensure continuous bubbling High flow- check for leaks (open mouth) Rule of 5

How do we know when to change CPAP pressure ? Clinical signs only – little research Observe grunting / chest wall retraction If obvious ? need more pressure How much oxygen? - high FiO 2 ? Need more pressure Observe the chest x-ray - very granular ? Need more pressure May need pressures > 5 cm H 2 O

Methods of weaning preterm babies <30 weeks gestation off CPAP: a multicentre randomized controlled trial Stability criteria( all 8 criteria for > 12hrs) Criteria for failed Trial Off (at least 2 of Following) CPAP 4-6cm H2O O2 requirement < 25% and not increasing RR < 60 No significant chest recession ( sternal /diaphragmatic) <3 episodes of self reverting apneas/ bradycardia / desaturations in 1hr for previous 6hrs Avg SpO2 > 86% most of time or PaO2/TcPO2 >45mm Hg Not currently treated for PDA/Sepsis Tolerated time off CPAP during cares up to 15min Increase work of breathing with RR> 75 Increased apnoea / bradycardia / desaturations > 2 in 1 hr for previous 6hr period Increase O2 requirement > 25% to maintain SpO2 >86% and/or PaO2/TcPO2 >45mm Hg PH < 7.2 PaCO2/ Tc PcO2 > 65 mm Hg Major apnea/ bradycardia requiring Resuscitation Arch Dis Child Fetal Neonatal Ed July 2012 Vol 97 No 4

When has CPAP failed? Apnoea Respiratory failure = PaCO 2 rising >60 mmHg (pH<7.20) Or FiO 2 is rising above ??? 60% Worsening of respiratory distress Agitation not relieved by simple measures But only after you have checked The prongs are in the nose They are the right size The nose has been cleared Place baby prone The mouth is closed The neck slightly extended You have tried higher pressures (?? ~ 10 cm H 2 O or more.)

HHHFNC (F&P)

HHHFNC oxygen therapy: definition Inspiration Expiration Heating and Humidification Dead space washout > 2 L/min Optimally warmed and humidified respiratory gases delivered by nasal cannula at flow rates between 2 and 8 L/min.

Mechanism of action

Clinical use of HHHFNC

How to use HHHFNC

Recommended Guidelines for Intubation From Optimized Noninvasive Respiratory Support with nCPAP or HHFNC Support Pediatrics 2013;131:e1482–e1490

Recommended Guidelines for Intubation From Optimized Noninvasive Respiratory Support with nCPAP or HHFNC Support Pediatrics 2013;131:e1482–e1490

Invasive Ventilation Disease PIP PEEP Ti Frequency Flow RDS 16-18 5-6 0.3-0.35 60 7-8 Pneumonia 14-16 3-4 0.35-0.4 50-60 6-8 MAS 14-16 3-4 0.35-0.4 40-50 5-7 Apnea 12-14 3 0.35 20-30 5-6 Air leak 14-16 3 0.3-0.35 60 5-6 BPD 15-20 4-5 0.4-0.7 20-40 5-6

Adjustments To affect oxygenation, adjust: FiO 2 PEEP I time PIP To affect ventilation, adjust: Respiratory Rate Tidal Volume

Weaning from Invasive Ventilation Clinically & Hemodynamically stable Effective respiratory efforts Basic Lung pathology/disease improving Associated illnesses (active Sepsis, PDA) improving Optimum blood gases Principle of weaning ( decrease the most harmful parameter first, limit change to one parameter at a time, avoid changes of a large magnitude)

High Frequency Ventilation Indications Failure of conventional ventilation (high PIP requirement 22-25 in preterm, 25-28 in term to maintain normal blood gases in conditions including HMD, Pneumonia, MAS, Pulmonary Hypoplasia ) Air Leak PPHN not responding to conventional ventilation

Surfactant therapy Prophylactic therapy a . Neonates with gestation less than 30 weeks of gestation b . Surfactant given within 15 minutes of birth before a diagnosis of RDS is made Early Rescue therapy a . Neonate with RDS (confirmed clinically , radiologically ). b . Surfactant given within first 2 hours of life Late Rescue therapy a . Neonate with RDS and requiring ventilation with a MAP of at least 8cms of water and/or an FiO2 > 30% or (a/A ratio < 0.22) b . Surfactant given after 2 hours of birth

Before Surfactant 1 hr after Surfactant SURFACTANT Therapy

Surfactant use 1. Prophylactic therapy a . Neonates with gestation less than 30 weeks of gestation b . Surfactant given within 15 minutes of birth before a diagnosis of RDS is made 2. Early Rescue therapy a . Neonate with RDS (confirmed clinically , radiologically ). b . Surfactant given within first 2 hours of life 3. Late Rescue therapy a . Neonate with RDS and requiring ventilation with a MAP of at least 8cms of water and/or an FiO2 > 30% or (a/A ratio < 0.22) b . Surfactant given after 2 hours of birth

Exogenous Surfactants in use Worldwide I. Organic solvent extracts of Minced animal lung tissue: Bovine: Surfactant-TA, Survanta Porcine: Curosurf , HL-10 Goat surfactant II. Organic solvent extracts of Lavaged animal lung surf: Alveofact (SF-R1-1), B LES , Infasurf III. Synthetic (protein-free): ALEC, Exosurf IV. Peptide-containing synthetic: Surfaxin ( KL-4) V. Surfactant with Recombinant apoproteins : Recombinant SP-C surfactant ( Venticute )

Types of natural surfactant name source Phospholipid (mg/ml) protein Dose (mg/kg) Dose vol (ml/kg) Survanta ( beractant ) bovine 25 (DPPC50%) SP B,SP C 100 4 Infasurf ( calfactant ) bovine 35 (DPPC74%) SP B,SP C 100 3 Curosurf ( poractant alfa ) Porci ne 80 (DPPC70%) SP B,SP C 100-200 1.25-2.5 Alveofact ( bovactant ) bovine 50 SP B,SP C 50-100 1-2 BLES (bovine lipid extract surfactant) NEOSURF bovine 27 SP B,SP C 135 5

Types of synthetic surfactant Trade name preparation protein Phosphplipid conc mg/ml Dose ml/kg Exosurf DPPC 9% hexadecanol,6% tyloxapol no 13.5 5 Surfact DPPC no 13.5 5 pumactant DPPC,PG no 40 1.2 surfaxin Trade name preparation protein Phosphplipid conc mg/ml Dose ml/kg Exosurf DPPC 9% hexadecanol,6% tyloxapol no 13.5 5 Surfact DPPC no 13.5 5 pumactant DPPC,PG no 40 1.2 Surfaxin ( lucinactant ) DPPC,POPG Kl 4 peptide as SP B ( sinapultide ) 30 5.8 venticute DPPC,POPG r SP C 50 Not studied in neonates

Technique of administration INSURE LISA or MIST

Surfactant in other conditions Meconium aspiration syndrome Bolus Lavage - better improvement in oxygenation in some studies Neonatal bacterial pneumonia -? Role Pulmonary hemorrhage Congenital diaphragmatic hernia – no benefit Chronic lung disease Expanded Use of Surfactant Therapyin NewbornsThierry Lacaze-Masmonteil . Clin Perinatol 34 (2007) 179–189.

Surfactants 2 types - synthetic & natural Natural > synthetic Prophylactic strategy > rescue Early rescue > late rescue Multiple doses > single dose ANCS + surfactant > either alone Useful in MAS Newer surfactants are being evaluated

Supportive Management Bronchodilation Chest Physiotherapy Sedation & Analgesia Nutritional Support

Summary Quantify Respiratory Distress Judicious O2 use Target O2 saturation 90-94% Lung Recruitment Avoid Ventilation Induced Lung Injury Supportive Care

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