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1 Neonatal Respiratoty distress. 2 3 Signs&symptoms 1. Intercostal retraction 2. tachypnea>60-80/minute 3. Grunting 4. cyanosis in room air; pao 2 0.4.

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Presentation on theme: "1 Neonatal Respiratoty distress. 2 3 Signs&symptoms 1. Intercostal retraction 2. tachypnea>60-80/minute 3. Grunting 4. cyanosis in room air; pao 2 0.4."— Presentation transcript:

1 1 Neonatal Respiratoty distress

2 2

3 3 Signs&symptoms 1. Intercostal retraction 2. tachypnea>60-80/minute 3. Grunting 4. cyanosis in room air; pao 2 0.4 5. Flaring of the ala nasi 6. reduced air exchange 7. Apnea 8. Stridor 1. Intercostal retraction 2. tachypnea>60-80/minute 3. Grunting 4. cyanosis in room air; pao 2 0.4 5. Flaring of the ala nasi 6. reduced air exchange 7. Apnea 8. Stridor

4 4 Downes, or RDS score 012 CyanosisNone In room air In 40%FIO2 RetractionsNoneMildSevere GruntingNone Audible with stethoscope Audible without stethoscope Air entry Clear Decreased or delayed Barely audible Respiratory rate Under 60 60-80 Over 80 or apnea Score: >4= Clinical respiratory distress; monitor arterial blood gases >8=Impending respiratory failure

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7 7 Normal ABG Respiratory Failure pao2> 55-80 mm Hg paco2 > 35-40 mm Hg PH= 7.35 – 7.40 pao2> 55-80 mm Hg paco2 > 35-40 mm Hg PH= 7.35 – 7.40 pao2 <50 mm Hg paco2 >60 mm Hg PH ≤ 7.2 pao2 <50 mm Hg paco2 >60 mm Hg PH ≤ 7.2

8 8 Evaluation: 1. History 2. Ph.E (Downes’or RDS score) 3. CHEST XRAY 4. BLOOD GLUCOSE 5. BLOOD CULTURE – CBC 6. ABG 7. ECHO, ECG

9 9 Respiratory distress syndrome(HMD) Disorder of premature infants Disorder of premature infants Respiratory distress Respiratory distress – tachypnea,grunting,flaring, retractions

10 10 Difficult to distinguish from pneumonia Difficult to distinguish from pneumonia Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy) Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy) Recovery prolonged by barotrauma or oxidative injury Recovery prolonged by barotrauma or oxidative injury

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12 12 Diagnosis 1. History  Time of onset of signs 2. C.xray  airbronchogram, reticular- granular patlern

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15 15Complications 1.Airleaks 2.Sepsis 3.IVH 4.PDA 5.BPD 6.ROP

16 16 Acute Complications Air Leak Syndromes Air Leak Syndromes – Consider with sudden change in condition – More common if baby receiving ventilatory support – Pneumothorax most common Therapy Therapy – None if stable – Oxygen 100% – Thorocentesis: Needle or tube

17 17 Acute Complications Intracranial Hemorrhage Intracranial Hemorrhage – High risk if HMD is severe – More common at lower gestational ages – Rare above 33 weeks gestation Suspect if there is a sudden change in condition Suspect if there is a sudden change in condition May coincide with development of air leak May coincide with development of air leak Signs: change in Fontanel, perfusion Signs: change in Fontanel, perfusion

18 18 Acute Complications Patent Ductus arteriosus Patent Ductus arteriosus – Usually evident during resolution phase Signs of Congestive Heart Failure Signs of Congestive Heart Failure – Increased oxygen need – Cardiomegaly – Acidosis, decreased urine output Therapy: Therapy: – Decrease fluid intake – Indomethacin

19 19 Prevention: Prevention of permature birth Prevention of permature birth Prevent of cold strass, birth asphyxia and hypovolemia Prevent of cold strass, birth asphyxia and hypovolemia Administration of corticosteroids to the mother at least 24-48 hours before delivery at gestatinl age< 34 weeks. Administration of corticosteroids to the mother at least 24-48 hours before delivery at gestatinl age< 34 weeks. Administration of surfactants in V.L.B.W Administration of surfactants in V.L.B.W

20 20 Treatment 1. Supportive care (treatment of acidosis,  Hypotension, Hypothermia) Decrease fluid Intake 2. Oxygen therapy (Pao 2 = 66-70 mmHg Sao 2 >90%)(CpAp-Mecliancal Ventilution) 3. Surfactant Therapy

21 21 Initial Care Maintain warmth- cold stress will mimic other causes of distress Maintain warmth- cold stress will mimic other causes of distress Monitor blood glucose levels- assure they are normal Monitor blood glucose levels- assure they are normal Provide enough oxygen to keep the baby pink Provide enough oxygen to keep the baby pink

22 22 Initial Care Ensure adequate hydration: Start fluids at 70-80 ml/kg/d 10% glucose solution Start fluids at 70-80 ml/kg/d 10% glucose solution Smaller babies may need more fluid Smaller babies may need more fluid Add electrolytes by the second day Add electrolytes by the second day On day 3-4 watch for diuresis On day 3-4 watch for diuresis

23 23 Initial Care Consider other etiologies: INFECTION,INFECTION INFECTION,INFECTION – Evaluate – Begin antibiotic therapy as prophylaxis – Continue as clinically indicated Anatomic malformations Anatomic malformations

24 24 Assess circulation Monitor heart rate Monitor heart rate Assess Blood pressure Assess Blood pressure Check peripheral perfusion and capillary refill Check peripheral perfusion and capillary refill Avoid excessive blood sampling Avoid excessive blood sampling

25 25 Respiratory DISTRESS(NICU) Respiratory Rate Fio2 Expiratory Grunt Lowerchest Retraction Xiphoid Retraction 060min<.30NoneNoneNone 160-80/min.30-.40 Stethoscope only Just visible 2>80min>040 Naked ear MarkedMarked If the score is <3 continue To observe. If the score is >4 insert an arterial line and monitor gasea. If the score is >6 consider CPAP. If the score is >8 consider mechanical ventilation.

26 26 CPAP Indications FiO 2 above 0.3 with clinical distress FiO 2 above 0.3 with clinical distress FiO 2 above 0.4 FiO 2 above 0.4 Significant retractions after extubation Significant retractions after extubation Hypoventilation: CPAP may be helpful Hypoventilation: CPAP may be helpful

27 27 CPAP risks Hard to control in spontaneously breathing baby, especially if vigorous or close to term Hard to control in spontaneously breathing baby, especially if vigorous or close to term Potential for airleak Potential for airleak Can’t give surfactant Can’t give surfactant May rarely worsen ventilation May rarely worsen ventilation

28 28 CPAP - Mechanism of action CPAP prevents collapse of unstable alveoli upon expiration Facilitates recruitment of unventilated alveoli Reduces right to left shunting across foramen ovale Reduces left to right shunting across the Ductus Arteriosus, improving cardiac output and blood pressure

29 29 Mechanical Ventilation FiO 2 more than 0.35 -0.4 on CPAP FiO 2 more than 0.35 -0.4 on CPAP Early treatment if condition is deteriorating Early treatment if condition is deteriorating Decreasing “work of breathing” Decreasing “work of breathing” Frequent apnea Frequent apnea Plan to give surfactant therapy Plan to give surfactant therapy Absolutely: for prolonged apnea or hypoxemia in absence of heart disease Absolutely: for prolonged apnea or hypoxemia in absence of heart disease

30 30 Mechanical ventilation - risks May require sedation, reducing spontaneous respiration May require sedation, reducing spontaneous respiration Airleaks, especially as compliance improves Airleaks, especially as compliance improves Baro-Volutrauma and risk of chronic lung injury Baro-Volutrauma and risk of chronic lung injury

31 31 Exogenous Surfactant Preparations Alveofact*:bovine lung surfactant extract Alveofact*:bovine lung surfactant extract Curosurf:porcine lung surfactant extract, lipids Curosurf:porcine lung surfactant extract, lipids Exosurf Neonatal*:colfosceril palmitate, cetyl alcohol, tyloxapol Exosurf Neonatal*:colfosceril palmitate, cetyl alcohol, tyloxapol Infasurf:calf lung surfactant extract Infasurf:calf lung surfactant extract Survanta:bovine lung surfactant extract, lipids Survanta:bovine lung surfactant extract, lipids *Not Available in USA

32 32 Functions of Surfactant Associated Proteins Hydrophilic Hydrophilic – SP-A: tubular myelin, host defense – SP-D: surfactant lipid homeostasis, host defense, antioxidant Hydrophobic Hydrophobic – SP-B: surface tension reduction, tubular myelin, type II cell functions – SP-C: surface tension reduction, film stability LeVine et al, 2001

33 33 Before Surfactant Treatment 45 Minutes Post-Treatment Radiographic Changes With Exogenous Surfactant Treatment

34 34 Relationship of Antenatal Corticosteroids and Postnatal Surfactant Neonatal Mortality Jobe et al, 1993 ** 57 46555566

35 35 Multi-Dose Studies Two-Year Follow- Up Survanta ® (beractant) Respiratory Complications Survanta Multi-Dose Study Group, 1994 ** 201226201225202226203226203226

36 36 Multi-Dose Studies Two-Year Follow-Up Survanta ® (beractant) CNS Complications 201226201226201226201226 Survanta Multi-Dose Study Group, 1994

37 37 Transien tachypnea of the Newborn(T.T.N) Wet lung, RDSII, Mild HMD

38 38 Delayed resorption of fetal lung fluid Risk Factors: Delayed resorption of fetal lung fluid Risk Factors: 1- delayed in cord clamping 2- c/s delivery 3- term- preterm neonates 4- the mother who received excessive fluid befor delivery.

39 39 Signs & symptom Mild respiratory distress present at birth or a few hour after birth Mild respiratory distress present at birth or a few hour after birth ABG  Normal or mild hypoxia & Acidosis ABG  Normal or mild hypoxia & Acidosis

40 40 C.XRay: Overaeration, flat- diaphragms, prominent pulmonary vacular marking sometimes fluid lines present in the fissures. Overaeration, flat- diaphragms, prominent pulmonary vacular marking sometimes fluid lines present in the fissures.

41 41 Delayed resorption of fetal lung fluid Delayed resorption of fetal lung fluid Most consider, and rule out pneumonia Treat with antibiotics if diagnosis is uncertain Treat with antibiotics if diagnosis is uncertain – Oxygen need beyond six hours – Oxygen need increasing – Worsening symptoms

42 42 Patients usually recover rapidly between 3-5 days Patients usually recover rapidly between 3-5 days Treatment= supportive therapy. Treatment= supportive therapy.

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44 44 MECONIUM ASPIRATION SYNDROME (MAS)

45 45 Approximately 13% of All live births are complicated by MSAF Approximately 13% of All live births are complicated by MSAF 5% of MSAF  MAS

46 46 MSAF>Term, post term, IUGR MSAF Term, post term, IUGR MSAF< Preterm <34 weeks

47 47 Risk factors for meconium- stained amniotic fluid Maternal hypertension Maternal hypertension Maternal diabetes mellitus Maternal diabetes mellitus Maternal heavy cigarette smoking Maternal heavy cigarette smoking Maternal chronic respiratory or cardiovascular disease Maternal chronic respiratory or cardiovascular disease Postterm pregnancy Postterm pregnancy Pre-eclampsia/ eclampsia Pre-eclampsia/ eclampsia

48 48 (cont.) Oligohydramnios Oligohydramnios Intrauterine growth retardation Intrauterine growth retardation Poor biophysical profile Poor biophysical profile Abnormal fetal heart rate patterns Abnormal fetal heart rate patterns

49 49 MAS MAS Mild  Less than 40% O 2 < 48H Moderate  More thon 40% O 2 >48H  No air leak Severe  Assisted ventilation >48  PPHN

50 50 Mechanism of injure: 1. Obstruction of air ways 2. Chemical pneumonitis 3. Vasoconstriction of pulmonary vessels 4. Inactivation of surfactant

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57 57 Management : 1. Fetal heart rate monitoring (Fetal Pulse oximetry) 2. Amnioinfusion 3. Intrapartum suctioning

58 58 Meconium Present? Suction mouth, nose, and posterior pharynx after delivery of head, but before delivery of shoulders Baby vigorous?* Suction mouth and trachea Continue with remainder of Initial steps: Clear mouth and nose of secretions Dry, stimulate, and reposition Give O 2 ( as necessary ) NO Yes

59 59 Treatment in NICU: Oxygen Therapy Oxygen Therapy Surfactant Therapy Surfactant Therapy Inhaled Nitric oxide Inhaled Nitric oxide ECMO ECMO

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61 61 پنومونی در نوزادان پنومونی بعد از HMD شايع ترين علت ديسترسی تنفسی می باشد و شامل : I- پنومونی مادر زادی و داخل رحمی II – پنومونی موقع تولد يا آسپيراسيون III- پنومونی بعد از تولد

62 62 -I پنومونی مادر زادی راه انتقال از طريق جفت می باشد. عامل بيماريزا : عفونت های مادر زادی (TORCH) ، ترپونما پاليدوم مايکوپلاسما و گاها ويروس ها ( ادنو ويروس ها و آنترو ويروس ها ) می باشند

63 63 علائم در ساعت های اول پس از تولد ظاهر ميشود. در ساعت های اول پس از تولد ظاهر ميشود. علاوه بر گرفتاری ريه ، گرفتاری در ساير احشاء نظير بزرگی کبد – طحال ، تظاهرات جلدی ( پتشی ) و اختلالات عصبی موجود است. علاوه بر گرفتاری ريه ، گرفتاری در ساير احشاء نظير بزرگی کبد – طحال ، تظاهرات جلدی ( پتشی ) و اختلالات عصبی موجود است. نوزادان يا مرده متولد ميشوند و يا در عرض چند ساعت اول حيات فوت می کنند. نوزادان يا مرده متولد ميشوند و يا در عرض چند ساعت اول حيات فوت می کنند.

64 64 II – پنومونی موقع تولد يا آسپراسيون راه انتقال کانال زايمان می باشد. عامل بيماريزا : ميکروبهای موجود در کانال زايمانی : نظير GBS ، E.coli ،.... می باشند.

65 65 علائم : ظهور علائم از چند ساعت تا چند روز پس از تولد متغيراست و بيشتر شبيه به HMD می باشد. عوامل مساعد کننده : پرماچوريتی ، PROM ، زايمان مشکل می باشند

66 66 III – پنومونی بعد از تولد : راه انتقال : تماس با افراد آلوده و يا وسائل آلوده در بخش نوزادان می باشد. عامل بيماريزا : اکثرا C.O.N.S ، C.O.P.S و گاها ويروس ها (RSV ) ، قارچ ها ( پس از اقامت زياد در بخش ) و کلامد يا می باشند. علائم : ظهور علائم در خلال ماه اول حيات می باشد

67 67 تشخيص : شرح حال شرح حال علائم بالينی علائم بالينی آزمايشگاهی آزمايشگاهی گرافی قفسه صدری گرافی قفسه صدری

68 68 درمان : I – پنومونی قبل از هفته اول حيات آمپی سيلين يا پنی سيلين + يک آمينوگليکوزيد II – پنومونی بعد از هفته اول حيات متی سيلين يا وانکوماسين + يک آمينوگليکوزيد يا سفالوسپرين نسل سوم III – پنومونی کلامديائی ارتيرومايسين يا تری متوپريم – سولفامتوکسازول طول مدت درمان ، در پنومونی استافيلوکوکی 4-3 هفته – در ساير جرم ها 10-14 روز است.

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