Neonatal conditions

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 FeedingOpisthotonos 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 CO
2
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