4. INTRACRANIAL INJURIES
Most common site of fatal and disabling injury –
intracranial cavity
Preterm – more prone to hypoxic cerebral injury –
spontaneous intraventricular hemorrhage
Term infants – more prone to subdural hemorrhages
which are traumatic in origin
6. INTRACRANIAL INJURIES
DIAGNOSIS:
Clinical history/course
Spinal taps (done in extreme caution)
Cranial ultrasount vs CT scan of the head
TREATMENT:
Minimal handling
Management of ICP – fluid restriction
Furosemide
paCO2 25-30 torr
Thermoregulation
Oxygen and ventilatory support, as warranted
Anticonvulsant for siezure
Vitamin K for coagulation defect
9. BRACHIAL PALSY
ERB-DUCHENNE PARALYSIS
Injury to the 5th
-6th
crevical root
Absent Moro on the affected side
KLUMPKE’S PARALYSIS
Injury to the 7th
cervical and 8th
thoracic root
Loss of sensory and motor fxn of hand and wrist
10. BRACHIAL PALSY
DIAPHRAGMATIC PARALYSIS
Injury to 4th
cervical root
HORNER’S SYNDROME
Injury to the sympathetic ganglion
Characterized by ptosis, enophthalmos, miosis, and
anhydrosis of the face on the affected side
14. INFECTIONS OF THE NEWBORN
INCIDENCE: 1-5 per 1000 livebirths
PREDISPOSING FACTORS
Prematurity
Male gender
Maternal infection
Difficult delivery
Congenital anomalies
15. INFECTIONS OF THE NEWBORN
ROUTES OF ENTRY
Hematogenous spread
Ascending infection
Direct contact along birth canal
Breaks in the skin
16. INFECTIONS OF THE NEWBORN
CHANGING SPECTRUM OF
PREDOMINANT PATHOGENS
EARLY ONSET SEPSIS
1930’s Grp A Strep Others:E.coli,Staph
1940’s E.coli Others:Streptococci
1950’s S. aureus Others:E.coli/Pseudo
1960’s E.coli Others:Pseudo/Kleb
1970’s Grp B Strep Others:E.coli/ Listeria
1980’s Grp B Strep
up to E.coli
present
17. LATE-ONSET SEPSIS
1970’s S. aureus Others:Grp D Strep
1980’s Coagulase(-) Others: G(-) enteric
Staph & Streptococci
up to S. aureus Untypable H.influenzae
Present
LATE LATE-ONSET SEPSIS
1990’s Candida sp.
Coagulase (-)Staph
18. INFECTIONS OF THE NEWBORN
EARLY-ONSET VS LATE-ONSET
VS LATE LATE-ONSET
EARLY LATE LATE-
LATE
Onset <4 days >4 days > 30 days
Incidence 0.1-0.4% 5-25% -
Transmission vertical vertical/ postnatal env.
postnatal env.
Clinical fulminant insiduous insiduous
Sxs pneumonia meningitis
multisystem
Morbidity neurologic prolonged prolonged
handicap hospitalization hospitalization
Mortality 15-50% 10-15%
19. INFECTIONS OF THE NEWBORN
DIAGNOSIS OF SEPSIS
Clinical judgment
Recovery of the organism from a
meaningful site: Blood culture
UA vs UV specimens - The best alternative is still
blood culture from a peripheral vein
Volume of blood – 0.5 ml should be adequate.
Larger specimens will often grow faster
Single vs multiple blood cultures- With early onset
sepsis, a single culture would suffice. With late-
onset sepsis esp with possible CONS, at least two
cultures should be obtained.
20. INFECTIONS OF THE NEWBORN
TREATMENT MODALITIES
AGAINST SEPSIS
METHODS GENERALLY USED:
Early Detection
Fluids, nutrition, antibiotics, ventilatory support
Catecholamines
AGENTS POSTULATED TO IMPROVE
OUTCOME OF SEPSIS:
Antiserum to endotoxin
Monoclonal antibodies to endotoxin
22. OTHER BACTERIAL INFECTIONS
TETANUS NEONATORUM
History of unhygienic cord practices
Clinical diagnosis characterized by TRISMUS
Prevention with tetanus immunization of the
mother
23. OTHER BACTERIAL INFECTIONS
CONGENITAL TUBERCULOSIS
Ghons complex in the liver
Diagnostics include:
AFB smear of gastric aspirate
Tuberculin test
Placental pathologic exam
24. OTHER BACTERIAL INFECTIONS
CONGENITAL SYPHILIS
May occur with other STDs
Characterized by jaundice, hepatosplenomegaly,
macular rashes with wet desquamating skin teeming
with spirochetes
VDRL for screening. Confirmatory test FTA-
ABS
29. JAUNDICE IN THE NEWBORN
BILIRUBIN METABOLISM
biliverdinHemoglobin bilirubin
Heme oxygenase
C0 Iron
biliverdin
reductase
1 mole of Hgb = 1 mole each of C0 & bilirubin
Transport = bilirubin is transported to liver bound to
serum albumin
Uptake = nonpolar bilirubin (dissociated from albumin)
crosses the hepatocyte plasma membrane,
binds to cytoplasmic ligandin (Y protein) for
transport to SER
Note: Phenobarbital increases concentration of ligandin
31. JAUNDICE
Color is due to accumulation in the skin
of unconjugated, nonpolar, lipid-soluble
bilirubin (indirect) formed from Hgb by
heme oxygenase, biliverdin reductase,
and nonenzymatic reducing agents in the
RES
32. RISK FACTORS FOR
HYPERBILIRUBINEMIA
History of previous sibling with
hyperbilirubinemia
Decreasing gestational age
Breastfeeding
Large weight loss after birth
33. CAUSES OF HYPERBILIRUBINEMIA
Enhanced enterohepatic circulation due
to:
High levels of intestinal B-glucuronidase
↑ bilirubin monoglucuronide
↑ intestinal bacteria
↓ gut motility with poor evacuation of
meconium
34. CAUSES OF HYPERBILIRUBINEMIA
Defective uptake of bilirubin from
plasma
↓ ligandin
Binding of ligandin by other anions
Defective conjugation due to ↓ UDPG-T
activity
Decreased hepatic excretion of bilirubin
35. PHYSIOLOGIC
HYPERBILIRUBINEMIA
Onset of jaundice beyond 24 hours of age
Rise in TSB less then 0.5 mg/dL/hour or
5mg/dl/day
Peaks at 3-5 days
Resolves in a week
Levels not rising above 12mg/dl
No associated illness
36. NONPHYSIOLOGIC
HYPERBILIRUBINEMIA
Onset of jaundice before 24 hours of age
Any elevation of TSB that requires
phototherapy
Rise in TSB over 0.5 mg/dL/hour
Signs of underlying illness eg. vomiting,
lethargy, poor feeding, excessive weight loss,
apnea, tachypnea, To
instability
Jaundice persisting after 8 days in FT, 14 days
in PT
37. PATHOLOGIC CAUSES OF
HYPERBILIRUBINEMIA
PRODUCTION
Isoimmunizatioin: Rh, ABO, minor blood
grps
Erythrocyte biochem. Defect: G6PD,
pyruvate kinase, hexokinase, porphyria
Structural abnormalities of RBCs:
hereditary spherocytosis, eliptocytosis
38. PATHOLOGIC CAUSES OF
HYPERBILIRUBINEMIA
PRODUCTION
Infection: bacterial, viral, protozoal (mixed
jaundice)
Sequestered blood: subdural hematoma,
cephalhematoma, ecchymoses, hemangiomas
Others: IDM, obstructive jaundice,
galactosemia, hemolysis (DIC, vit K
deficiency)
43. WORK-UP FOR JAUNDICE
Total serum bilirubin, B1, B2
Blood type, Rh, direct Coombs test of
the infant
Blood type, Rh, antibody screen of the
mother
Peripheral smear and reticulocyte count
Hct
44. WORK-UP FOR JAUNDICE
If direct Coombs + - antibody on
infant’s RBC
G6PD screen, congenital
hypothyroidism, metabolic defects
(urine metabolic screen)
For neonatal cholestasis: Liver function
test, TORCH assay, UTZ, liver biopsy
45. TREATMENT OF
HYPERBILIRUBINEMIA
Phototherapy
Exchange Transfusion
Phenobarbital ?
Tin (Sn) protoporyhyrin or tin mesoporphyrin:
inhibits conversion of biliverdin to bilirubin by
heme oxgenase
Dose: single IM on D1 of life
Complications:transient erythema
49. CLINICAL MANIFESTATIONS OF
KERNICTERUS
Onset of symptoms: 2-5 d (FT), 7 d (PT)
Early phase: lethargy, poor feeding, loss of
Moro reflex
Second phase: prostration, dec. DTRs,
respiratory distress
Late phase: opisthotonus, bulging fontanel.
Twitching of face & limbs, high-pitched cry
Advanced cases: convulsions, spasm, stiff
extension of arms inward rotation with fists
clenched
67. CARDIOVASCULAR DISTURBANCES
CONGENITAL HEART DEFECTS
COMMON ACYANOTIC ABNORMALITIES:
Patent ductus arteriosus: Fetal blood vessel
that usually closes soon after birth remains open with
oxygen-rich blood returning from the lungs pumped to
the lungs again, placing extra strain on the right
ventricle and on the blood vessels leading to and from
the lung.
69. CARDIOVASCULAR DISTURBANCES
CONGENITAL HEART DEFECTS
COMMON CYANOTIC ABNORMALITIES:
Coarctation of the aorta: a portion of the
aorta is abnormally narrow and unable to carry
sufficient blood to the body, placing extra strain on the
left ventricle with high blood pressure in the upper
body and rupture of blood vessel in the brain
70. CARDIOVASCULAR DISTURBANCES
CONGENITAL HEART DEFECTS
COMMON CYANOTIC ABNORMALITIES:
Tetralogy of Fallot: a combination of
four different heart malformations allows mixing of
oxygenated and deoxygenated blood pumped by the
heart.
72. CARDIOVASCULAR DISTURBANCES
CONGENITAL HEART DEFECTS
Treatment: Surgical correction of the defect
Patch made from pericardium or
synthetic fabric for septal defect
Ligation of ductus arteriosus
Snipping out narrowed portion of the aorta
while sewing the normal ends togetherin
coarctation of the aorta,
Corrective procedure for each part of the
defect in Tetralogy of Fallot
Note: Success rates are well above 90 percent,
with treated children living healthy, normal lives.
79. HEMATOLOGIC DISTURBANCES
ANEMIA
TREATMENT OF ANEMIA
Replacement of blood loss
PRBC transfusion 10cc/k
Treatment of underlying cause
Vitamin K of HDN
Vitamin E and Iron
Erythropoietin
Specific factor repolacement for
hemophilia
83. ENDOCRINE DISORDERS
INFANT OF DIABETIC MOTHER
May be asymptomatic
Symptoms of hypoglycemia:
Tremors
Apnea
Limpness
Feeding difficulty
High-pitched cry
89. ENDOCRINE DISORDERS
CONGENITAL ADRENAL HYPERPLASIA
Usually present with ambiguous
genitalia
75% may go into adrenal crisis –
salt-losing type due to 21-hydroxylase
deficiency
