The prevalence of prematurity has increased in recent years in developing countries. Here we report premature baby and its complication

1. god's littlest angel
Preterm Babies
Dr. Leen Doya
Department of pediatric
Tishreen university

2. Background (WHO)
 full term : 37-42 weeks' gestation.
 Prematurity , preemies , Preterm birth : neonates
born at <37 weeks' gestation.
 Sub- categories of preterm birth:
7.1%
9.5%
32-33 W
12.1%
34-36W
71.3%

3. Prevalence
(AAP)
Every year:
 15 million babies are born preterm worldwide.
 1 million children die due to complications of
preterm birth.
 Across 184 countries, the rate of preterm birth
ranges from (5-18)% of babies born.
 the most common reason for hospitalization and
mortality.

4. Epidemiology
 preterm births during 2014 ranged from 13.4% in North
Africa to 8.7% in Europe.
 Asian and sub-Saharan African countries accounted for
81·1% of preterm births globally in 2014.

5. CAUSES OF PREMATURITY
 The mechanisms are not clearly understood .
I. Spontaneous:( 2/3 of all premature ).
 No matter when it begins.
 labor starts early and are not able to stop .
 start with typical labor contractions or premature
rupture of membranes.
II. Induced:
 The labour is often induced before term when there is
impending danger to mother or foetal life in-utero

6. I. SPONTANEOUS RISKS FACTORS
1. Infection:
 Any kind of systemic inflammation or infection
including infections in the mouth (such as gum
disease), vagina, uterus, and kidneys.
2. Cervical Problems:
 Insufficient cervix or short cervix both increase the
risk of preterm birth.
3. Bi-cornuate uterus.
4. Low maternal weight /maternal age <16 - >35.
5. Chronic and acute systemic maternal illness.
6. Trauma and Physical exertion
7. Sexual activity.

7. I. SPONTANEOUS RISKS FACTORS
8. Smoking:
 causes blood vessels in the uterus to constrict, which
prevent nutrients and oxygen from getting to the
baby or contribute to early labor.
9. Stress.
10. Short Time Between Pregnancies: < six months.
11. Carrying Twins, Triplets, and More.
12. Genetics:
 if mom or sister went into labor early.
 previous premature baby .
13. Poor socio-economic status .
14. Threatened abortion / Congenital malformations.

8. II. Induced
1. Maternal diabetes mellitus.
2. Placental dysfunction .
3. Placental Abruption.
4. Eclampsia.
5. Fetal hypoxia.
6. Antepartum hemorrhage.

9. How to confirm the baby is
premature?

10. gestational age is assessed
1. History:
LMP & EDD and quickening (Date of first reported fetal
activity , usually occurs at 16-18 weeks).
2. Examination:
Fundal height by obstetrician Examination .
3. Investigations:
 First reported fetal heart sounds (10-12 weeks by
Doppler ultrasound examination) .
 Ultrasound examination (very accurate if obtained
before 20 weeks' of gestation).

11. Ballard
scoring
(postnatal scoring
system)

14. Clinical Feature and
Complication

15.  Their size is small with
relatively large head.
 Crown-heel length is less than
47 cm
 Head circumference is less
than 33cm but exceeds the
chest circumference by more
than 3cm.
Measurement

16. Activity and Posture
 The general activity is poor .
 Their automatic reflex responses
such as moro response, sucking
and swallowing are incomplete.
 The baby assumes an extended
posture due to poor tone.

17. FACE AND HEAD
 Disproportionately large head
size .
 Sutures are widely separated
and the fontanels are large .
 Small chin, protruding eyes
due to absent buccal pad of
fat.

18. FACE AND HEAD
 Optic nerve is often un-
myelinated but presence of
papillary membrane makes its
visualization difficult.
 Hair appear woolly and fuzzy
 hair fibers can be seen
separately.

19. Ear cartilage is deficient or absent
with poor recoil

20. Skin and Subcutaneous Tissues
 Skin is thin, gelatinous, shiny and
excessively pink .
 Edema may be present.

21. Subcutaneous fat is deficient and
breast nodule is small or absent

22. Deep sole creases are often not
present

23. GENITALS
 In male testes are undescended
and scrotum is poorly
developed.
 In female infants, labia majora
are widely separated exposing
labia minora and hypertrophied
clitoris

24. PHYSIOLOGICAL HANDICAPS
 CNS :
 Immaturity of CNS is expressed
as inactivity , poor cough reflex
and in-coordinated sucking and
swallowing.
 Inefficient blood brain barrier.

25. RASPIRATORY SYSTEM
 Breathing is mostly diaphragmatic, periodic and
associated with intercostal recessions.
 Pulmonary aspiration and atelectasis .
 They are vulnerable to develop chronic pulmonary
insufficiency.

26. CARDIOVASCULAR SYSTEM
 The closure of ductus arteriosus is delayed.
 In grossly ( less than 32 weeks) ECG shows left
ventricular preponderance.
 Risk to develop thrombo- embolic complications and
↑BP.

27. GASTRO-INTESTINAL SYSTEM
 Due to coordinated sucking and swallowing ,
regurgitation and aspiration are common.
 Hypoglycemia.
 Abdominal distention and functional intestinal
obstruction.
 Immaturity of the glucuronyl transferase system in
the liver leads to hyper-bilirubinemia.
 Development of kernicterus at lower serum bilirubin
levels.

28. RENAL IMMATURITY
 The urea is high due to low GFR.
 They vulnerable to develop late metabolic
acidosis especially when fed with a high
protein milk formula.
 Concentration of urine is poor.
 The solute retention and low serum proteins
explain occurrence of edema in preterm
infants.

29. TOXITY DRUG
 Poor hepatic detoxification and reduced renal
clearance make a preterm baby vulnerable to
toxic effects of drugs.

30. THERMO REGULATION
 Hypothermia is invariable.
 high surface area to body weight ratio (5 times
than the adult) that lead Excessive heat loss.
 decreased brown fat and glycogen stores.
 immature heat regulation mechanism.

32. Apnea of preterm (AOP)
 Sudden absence of breathing that lasts at least 20
seconds, or is associated with bradycardia or cyanosis
(oxygen desaturation) in an infant less than 35 weeks’
gestational age.
 It’s a developmental disorder ( physiologic immaturity
of respiratory control) .
 AOP usually presents on day 2-7.

33.  AOP is diagnosis of exclusion.
 An other causes:
hypoxia, infection, anemia, electrolyte disturbance,
hypoglycemia, IVH, seizures, heart failure or
aspiration due to gastro-oesophageal reflux .
 Breathing will usually start again after gentle
physical stimulation.
(AOP)

34. Apnea of preterm (AOP)
Treatment
 respiratory stimulant: caffeine ,
Theophylline , aminophylline ( if
central).
 CPAP ( if obstructive) .
 mechanical ventilation may be
necessary if apneic episodes are
frequent.

35. Intra ventricular Hemorrhage (IVH)
 A hemorrhage in the brain that begins in the
germinal matrix can progress into the ventricular
system.
 Inversely proportional to gestational age and birth
weight.
 Major cause of death in the NICU.
 lead to neurodevelopmental disability.

36. Risk Factors of IVH
I. Infection /Acidosis/ Hypoxic episodes.
II. Assisted Ventilation with high inspiratory pressures
III. CPAP.
IV. Caretaker activities such as suctioning or handling.
V. Coagulopathy.
VI. Decreased HCT/ Rapid Volume expansion.
VII. Hyperosmolar.
VIII. ↑ ∆ / ↓ ∆ .
IX. ↑BP / ↓BP .
X. Medications.
XI. PDA.
XII. Pneumothorax.

37. Clinical Presentation
 can be asymptomatic (most common) or catastrophic
depending on the degree of the hemorrhage.
Most common Presentation of IVH:
I. Apnea.
II. ↑BP / ↓BP .
III. Sudden anemia.
IV. Acidosis.
V. Changes in muscular tone.
VI. Seizures.

38. Diagnosis - Cranial Ultrasound
 All babies < 1500 grams or < 32 weeks.
 Approximately 60% will occur in the first 24hours.
 85% in the first 72 hours.
 90% will occur within the first week of life.

39. classification system divides
Grade IV
IVH with extension into the parenchyma
Grade I
Germinal matrix hemorrhage
Grade II
IVH without ventricular dilatation
Grade III
IVH with ventricular dilatation

40. Prognosis
 correlated with the grade of IVH.
 The outcome in infants with grades I and II is good.
 ( 40% ) grade III IVH have significant cognitive
impairment.
 (90% ) grade IV IVH have major neurologic sequelae
, requiring lifetime care.

41. Prevention of IVH
Antenatal:
Prevention of preterm birth is the most effective
method of preventing IVH.
Corticosteroids (Given for lung maturity , Decrease in
IVH ).

42. Patient Care:
 minimize gently handling and stimuli (visual & auditory).
 Don't raise feet above head
 prevent neutral thermal environment.
 Suctioning: allow recovery time between suctioning
 Slow administration of hyperosmolar medications, volume
replacement (can cause rupture of capillaries in the
germinal matrix )or NaHCO3 (rapid infusions may cause
elevations in CO2 which can dilate cerebral vessels).
 Prophylactic Indomethacin (if the mother did not receive of
steroids) was associated with a lower risk incidence of
severe IVH.
Prevention of IVH

43. Patent Ductus Arteriosus in the Preterm
(PDA)
 The most common cardiac
complication in premature
infants .
 Incidence inversely related
to gestational age.

44.  bounding pulses/ wide pulse pressure.
 systolic or continuous murmur.
 Tachycardia.
 hyperactive precordium.
 Apnoea.
 increase in ventilatory requirements.
 congestive heart failure.
 Echocardiogram most useful to evaluate PDA.
Signs and Symptoms

45. PDA
Complication
CHD
IVH
pulmonary
hemorrhage
BPDrenal
impairment
NEC
CLD

46. PDA treatment
 Fluid restriction (avoid dehydration).
 symptomatic:
 IV or PO Indomethacin ( 3 days ).
 IV or PO Ibuprofen .
 monitor urine output, renal function and GIT complications
 Contraindicated :
 Infant has untreated infection
 Bleeding
 Platelet < 60x109/L
 surgical ligation fail to close a symptomatic duct.
NEC
Impaired renal function

47. Necrotizing enterocolitis
( NEC)
 characterized by various degrees of mucosal or trans
mural necrosis of the intestine.
 The incidence increases with increasing prematurity
(10% < 1500 g).
 it is typically seen in the first few weeks of life.
 The disease has significant morbidity an a mortality of
about 20%.

48. Pathogenesis
 Immaturity of the circulatory, gastrointestinal, and
immune systems.
 Asphyxia, as it leads to low cardiac output and
intestinal perfusion.
 Enternal feeding.
 Lack of breast feeding.
 Umbilical catherisation.
 septicemia.

49. Early signs of NEC
 The infant stop tolerating feeds.
 Bile-stained vomiting.
 Abdominal distension.
 Stool contained fresh blood.
 The infant may rapidly become shocked and
require mechanical ventilation.

50. Lissauer T, Clayden G, Craft A. Illustrated textbook of paediatrics. 4th ed. Edinburgh [etc.]: Mosby; 2012.
DIAGNOSIS

51. Stages I
ClinicalSigns
Lethargy.
temperature
instability.
Apnea
bradycardia
Emesis
abdominal
distension
haematochezia
Radiographicfindings
intestinal
dilation

52. Stages II
ClinicalSigns
as in stage I
metabolic
acidosis.
thrombocytopenia
abdominal
tenderness.
absent bowel
signs
Radiographicfindings
intestinal dilation
portal venous gas

53. STAGE IIIA
ClinicalSigns
as in stage II
respiratory or
circulatory
arrest
Shock
Radiographicfindings
as in stage II
Ascites

54. STAGE IIIB
ClinicalSignsPerforation
Radiographicfindings
Pneumoperitoneum
Football Sign

55. Treatment
 stop oral feeding.
 broad spectrum antibiotics to cover both aerobic
and anaerobic organisms.
 Parenteral nutrition is always needed .
 mechanical ventilation.
 circulatory support are often required.
 Surgery is performed for bowel perforation.

56. Infection
are the important cause of neonatal mortality.
Preterm have higher incidence :
1. maternal genital tract infection is an important cause of
preterm labor.
2. immune dysfunction (↓IgG antibodies and
inefficient cellular immunity).
3. premature often require prolonged IV access,
endotracheal intubation, or other invasive procedures .

57. Signs and Symptoms
I. temperature instability : ↑ ∆ / ↓ ∆ .
II. change in behaviour : lethargy, irritability
III. skin : poor perfusion, pallor, jaundice, petechial.
IV. feeding problems : poor feeding, vomiting, diarrhea,
abdominal distension
V. cardiovascular : tachycardia, ↓BP.
VI. respiratory: AOP / tachypnea, cyanosis, RDS .
VII. metabolic : ↑ GLU / ↓ GLU, metabolic acidosis.

58. Early-onset
• <48 hours
• ascended from birth canal
• Viral(acquired via placent)
• Risk factors:
• prolonged or premature
rupture of amniotic
membrane
• chorioamnionitis. Late-onset
• >48 h
• Nosocomially acquired.
• Staphylococcus
epidermidis the most
common
• organisms is broad, and
includes G+
(Staphylococcus aureus
..etc) and G-(Escherichia
coli and Pseudomonas,
Klebsiella and Serratia
species ).

59. Management
Empirical antibiotics:
 start immediately when diagnosis is suspected.
 do not wait for culture results after 48-72 hours
Adjust antibiotics accordingly.

60. ANEMIA OF PREMATURITY
 In a premature infants, have lower Hb concentration
in which make the postnatal Hb level decline rapidly
 Develop anemia around 6 to 8 weeks of age.
 Causes:
– Decreased red cell production .
– Increased red cell destruction.
– Blood loss.
 Management:
– Blood transfusion.
– Iron supplementation .

61. NUTRITIONAL HANDICAPS
Deficiencies of folic acid and vitamin E.
 Develop hemolytic anemia.
 thrombocytopenia and edema 6 to 10 weeks
of age.
 Osteopenia and rickets.

62. MANAGMENT
I. ARREST OF PREMATURE LABOR
Bed rest and sedation.

63. Maternal steroids
 Betamethasone 12mg IM / 24 hours --2 doses.
 or Dexamethasone 6mg IM every 12 hours for 4
doses.
 Improved neonatal outcomes:
Given between (28 – 34)w gestation and within
7 days of delivery.
Every weekly for at least 3 w before delivery for
high risk mother.
 Not indicated for prem<24w
 Maximum benefit after 48 h.

64. Tocolytics
 Nifedipine, indomethacin, magnesium sulphate.
 To complete steroid therapy for fetal fetal lung
maturation
 Broad spectrum Abx for prophylaxis of clinical
infections (chorioamnionitis)

65. Maturity of fetus
 examination of amniotic fluid for phosphatidyl
glycerol or L/S ratio.

66. CARE OF PRETERM BABY
 OPTIMAL MANAGEMENT AT BIRTH:
 Delayed clamping of cord.
 Elective intubation of extremely LBW babies (<1000g).
 Should be promptly dried, kept effectively covered and
warm.
 Vitamin K 1mg ( 0.5mg in babies < 1500g) should be
given intra-muscularly.
 Transferred by the doctor or nurse to the NICU as soon as
breathing is established.

67. CARE OF PRETERM BABY
OXYGEN THERAPY:
The lowest concentration and flow rates should be used
to maintain SpO2 ( 85-95%) and PaO2 ( 60-80 mm Hg).
PHOTOTHERAPY:
Early phototherapy is advised to keep the serum
bilirubin level within safe limits (to obviate the need for
exchange blood transfusion).

68. • Within first week of life IVH
• Around day 28 periventr
leukomalacia
Cranial US for
prem <32weeks
• Infants<32w POG/ BW<1.5kg
• Preterm<36w (received O2 therapy)
Screening for
ROP at 4-6w

69.  Can be given trough:
 Parenteral feeding
 enteral feeding should be introduced as soon as possible.
 PRETERMS :
 <1200 g / <32 wk: IV fluids for first 2-3 days, once
stable start gavage feeding.
 1200-1800 g/ 32-34 wk : Start gavage feeding.
 >1800 g/ >34 wk: Start breast feeding directly( if
trial feed takes>20 min or intake is less than
required, switch to gavage feeding)
Nutrition
FEEDING GUIDLINES

70. Total parenteral nutrition
(TPN)
 intravenous infusion of all nutrients necessary for
metabolic requirements and growth (120-130
KCal/kg/day ).
 Indication for TPN:
1. Birth weight ≤ 1000 g
2. Birth weight 1000-1500 g and anticipated to be not
on significant feeds for 3 or more days.
3. Birth weight > 1500 g and anticipated to be not on
significant feeds for 5 or more days.
4. Surgical conditions in neonates.

71. EARLY ENTERAL NUTRITION
Trophic feeding:
 feeding very small amounts to stimulate development
of the immature GIT.
 Breast milk or ½ or full strength preterm formula at
10ml/kg/d by intermittent gavage/ continuous
nasogastric drip , Increase by 10-15 ml/kg/d .
 Preterm 28w double its birth weight in 6w, and treble
in 12w.
 Advantages:
I. Improves GI motility Enhances enzyme maturation.
II. Improves mineral absorption.
III. Lowers incidence of cholestasis.
IV. Shortens time to regain birth weight

72. Breast milk
 Advantages:
 ↓amino acids.
 ↑essential fatty acids.
 ↓ renal solute load.
 IgA ( protection against pathogens).
 Promotes intestinal maturation.
 Low risk of necrotising enterocolitis.
 Disadvantages:
↓Vitamin D, Ca, P .
Inadequate iron.

73. Vitamin and mineral
supplementation
 Multivitamins:
 can be given after day 14 of life when on feeding
of 150 ml/s kg/day.
 Iron:
 babies of BW< 2000g should receive iron
supplements 3 mg/kg elemental iron per day.
 Vitamin E supplementation.
 Ca (220mg/day) and P (100mg/day).

74. VACCINATION
 TIMING :
 at the same chronologic age as recommended for FT
infants.
 All of the available vaccines are safe when given.
 NICU should have immunization programs in place.
Dosing :
 Vaccine dosages normally given to FT infants.
 Any side effects associated with the vaccines are
similar in both full-term and preterm babies

75.  The response (HBV) may be diminished in premature
with BW <2,000 grams.
 IF the 1st dose of HBV is routinely given at birth,
routine HB immunization of infants should be delayed
until the infant reaches 2,000 grams or upon hospital
discharge .
 BCG most immunogenic if delayed until at least 34-35
weeks' postmenstrual age in very premature infants.
VACCINATION

77. PROGNOSIS
 prognosis depend on the gestation age and clinical.
 catch up in their physical growth with term
counterparts by the age of 1 to 2 years.
 (15 – 20) % of neurological handicaps :
 CP.
 seizures.
 ROP.
 Hydrocephalus.
 deafness.
 MR.

79. From the world