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Neonatal Respiratoty

distress

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Signs&symptoms

1. Intercostal retraction

2. tachypnea>60-80/minute

3. Grunting

4. cyanosis in room air; pao2<60minHg in fio2>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; pao2<60minHg in fio2>0.4

5. Flaring of the ala nasi

6. reduced air exchange

7. Apnea

8. Stridor

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Downes, or RDS score

0 1 2Cyanosis None In room air In 40%FIO2

Retractions None Mild Severe

Grunting None 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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6

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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

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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

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Respiratory distress syndrome(HMD)

•Disorder of premature infants

•Respiratory distress–tachypnea,grunting,flaring, retractions

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• Difficult to distinguish from pneumonia

• Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy)

• Recovery prolonged by barotrauma or oxidative injury

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Diagnosis

1. History Time of onset of signs

2. C.xray airbronchogram, reticular-granular patlern

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Complications 1. Airleaks

2. Sepsis

3. IVH

4. PDA

5. BPD

6. ROP

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Acute Complications

• Air Leak Syndromes–Consider with sudden change in

condition–More common if baby receiving

ventilatory support– Pneumothorax most common

• Therapy–None if stable–Oxygen 100%– Thorocentesis: Needle or tube

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Acute Complications

• 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

• May coincide with development of air leak• Signs: change in Fontanel, perfusion

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Acute Complications

• Patent Ductus arteriosus–Usually evident during resolution

phase• Signs of Congestive Heart Failure– Increased oxygen need–Cardiomegaly–Acidosis, decreased urine output

• Therapy:–Decrease fluid intake– Indomethacin

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Prevention:

• Prevention of permature birth• 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 surfactants in V.L.B.W

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Treatment 1. Supportive care (treatment of acidosis,

Hypotension, Hypothermia) Decrease fluid Intake

2. Oxygen therapy (Pao2 = 66-70 mmHg Sao2>90%)(CpAp-Mecliancal Ventilution)

3. Surfactant Therapy

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Initial Care

• Maintain warmth- cold stress will mimic other causes of distress

• Monitor blood glucose levels- assure they are normal

• Provide enough oxygen to keep the baby pink

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Initial Care

Ensure adequate hydration:• Start fluids at 70-80 ml/kg/d 10% glucose

solution• Smaller babies may need more fluid• Add electrolytes by the second day

• On day 3-4 watch for diuresis

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Initial Care

Consider other etiologies:• INFECTION,INFECTION

– Evaluate– Begin antibiotic therapy as prophylaxis– Continue as clinically indicated

• Anatomic malformations

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Assess circulation

• Monitor heart rate• Assess Blood pressure• Check peripheral perfusion and capillary

refill• Avoid excessive blood sampling

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Respiratory DISTRESS(NICU)Respiratory

RateFio2 Expiratory

Grunt Lowerchest Retraction

Xiphoid Retraction

0 60min <.30 None None None

1 60-80/min .30-.40 Stethoscope only

Just visible Just visible

2 >80min >040 Naked ear Marked Marked

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.

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CPAP Indications

• FiO2 above 0.3 with clinical distress

• FiO2 above 0.4

• Significant retractions after extubation• Hypoventilation: CPAP may be helpful

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CPAP risks

• Hard to control in spontaneously breathing baby, especially if vigorous or close to term

• Potential for airleak• Can’t give surfactant• May rarely worsen ventilation

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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

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Mechanical Ventilation• FiO2 more than 0.35 -0.4 on CPAP

• Early treatment if condition is deteriorating

• Decreasing “work of breathing”• Frequent apnea• Plan to give surfactant therapy• Absolutely: for prolonged apnea or

hypoxemia in absence of heart disease

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Mechanical ventilation - risks

• May require sedation, reducing spontaneous respiration

• Airleaks , especially as compliance improves

• Baro-Volutrauma and risk of chronic lung injury

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ExogenousSurfactant Preparations

•Alveofact*: bovine lung surfactantextract

•Curosurf: porcine lung surfactant extract, lipids

•Exosurf Neonatal*: colfosceril palmitate, cetyl alcohol, tyloxapol

• Infasurf: calf lung surfactant extract

•Survanta: bovine lung surfactant extract, lipids

*Not Available in USA

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Functions of SurfactantAssociated Proteins

• Hydrophilic– SP-A: tubular myelin, host defense– SP-D: surfactant lipid homeostasis,

host defense, antioxidant

• Hydrophobic– SP-B: surface tension reduction,

tubular myelin, type II cell functions– SP-C: surface tension reduction,

film stabilityLeVine et al, 2001

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Before SurfactantTreatment

45 MinutesPost-Treatment

Radiographic Changes WithExogenous Surfactant Treatment

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Relationship of Antenatal Corticosteroidsand Postnatal Surfactant

Neonatal Mortality

Jobe et al, 1993

17.715.2

24.9

0.5

0

5

10

15

20

25

30

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Maternal Corticosteroids No Maternal Corticosteroids

Mor

talit

y (%

)

Surfactant No Surfactant

**

**

57 46 555 566

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Multi-Dose Studies Two-Year Follow-Up Survanta® (beractant)

Respiratory Complications

Survanta Multi-Dose Study Group, 1994

13.3

20.2

4.4

6.9

3

16

3.51.8

11.1

0.2

0

5

10

15

20

25

Allergies ReceivingBronchodilator

ReceivingOxygen

Wheezing Tachypnea

%

Control Survanta

**

**

201 226 201 225 202 226 203 226 203 226

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Multi-Dose Studies Two-Year Follow-Up

Survanta® (beractant)CNS Complications

6.9 6.4

1.5

14.3

4.9 5.3

2.7

8.9

0

5

10

15

20

25

Hydrocephalus Shunt Seizures Cerebral Palsy

%

Control Survanta

201 226 201 226 201 226 201 226

Survanta Multi-Dose Study Group, 1994

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Transien tachypnea of the Newborn(T.T.N)

Wet lung, RDSII, Mild HMD

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• Delayed resorption of fetal lung fluid Risk Factors:

1- delayed in cord clamping2- c/s delivery 3- term- preterm neonates 4- the mother who received excessive fluid befor

delivery.

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Signs & symptom

• Mild respiratory distress present at birth or a few hour after birth

• ABG Normal or mild hypoxia & Acidosis

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C.XRay:•Overaeration , flat-

diaphragms, prominent pulmonary vacular marking sometimes fluid lines present in the fissures.

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• Delayed resorption of fetal lung fluid

Most consider, and rule out pneumonia• Treat with antibiotics if diagnosis is

uncertain–Oxygen need beyond six hours–Oxygen need increasing–Worsening symptoms

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• Patients usually recover rapidly between 3-5 days

• Treatment= supportive therapy.

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MECONIUM ASPIRATION SYNDROME (MAS)

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Approximately 13% of All live births are complicated by MSAF5% of MSAFMAS

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MSAF>Term, post term, IUGRMSAF< Preterm <34 weeks

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Risk factors for meconium- stained amniotic fluid

• Maternal hypertension • Maternal diabetes mellitus • Maternal heavy cigarette smoking• Maternal chronic respiratory or

cardiovascular disease• Postterm pregnancy• Pre-eclampsia/ eclampsia

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

patterns

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•MAS

Mild Less than 40% O2 < 48H

Moderate More thon 40% O2>48H No air leak

Severe Assisted ventilation >48 PPHN

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Mechanism of injure:

1. Obstruction of air ways

2. Chemical pneumonitis

3. Vasoconstriction of pulmonary vessels

4. Inactivation of surfactant

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Management :

1. Fetal heart rate monitoring (Fetal Pulse oximetry)

2. Amnioinfusion

3. Intrapartum suctioning

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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 O2 ( as necessary )

NO

NO

Yes

Yes

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Treatment in NICU:

• Oxygen Therapy• Surfactant Therapy• Inhaled Nitric oxide • ECMO

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پنومونی در نوزادان

شايع ترين علت HMDپنومونی بعد از ديسترسی تنفسی می باشد و

شامل :

I پنومونی مادر زادی و داخل -رحمی

II – پنومونی موقع تولد يا آسپيراسيون

III پنومونی بعد از تولد -

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-Iپنومونی مادر زادی

راه انتقال از طريق جفت می باشد .

عامل بيماريزا : عفونت های مادر ( ، ترپونما پاليدوم TORCHزادی )

) ادنو مايکوپالسما و گاها ويروس ها می ويروس ها و آنترو ويروس ها (

باشند

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عالئم

در ساعت های اول پس از تولد •ظاهر ميشود .

عالوه بر گرفتاری ريه ، گرفتاری در • –ساير احشاء نظير بزرگی کبد

طحال ، تظاهرات جلدی )پتشی( و اختالالت عصبی موجود است .

نوزادان يا مرده متولد ميشوند و يا در •عرض چند ساعت اول حيات فوت می

کنند .

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II – پنومونی موقع تولد يا آسپراسيون

راه انتقال کانال زايمان می باشد . عامل بيماريزا : ميکروبهای موجود

، GBSدر کانال زايمانی : نظير E.coli . می باشند .... ،

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عالئم :ظهور عالئم از چند ساعت تا چند

روز پس از تولد متغيراست و می باشد .HMDبيشتر شبيه به

عوامل مساعد کننده : ، زايمان PROMپرماچوريتی ،

مشکل می باشند

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III – : پنومونی بعد از تولد

راه انتقال : تماس با افراد آلوده و يا وسائل آلوده در بخش نوزادان می

باشد .

C.O.N.S ، C.O.P.Sعامل بيماريزا : اکثرا ( ، قارچ ها RSVو گاها ويروس ها )

) پس از اقامت زياد در بخش ( و کالمد يا می باشند .

عالئم : ظهور عالئم در خالل ماه اول حيات می باشد

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: تشخيص

شرح حال •عالئم بالينی •آزمايشگاهی •گرافی قفسه صدری •

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: درمانI – 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 کالمديائی ارتيرومايسين يا تری سولفامتوکسازول –متوپريم

3-4طول مدت درمان ، در پنومونی استافيلوکوکی روز است.14-10 در ساير جرم ها –هفته

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