Neonatal jaundice

Introduction - Prolonged neonatal jaundice:

è Jaundice > 2 weeks in term & > 3 weeks in preterm.
- Jaundice: è Unconjugated:
è Yellowish discoloration of skin, sclera, mucus membrane
P Physiological or breast milk jaundice.
due to increase serum bilirubin > 2 mg/dl. P Infection (UTI), Hypothyroidism, Crigler-Najjar syndrome.
è Jaundice appear clinically when ser. bilirubin > 5 mg/dl.
P Hemolytic anemia (G6PD deficiency).
P High obstruction (pyloric stenosis).
- Types of hyperbilirubinemia: P Trisomy 21.
è Unconjugated (indirect): high TB and mainly indirect.
è Conjugated:
è Conjugated (direct): high TB and mainly direct.
P Bile obstruction (Biliary atresia, Choledochal cyst)
P Neonatal hepatitis (TORCH, galactoasemia, CF, tyrosinemia I).

Unconjugated hyperbilirubinemia
- Causes:
- Types of neonatal jaundice è # Production:
P Hemolytic disease:
§ Isoimmune (Rh or ABO incompatibilities).
§ Non-immune (G6PD deficiency, H. spherocytosis,
alpha thalassemia, pyruvate kinase deficiency).
P Extravasated blood (cephalohematoma, IC HgE).
P Polycythemia, sepsis.
è $ Uptake: gilbert syndrome.
è $ Conjugation (glucuronyl transferase enzyme):
P Crigler-Najjar syndrome I (absent) & II (deficient).
P Immature: preterm baby.
P Under stimulated: hypothyroidism, galactosemia.
P Inhibited: breast milk jaundice.
è # EHC: pyloric stenosis, breastfeeding jaundice.
è Drugs: sulfonamide, indomethacin.
 Neonatal jaundice

è Rhesus incompatibility: P Investigation:

P Occur when the mother is Rh - & the baby is Rh +. § Blood group and Rh.
P Pathophysiology: § CBC: decrease hemoglobin.
§ TB and SBR: increase TB and increase indirect.
§ Retic count: increase.
§ Coombs test (direct): positive.

§ When the mother is Rh – and the fetus is Rh +. P Prevention:

§ Isoimmunization happens when fetal blood is § Anti D (IM) to Rh – ve mother and Rh + fetus
exposed to the mother blood (FMT). § Given within 72 hours after delivery.
§ Mother develop IgM = cannot cross placenta.
§ In the subsequent pregnancy, if the fetus is Rh +. P Treatment:
§ The mother now develops IgG = can cross placenta. § Adequate resuscitation
§ The result is extravascular hemolytic anemia. § Phototherapy and exchange transfusion.

P Causes of RBC Transfer “A break in the barrier” è ABO incompatibility:

§ Abortion, ectopic pregnancy P Mother’s blood group O & Infant’s blood group A or B.
§ Partial molar pregnancy, Blighted ovum P Maternal anti A or anti B IgG cross the placenta and
§ Antepartum bleeding cause hemolysis in infant.
§ Postpartum (Rh + baby) (MC period to have FMH) P Generally, less severe than rhesus disease but might
§ Procedures (amniocentesis, cordocentesis, CVS). affect first baby.
§ Platelet transfusion, transfusion Rh + blood. P Still cause significant hemolysis (anemia) and
hyperbilirubinemia.
P Clinical presentation: P Treatment: phototherapy or exchange transfusion.

è Crigler-Najjar syndrome (AR):

Type I Type 2
Absent glucuronyl transferase Partial decrease.
Severe type: kernicterus, death. Less severe than type I.
Unresponsive to phenobarbitone. Responsive to phenobarbitone trial.
Treatment by exchange transfusion Treatment by phenobarbitone.
and phototherapy
 Neonatal jaundice

è Gilbert syndrome (AD): - Investigation:

P Epidemiology: MC inherited disorder of bil. Meta.
P $ UDP glucuronosyltransferase activity & conjugation
P Clinical features:
§ Recurrent episodes of mild jaundice
§ Provoked by stress (febrile ill, fasting, dehydration,
vigorous exercise, menstruation, surgery)
P Diagnosis:
§ # Unconjugated bilirubin.
§ Normal CBC, blood smear, reticulocyte count.
§ Normal AST, ALT, alkaline phosphatase.
P Treatment: benign, no treatment required.

è Breast feeding & breast milk jaundice:

- Treatment:
è Determined by plotting the total bilirubin
level on graph of bilirubin against age in
hours this will determine if:
P No treatment needed.
P Treatment by phototherapy.
P Treatment by exchange transfusion.

è Phototherapy:
P Blue – green light (wavelength 425 – 475nm)
P Converts the toxic bilirubin (indirect) by photo-
oxidization & isomerization into harmless water
soluble pigment (lumirubin) excreted in bile & urine.
P Indication:
§ If bilirubin level above phototherapy line.
§ During waiting for exchange transfusion.
P Contraindication: in case of direct hyperbilirubinemia,
because will lead to bronze baby syndrome.
 Neonatal jaundice

P Technique: P Complication:
§ Infant should be undressed expect eyes & genitalia § Hypocalcemia, metabolic acidosis, hyperkalmeia.
§ The lamp should be 45cm above the infant. § Heart failure.
§ The infant should be turned every 2 hours. § Hazards and blood transfusion infection (HBV, HIV).
§ Increase frequency of feeding or IVF (10-20%). § Complication of UVC (sepsis –thrombosis).
§ Monitor temperature and hydration state.
§ TB – SBR every 6 hours. è Intravenous immunoglobulin (IVIG): can be used in Rh
disease or ABO incompatibility when total bilirubin levels
P Complication: are rising despite continuous multiple phototherapy or
§ Dehydration (hyperthermia). level is near exchange transfusion level.
§ Diarrheal (watery), hypocalcemia.
§ Dermatitis (macular rash and erythema). - Complication (Kernicterus):
§ Damage to retina and genitalia. è Pathologic term that refers to yellow staining of the brain
§ If used in direct jaundice, bronze baby syndrome. (basal ganglia & brainstem) with irreversible brain damage.
è Factors increases risk of kernicterus:
è Exchange transfusion: P # BBB permeability: preterm (VLBW), acidosis, sepsis,
P Benefits: hypoxia (asphyxia), anemia.
§ Removes toxic unconjugated bilirubin. P Long duration of exposure to increase bilirubin.
§ Removes antibodies & correct anemia. P Completion for binding site (displacement from albumin):
§ Drugs (aspirin – gentamycin).
P Indication: § Hypoalbuminemia.
§ Rh and ABO incompatibility. § Hypothermia & Hypoglycemia.
§ If bilirubin level high (# risk of kernicterus).
§ May be also done in sepsis and NEC (rare). è Clinical manifestation:
P Acute encephalopathy:
P Procedure: § Early (LMN):
§ Amount: double blood volume (2 x 80 ml/kg). v Hypotonia, lethargy, poor feeding
§ Type: fresh blood O -ve. v High pitched cry, lost Moro and suckling reflex.
§ Small amount of blood (10-20 ml) are removed &
replaced by equal amount through UVC. § Late (UMN):
§ IV D10% and Ca gluconate are given at 100 ml v Hypertonia, arched back (opisthotonus).
blood intervals. v Seizures, coma and may die.
 Neonatal jaundice

P Chronic encephalopathy: - Clinical presentation:

§ Choreoathetoid, cerebral palsy, upward gaze palsy. è Skin and sclera: greenish in color.
§ Learning difficulties, SNHL, MR, seizures. è Color of urine: dark.
è Color of stool: pale.
è Prevention: è Hepatomegaly, liver dysfunction, malabsorption, FTT.
P If bilirubin toxicity is suspected treatment is an è No risk of kernicterus.
immediate exchange transfusion.
P Prevention and treatment of risk factors. - Investigation:
P Treatment: no curable, only supportive. è TB- SBR.
è LFT.
Conjugated hyperbilirubinemia è Ultrasound abdomen.
è TORCH screen.
- It’s a sign of hepatobiliary dysfunction. è Sepsis screen.
- Its defined as
è Direct > 15% of total bilirubin.
- Treatment: treatment the underlying cause.
è Direct > 1.5 - 2 mg/dl
è Increase > 0.5 mg/dl/hr.
Biliary atresia
è Increase > 5 mg/dl/day.
- Biliary atresia is characterized by obliteration or
- Causes: discontinuity of extrahepatic or intrahepatic biliary ducts,
è Obstruction: biliary atresia, choledochal cysts. lead to obstruction of bile flow.
è Infection: TORCH, viral hepatitis (A, B, C), sepsis.
è Genetic: Alagille syndrome, cystic fibrosis, alpha 1- - Groups:
antitrypsin deficiency, tyrosinemia. è Isolated biliary atresia 65-90%.
è Metabolic: galactosemia, rotor syndrome, dubin- è Associated with situs inversus and polysplenia 10-35%.
johnson syndrome, progressive familial intrahepatic
cholestasis. - Types:
è Idiopathic neonatal hepatitis. è Type I: obliteration of common duct.
è Type II: atresia of hepatic duct.
è Type III (90%): atresia of right and left hepatic ducts.
 Neonatal jaundice

- Epidemiology: - Complication:
è Incidence: 1:10000-15000 live births. è FTT, ascites, bleeding.
è Race: more in black – Asian population. è Liver cirrhosis & portal HTN.
è Sex: more in females. è Hepatic encephalopathy, death (HF).
è Present in neonatal period (1st 2 weeks of life).

- Clinical presentation (neonatal cholestasis):

è Early:
P Jaundice (in the 1st 2 weeks), may delayed up to 8 w.
P Dark urine and pale stool.
P Hepatomegaly.
è Late:
P Deep jaundice.
P Biliary cirrhosis: ascites, portal HTN, splenomegaly,
clubbing, itching.
P Fat malabsorption: $ fat soluble vitamin (ADEK) = FTT.

- Investigation:
è TB-SBR (increase direct).
è LFT (increase ALP and GGT).
è US abdomen: absent GB and exclude choledochal cyst.
è HIDA scan: good uptake but failure to excrete to
intestine.
è ERCP or MRCP.
è Intraoperative cholangiography (definitive).

- Treatment:
è Kasai operation
P Hepato – porto – enterostomy.
P Successful if performed < 2months age.
è Liver transplantation.
 Introduction, Pre & Postmaturity

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Introduction to neonatology Skin:

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è Color = pink (acrocyanosis normal 1st day).
- Neonatal period: è May be covered by vernix caseosa.
è The 1st 28 days of life.
è Transient skin manifestation may be present (no Rx).
è Early neonatal period: birth - 7th day. Lesion Description
è Late neonatal period: 7th - 28 day . Milia • White papule on the nose, cheeks
• Due to obstruction of sebaceous gland, resolve spontaneously.
- Gestational age: Miliaria • White crops over the scalp and face
è Time from the 1st day of LMP. • Due to obstruction of the sweat gland
Erythema • Pustular rash on erythematous base on the trunk and face,
è Pattern: before 37 weeks of gestation.
toxicum appear at 2-3 days of age, the fluid contains eosinophils
è Term: between 37 and 42 weeks of gestation. • Usually disappear within 5-7 days
è Post term: after 42 weeks of gestation. Mongolian • Blue/black macular discoloration at lumbosacral area and
spots buttocks more common in black –fade over 1st few years
- Birth weight: • Differential diagnosis is child abuse or bruises.
Cutis • Reticular vascular pattern over most of body when the baby is
è Normal birth weight = 2.5-4.5 kg.
marmorata cooled, improves over 1st month abnormal if persists.
è Low birth weight (LBW) = < 2500 g.
Salmon • Pale, pink macules
è Very low weight (VLBW) = < 1500 g. patch • Usually disappears with time.
è Extremely low weight (ELBW) = < 1000 g. Pustular • More common in black neonates smear from pustules reveals
è SGA: birth weight <10th centile for GA. melanosis neutrophils and resolves spontaneously.
è LGA: birth weight > 90th centile for GA. Neonatal • Multiple - yellowish white papules - located over the nose,
Large of Gestational & Acne • Due to normal physiological response to maternal hormones
age

Neonatal physiology normal variations

- Anthropometric measurement:
è Birth weight = 2.5 – 4.5 kg. Physiological weight loss
è OFC = 35 ± 2 cm.
Head circu
• Loss 10% of BW in 1st 3-5 days
• Regain it in age 10 days
è Length = 50 cm. • Normal weight gain 25-30 g/d

- Vital signs: è Pathological skin lesions

è Heart rate P Port wine stain: Sterger Weber & Klippel–Trénaunay
è Respiratory rate P Strawberry hemangioma: present after 1 month and
è Blood pressure increase until 3 – 15 months then regress.
P Club foot, extra digit, natal teeth, abnormal head shape.
 Introduction, Pre & Postmaturity

- Head: - Chest and respiration:

è OFC = 35 ± 2cm. è Normal RR = 40-60 breath/minute.
è Fontanelle: è Type = periodic breathing, irregular in rate and depth.
P Anterior closed at 9 - 18 months. è Is obligatory nasal breathing and mainly abdominal.
P Posterior closed at birth - 2 months. è Breath sounds is broncho-vesicular breathing.
è Sutures: è Breast size about 4-20 mm in term newborn.
P Coronal – sagittal – lambdoidal – metopic. è Neonatal gynecomastia:
P Moulding (overlapping) may present at birth. P Seen in both girls and boys (breast enlargement)
è Caput succedaneum and cephalohematoma. P May secrete small amount of milk (witch’s milk).
P Its due to withdrawal of maternal hormones.
- Eyes: P Start in the 1st week and resolves within few weeks.
è Pupillary light reflex is present at birth. P Don’t squeeze (risk of mastitis and breast abscess).
è Absent of tear. P Resolves without treatment.
è Red reflex: should be examined for all newborns.
è Ophthalmia neonatum: in the 1st 48 hours (gonococcal). - Cardiovascular system:
è Subconjunctival hemorrhage: due to precipitate è HR = 110 – 160 beats/min.
deliveries – harmless and resolves within weeks. è Apex beat: lies in the 4th ICS midclavicular line.
è Blood pressure: 70/50 mmHg in neonate.
- Mouth: è Innocent murmur: systolic, soft, short, grade 1-2.
è Epstein’s pearls: cyst on palate/gum (self-resolving). è Normal blood volume in term infant (80-85 mL/kg).
è Tongue – tie.
è Ranula: mucous cyst in the mouth floor (self-resolve). - Abdomen and genetalia:
è Bohn’s nodule: mucus gland cyst. è Umbilical stump: dry, loughs down between 7-10 days of age.
è Umbilical cord contains 2 arteries and 1 vein.
- Neck: è Gentalia in boys: scrotum well develop.
è Normally the neck of a newborn is short. è Gentelia in girls: labia mijora cover labia minora.
è Neck webbing (in turner & Noonan's syndrome). è Vaginal bloody discharge: due to maternal hormonal withdraw.
è Neck swelling:
P Central: thyroglossal cyst Delayed passage of meconium Delayed passage of urine
(normally 1st 24-48 of life) (normally 1st 24, 1-3 mL/kg/h)
P Peripheral: SCM tumor, cystic hygroma, LN
Anal atresia (imperforated anus). Renal agenesis
Hirschsprung disease. Renal outlet obstruction
Meconium ilius (CF). Shocked neonate
Organic obstruction (IO).
 Introduction, Pre & Postmaturity

Newborn screening
- Investigation should done to all newborns.
- A blood sample, usually a heel prick.
- Taken when feeding has been established on day 5.
- Tests:
è Congenital hypothyroidism
è Sickle cell and thalassemia
è Cystic fibrosis.
è Phenylketonuria, MCAD
è Maple syrup urine disease
è Isovaleric acidemia, glutaric aciduria, homocystinuria

Neonatal resuscitation Prematurity

- High risk deliveries: - Preterm: baby born before completed 37 weeks of gestation.
è Preterm deliveries.
- Incidence ≈ 6-8% of all births.
è Cesarean section delivery.
è Meconium stained amniotic fluid.
- Causes:
è Maternal diabetes.
è Idiopathic (most common) 40%.
è Diminished fetal activity or known fetal malformation.
è Maternal factors: extreme age and chronic disease.
è Multiple gestation, polyhydramnios, oligohydramnios.
è Fetal factors: twins and congenital infection.
è Obstetric factors: polyhydramnios.
- Resuscitation steps:
è Place to newborn under radiant warmer.
- Features of preterm newborn:
è Dry the newborn (wrap).
è Physical appearance:
è Suction the mouth (nose gently).
P Weight < 2.5 kg (expect IDM).
è Evaluation of the newborn by APGAR scoring system.
P Birth length < 47cm.
P At 1 min and 5 min and every 5 minutes thereafter as
P OFC < 33cm.
long as the resuscitation is continuing. P Skin: thin, shiny – little S.C fat covered with lanugo hair.
P 1 min score: idea about method of resuscitation.
P Nails: don’t reach the finger-tip.
P 5 minute score: idea of response to resuscitation.
P Ear: soft – no cartilage – no recoil.
P If score < 7: ABC
 Introduction, Pre & Postmaturity

P Breast nodule: small <3 mm in diameter. - Management:

P Genitalia: è Senior pediatrician should be present at birth.
§ Males: smooth scrotum – undescended tests. è Place baby under radian warmer and dry infant.
§ Females: prominent clitoris. è Assess viable gestation: if needed resuscitate as for term
P Sole creases: no creases or just cover Ant 1/3. infant (electively intubate if very preterm).
è Complete examination and vitamin K IM.
è Physiological features: è Transfer to NICU: incubator care – thermal regulation –
P Weak sucking. IVF – antibiotic – treatment complication.
P Incoordination between sucking and swallowing. è Temperature control (avoid hypothermia):
P Growth: rapid growth. P Prevent heat loss.
P Weak activity. P Infant should be in “neutral thermal environment”.
P Weak crying. § Its range of environmental temp. at which oxygen O2
P Hypotonic with frog posture. consumption is minimal and growth is maximum.
§ Core body temperature of 37C.
- Complication of prematurity and etiology:
RS • Respiratory distress syndrome: surfactant deficiency
• Apnea of prematurity: immature respiratory center.
• Aspiration syndromes.
• Pneumothorax: positive pressure ventilation.
• Bronchopulmonary dysplasia: prolonged O2 therapy.
CVS • Patent ductus arteriosus è Feeding (dehydration – hypoglycemia):
GI • NEC: immature GIT & weak intestinal mucosal barrier.
P Methods: breast feeding, bottle feeding, tube feeding.
• GERD: immature LES (weak).
P Trophic feeding: feeding small milk volumes (0.5 – 1
NS • IVH: fragile and immature cerebral blood vessels.
• Kernicterus: immature BBB (blood brain barrier). mL/kg/hour) to enhance gut structure & function in infants
• Hypoxic ischemic encephalopathy: decrease O2. too ill or immature to tolerate substantive milk feeds.
• Retinopathy of prematurity: prolonged O2 therapy. P IVF: preterm baby needs more fluid than term baby
• Periventricular leukomalacia: perinatal cerebral hypoxia
Hemato • Anemia: $ life span RBC, $ iron store, # sampling
• Coagulopathy and DIC: defect in coagulation factors.
Immune • Increase infection (sepsis)
Renal • Impaired fluid and electrolyte homeostasis
• Hypocalcemia, hypokalemia, hypomagnesemia
Liver • Indirect jaundice, hypoglycemia, hypoalbuminemia
Temp. • Hypothermia: large surface area, little SC fat, immature
heat regulatory center, lack of shivering process.
 Introduction, Pre & Postmaturity

Complications of preterm - Patent ductus arteriosus (PDA):

è Failure of ductus arteriosus to close within 24 hours of birth.
- Respiratory distress (RD): è Clinical presentation:
è Clinical signs: apnea, desaturation.
P Small: asymptomatic.
è Prevention: antenatal dexamethasone / betamethasone.
P Large: poor growth, apnea, systolic murmur.
P 2 doses 12 – hourly, give to mother 1-7 days before.
è Treatment:
P Used at gestational age 24 to 34+6 weeks.
P Restrict fluids.
P Decrease incidence and mortality by 40%.
P Pharmacological closure (indomethacin).
è Treatment:
P Treatment HF and Surgical closure.
P Surfactant through ETT as early as possible.
P CPAP or Mechanical ventilation.
- Necrotizing enterocolitis (NEC):
è Syndrome of acute intestinal necrosis of unknown cause
- Intraventricular hemorrhage (IVH): usually affect sick preterm and VLBW newborn.
è Usually occur within 1st 72 hours of life.
è Incidence: 2-10% of VLBW, Mortality rate is 25-30%.
è Common with sever RDS or perinatal asphyxia.
è Risk factors (4 P’s):
è Prevention: antenatal dexamethasone / betamethasone.
P Prematurity, Perinatal asphyxia, Polycythemia, PDA, UVC.
è Clinical presentation:
P Feeding:
P Asymptomatic 50%
§ Rapid increase enteral feeding.
P Symptomatic: pallor, jaundice, bulging AF, apnea,
§ Bottle feeds > breast feeds.
convulsion, collapse, death. § Hyperosmolar milk feeds.
è Diagnosis: US, CT scan.
è Treatment: supportive care NICU, blood transfusion.
è Clinical presentation (onset 1-2 weeks of life):
P Early: vomiting (bilious), feeding intolerance,
- Periventricular leukomalacia (PVL): abdominal distension, bloody stool.
è Occurs in up to 10% VLBW infants.
P Late (features of sepsis): temperature instability,
è Cerebral hypoxia/ischemia: causes bilateral necrosis of
jaundice, apnea, bradycardia, lethargy, abdominal
periventricular white matter. tenderness & erythema, hypoperfusion and shock.
è Clinical presentation:
P Early asymptomatic.
è Investigation:
P Late 6-8 weeks: cognitive & behavior disability,
P Laboratory:
diplegic cerebral palsy (80 – 90%). § CBC ($ platelets $ RBCs # WBCs), # CRP, blood C & S.
è Treatment: supportive.
§ Urea and electrolytes – ABG (metabolic acidosis).
 Introduction, Pre & Postmaturity

P Radiological findings: - Retinopathy of prematurity:

§ X-ray abdomen: è Abnormal retinal vascular proliferation which lead to
v Intramural air “Pneumatosis retinal detachment and blindness.
intestinalis” (specific sign). è Risk factors: VLBW, preterm.
v Dilated loops of bowel “Tram-Tark sign”. è No warning sign, so ophthalmic screening is mandatory.
v Air under diaphragm “Pneumoperitoneum”. è Management:
v Free peritoneal gases “Football sign”. P Prevention: low O2 for the least time.
v Portal vein gases. P Treatment: laser therapy, anti-VEGF.
P Abdominal ultrasound. Oxygen therapy in preterm infants:
• Oxygen therapy should be provided to correct hypoxaemia.
• In neonatal resuscitation, recommended to start with 21%-30% oxygen.
è Treatment: • Avoid Low saturations (<91%): # risk of NEC and death.
P Admission to NICU. • avoid high saturation (>95%): # risk of retinopathy of prematurity.
P NPO – IVF – nasogastric tube on free drainage.
P IV antibiotic (3rd cephalosporin + metronidazole). - Pneumothorax
P Systemic support (O2 – IPPV – correct BP). è Air leaks into the pleural cavity
P Surgical: GI perforation or obstruction, failed medical. è Causes: iatrogenic (MV -Ambu bag), server RDS
è C/P: sudden deterioration, apnea, desaturation, cyanosis, death.
è Prevention: è PE absent air entry in affected side.
P Avoid aggressive feeding. è Diagnosis: chest x ray.
P Breast feeding decrease incidence of NEC. è Treatment:
P Antenatal steroid. P Immediate needle decompression.
P Early treatment of risk factors (sepsis). P Subsequent insertion of a chest drain.

- Bronchopulmonary dysplasia - Late onset complications

è Definition: O2 dependence at 28 days. è 5%-10% of VLBW infants develop cerebral palsy, but the
è Causes: lung damage due to pressure and volume most common impairment is learning difficulties.
trauma from assisted ventilation and O2 toxicity. è Hearing impairment, with 1%-2% requiring amplification.
è Clinical presentation: dyspnea, O2 dependence, FTT. è Visual impairment, with 1% blind in both eyes, refraction
è CXR: generalized opacity, lung collapse, cystic changes. errors and squints are common.
è Complication: recurrent chest infection & wheezy chest. è At an increased risk of respiratory failure from
è Prognosis: death rate (10-20%) due RF. bronchiolitis and other LRTIs especially if one has BPD
 Introduction, Pre & Postmaturity

Post maturity Intrauterine growth restriction (IUGR)

- Baby born after 42 completed weeks of gestation. - Failure of a fetus to achieve genetic growth potential.
- Causes: - Most of IUGR are SGA, although the two terms aren’t synonyms.
è Unknown (most common).
è Mother with previous history of post term delivery. - Types:
è Anencephaly. è Symmetrical IUGR
P Weight, length and OFC all < 10 centile.
- Features: P Onset usually early (1st trimester).
è Face: open eyes, alert, abundant scalp hair. P Fetal anomalies are common.
è Skin: dry, wrinkled, peeling, meconium staining. P Cause:
è Nails: ling nails. § Chromosomal disorders: trisomy (13,21,18).
è Weight: average or decreased. § Congenital malformation.
§ Congenital infection “TORCH”.
- Complication: P Bad prognosis.
è Perinatal asphyxia, Polycythemia, MAS.
è Hypocalcemia, hypoglycemia. è Asymmetrical IUGR:
è Persistent pulmonary HTN. P Weight is much more affected (head sparing).
P Onset usually late (2nd - 3rd trimester).
Large for gestational age (LGA) P Fetal anomalies less common.
P Causes:
- LGA: birth weight > 90th centile for GA. § Maternal disease:
- Causes: v Undernutrition.
è Constitutional: large parents (most common).
v DM – preeclampsia.
è Infant of diabetic mother (IDM).
v Smoking or alkaline.
è Beckwith-Weidman syndrome.
§ Placental insufficiency:
è Hydrops fetalis.
v Preeclampsia.
v Multiple gestation.
- Complication: v Antiphospholipid syndrome.
è Birth injury.
P Good prognosis.
è Hypoglycemia (IDM).
 Introduction, Pre & Postmaturity

- Complication
è Birth asphyxia, MAS.
è Hypoglycemia (decrease glycogen stores).
è Hypothermia (decrease weight SC fat).
è Polycythemia (chronic hypoxia intrauterine).
è Thrombocytopenia, coagulopathy.

- Management
è Routine postnatal care.
è Attention to thermal care and blood sugar.
è Admit to NICU if birth weight < 1800 g.
è Discharge when:
P Sucking well
P Weight gain
P Body temperature is maintained at room temp.
P Mother is capable to care for infant.
 Neonatal Respiratory Distress

Respiratory distress è CNS:

P Perinatal asphyxia.
- Signs of respiratory distress: P Intracranial hemorrhage .
è Tachypnea.
è Others:
è Recession (SC – IC – SS).
P Congenital diaphragmatic hernia.
è Nasal flaring.
P Metabolic acidosis.
è Grunting.
P Severe anemia.
è Cyanosis.
P Hypoglycemia – hypothermia – polycythemia.

- Respiratory: Respiratory distress syndrome (RDS) “Hyaline membrane disease”

è Lungs:
P Respiratory distress syndrome (RDS). - Most common respiratory illness in NICU
P Meconium aspiration syndrome (MAS). - Occurs mainly in premature neonate (may affect term babies).
P Transient tachypnea of newborn (TTN). - Cause: surfactant deficiency.
P Pneumonia (congenital). - Major cause of morbidity and mortality in preterm infant.
P Congenital emphysema. - Incidence and severity of RDS are related inversely to
P Chronic lung disease (CLD). gestational age of newborn infant
P Pulmonary hemorrhage. è 26-28 weeks' gestation: 90%
P Lung hypoplasia, lung collapse. è 30-34 weeks' gestation: 20-30%
è Airways:
P Choanal atresia (bilateral). - Surfactant
P Subglottic stenosis. è Produced from pneumocytes Il.
P Pierre robin syndrome. è Starting at 22 weeks and mature at 35-36 weeks.
P Trachea-oesophageal fistula. è Appeared in AF at 34 weeks.
è Pleura: è Composition of surfactant:
P Pneumothorax. P Lipid (90%):
P Pleural effusion. § Phosphatidylcholine (lecithin) about 80%.
§ Phosphatidylglycerol about 10%.
- Non respiratory: § Neutral lipids and phospholipids about 10%.
è CVS: P Surfactant proteins (10%): (A,B,C,D).
P CHD. è Recycling and regeneration (including externally given
P Heart failure. surfactant)
 Neonatal Respiratory Distress

è Function: - Diagnosis
P It decreases alveolar surface tension. è Based on HX of prematurity + signs + characteristic x-ray.
P Equalizes tension in alveoli of different size. è Signs
P Increases lung compliance. P Tachypnea > 60 RR.
P Retraction (SC, IC, SS).
- Assessment of Fetal Lung Maturity P Grunting.
è Lecithin/sphingomyelin (L/S) ratio P Nasal flaring.
P >2.5 mature lung P Recurrent apnea’s.
P 1.5-2 transitional lung P Duskiness, Cyanosis.
P <1.5 immature lung. P Bilateral crepitation, bilateral decreased air entry.
è Lamellar body counts (most available)
è Phosphatidylglycerol: after 35 GA (most accurate) è Chest X-ray
P Ground glass appearance.
- Risk factors Risk of RD reduced in: P Air bronchograms (interstitial edema).
è Prematurity • IUGR. P Reticulogranular shadows.
è C/S delivery • Maternal smoking P White-out lungs (late).
• Narcotic addiction.
è Maternal DM
• PROM.
è Asphyxia and stress è ABG:
• Antenatal steroids.
è Second twin, white race, male • Female sex. P Mild RDS: hypoxemia
è Sepsis, hypothermia, acidosis. P Severe RDS: $ PaO2 – # PaCO2 – $ PH.

- Physiologic abnormalities è Septic work up workup.

è Decrease alveolar ventilation
è Reduce lung volume - Complications
è Decreased lung compliance è Pneumothorax
è V/Q mismatch è PIE
è Decreased oxygenation and air exchange è Chronic lung disease
è VAP/ Sepsis
è Pulmonary hemorrhage
è IV access complications
è Intraventricular hemorrhage, PDA, NEC
è Bronchopulmonary dysplasia
 Neonatal Respiratory Distress

- Prevention Meconium aspiration Syndrome (MAS)

è Antenatal glucocorticoids
P Agents: betamethasone or dexamethasone
- Definition: its severe respiratory distress in post term and
P Dose: 2 doses 12 hours apart.
full term babies exposed to intrauterine asphyxia.
P Given between 24-34 weeks’ gestation.
- Pathophysiology:
è Intrauterine asphyxia
P Enhances lung maturity.
è Paralysis of anal sphincter
P Stimulate phospholipid and surfactant synthesis
è Meconium stained liquor
P All pregnant mothers at risk for preterm delivery
è Meconium aspiration
below 34 weeks’ gestation should receive ACS
è Complete airway obstruction (collapse)
è Prophylactic surfactant.
è Incomplete airway obstruction (air trapping)
P Given immediately after birth to extremely preterm.
è Subsequent chemical pneumonitis or secondary infection.
P Type 1: natural (survanta, curosurf).
P Type 2: synthetic.
P Route: through ETT, 4mL/kg , 2 doses (12 hour apart).
- Risk factors:
è Perinatal asphyxia.
P S/E: bradycardia, pulmonary Hge, pneumothorax
è Oligohydramnios.
è Elective intubation.
è Maternal infection and chorioamnionitis.
è Early use of CPAP or mechanical ventilation.

- Treatment - Mechanism of distress:

è Chemical pneumonitis
è Respiratory support via NC, CPAP, MV.
è Surfactant deactivation
è Oxygen therapy to maintain target sat 90-95%
è Ball valve air trapping
è Surfactant through ETT
è Atelectasis
è IV hydration
è V/Q mismatch
è IV antibiotics
è Hypoxia/ acidosis
è Respiratory stimulants
è Pulmonary HTN.
è Vitamin A

- Diagnosis (clinical & radiological):

è Clinical presentation:
P Severe RD with grunting and cyanosis.
P Meconium staining of skin nails and umbilical cord.
P Ronchi or crepitation on auscultation.
 Neonatal Respiratory Distress

è Chest x-ray: - Diagnosis:

P Hyperinflated chest. è Clinically:
P Patchy consolidation and collapse. P Mild RD within few hours after birth.
P Pneumothorax. P Spontaneous resolution within 24-72 hours.
è Chest x-ray:
- Care at delivery (delivery room): P Prominent perihilar vascular marking.
è No airway suction at the perineum by OB. P Fluids in the fissures (wet lung disease).
è Vigorous babies: routine care.
è Non-vigorous babies: suction of the mouth before giving Congenital diaphragmatic hernia
respiratory support or stimulation.
- Definition: its congenital malformation of diaphragm with
- Treatment: herniation of abdominal content into the thorax.
è Admission to NICU.
- The primary concern is not the diaphragmatic hernia itself
è Respiratory support: O2 & MV (avoid CPAP).
but the associated pulmonary hypoplasia.
è Surfactant through ETT.
- 50% of cases are asso. with other anomalies (NTD, 20% CHD).
è IVF, IV antibiotics.
- Usually diagnosed antenatally (U/S), M:F = 1:1
è PPHN: sedation, NO, adequate BP & perfusion, ECOM.
- Types:
è Bochdalek (90%): posterolateral, Lt. (80%).
- Long term complications:
è Morgagni: retrosternal, Rt. (90%).
è Reactive airway disease (asthma)
è Persistent pulmonary hypertension (PPHN)
- Clinical presentation:
è Antenatal: polyhydramnios.
Transient tachypnea of newborn (TTN)
è Postnatal presentation:
- It’s self-limited respiratory distress in full term baby. P Severe RD immediately after birth.
- More in C/S deliveries. P Scaphoid abdomen.
- Related to delayed clearance of interstitial lung fluids. P Hear sounds on right side of chest.
- Usually, tachypnea without major signs of respiratory P Absence of left sided breath sounds.
distress or any O2 requirement. P Bowel sound on left side of chest.
- Resolves in 24-72 h. è CXR:
- May need respiratory support and NICU admission. P Loops of bowel in hemi thorax
- Risk factors: CS, maternal DM, maternal excess analgesia. P Mediastinal shift.
 Neonatal Respiratory Distress

- Management: - Treatment
è Resuscitation after birth: ETT and MV (avoid ventilation è Proper positioning
the baby with bag and mask à distension stomach). è Frequent suctioning
è IV line, NGT for decompression. è Minimize mechanical ventilation
è Surgical repair (stabilize Pulmonary HTN before). è HTS nebulization
è Postoperative respiratory support (NO, ECMO).
Pleural effusion
- Complication:
è Pulmonary hypoplasia (main concern, irreversible).
- Causes
è Hydrops
è PPHN.
è CHF
è GERD.
è Infection
è Chylothorax
- Prognosis: MR about 40% (due to pulmonary hypoplasia).

Congenital pneumonia - Chylothorax

è Etiology
- Sepsis risk factors P Idiopathic
è PROM P Post cardiac surgery
è Prematurity P Syndromic (Turner, Noonan’s)
è Maternal fever & chorioamnionitis. P Lymphangiectasia
è GBS colonization
è Fluid analysis
- Same signs of RDS P High lymphocyte count.
- CXR mimics RDS in GBS pneumonia. P High TG.
P Foamy appearance.
Atelectasis
è Treatment
- Risk factors P Respiratory support, NPO.
è Mechanical ventilation
P Aspiration/ Chest tube.
è Increased respiratory secretions
P Fluid replacement with Albumin, FFP.
è Impaired swallowing
P High MCT formula.
è Prolonged intubation
P Octreotide infusion or Pleurodesis.
è Immobilization.
 Neonatal Respiratory Distress

Choanal atresia Neonatal cyanosis

- Definition: its failure of completion of bucconasal - Is a clinical description of bluish discoloration of the skin
membrane breakdown in early life (bony or membrane). and MM due to presence of > 5g/dl of deoxy Hb in blood.
- Incidence: (1:8000) more common in female. - Types:
è Peripheral cyanosis:
- Types: P Acrocyanosis normal at birth.
è Unilateral (detected later in life). P Hypothermia.
è Bilateral: RD immediately after birth with and cyanosis P Shock.
P Worse: calm or feeding
P Improved: crying. è Central cyanosis:
P Pulmonary: RDS, MAS, CDH.
- CHARGE (60% associated with other congenital anomalies): P Cardiac: cyanotic CHD.
è C (coloboma) P Other: Polycythemia, Methemoglobinemia.
è H (heart defect)
è A (atresia) - If you have a newborn with central cyanosis and have low
è R (retardation of growth / development) O2 sta. ≤94%,: is it cardiac or respiratory disease?
è G (genital abnormalities) è Hyperoxia Test (Nitrogen washout test):
è E (ear deformity). P The infant is placed in 100% oxygen for 10 minutes
P Look for O2 sta. or PaO2 changes in ABG.
- Diagnosis: § If remains low = cyanotic CHD.
è Inability to pass NGT. § If improved = RD or PPHN
è Confirmed by CT scan. è Immediate management:
P Stabilize the airway, breathing, and circulation (ABC),
- Treatment: surgery. P Start prostaglandin E infusion (5 ng/kg per min).
P Urgent cardiac consultation, echocardiography
 Neonatal Respiratory Distress

Neonatal apnea
- Definition: pause (cessation) in breathing > 20 seconds.
- Causes:
è Apnea of prematurity:
P Central 40%.
P Obstruction 10%.
P Mixed 50%.
è Systemic disease: sepsis, IVH, NEC, anemia,
hypothermia, GERD, drugs (sedative), PDA.

- Management:
è Tactile stimulation and gentle oral suction.
è Positioning (ovoid extreme flexion or extension).
è Respiratory stimulant (theophylline, caffeine citrate).
è O2 supplement or ETT and MV.
è Good monitoring.