Nicu 3 2012 - interdepartment case copy - copy

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  • Nicu 3 2012 - interdepartment case copy - copy

    1. 1. NICU CASE Presented by: Airamsherlyn P. Natinga, MD
    2. 2. General Data:  A case of B. Bb. Boy  admitted to NICU-B  March 06, 2012  @ 4:32 pm
    3. 3. Maternal History - Born to a 30 y.o. G2P2 (2002) mother - Regular PNCU - No teratogenic nor radiation exposure - No hypertension, no DM, no BA - No thyroid nor cardiac diseases - With multivitamins intake - Mother‟s blood type: “O+”
    4. 4. Had UTI @ 6 mos AOG with Cefalexin 500mg 1 cap TID x 7 days, completed  Admitted @ Catbalogan Provincial Hospital on March 4, 2012 due to labor pains 1st HD: Had fever, T= 38.4ºC, lysed with Paracetamol 500mg tablet q 4H and started with Cefuroxime 750mg IVTT q 8H 2nd HD: Referred to this center as HOC for CS, re: meconium-stained AF with NRFHS
    5. 5. Interpregnancy intervals: G1 – 2000 – full term, NSVD @ Catbalogan Provincial Hospital G2 – present pregnancy
    6. 6. BIRTH HISTORY - delivered term, 39 wks by BS, via NSVD - cephalic presentation - no cyanosis - thickly meconium - stained amniotic fluid - AS 4,6
    7. 7. PHYSICAL EXAMINATION SIGN 0 1 2 Heart rate Absent Below 100 Over 100 Respiratory effort Absent Slow, irregular Good, crying Muscle tone Limp Some flexion of extremities Active motion Response to catheter in nostril (tested after oropharynx is clear) No response Grimace Cough or sneeze Color Blue, pale Body pink, extremities blue Completely pink A P G A R 1‟ 0 1 1 1 1 5‟ 1 2 1 1 1
    8. 8. PHYSICAL EXAMINATION With irregular cry and activity With alar flaring, with sl retractions, no grunting, no apnea Suctioned secretions oropharyngeal, thick greenish fluid Vital signs: HR 120‟s bpm RR 65 cpm O2 sat 85% at room air
    9. 9. ANTHROPOMETRIC : BW : 3.39 kg ( p 90) HC : 35 cm ( p 90) CC : 33 cm AC : 32 cm BL : 51 cm (p 10) AGA
    10. 10. BALLARD SCORE: 39 Weeks
    11. 11. BALLARD SCORE: 39 Weeks
    12. 12. SKIN: pinkish, (-) jaundice HEAD & NECK: normocephalic, (+) caput succedaneum, (-) cephalhematoma, open & flat anterior & posterior fontanelles, with alar flaring CHEST & LUNGS: SCE, harsh breath sounds, no crackles, no wheeze, with retractions HEART: AP, NRRR, no murmur
    13. 13. ABDOMEN: globular, NABS, greenish tinged umbilical cord with 2A 1V, full pulses BACK : no dimpling, no lumps, no tuffs of hair GENITALIA : grossly male, descended testes with good rugae ANUS: patent EXTREMITIES: full pulses, no deformities NEUROLOGIC EXAM: No neurologic deficit
    14. 14. Admitting Impression: Live Full Term Baby Boy, 39 weeks AOG by Maturity Aging delivered via NSD to a G2P2 (2002) 30yrs old mother , Cephalic, Thickly MS Amniotic Fluid, Apgar Score 4,6 BW 3.39kg BL 51cms, AGA T/C MAS
    15. 15. COURSE IN THE WARD Admitted to NICU-B: O2 sat 85% @ room air HR 120 bpm RR 65 cpm - Routine NB care done - TPR q 4h - V/S q hourly until stable - Vit. K 1mg IM - Hepa B vaccine 0.5ml IM ® - IVF: D5W at 60cc/kg/day - Meds: Ampicillin 100mg/kg/day q12h Gentamycin 5mg/kg/dose
    16. 16. COURSE IN THE WARD - Hook to NCPAP, FiO2 @ 60%, PEEP 6 - pulse oximeter - OGT - HGT monitoring q 8h - NPO temporarily - CBC, Platelet Count - Blood typing - Blood C/S - CXR: APL Hgb 136 Hct . 0.40 Rbc 4.49 Wbc 21.0 Pmn 0.34 Lymphocytes 0.33 Monocytes 0.10 Stabs 0.23 Plt ct. 186 Bld type “A+” NRBC 21/100WBC
    17. 17. 2 HOURS OF LIFE: S = (+) grunting (+) subcostal retractions (+) tachypnea (+) alar flaring ( -) cyanosis O = O2 sat 90%, HR = 150 bpm RR = 65 cpm, afebrile SCE, harsh BS CRT 2 sec A= T/C Meconium Aspiration Syndrome; Sepsis Neonatorum P = NCPAP : FiO2 = 60%; PEEP 6  d/c Ampicillin, shifted to Cefuroxime 100mk q 12H  ABG detn  Referred to Neonatologist for further evaluation and co- management
    18. 18. 3 HOURS OF LIFE: S = (+) grunting (+) subcostal retractions (+) circumoral cyanosis (-) seizure O = O2 sat 80% HR 140s bpm RR 70 cpm afebrile SCE, harsh BS CRT 4 sec A= MAP; Sepsis Neonatorum P = Emergency ET Intubation (3.5cm)  Hook to Mech. Vent : FiO2 = 100% RR = 60 PIP = 20-30 PEEP 4-5cm H2O IT = 0.5 I:E =1:2  Dopamine 5ug/kg/hr  PNSS IV push 20cc/kg  ABG determination
    19. 19. ABG det‟n CXR: APL CXR Reading:  Haziness is seen in both lung fields.  Lung fields appeared hyperaerated.  The heart is not enlarged.  ET tube seen with tip at the level of T2.  Impression:  Hyaline Membrane Disease is primarily considered. But on review of the film it is more consistent with MAP. pH = 6.9 pCO2 = 102.6 pO2 = 30
    20. 20. 4 HOURS OF LIFE: S = (+) desaturation (+) cyanosis (-) seizure O = O2 sat 80% (+) HR 140s (+) tachypnea (-) seizure, afebrile A = MAS; Sepsis Neonatorum P= the same mechanical vent set-up • NaHCO3 2meq/kg IV push • PNSS 10cc/kg IV push • ABGs det‟n • Amikacin 15mg/kg OD, IV drip
    21. 21. 10HOURS OF LIFE: S = (+) desaturation (+) bradycardia (+) apnea (+) cyanosis O = O2 sat 80s % rt. hand O2 sat 60% LL Ext HR 90 bpm; RR 70 cpm afebrile SCE, (+) crackles all over LF faint pulses, CRT 4 sec A = MAP; t/c PPHN; Sepsis Neonatorum P= mech vent RR adjusted up to 150, still no improvement  NaHCO3 2meq/kg IV push  Suction secretions  PNSS 10cc/kg IV push  Dopamine increased to 10ug/kg/hr  Dexamethasone 0.5mg IVTT q 6H x 4 doses  Furosemide 2mk IV push  ABGs det‟n
    22. 22. 24 HOURS OF LIFE: S = (+) desaturation (+) tachynea (+) pallor (-) UO; (+)BM O = O2 sat 80s%; afebrile HR 134 bpm; RR 60 Sclerematous SCE, (+) crackles Faint pulses, CRT 4 sec A= MAP; t/c PPHN; Sepsis Neonatorum P = • Foley catheter inserted, (+) tea-colored urine • Rpt cbc, plt ct • For FFP transfusion • Parents requested to transfer EVRMC • Bld c/s in 24H no growth
    23. 23. A= MAP; PPHN P = Epinephrine 0.5mg via ET Tube  Continuous CPR and ambubagging  Parents decided DNR 32 HOURS OF LIFE: S = (+) desaturations (+) bradycardia (+) cyanosis (+) apnea O = O2 sat 40s% Mottled skin sclerematous Dilated pupils no spontaneous breathing Faint pulses
    24. 24. 33 HOURS OF LIFE:  Hr = 0  Rr = 0  Pr = 0  Pupils fixed and dilated  Ecg LLII = flat tracings Cardiopulmonary Arrest, Secondary Meconium Aspiration Pneumonia with PPHN Sepsis Neonatorum Term Baby Boy, delivered via NSVD, cephalic, Thickly Meconium-stained Amniotic Fluid, AS 7,8 to a G2P2 (2002) mother, BW 3.39 kg, BL 51 cm, AGA
    25. 25. Salient Features  Birth:  Full term NB  Male  TMS amniotic fluid  AS 4,6  P.E.  (+) caput succedaneum  Greenish tinged umbilical cord  (+) grunting  (+) tachypnea  (+) alar flaring  (+) apnea  (+) subcostal retractions  (+) crackles  Thick greenish (ms) secretions  Perinatal Hx - maternal infection (UTI) - maternal fever - NRFHS  Diagnostics:  ABG = respiratory acidosis  CXR - consistent with meconium aspiration pneumonia
    26. 26. Final Diagnosis Cardiopulmonary Arrest from Severe Hypoxia, secondary to Persistent Pulmonary Hypertension; Meconium Aspiration Pneumonia Sepsis Neonatorum; Term Baby Boy delivered via NSVD, Cephalic, Thickly meconium stained Amniotic Fluid, Apgar Score 4,6 to a G2P2 (2002) Mother, BW 3.39 kg, BL 51 cm
    27. 27. Differential Diagnosis
    28. 28. Respiratory Distress in Newborn Pulmonary Transient Tachypnea of the Newborn Hyaline Membrane Disease Meconium Aspiration Syndrome Neonatal Pneumonia Behrman’s Pediatric 5th edition Non-Pulmonary Cardiac: CHD Anatomical Anomalies: CDH Metabolic Disorders: Galactosemia Establish degree of Distress
    29. 29. mild moderate severe Supplemental O2 IVF NG feeds if BP stable Pulse oximetry Monitoring Consider antibiotics CPAP BP/ABG monitoring IVF, NG feeds (if BP stable) Cont. Pulse Ox monitoring Empiric antibiotics Intubation & ventilation BP/ABG monitoring TPN if BP is unstable NG feeds if BP stable Cont. Pulse Ox monitoring Transcutaneous O2/CO2 Empiric antibiotics Worsening resp distress Worsening resp distress Hemodynamic instability Consider surfactant replacement ECG if FiO2 >0.6 prior to surfactant in near term and term infants Follow up Oxygenation and & ventilation
    30. 30. 1.Transient Tachypnea of the Newborn • is a self-limited disease common in infants throughout the world as an early onset of tachypnea, following vaginal or cesarian delivery, normal preterm or term, present within the first few hours of life with retractions, expiratory grunting, or cyanosis, increased oxygen requirement. • Features:  presents as respiratory distress in full-term or near-term infants that become evident shortly after birth  Tachypnea  Nasal flaring  Grunting  Retractions  Cyanosis in extreme cases
    31. 31. 1.Transient Tachypnea of the Newborn ABG: do not reflect carbon dioxide retention, resolves over a 24-hour to 72-hour period. × partial carbon dioxide tensions are usually normal CXR × prominent perihilar streaking, which correlates with the engorgement of the lymphatic system with retained lung fluid, and fluid in the fissures × Small pleural effusions may be seen. × Patchy infiltrates have also been described.
    32. 32. 2.Congenital Diaphragmatic Hernia  Herniation of the abdominal contents into the thoracic cavity through an opening in the diaphragm causing varying degree of pulmonary hypoplasia  2 types:  Bochdalek Hernia (posterolateral location)  Morgagni Hernia retrosternal location)  Symptoms are critical in the 1st 72 hours Features:  Infant sex: higher in males  Signs of respiratory distress  Alar flaring, grunting, retractions  tachypnea  Cyanosis  ABG – dec pO2 shows evidence of severe hypoxia, pCO2 elevated, decreased pH and HCO3
    33. 33. 2. Congenital Diaphragmatic Hernia  Maternal Hx: × underweight women × Smoking during pregnancy × Epileptic mothers, taking anticonvulsant drugs × Tachycardia × Scaphoid abdomen × Decreased breath sounds on the affected side × Hyperresonce to percussion on the affected side × Asymmetry of the wall × Increased diameter of the chest wall  Chest Xray × Mediastinal structures shifted away from the affected side × Heart shifted away from the affected side × Decreased lung volume × Loops of bowel in the thoracic cavity × Ngt tubes inserted inserted into the stomach seen in the thoracic cavity × Gasless abdominal bowel  Prenatal utz: between 16 & 24 week × Polyhydramnios × Chest mass
    34. 34. 3. Congenital Heart Disease Common Types:  Acyanotic Congenital Heart Disease  Atrial Septal Defect (ASD)  Ventricular Septal Defect (VSD)  Patent Ductus Arteriosis (PDA)  Coarctation of the Aorta (CoA)  Aortic Valve Stenosis (AVS)  Pulmonary Valve Stenosis  Cyanotic Congenital Heart Disease  Tetralogy of Fallot  d-Transposition of the Great Arteries  Tricuspid Atresia  Total Anomalous Pulmonary Venous Connection (TAPVC)  Congenital heart defects are structural problems with the heart present at birth, when a mishap occurs during heart development soon after conception and often before the mother is aware that she is pregnant.
    35. 35. 3. Congenital Heart Defects  the reason defects occur is presumed to be genetic  Environmental exposure: × ingestion of some drugs × Smoking during pregnancy  infections during  PE  Signs of respiratory distress  Tachypnea  Alar flaring  Grunting  cyanosis (skin, lips and fingernails × Usually in preterm infants × Most commonly with genetic disorders such as Down syndrome × O2 sats 75%-85% × Murmur × Rales (VSD)  Diagnostics:  Cxr /2D-Echo: × Cardiomegaly × Engorged pulmonary vessels (VSD) × RVH × Pulmonary edema (CAA)
    36. 36. Meconium - Stained Amniotic Fluid
    37. 37. Meconium:  a viscous, sticky, dark green substance composed of:  intestinal epithelial cells  Swallowed vernix caseosa  Lanugo  Mucus  Blood and cellular debris  3 major solid constituents of intestinal secretions of meconium  Bile  mucosal cells  solid elements of swallowed amniotic fluid  Water is the major liquid constituent, making up 85- 95% of meconium. Medscape Updated July 2011
    38. 38. Meconium-stained amniotic fluid  10-15% of births  usually occurs in term or post-term infants Meconium Aspiration Syndrome • is a respiratory disorder in a term and or near term infant born through meconium stained amniotic fluid whose symptoms is a serious condition in which a newborn breathes a mixture of meconium and amniotic fluid into the lungs around the time of delivery.
    39. 39.  Although meconium is sterile, its passage into amniotic fluid is important because of the risk of meconium aspiration syndrome (MAS) and its sequelae.  Meconium-stained amniotic fluid may be aspirated during labor and delivery, causing neonatal respiratory distress.  Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration chiefly affects infants at term and postterm. Medscape Updated July 2011
    40. 40. Meconium Aspiration Pneumonia  develops in 5% of such infants  30% of them require mechanical ventilation  3-5% expire  fetal distress and hypoxia occur with passage of meconium into amniotic fluid  infants may be depressed and require resuscitation at birth  Meconium inactivates surfactant
    41. 41. Physiology  The passage of meconium from the fetus into amnion is prevented by:  lack of peristalsis (low motilin level)  tonic contraction of the anal sphincter  terminal cap of viscous meconium  MSAF may be a natural phenomenon that doesn‟t indicate fetal distress.  mature GI tract in post term fetus:  increased motilin level  vagal stimulation by cord or head compression (may be associated with passage of meconium in the absence of fetal distress)
    42. 42. Factors that promote the passage in-utero include:  Placental insufficiency  Maternal hypertension  Maternal chronic respiratory or CV Disease  Post term pregnancy  Oligohydramnios  Poor biophysical profile  Maternal drug abuse, especially of tobacco and cocaine  Abnormal fetal HR pattern
    43. 43. Incidence:  Passage of meconium is increasingly common in  infants >37 weeks' gestation  occurs in up to 50 % of post-mature infants ( >42 weeks)  MAS varies between 1 and 5 % of all deliveries where there has been meconium-stained fluid.
    44. 44. Cleary & Wiswell proposed severity criteria to define MAS:  Mild: requires <40%O2 for <48hrs  Moderate: >40%O2 for >48hrs, no air leak. Severe: assisted ventilation for >48hrs often with PPH. International Journal of Pediatrics October 9, 2011
    45. 45. Pathophysiology:  In utero, meconium passage may occur either:  in response to fetal hypoxia, with transient period of hyperperistalsis and relaxation of anal sphincter tone  or as a normal physiologic event in fetal gut maturation  Meconium in the lungs causes:  ventilation-perfusion mismatch secondary to ball valve effect (mechanical obstruction)  chemical pneumonitis (surfactant inactivation)
    46. 46. Pathophysiology  The pathophysiology of MAS is complex.  Intrauterine fetal gasping  mechanical airway obstruction  Pneumonitis  surfactant inactivation  damage of umbilical vessels all play roles in the pathophysiology of meconium aspiration
    47. 47. Pathophysiology  There is also a strong association between MAS and persistent pulmonary hypertension of the newborn (PPHN).  The timing of the initial insult resulting in MAS remains controversial.  Chronic in-utero insult may be responsible for most cases of severe MAS.  In contrast to these severe cases, the vigorous infant who aspirates meconium-stained fluid from the nasopharynx at birth usually develops mild to moderate disease.
    48. 48. Mechanism of Injury: 1.Mechanical Obstruction of the Airway  the initial and most important problem of the infant with MAS  the exact incidence of large-airway obstruction is unknown  mechanism can create:  ball valve phenomenon  air flows passed the meconium during inspiration but is trapped distally during expiration  increases in:  expiratory lung resistance  functional residual capacity  anterior posterior diameter of the chest
    49. 49. Mechanism of injury  total obstruction of the small airways: regional atelectasis and ventilation/perfussion mismatches can be developed  Adjacent areas often are partially obstructed and over expanded, leading to: Pneumothorax pneumomediastinum air leaks  Pulmonary air leaks are 10x more likely to develop in infants with MAS than those without, and leaks often develop during resuscitation.
    50. 50. Mechanism of injury 2. Pneumonitis  usual feature of MAS, occurring in about ½ of the cases  Meconium has a direct toxic effect mediated by inflammation.  An intense inflammatory response in the bronchi and alveoli can occur within hours of aspiration of meconium.  airways and lung parenchyma become infiltrated with large numbers of PMNs, leukocytes and macrophages.  Produce direct local injury by release of inflammatory mediators-cytokines:  TNF-α  IL-1β  IL-8and reactive oxygen species.
    51. 51.  Lead to vascular leakage, which may cause toxic pneumonitis with hemorrhagic pulmonary edema.  Meconium contains substances such as bile acids that also can cause direct injury.  Clinicians should maintain a high index of suspicion for bacterial pneumonia in infants with MAS.  Indications of bacterial pneumonia and/or sepsis and should prompt the clinician to obtain relevant cultures and initiate antimicrobial therapy in the presence of:  fever  an abnormal WBC  decline in respiratory function
    52. 52. Mechanism of injury 3.Pulmonary vasoconstriction  the release of vasoactive mediators, such as:  eicosanoids  endothelin-1  prostaglandin E2 (as a result of injury from meconium seems to play role in the development of persistent PHN)  The pulmonary vasoconstriction is, in part, the result of the underlying in utero stressors.
    53. 53. Mechanism of injury 4. Surfactant inactivation  Meconium displaces surfactant from the alveolar surface and inhibits its surface tension lowering ability.  A full term baby born with a sufficient quantity of surfactant may develop surfactant deficiency by inactivation that leads to:  Atelectasis  decreased lung compliance/volume  poor oxygenation
    54. 54.  http://video.about.com/pregnancy/MAS.htm
    55. 55. Clinical Manifestations  Either in utero  first breath, thick, particulate meconium is aspirated into the lungs.  small airway obstruction  respiratory distress within 1st hours  Tachypnea  Retractions  Grunting  cyanosis observed in severely affected infants.
    56. 56. Clinical Manifestations  Partial obstruction of some airways may lead to  pneumothorax  Pneumomediastinum  both  Overdistention of the chest may be prominent  condition usually improves w/in 72 hr  assisted ventilation: may be severe with a high risk for mortality  Tachypnea may persist for many days or even several weeks  assisted ventilation: may be severe with a high risk for mortality
    57. 57. Clinical Manifestations  typical chest roentgenogram is characterized by :  patchy infiltrates  coarse streaking of both lung fields  increased anteroposterior diameter, and flattening of the diaphragm  Nº CXR in an infant with severe hypoxia and no cardiac malformation suggests the diagnosis of pulmonary hypertension.  ABG  Arterial Po2 may be low in either disease, and if hypoxia has occurred, metabolic acidosis is usually present
    58. 58. Diagnosis Coarse interstitial infiltrates +L side pneumothorax Hyperinflation and patchy asymmetric airspace disease that is typical of MAS. B., BB. BOY CXR
    59. 59. Diagnosis Coarse interstitial infiltrates +L side pneumothorax Areas of opacification due to atelectasis bilaterally.
    60. 60.  Close up of left lung demonstrating the streaky lucencies of the air in the interstitium (red arrows) complicated by a pneumothorax (yellow arrow).
    61. 61.  Homogeneous density similar to respiratory distress syndrome (RDS). B., BB. BOY CXR
    62. 62.  In infants with severe disease who require high concentrations of supplemental oxygen and mechanical ventilation, the lungs may develop an appearance of homogeneous density similar to respiratory distress syndrome (RDS).  Radiographic changes resolve over the course of 7 to 10 days but sometimes persist for several weeks.
    63. 63.  Air leak occurs in 10 to 30 percent of infants with MAS.  Arterial blood gas measurements typically show hypoxemia and hypercarbia.  Infants with pulmonary hypertension and right-to-left shunting may have a gradient in oxygenation between preductal and postductal samples.  2D Echocardiogram for evaluation of PPH.
    64. 64. Management  Sept 2007 the ACOG revised recommendations and recommended that: “all infants with MSAF should not longer receive intrapartum suctioning. If meconium present and the newborn depressed, the clinician should intubate the trachea and suction meconium from beneath the glottis”.  Intrapartum suctioning not effective in removing meconium aspirated by the fetus into the lungs prior delivery.
    65. 65.  Skilled resuscitation team should be present at all deliveries that involve MSAF.  Pediatric intervention depends on whether the infant is vigorous.  Vigorous infant is if has: 1. Strong resp. efforts 2. Good muscle tone 3. Heart rate >100b/m  When this is a case-no need for tracheal suctioning, only routine management.
    66. 66.  When the infant is not vigorous:  Clear airways as quickly as possible.  Free flow 02.  Radiant warmer but drying and stimulation should be delayed.  Direct laryngoscopy with suction of the mouth and hypopharynx under direct visualization, followed by intubation and then suction directly to the ET tube as it slowly withdrawn.  When the infant is not vigorous:  The process is repeated until either „„little additional meconium is recovered, or until the baby‟s heart rate indicates that resuscitation must proceed without delay‟‟.
    67. 67. Postnatal Management Apparently well child born through MSAF  Most of them do not require any interventions besides close monitoring for RD.  Most infants who develop symptoms will do so in the first 12 hours of life. Approach to the ill newborns:  Transfer to NICU.  Monitor closely.  Full range of respiratory support should be available.  Sepsis: ABx indicated.  Transfer to ECMO center may be necessary.
    68. 68. Treatment in NICU Goals:  Increased oxygenation while minimizing the barotrauma (may lead to air leak) by minimal MAP and as short IT as possible.  Prevent pulmonary hypertension.  Successful transition from intrauterine to extrauterine life with a drop in pulmonary arterial resistance and an increase in pulmonary blood flow.
    69. 69.  Severe MAS can spiral into vicious cycle of hypoxemia that leads to acidosis, which together cause pulmonary vein constriction.  May lead to persistent pulmonary hypertension.  The resultant right-to-left shunting at the level of the ductus arteriosus, the atrial level, or both causes further cyanosis and hypoxemia, which perpetuate the cycle.
    70. 70. Ventilatory support depends on the amount of respiratory distress:  O2 hood  CPAP (10%).  Mechanical ventilation (40%).  Observational study showed worse outcome for infants treated with hyperventilation.  High-frequency ventilators may slow the progression of meconium down the tracheobronchial tree and allow more time for meconium removal.
    71. 71. Surfactant  Two randomized controlled studies have evaluated the efficacy of exogenous surfactant administration.  Results showed decreased number of infants requiring ECMO and possible reduction of pneumothorax, but no difference in mortality.  A Cochrane meta-analysis of 4 randomized trials confirmed that surfactant replacement showed no effect on mortality but reduce the use of ECMO.  Lavage with dilute surfactant-increases oxygenation and decrease the need of MV.
    72. 72. Inhaled NO  Randomized clinical trials have demonstrated that iNO therapy decreases the need for ECMO in addition to mortality in full-term and near-term neonates with hypoxic respiratory failure and PPHN  For hypoxic respiratory failure due to MAS, infants responded well to combined iNO and HFV as compared to either treatment alone  The response to combined treatment with HFV and iNO reflects both decreased intrapulmonary shunt and augmented nitric oxide delivery to its site of action.
    73. 73. ECMO  40% of infants with MAS treated with inhaled NO fail to respond and require bypass.  35% of ECMO patients are with MAS.  Survival rate after ECMO 93-100%.
    74. 74. Treatment  Routine intubation to aspirate the lungs of vigorous infants born through meconium-stained fluid is not recommended.  Depressed infants (those with hypotonia, bradycardia, fetal acidosis, or apnea) should undergo endotracheal intubation, and suction should be applied directly to the endotracheal tube to remove meconium from the airway.
    75. 75.  The risk associated with laryngoscopy and endotracheal intubation:  Bradycardia  Laryngospasm  Hypoxia  posterior pharyngeal laceration with pseudodiverticulum formation  less than the risk of meconium aspiration syndrome in these severe circumstances.
    76. 76.  Treatment of meconium aspiration pneumonia includes:  supportive care  standard management for respiratory distress.  The oxygenation benefit of PEEP must be weighed against the risk of pneumothorax.  Severe meconium aspiration may be complicated by persistent pulmonary hypertension and requires similar treatment.
    77. 77.  Patients who are refractory to conventional mechanical ventilation or HFV may benefit from:  surfactant therapy  regardless of gestational age  iNO  or extracorporeal membrane oxygenation (ECMO)
    78. 78. Prevention of MAS  The risk of meconium aspiration may be decreased by:  Antepartum Period: elective induction of labor for pregnancies at or beyond 41 weeks  Intrapartum Fetal Monitoring: paying careful attention to fetal distress  Initiating prompt delivery in the presence of fetal acidosis, late decelerations, or poor beat-to-beat variability.  Amnioinfusion: ACOG 2007, conclude that routine prophylactic amnioinfusion for the dilution of MSAF is not recommended
    79. 79. Prevention  Routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born with clear or meconium-stained amniotic fluid is no longer recommended.  Postpartum Endotracheal Suctioning  NRP recommends intubation and direct endotracheal suctioning soon after delivery for non-vigorous infants born through MSAF, depressed respiratory efforts, poor muscle tone, HR less than 100/min  According to Int‟l Consensus on CP Resuscitation and Emergency CV Care, available evidence does not support or refute the routine endotracheal suctioning of depressed infants born through MSAF International Journal of Pediatrics Oct 2011
    80. 80. Prognosis  The mortality rate of meconium-stained infants is considerably higher than that of non-stained infants.  Meconium aspiration used to account for a significant proportion of neonatal deaths.  Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to 5-10 yr.  The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension.
    81. 81. Neurologic outcome  Outcome is good in uncomplicated MAS with no underlying disorder.  Most cases of severe MAS are associated with intrauterine asphyxia and/or infection and neurologic outcome depends upon these conditions.
    82. 82. Potential Future Therapy  Currently MAS treatments are all supportive in nature and do not directly affect the injurious actions of meconium on the lung.  There is still no effective and safe treatment or prophylactic measure for MAS once the meconium has passed below the vocal cords into the lungs.  It has been suggested that fetal pancreatic digestive enzymes play an important role in the lung damage after meconium aspiration by causing disruption of intercellular connections and cell detachment from the basement membrane.
    83. 83. Potential Future Therapy  Recent data show that some of the cell death induced by meconium occurs by apoptosis, and therefore has the potential for pharmacologic inhibition through the use of apoptosis blockers or other strategies.
    84. 84. Summary  Optimal care of an infant born through MSAF involves close collaboration between OBs and Pediatricians.  Effective communication and anticipation of potential problems is a corner stone of the successful partnership.
    85. 85. References: 1. Nelson‟s Textbook of Pediatrics 18th and 19th Ed; Respiratory Tract Disorders 2. Standards of Newborn Care 3rd Edition; Management of Newborns with Acute Respiratory Disorders; Hernandez. Matias. Santos; Phil. Society of Newborn Medicine 2008 3. Behrman‟s Pediatric Decision Making 5th Ed; Neonatal; 2011 4. Meconium-stained amniotic fluid (MSAF) Pediatrics point of view . Fostersom / Pediatrics / Neonatology. February 2009 5. The epidemiology of meconium aspiration syndrome: incidence, risk factors, therapies, and outcome. Dargaville PA; Copnell B Pediatrics. 2006 May;117(5):1712-21. 6. Surfactant and surfactant inhibitors in meconium aspiration syndrome. Dargaville PA; South M; McDougall PN J Pediatr 2001 Jan;138(1):113-5.
    86. 86. Persistent Newborn Pulmonary Hypertension  Medscape Pediatrics Updated Dec 20, 2011  Robin H Steinhorn, MD Raymond and Hazel Speck Berry Professor of Pediatrics, Division Head of Neonatology, Vice Chair of Pediatrics, Northwestern University, The Feinberg School of Medicine Member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Heart Association, American Pediatric Society, American Thoracic Society and Society for Pediatric Research Meconium Aspiration Syndrome  Medscape Pediatrics Updated March 30, 2010  Melinda B Clark, MD Assistant Professor of Pediatrics, Department of Pediatrics, Albany Medical College Member of the following medical societies: Alpha Omega Alpha, Ambulatory Pediatric Association, American Academy of Pediatrics, and Medical Society of the State of New York
    87. 87. Transient Tachypnea of the Newborn  Medscape Pediatrics updated Jan 13, 2010  KN Siva Subramanian, MD Professor of Pediatrics and Obstetrics/Gynecology, Chief of Neonatal Perinatal Medicine, Hospital Ethicist, Georgetown University Hospital Member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Nutrition,American Society for Parenteral and Enteral Nutrition, American Society of Law, Medicine & Ethics,New York Academy of Sciences, and Southern Society for Pediatric Research “The frequency of meconium-stained amniotic fluid increases as a function of the duration of labor.”  The Journal of Maternal-Fetal & Neonatal Medicine : Official Journal of the European Association of Perinatal Medicine  PubMed Articles, 2009
    88. 88. Journal Updates
    89. 89. Journal Updates Glucocorticoids in the treatment of neonatal meconium aspiration syndrome  England Journal of Pediatrics 2011 December; 170(12): 1495– 1505.  Published online 2011 April 6. doi: 10.1007/s00431-011-1453-2  PMCID: PMC3221844  Copyright © The Author(s) 2011
    90. 90. Journal Updates  Meconium-induced lung edema, inflammation and vasoconstriction on the course of the disease, glucocorticoids are increasingly used in the treatment of MAS despite the fact that principal questions on the choice of GCs derivative, mode of delivery and dosing have not been answered yet.  To bring a complex insight into the topic, this article reviews the pathomechanisms of MAS, mechanisms of action of GCs, as well as the advantages and disadvantages of GCs administration in experimental models and newborns with MAS.
    91. 91. Journal Updates  The anti-inflammatory effect of GCs is supplied also through enhancing the activity of lipocortines.  Lipocortines inhibit the activity of PLA2 and thereby decrease the production of arachidonic acid and mediators of lipooxygenase and cyclooxygenase pathway as well as of PAF.
    92. 92. Journal Updates  GCs  reduce the penetration of neutrophils into the lungs,  decreasing their adherence to the endothelium  thereby increasing secondarily a count of  circulating neutrophils  circulating mononuclears  eosinophils  basophils  as well as the synthesis of cytokines by  Macrophages  eosinophils  T lymphocytes.
    93. 93. Journal Updates  GCs stimulate the production of secretion leukocyte protease inhibitor, an important antiprotease, which may suppress an inflammation in the airways.  GCs facilitate the transcription of β2-receptor gene and reduce the mast cells count and production of mucus in the airways.  By stabilizing the cell membranes and decreasing the production of pro-inflammatory and vasoactive substances, GCs reduce microvascular permeability.  By direct modulation of the pulmonary vasomotoric tone, GCs diminish pulmonary vasoconstriction and inhibit fibrogenesis.
    94. 94. Journal Updates  GCs may effectively suppress:  pmn‟s inflammation  lung edema formation  pulmonary vasoconstriction. However, the effect of the treatment depends on:  the specific properties  dose  mode of delivery of the individual GCs  as well as on the current status of the newborn or experimental animal with MAS.
    95. 95. Journal Updates Dexamethasone  is a synthetic GC with potent anti-inflammatory and immunosuppressive action.  It is >30 times stronger than hydrocortisone and about five times stronger than prednisone.  is also used for diagnostic procedures (to suppress the natural pituitary–adrenal axis) in obstetrics to promote the maturation of foetal lungs as well as in a wide spectrum of endocrine, oncological and other diseases.  the action is fast, but of a short term.  In newborns, the plasma half-life of dexamethasone is 150–300 min and the biological half-life is between 36– 54 h.
    96. 96. Journal Updates  The half-life of dexamethasone in adults is 110– 190 min, with the biological half-life of 36–72 h.  Considering time-related inflammatory changes in MAS, limitations of the treatment efficacy in late administration of GCs may be reduced by repetitive administration, every 2–4 h is recommended (data given by the producer, Dexamed, Medochemie, Cyprus).  Although the acute cardiovascular changes may be critical for neonates with meconium-induced lung injury, the side effects of repetitive GCs administration in MAS have not been investigated yet in a clinical study
    97. 97. Journal Updates Concluding remarks  Despite the increasing number of trials with GCs in experimental models and newborns with MAS, their administration is still missing in the generally accepted therapeutic protocol of MAS.  However, favourable results from the studies indicate that GCs may be beneficial, particularly in severe forms of MAS with apparent lung edema, pulmonary vasoconstriction and inflammation.  The authors found that the surfactant lung lavage in combination with dexamethasone pretreatment may improve the status of the newborns with MAS more effectively than the surfactant lavage alone.
    98. 98. Journal Updates International Journal of Pediatrics Volume 2012 (2012), Article ID 359571, 7 pages doi:10.1155/2012/359571 Review Article Advances in the Management of Meconium Aspiration Syndrome Kamala Swarnam,1 Amuchou S. Soraisham,1,2,3 and Sindhu Sivanandan1 1Division of Neonatology, Department of Pediatrics, University of Calgary, Calgary, AB, T2N 1N4, Canada 2Alberta Children's Hospital Research Institute for Child and Maternal Health, University of Calgary, Calgary, AB, T2N 4N1, Canada 3Department of Pediatrics, Foothills Medical Centre, Rm C211 1403-29th Street NW, Calgary, AB, T2N 2T9, Canada Received 25 July 2011; Accepted 9 October 2011
    99. 99. Journal Updates Abstract  Meconium aspiration syndrome (MAS) is a common cause of severe respiratory distress in term infants, with an associated highly variable morbidity and mortality.  MAS results from aspiration of meconium during intrauterine gasping or during the first few breaths.  The pathophysiology of MAS is multifactorial and includes acute airway obstruction, surfactant dysfunction or inactivation, chemical pneumonitis with release of vasoconstrictive and inflammatory mediators, and persistent pulmonary hypertension of newborn (PPHN).  This disorder can be life threatening, often complicated by respiratory failure, pulmonary air leaks, and PPHN.
    100. 100. Journal Updates Abstract  This disorder can be life threatening, often complicated by respiratory failure, pulmonary air leaks, and PPHN  Approaches to the prevention of MAS have changed over time with collaboration between obstetricians and pediatricians forming the foundations for care.  The use of surfactant and inhaled nitric oxide (iNO) has led to the decreased mortality and the need for extracorporeal membrane oxygenation (ECMO) use.  In this paper, we review the current understanding of the pathophysiology and management of MAS.
    101. 101. Journal Updates Conclusions  Despite improvement in obstetrical and neonatal care, MAS continues to be a neonatal disorder with high morbidity and mortality.  The lung injury caused by meconium is complex and can be attributed to mechanical obstruction of airways, surfactant inactivation, chemical pneumonitis, and PPHN.  Among preventive strategies, elective induction of labor for pregnancies at or beyond 41 weeks is associated with significant reduction in the incidence of MAS and amnioinfusion reduces the risk of MAS only in clinical settings with limited peripartum surveillance.
    102. 102. Journal Updates Conclusions  Intrapartum management includes endotracheal suctioning to clear meconium only in nonvigorous infants born through MSAF.  The management of a symptomatic infant with MAS is primarily supportive.  These infants are at high risk of developing PPHN and air leaks. Invasive ventilation if required should use lower PIP, moderate PEEP, higher rates (40–60/min), and adequate expiratory time and permissive hypercapnea should be tolerated to facilitate gentle ventilation.
    103. 103. Journal Updates Conclusions  MAS complicated with PPHN and not responsive to conventional ventilation may require HFV and iNO.  iNO therapy has decreased the need for ECMO in MAS complicated by hypoxic respiratory failure and PPHN.  Surfactant replacement should be considered in ventilated infants requiring more than 50% FiO2.  Unless there is definite risk for infection, prophylactic use of antibiotics in MAS does not reduce infection or alter the clinical course of illness.
    104. 104. Journal Updates Conclusions  ECMO has been used as a final rescue therapy in infants with severe and refractory hypoxemia associated with MAS.  The role of steroids and other adjuvant pharmacotherapies like magnesium sulfate, free radical scavengers, and protease inhibitors is still experimental and they are not routinely recommended.  As MAS is a major cause of mortality in developing countries, studies focusing on prevention and early treatment should be continued to reduce mortality and morbidity.
    105. 105. CLINICAL REPORT Surfactant-Replacement Therapy for Respiratory Distress in the Preterm and Term Neonate By: William A. Engle, MD, and the Committee on Fetus and Newborn PEDIATRICS Volume 121, Number 2 February 2008
    106. 106. ABSTRACT  Respiratory failure secondary to surfactant deficiency is a major cause of morbidity and mortality in preterm infants.  Surfactant therapy substantially reduces mortality and respiratory morbidity for this population.  Secondary surfactant deficiency also contributes to acute respiratory morbidity in late-preterm and term neonates with meconium aspiration syndrome, pneumonia/sepsis, and perhaps pulmonary hemorrhage; surfactant replacement may be beneficial for these infants.
    107. 107.  This statement summarizes indications, administration, formulations, and outcomes for surfactant-replacement therapy.  Because respiratory insufficiency may be a component of multiorgan dysfunction, preterm and term infants receiving surfactant-replacement therapy should be managed in facilities with technical and clinical expertise to administer surfactant and provide multisystem support.
    108. 108. CLINICAL IMPLICATIONS 1. Surfactant should be given to infants with respiratory distress syndrome as soon as possible after intubation irrespective of exposure to antenatal steroids or gestational age. 2. Prophylactic surfactant replacement should be considered for extremely preterm infants at high risk of respiratory distress syndrome, especially infants who have not been exposed to antenatal steroids.
    109. 109. 3. Rescue surfactant may be considered for infants with hypoxic respiratory failure attributable to secondary surfactant deficiency (eg, meconium aspiration syndrome, sepsis/pneumonia, and pulmonary hemorrhage). 4. Preterm and term neonates who are receiving surfactant should be managed by nursery and transport personnel with the technical and clinical expertise to administer surfactant safely and deal with multisystem illness.
    110. 110. RESEARCH IMPLICATIONS 1. Randomized trials of continuous positive airway pressure, with or without surfactant, during a brief intubation compared with prophylactic or early surfactant replacement in preterm infants are needed. 2. Improved surfactant preparations, surfactant- dosing strategies for infants born to mothers who are receiving antenatal steroids, and noninvasive techniques for surfactant administration need additional study.
    111. 111. 3. Surfactant replacement for illnesses other than respiratory distress syndrome needs additional study. 4. It is no longer necessary to include first-generation synthetic surfactants in future studies.
    112. 112. Take Home Points  The initial assessment of a patient in respiratory distress should be rapid and focused on quickly determining the severity of respiratory distress and need for emergent interventions.  Specific causes of respiratory distress can be categorized as pulmonary and non-pulmonary and require specific interventions.
    113. 113. Thank You

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