1

Frequent  Premature & low birth weight

 born in hospital without rooming in

Patogenesis 

1. Antenatal :
Viral
 Transplacenter Spirochaeta
Bacteri
 Amnionitis

2. Intranatal
Long labor
 Ascending bacteria
Rupture of membrane
 Direct contact
2
3. Post natal

 Continue 1 & 2

 Immediately after birth

 Almost fatal  resistance from all antibiotic

Clinical manifestation :

 Not characteristic

 Suspect if there is “NOT DOING AS WELL AS BEFORE"

3
DIAGNOSIS

Carefully Observation

Risk factor

Clinical presentation

Laboratory

Radiologic (Chest x-ray, USG)

4
 Prematurity and low birth weight

 Prematue Rupture of membranes

 Maternal peripartum fever

 Amniotic fluid problems

 Resuscitation at birth

 Multiple gestation

 Invasive procedures
Not spesific
  Body weight
 Poor feeding
 Lethargy
 Minimal acitivity
 Vomiting, diarrhea
 Jaundice
 Hepatomegaly
 Body temperature : N /  / 
 Edema, bleeding
LBW baby  hypothermia & sclerema

6
 LABORATORY
 Blood :
 White blood cell count with differential

 Platelet count

 Urine : leucocyte > 5 – 10/LPB

 Cultures (blood & other body fluids)

 Gram’s stained smears

 CRP  increases in the presence of inflammation

caused by infection or tissue injury.
THERAPY

Risk Factor (+)  profilactic with antibiotic

Gram (+) & (-)  combination :
Ampicillin / Penicillin
50 – 100 mg/kgBW 100.000 IU/kgBW
With :
Kanamicin / Gentamicin
15 mg/kgBW 2 – 4 mg/kgBW
1. Severe Infection
Sepsis, meningitis, pneumonia, diarrhea
pyelonefritis, tetanus neonatorum, etc.

2. Mild Infection
Skin, eye, umbilical, mouth, etc.

9
 At first  vesicle
 Purulent encounter hyperemic area
 Multiple  severe systemic infection

R/ :
Isolation + aseptic treatment
A.B : Cloxacillin 50 mg/kgBW
Incise the bullous
R/ topical
A.B ointment
10
 Infection with Neisseria gonorrheae ( a gram-negative
diplococcus)  a reproductive tract infection
 transmission to the fetus/ neonate in pregnancy

Clinical presentation :
 Hyperemic
 Palpebra Edema
 Purulent secret
 Unilateral/ bilateral
  cornea  Blind
11
D/ : Gram’s stain of exudate  diplococcus  gram (-)

R/ :

Isolation

A.B. eye drop/ ointment

A.B. injection  for severe cases

12
 UMBILICAL INFECTION

E/ : Staphylococcus aureus
Hyperemic, edema, exudate
Severe  lig. falciforme  multiple abscess

R/ :
 Topical : A.B ointment
 A.B. injection  for severe cases

13
 Oral Thrush

Whitish patches appear on the tongue, ginggiva or buccal

mucosa.
E/ fungus : Candida albicans
If : - immunocompromize Overgrowth
- Using A.B. for long period  Infection
- Using corticosteroid for long period
Moniliasis
diarrhea +
Parenteral infection/ sepsis
14
R/ :

 Gentian violet 0,5 %  4x / day

 Nistatin oral solution 3 x 100.000 U/day

 Severe : amphotericin / fungilin

15
16
 Definition of Neonatal Sepsis

 Disease of infants who are younger < 1 month of age

 are clinically ill

 Positive blood cultures (or positive cultures from other normally

sites)
 Infections 32%
 Asphyxia 29%
 Complications of prematurity 24%
 Congenital anomalies 10%
 Other 5%

Case fatality due to neonatal sepsis is 12 to 68% in

developing countries
Neonatal sepsis- morbidity

 Brain damage due to

meningitis, septic shock, or
hypoxemia
 Other organ damage -
lung, liver, limbs, joints
 Neonatal Sepsis

Early Onset Late Onset

 < 72 hours of age  > 72 hours of age

 Acquired around birth  Acquired from the

environment
 Vertical transmission
 Nosocomial or hospital
from mother to baby
acquired

Distinction between Early & Late onset sepsis

 not clear in developing countries:
• baby born at home & brought to the hospital at 3 days of age
• baby referred from another hospital
 Early Onset Sepsis - risk factors

 Maternal chorioamnionitis

 Prolonged rupture of membranes >18 h

 Foul smelling amniotic fluid

 Handling by untrained midwife

 Maternal urinary tract infection

 Premature labor
Chorioamnionitis

Maternal fever during labor  38ºC

± uterine tenderness

± leucocytosis

± fetal tachycardia

High risk of neonatal sepsis

Late Onset Sepsis -
risk factors

 Prematurity/ LBW
 In hospital  Invasive procedures- ventilator, IV
lines, central lines, urine catheter, chest tube
 Contact with infectious disease - doctors, nurses,
babies with infections,
 Not fed maternal breast milk
 POOR HYGIENE in NICU
Bacterial Pathogens Responsible for Sepsis in
Developing Countries

 Early onset sepsis  Late onset sepsis

 Gram negative bacilli  Gram negative bacilli
 E.coli  Pseudomonas
 Klebsiella  Klebsiella
 Enterococcus  Staph aureus
 Group B streptococcus  Coagulase negative
staphylococci
 Diagnosis of Neonatal Sepsis
 Clinical signs and symptoms

 Laboratory tests

 culture of bacterial pathogen

 other laboratory indicators

 Radiologic
 Clinical signs and symptoms
Clinical Signs: early signs non- specific, may be subtle
 Respiratory distress- 90%
 Apnea
 Temperature instability-  temp more common
 Decreased activity
 Irritability
 Poor feeding
 Abdominal distension
 Hypotension, shock, purpura, seizures- late signs
Laboratory Tests

 Cultures to identify bacterial pathogen

 blood, CSF, urine, other

 Hematological tests
 WBC count (normal 5.000 – 25.000/uL)

 Platelet count (Trombocytopenia  < 100.000/mm3)

 Erythrocyte Sedimentation Rate (ESR)

 Other tests

 C- reactive protein
Lumbar Puncture

 Possibility of meningitis + 30%

 Babies with meningitis may not have specific symptoms

 15% of babies with meningitis will have negative blood

cultures
 First line therapy in facility setting

 Ampicillin 50 mg/ kg
 every 12 hours in 1st week of life
 every 8 hours from 2- 4 weeks

PLUS
 Gentamicin once daily.
 > 35 weeks gestation: 4 mg / kg every 24 hours
 30 - 34 weeks gestation:
 0 - 7 days: 4.5 mg/kg every 36 hours
 > 8 days: 4 mg/kg every 24 hours
Supportive Care

 Temperature support

 GI support - vomiting, ileus

 Cardiorespiratory support

 hypoxia, apnea, ARDS, shock

 Hematological support: anemia, thrombocytopenia, DIC

 Neurological support- seizures

 Prevention of
Nosocomial Infection

 Hand washing

 Early feeding

 Maternal breast milk

 Decrease use of broad spectrum antibiotics

 Decreased use of invasive procedures

 Proper sterilization procedures

32
 Definition of Seizure

Seizures are transient disturbances in brain function

manifesting as episodic impairments in consciousness in

association with abnormal motor or automatic activity.

33
 Types and Clinical Presentations of
Neonatal Seizures

Four types of seizures are frequently encountered in neonates:

Tonic Seizures

Clonic Seizures

Myoclonic Seizures

Subtle (Fragmentary) Seizures

34
 Subtle (Fragmentary) Seizures
Usually occurs in association with other types of seizures and
may manifest with:

 Stereotypic movements of the extremities such as bicycling

or swimming movements.
 Deviation or jerking of the eyes with repetitive blinking.
 Drooling, sucking or chewing movements.
 Apnea or sudden changes in respiratory patterns.

35
 Benign Movements
that are Not Seizures

 Jitteriness
 Sleep apnea

36
 Jitteriness
 Jitteriness is often misdiagnosed as clonic seizures.

 Clinically they differ from clonic seizures in the following

aspects:
 The flexion and extension phases are equal in amplitude.

 Neonates are generally alert, with no abnormal gaze or eye

movements.

 Passive flexion or repositioning of the limb diminishes the

tremors. Tremors are provoked by tactile stimulation, though
they may be spontaneous.
37
 No EEG abnormalities.
 Jitteriness (cont)

 Often seen in neonates with hypoglycemia, drug

withdrawal, hypocalcemia, hypothermia and in (SGA)
neonates.

 Spontaneously resolve within few weeks.

38
 Sleep Apnea

Not associated with abnormal movements and is usually

associated with bradycardia.

When seizures are present with apnea abnormal movements,

tachycardia and increased blood pressure are present as well.

39
 Seizures

 Abnormal gaze or eye movements.

 Staring
 Blinking
 Nystagmoid jerks
 Horisontal eye deviation

 The hands continue to move if grasped

 Movement  coarser

 EEG abnormalities.
 Most Common
Causes of Seizures
 HIE

 Infections (TORCH, meningitis, septicemia)

 Metabolic disorders (Hypoglycemia, hypocalcemia,

hypomagnesemia)

 CNS bleed (intraventricular, subdural, trauma, etc.)

41
 Less Common
Causes of Seizures
 Congenital brain anomalies
 Inborn errors of metabolism
 Maternal drug withdrawal (heroin, barbiturates,
methadone, cocaine, etc.)
 Kernicterus
 Pyridoxine (B6) dependency, and hyponatremia

42
Hypoglicemia

 WHO : Blood glucose < 45 mg/dl  Term & Preterm baby

 Incidence :

 LGA, SGA, Preterm baby

 Severe asphyxia

 Baby from Diabetic mother (Uncontrolled)

 Preterm baby  combined with asphyxia, Hypocalcemia,
Infection, Hemorrhage
Hypocalcemia

Blood Calcium < 7 mg%

In the first 2-3 daysof life Early onset hypocalcemia

Incidence :
SGA baby
Born from DM mother
Preterm baby
HIE

Can combined with the other metabolic disorders :

Hypoglicemia
Hypomagnesemia
Hypofosfatemia
Hypocalcemia

 1/ 2 weeks of life  Late onset Hypocalcemia

 Incidence :

 Term baby
 LGA baby
 Baby with Cows milk feeding :
 Low fosfat level
 Comparation of fosfat - calsium, fosfat -
magnesium  not optimal
Hypomagnesemia

Blood Magnesium < 1,2 mg/dl

Frequently combined with Hypocalcemia

Mechanism : not clear

Secondary  caused by asphyxia perinatal

Seizure  24 hours of life

R/ Anticonvulsant  difficult

FOKAL & UNILATERAL

Renen et al  40% neonatal seizures  HIE

47
 Intracranial bleeding

Type of seizure  Depend on type of bleeding

After the first of life

3 types :

Subarachnoid Primer bleeding

Intraventricular – Periventricular bleeding

Subdural bleeding
 Subarachnoid Primer bleeding

 Cause : rupture of superficial vein caused by prolonged labor

 Associated with HIE

 Most common  asymptomatic

 After the second day of life

 Term baby

 Between episodes of seizures  the baby active

Intraventricular – Periventricular bleeding

 Bleeding come from :

 Subependimal matriks germinalis capillary /
 Lession on this area
 Several hours up to 3 days of life
 Tonic seizure
 Progressive poor (several minutes – several hours) &
death
 > Preterm baby, gestational age < 34 weeks
 Subdural bleeding
 Caused by rupture of tentorium falx cerebral
 The first day of life
 Local & subtle
 Incidence :
 Term & LGA baby
 Breech Presentation
 Forceps Extraction
 Partus precipitatus  cerebral contusion
 The bleeding  can not seen by USG
 Depress midbrain  Sudden death
 Intracranial infection
Occur during :

 Intrauterine
 During labor
 Immediately after birth
Cause by  intrauterine infection :Toxoplasmosis,
Cytomegalovirus, Rubella, Herpes
The third day of life
5-10% caused by :

Bacterial & non-bacterial infection

 Congenital abnormally

Microgyria, Pachygyria, Heteropia

 5-10%  seizures

 Seizure  occur every time

Mostly because of :

Cortex cerebral associated with neuron migration disorder

 IDIOPATHIC
2 Types :
1. “Benign Familial Neonatal Seizure”
Occur between 2nd – 3 rd day
Disappear after several months
Recurrent seizures  10-12x/day,
Among seizures  neonate is normal
Type of seizures :  Focal clonic
 Focal tonic
 Apnea
D/ base on history of family
Autosomal Dominant
2. “Benign Idiopatic Neonatal Seizure” (Fifth – Day Fits)
Clinical sign :
 Occur  the end of the first week (the 4 -5
days of life) and disappear within 15 days
 Term baby & spontaneous delivery
 Type of seizure :  Focal Clonic /
 Multifocal
 Apnea
 Occur 24 hours
80% : Epileptic statue during this interval
55
 Laboratory Investigation
Primary tests
 Blood glucose, calcium and magnesium
 Complete blood count, differential leukocyte count
and platelet count
 Electrolytes
 Arterial blood gas
 Cerebral spinal fluid analysis and cultures
 Blood cultures & sensitivity test
56
 Laboratory Investigations (cont)

 TORCH titers, ammonia level, head sonogram and

amino acids in urine.

 EEG (Normal in about 1/3 of cases)

 Cranial ultrasound for hemorrhage and scarring

 CT  To diagnose cerebral malformations &

hemorrhage

57
 Management of Seizures
Management goals
 Achieve systemic homeostasis (airway, breathing and
circulation).
 Correct the underlying cause if possible.
 10% dextrose solution (2cc/kg IV) empirically to
any seizuring neonate.
 Calcium gluconate (200mg/kg IV), if hypocalcemia
is suspected .
 Anticonvulsant drugs 58
 Anticonvulsants
Drug Dose Comments Side Effects

Phenobarbital  Loading dose:  It is the drug of  Hypotension

10-20 mg/kg. choice.  Apnea
Add 5 mg/kg to  Administer IV
a maximum of over 5 minutes.
40 mg/kg  Therapeutic
level: 20-40
g/ml.
 Maintenance:  Administer IM,  Monitor
3-5 mg/kg/day IV, or PO every respiratory
in divided 12 hours. status during
doses every 12  Begin therapy administration
hours. 12 hours after and assess IV
loading dose. site. 59
 Anticonvulsants (cont)

Drug Dose Comments Side Effects

When seizures are not controlled with phenobarbital alone.

Phenytoin  Loading dose:  Administer IV at  Do not give IM.

15-20 mg/kg IV a maximum rate  Toxicity is a
over 30 min. of 0.5 mg/kg/min problem with this
 Maintenance: 4- drug.
 Maintenance: 8 mg/kg/day by  Cardiac
3-5 mg/kg/day. IV push or PO. arrhythmias
 Divide total dose  Cerebellar
and administer damage
IV every 12
hours.

60
 Anticonvulsants (cont)

Drug Dose Comments Side Effects

For treatment of status epilepticus.

Benzodiazepines  Lorazepam:  Administer IV.  Respiratory

0.05 – 0.1 mg/kg  Repeat every 15 depression,
 Diazepam: 0.1 – minutes for 2-3  Interferes with
0.3 mg/kg/dose. doses if needed. bilirubin binding to
 Maximum dose is albumin
2-5 mg.
 It can be given
once as a PO
dose of 0.1-0.3
mg/kg. 61
 Magnesium sulfate 50%, 0.2ml/kg or 2mlEq/kg.

 In pyridoxine dependency give pyridoxine 50mg IV as a

therapeutic trial. Seizures will stop within minutes.

 Antibiotics in suspected sepsis.

 Stopping AEDs two weeks after last seizure episode is

acceptable as prolonged medication can adversely affect

the developing brain.

62
 Prognosis
 Best prognosis with:  Hypocalcemia
 Pyridoxine dependency
 Subarachnoid hemorrhage

 Hypoglycemia
 Worse prognosis with:  Anoxia
 Brain malformation

 Chronic seizures 15-20%

 Sequelae:  Mental retardation
 Cerebral palsy

63
THE END