Neonatal Jaundice, neonatal sepsis and perinatal asphyxia

1. NEONATAL
CONDITIONS
REINFRIED HAULE

2. Neonatal Jaundice
Neonatal Sepsis
Perinatal Asphyxia

3. Neonatal Jaundice

4. OBJECTIVE
 Define Neonatal Jaundice
 Pathophysiology
 Epidemiology
 Clinical Manifestations
 Investigations
 Treatment

5. Definition of Jaundice
 Jaundice = Yellow coloration of skin & sclera as result of
accumulation of unconjugated bilirubin
 One of the most common problems encountered in newborns
 Normal transitional phenomenal in most infants (Neonatal physiologic
jaundice)
Sclera
Icterus

7. Definition of Jaundice
 High levels of unconjugated bilirubin is neurotoxic
 Kernicterus = form of brain damage from unconjugated bilirubin
passing through the blood brain barrier (BBB) into brain
 Mental retardation
 Seizures
 Movement disorders
 Speech difficulties
 Hearing loss

8. Staining of the thalamus and basal ganglia

9. PATHOPHYSIOLOGY
Unconjugated Bilirubin
(Indirect Bilirubin)
Insoluble
Conjugated Bilirubin
(Direct Bilirubin)
Soluble
+ Glucuronic Acid

10. PATHOPHYSIOLOGY
 Neonatal physiologic jaundice occurs from 2 phenomena:
1. Increased breakdown of fetal erythrocytes
2. Low activity of glucuronyl transferase

11. PATHOPHYSIOLOGY
 Neonatal pathologic jaundice occur from:
Increased bilirubin load
Decreased bilirubin
conjugation
Impaired bilirubin excretion

12. PATHOPHYSIOLOGY
 Neonatal pathologic jaundice occur from:
1. Increased bilirubin load
 Hemolytic causes
 Rh factor incompatibility
 ABO incompatibility
 RBC membrane defects
 RBC enzyme defects (G6PD deficiency)
 Non-hemolytic causes
 Cephalohematoma / Caput Succedaneum
 Bruising
 Swallowed blood
 Exaggerated enterohepatic circulation: Intestinal atresia, pyloric stenosis,
Hirschsprung's disease, breast milk jaundice

13. Caput Succedaneum

14. PATHOPHYSIOLOGY
 Neonatal pathologic jaundice occur from:
2. Decrease bilirubin conjugation
 Gilbert Syndrome
 Crigler-Najjar syndrome types 1 and 2
 Congenital Hypothyroidism

15. PATHOPHYSIOLOGY
 Neonatal pathologic jaundice occur from:
3. Impaired bilirubin excretion
 Biliary obstruction
 Biliary atresia, Choledochal cyst, Primary sclerosing cholangitis, Gallstones,
Neoplasm, Dubin-Johnson syndrome

16. PATHOPHYSIOLOGY
 Neonatal pathologic jaundice occur from:
3. Impaired bilirubin excretion
 Infection:
 Sepsis, Urinary Tract Infection, Syphilis, Toxoplasmosis, Tuberculosis, Hepatitis,
Rubella, Herpes
 Metabolic Disorders:
 Congenital Hypothyroidism

17. EPIDEMIOLOGY
 Jaundice occurs in >50% normal newborns
 More common in preterm infants (80%)
 Incidence is higher in East Asians and American Indians and lower
in blacks

18. CLINICAL MANIFESTATION
 Jaundice first becomes visible in the face and progresses
downward as bilirubin increases.
DOWNWARD

19. CLINICAL MANIFESTATION
 Neurologic effects of bilirubin toxicity:
Early Late Chronic
Lethargy Irritability Mental Retardation
Poor Feeding Opisthotonos Seizures
Hypotonia Apnea Hearing Loss
Seizures

20. CLINICAL MANIFESTATION
 Neonatal physiologic jaundice normally presents on the second or
third day of life
 Peaks at 3-5 days of life
 Resolves after 1-2 weeks
 Neonatal pathologic jaundice can
 start on first day life
 last longer than 14 days (term) or 21 days (preterm)

21. INVESTIGATIONS
 Depends on whether jaundice is physiologic or pathologic:
 Total serum bilirubin (conjugated/unconjugated)
 Maternal and infant blood group
 Coombs test
 Full Blood Count
 G6PD
 Thyroid function test
 Syphilis serology (VDRL)
 Abdominal ultrasound

22. WHO Guildelines for Treatment

23. TREATMENT
 Phototherapy is first line treatment for neonatal jaundice
 Reduces jaundice by using UV light to cause insoluble bilirubin ->
water-soluble bilirubin, and be excreted in the bile and urine without
conjugation
 Caution with use:
Protect Infant’s Eyes
Beware of dehydration, hyperthermia or
hypothermia

24. Phototherapy

25. TREATMENT
 Exchange Blood Transfusion may be required for severe jaundice
 Removes partially hemolyzed and antibody-coated erythrocytes and
replaces them with uncoated donor RBCs that lack the sensitizing
antigen.

26. Summary
 Neonatal Jaundice is a very common condition is newborns.
 Important to differentiate between physiologic vs. pathologic
jaundice.
 Onset of jaundice
 Duration of jaundice
 Treatment of jaundice depends on level of serum bilirubin.

27. Neonatal Sepsis

28. Objectives
 Definition of Neonatal Sepsis
 Early-Onset vs. Late-Onset Sepsis
 Epidemiology of Neonatal Sepsis
 Clinical Features of Neonatal Sepsis
 Diagnosis of Neonatal Sepsis
 Treatment of Neonatal Sepsis

29. Definition
 Neonatal Sepsis = Invasive bacterial infection in the first 90
days of life
 Early-Onset Sepsis:
Within 7 days of birth
Organisms acquired from trans-
placental or passage through birth
canal
 Late-Onset Sepsis:
Symptoms between 7-90 days of life
Often acquired from environment

30. Early-Onset Sepsis
 Timing of onset:
 85% of newborns within 24 hours
 5% of newborns 24-48 hours
 Onset most rapid in premature infants
 Pneumonia more common in early-onset
 Transmission:
 Trans-placental infection
 Ascending infection from cervix by organisms that colonize in the
mother's GU tract

31. Early-Onset Sepsis
 Organisms most common:
Group B Streptococcus (GBS)
Escherichia coli (E. coli)
Listeria monocytogenes
Coagulase-negative Staphylococcus
Staphylococcus aureus
Haemophilus influenzae

32. Late-Onset Sepsis
 Timing of onset:
 7 to 90 days of life
 Meningitis and bacteremia more common in late-onset
 Transmission:
 Care-giving environment
Colonization include indwelling lines
(vascular or urinary catheters), or
contact from caregivers with bacterial
colonization.

33. Late-Onset Sepsis
 Organisms most common:
Staphylococcus aureus
Group B Streptococcus (GBS)
Escherichia coli (E. coli)
Coagulase-negative staphylococci (S. epidermidis)
Klebsiella
Pseudomonas
Enterobacter
Serratia
Acinetobacter
Anaerobes

34. Epidemiology
Under 5 years old Mortality in Tanzania
Neona
tal
30%
Malari
a
23%
Pneu
monia
19%
Diarrh
ea
16%
HIV
12%

35. Epidemiology
 Culture-proven sepsis ~ 2 / 1000 live births
**Many newborns undergo start of treatment before presence of
sepsis has been proven**
 Premature infants have increased incidence
 Very low birth weight (<1000g): 26/1000 live births
 Birth weight of 1000-2000g: 8-9/1000 live births

36. Epidemiology
 Risk is greater in males (2:1)
 Mortality rate as high as 50% for infants without treatment

37. Risk Factors
 Most common risk factors:
Premature rupture of membranes (PROM)
Occurring ≥ 18 h before birth
Prematurity
Maternal infection (urinary tract or
endometrium)
Chorioamnionitis
Maternal GBS Colonization
Especially untreated during labor

38. Risk Factors
 Other risk factors:
Low APGAR score (<6 at 1 or 5 min)
Maternal fever greater than 38°C
Poor prenatal care
Poor maternal nutrition
Low socioeconomic status
Recurrent abortion

39. Risk Factors
 Other risk factors:
Maternal substance abuse
Low birth weight
Difficult delivery
Birth asphyxia
Meconium staining
Congenital anomalies
Indwelling catheter

40. Clinical Features
 Clinical signs are NONSPECIFIC and associated
with other neonatal diseases:
 Temperature instability (hypo- or hyperthermia)
 Diminished spontaneous activity
 Less vigorous sucking
 Apnea
 Bradycardia or tachycardia
 Respiratory distress
 Neurologic findings (eg, seizures, jitteriness, hypotonia)
 Jaundice, pallor, cyanosis, purpura, petechiae
 Vomiting, diarrhea, and abdominal distention.

41. Clinical Features
Hypotonia

42. Clinical Features
Petechiae and purpura

43. Clinical Features
Diffuse mottled, bluish-gray appearance of this
infant's skin suggestive of systemic poor perfusion.

44. Clinical Features
 Specific signs of an infected organ may
pinpoint the primary site of infection.

45. Clinical Features
 Periumbilical erythema, discharge, or bleeding
suggests omphalitis.

46. Clinical Features
 Coma, seizures, opisthotonos, or a bulging fontanelle
suggests meningitis or brain abscess.

47. Clinical Features
 Decreased spontaneous movement of an extremity
and swelling, warmth, erythema, or tenderness over a
joint indicates osteomyelitis.

48. Clinical Features
 Unexplained abdominal distention may indicate
peritonitis or necrotizing enterocolitis.

49. Diagnosis
 Laboratory Studies:
 Blood, cerebrospinal fluid (CSF), and urine cultures
 Gram stain provides early identification
 FBP with differential
 WBC remain non-specific: < 4,000/μL or > 25,000/μL are abnormal
 Normal WBC counts in 50% of culture-proven sepsis cases
 Thrombocytopenia (<100,000) may occur in neonatal sepsis.

50. Diagnosis
 Laboratory Studies:
 Cerebrospinal fluid :
 ↑ WBC count (predominately neutrophils)
WBC within the reference range in 29% of GBS
meningitis infections
 ↑ Protein
 ↓Glucose
Protein and glucose within reference range in
50% of patients with GBS meningitis
 Positive gram stain or culture

51. Treatment
 When sepsis is suspected, treatment should be
initiated immediately.
 Begin antibiotics as soon as diagnostic tests are performed.
 Don’t need to wait for results.

52. Treatment
Risks of starting
antibiotics in a
concerning
child for sepsis
who is
negative are
minimal. Risks of post-
poning
antibiotics in a
concerning child
for sepsis are
significant.
Risk Meter

53. Treatment
 Prior to 1 month of Age:
Triple Therapy
1. Ampicillin – Covers GBS and Listeria
2. Gentamicin – Covers E. coli
 Potential to produce ototoxicity and
nephrotoxicity
1. Cloxacillin – Covers Staph aureus
 Most strains of S. aureus produce beta-
lactamase, which makes them resistant to
penicillin

54. Treatment
 After 1 month of age:
 Cetriaxone – covers E. Coli and GBS
 +/- Cloxacillin

55. Summary
 Neonatal sepsis is divided into early vs. late onset sepsis.
 High mortality if patient untreated.
 Clinical signs are NONSPECIFIC and associated with other
neonatal diseases.
 Work-up needs to include cultures of blood, spinal fluid and urine.
 Treatment needs to start immediately.

56. Perinatal Asphyxia

57. OBJECTIVE
 Definition Perinatal Asphyxia
 Epidemiology
 Risk Factors
 Signs & Symptoms
 Diagnosis
 Treatment

58. Definition Perinatal Asphyxia
 Perinatal Asphyxia: A condition when there is extreme decrease
in the amount of oxygen in the body accompanied by an
increase of carbon dioxide around the time of delivery
 Hypoxia, Acidosis and CO2 accumulation
 Prolonged asphyxia may lead to hypoxic-ischemic encephalopathy

59. EPIDEMIOLOGY
 Accounts for much neonatal mortality and long-term morbidity.
 Birth asphyxia is the cause of 23% of all neonatal deaths worldwide.
 Largely preventable with improved obstetric care, prompt
resuscitation, and supportive care of neonates.

60. RISK FACTORS
 Maternal medical or obstetric factors:
 Hyper or hypotension
 Heart failure
 Diabetes
 Severe anaemia
 Haemoglobinopathies
 Infections
 Respiratory illness (e.g. pneumonia, asthma)
 Smoking or alcoholism
 Pre-eclampsia/eclampsia
 Prolonged rupture or membranes

61. RISK FACTORS
 Fetal Factors:
 Multiple gestation
 Prematurity or post term
 Intra-uterine growth retardation
 Intrauterine infections
 Congenital abnormalities
 Abnormal presentation
 Placental Factors:
 Placenta Abruption
 Placenta previa
 Cord compression

62. SIGNS & SYMPTOMS
 Each baby may experience signs & symptoms of birth asphyxia
differently.
 Before delivery, symptoms may include:
 Abnormal heart rate or rhythm
 An increased acid level in a baby's blood
 At birth, signs & symptoms may include:
 Bluish or pale skin color
 Low heart rate
 Weak muscle tone and reflexes
 Weak cry
 Gasping or weak breathing
 Meconium — the first stool passed by the baby — in the
amniotic fluid, which can block small airways and interfere
with breathing

63. DIAGNOSIS
 Indicators of asphyxia at birth:
 Apgar scores < 3 at 1 minute, < 7 at 5 minutes
 Resuscitation > 10 min before spontaneous
respiration established
 Cord blood pH < 7

64. TREATMENT
 Prompt treatment is important to minimize the
damaging effects of decreased oxygen to the
baby
 All health care providers at deliveries should be trained in Neonatal
Resuscitation

67. SUMMARY
 Perinatal asphyxia is a common newborn
condition that can be preventable
 Indicators of asphyxia at birth include:
 Apgar scores < 3 at 1 minute, < 7 at 5 minutes
 Resuscitation > 10 min before spontaneous
respiration established
 Cord blood pH < 7
 Prompt treatment is important to minimize the
damaging effects