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31

What are the most common malformation syndromes  

– Down syndrome - 1:660

– XXY syndrome - 1:500 males

32

Preterm is considered what 

<37 wks 

33

Appropriate for gestational age (= AGA):

Is a birth weight between

10th and 90th percentile for GA. (gestational age) 

34

Low-birth weight (LBW) infants

 <2,500 g at birth

– Premature

and/or

– IUGR for their gestational age i.e. SGA.

35

Fetal causes of growth restriction

– Chromosomal disorders (17%)

– Congenital malformations

– Congenital infections (eg. TORCH)

36

Placental causes of fetal growth restrictions

– Placenta previa

– Placental abruption

– Placental infarction

37

Maternal causes of fetal growth restrictions

– Toxemia of pregnancy

– Chronic hypertension

– Alcoholism, narcotic abuse and smoking

– Drugs (dilantin)

– Malnutrition (esp. prolonged hypoglycemia)

38

SMOKING is associated with what birth defects 

• Spontaneous abortion

• Premature labor

• Low birth weight

• SIDS

• Placental abnormalities

39

Major risk factors for Prematurity

• Premature rupture of membranes

• Intrauterine infections

• Structural abnormalities of the uterus, cervix, placenta

• Multiple gestation

40

APGAR score 

41

How often is APGAR administered 

1min and 5 min 

1min- tests post toleration to birthing 

5min- tests toleration to new environment

42

Complications of Prematurity

• Hyaline membrane disease ( Respiratory distress syndrome)

• Necrotizing Enterocolitis

• Intraventricular and germinal matrix hemorrhage

• Long term sequelae, including developmental delay

43

Leading cause of morbidity and mortality among premature infants

Respiratory Distress Syndrome (RDS) of the New Born

(hylaine membrane disease) 

44

Risk factors for Respiratory Distress Syndrome (RDS) of the New Born

• Prematurity

• Perinatal asphyxia

• Maternal diabetes

• Cesarean section before onset of labor

• Twin gestation

• Male sex

45

Microscopic alterations in RDS timeline

First several hours- Necrotic cellular debris in terminal bronchioles and alveolar ducts

 If survives for 12-24 hours: Smooth homogenous pink membranes lining terminal and respiratory bronchioles and alveolar duct •Membranes are composed of necrotic alveolar type II pneumocytes and fibrin; neutrophilic inflammatory reaction is not associated with these membranes

infantdiesafter several days,: reparative changes, including proliferation of type II pneumocytes and interstitial fibrosis, is seen.

46

Prevention of RDS 

• Delay labor until lung matures

• Induce maturation (steroids)

• Evaluate amniotic fluid phospholipids

47

Long term sequelae of RDS 

– Retrolental fibroplasia (retinopathy of prematurity) - oxygen toxicity - vascular endothelial growth factor (VEGF)

– Bronchopulmonary dysplasia

48

Bronchopulmonary dysplasia

Decrease in alveolar septation resulting in large, simplified alveolar structures and a dysmorphic capillary configuration.

49

Bronchopulmonary dysplasia caused by

Most likely caused by an arrested development of alveolar septation at the so-called saccular stage of development.

50

Contributing Factors to Bronchopulmonary dysplasia

• Hyperoxemia

• Hyperventilation

• Prematurity

• Inflammatory cytokines (IL1β, IL6 and IL8)

• Vascular maldevelopment

51

Prevention of Bronchopulmonary dysplasia

gentler ventilation,

glucocorticoids and prophylactic surfactant

52

Bronchopulmonary dysplasia pathology

• Hyperplasia and squamous metaplasia of bronchial epithelium

• Peribronchial fibrosis

• Fibrotic obliteration of bronchioles

• Overdistended alveoli.

53

Neonatal Necrotizing Enterocolitis

Disease of premature infants along with term infants of low birth weights (small for gestational age)

54

Neonatal Necrotizing Enterocolitis (NEC) 

 Predisposing factors

– Intestinal ischemia

– bacterial colonization of the gut

– administration of formula feeds

 

55

Neonatal Necrotizing Enterocolitis (NEC)

CLinical features 

Preterm or SGA infant with history of asphyxia requiring ventilation develops signs of obstruction after oral feedings have begun

• Abdominal distension, bloody stools, shock, DIC progressing to death

56

Neonatal Necrotizing Enterocolitis (NEC)

Diagnosis

– Abdominal radiographs show dilated loops of bowel

– pneumatosis intestinalis

57

Neonatal Necrotizing Enterocolitis (NEC)

Pathology involves what parts of GI

Typically involves terminal ileum, caecum and right colon

58

Microscopy signs in Neonatal Necrotizing Enterocolitis (NEC)

• Mucosalcoagulative necrosis extending into and often through the submucosa and muscular layers

• Small air filled spaces beneath mucosa – pneumatosis intestinalis

59

Neonatal Necrotizing Enterocolitis (NEC) 

Complications 

• Early – sepsis, shock, acute tubular necrosis, DIC, intestinal perforation

• Delayed – short gut syndrome, malabsorption, strictures.

60

Neonatal Intraventricular hemorrhage

Bleeding into the germinal matrix with extension into ventricles and beyond