SlideShare una empresa de Scribd logo
1 de 124
Descargar para leer sin conexión
MEKELLE
UNIVERSITY
CHS
DEPARTMENT OF

PEDIATRICS &
CHILD HEALTH

SEMINAR ON MANAGEMENT OF COMMON NEONATAL PROBLEMS
By:
KIROS W/GERIMA
KIBRA SEBUH
KIFLOM SEYOUM
KESATEA G/WAHD
WORKU ASFAW
12/23/2013

1
Seminar outline
Neonatal Sepsis
Hypothermia
Respiratory distress syndrome
Perinatal Asphyxia
Neonatal Seizure
Neonatal Jaundice
Rh and ABO incompatibility
New born Anemia
Hypoglycemia
References and Sources


12/23/2013

2
NEONATAL SEPSIS
by Kiros Weldegerima

12/23/2013

3
Sepsis Outline of presentation
•
•
•
•
•
•
•
•

Classifications
Risk factors
Clinical Manifestations
Meningitis and Pneumonia
Diagnostic work up
Management principles
Prevention Strategies of Sepsis
Hypothermia and its management

12/23/2013

4
Neonatal Sepsis
Infection or sepsis is a problem faced to all new
borns
But the risk and severity is high in small and
premature infants
It is the cause of 30-50 % of Neonatal mortality
in developing countries
Sepsis in the Neonate includes
meningitis, septicemias, pneumonia, Arthritis, o
steomyelitis, and UTI or combinations of those.
12/23/2013

5
• Neonatal Sepsis can be divided as early and
late onset depending on the time of
occurrence
• Early-onset neonatal sepsis occurs with in the
first 72 hrs of life in 90% of cases
– Is caused by organisms prevalent in the
maternal genital tract
– Or in the labor room or operation theatre
where the neonate exposes initially to the
Environment
12/23/2013

6
Early onset Causative Agents
– Majority are caused by Group B
streprococcus, E-coli, klebsiela and
enterobacter
– Majority manifest with respiratory distress
due to an early intrauterine pneumonia
– The manifestation of illness is earlier than
the time limit of 1 week (24hr=85%, 2448hr=5%, 2-6 days=10)

12/23/2013

7
RISK FACTORS
Neonatal sepsis is associated with certain high
risk obstetric factors;
-Birth asphyxia
-Unclean vaginal examination
-foul smelling liquor
-prolonged labor(>24 hours)
-preterm and low birth weight Neonates
-prolonged rupture of membranes(>18 hours)
-maternal pyrexia
12/23/2013

8
Late onset causative Agents
• Late onset neonatal sepsis occurs after 7 days
most of which is after the first week of life up to
90 days.
• Most are caused by gram negative bacteria
– Klebsiela, enterobacter, E-coli, pseudomonas
and salmonella
– Gram positives like staphylococcus aureus
also contribute as causes of late onset sepsis.

12/23/2013

9
Infection Acquiring areas
Late onset infections are acquired as
nosocomial after delivery in:
-the normal newborn nursery
-Neonatal Intensive care Unit or
-the Community.

12/23/2013

10
Sources of infection in late onset
The usual sources of late onset neonatal sepsis:
-Incubators
-Resustation Equipment
-Feeding bottles
-Catheters
-Infusion sets and sites

12/23/2013

11
Clinical features
• It may be subtle especially in those who
are very small and premature
• This is mostly due to depressed immunity
of the premature neonates
• Early manifestations could be change in
behavior or feeding patterns
• But Gradually/sometimes suddenly they
develop signs and symptoms

12/23/2013

12
Clinical features of sepsis
Common clinical Features are
-Lethargic/Unconscious
-Inactive/Unresponsive
-failure to suck
-Hyperthermia/Hypothermia
-Respiratory Distress/Apnea
-failure to gain weight/weight loss
-Anemic/pale conjunctiva, palms
12/23/2013

13
Bacterial meningitis
• About a third of babies with neonatal sepsis can
have coexisting meningitis
• It is more common with late onset neonatal
sepsis
• Clinical evidence of meningial irritation are
usually absent in the new born period
• So to diagnose meningitis in New born we should
see other Clinical clues
12/23/2013

14
Meningitis cont.…
In a baby with sepsis the findings of
-convulsion/twitching
-staring look/fixed eye
-Bulged anterior fontanel
-abnormal excessive high pitched cry
Should arouse the suspicion of meningitis and
proceed with lumbar puncture.

12/23/2013

15
Lumbar puncture result that Indicates
meningitis

12/23/2013

> 30 cells/ml in Neonates , other than
Neonate >5 cells/ml of CSF
>60% polymorphs cells
–CSF glucose /blood glucose ratio <50%
–Protein>150 mg/dl in Terms and >175
in preterm
–Presence of microorganisms
–If the CSF not clear may also suggest
abnormality.

16
Pneumonia in the newborn
• Is more common in early onset neonatal sepsis
• Some peculiarities of pneumonia in the NB
– Minimal clinical signs
– Generalized signs of sepsis predominate esp in
premature NBs
– Some neonates can have apnea rather than
tachypnea.
– Clinical signs of pneumonic consolidation may not be
evident in the neonatal period

12/23/2013

17
Diagnostic work up of sepsis
• Clinical features + presence of high risk
obstetric factors
• Blood culture and sensitivity
• CSF analysis when indicated
• Chest X-ray
• Urine analysis and /or urine culture
• Head to Toe physical examination to identify
focus of infection (bone, joint, skin, GI)
12/23/2013

18
Management
• Depending on the etiologic agent but
Till etiologic agent is identified:– Good broad spectrum coverage i.e. for gram +ve
and gram –ve organisms is essential

• First line drugs
– Crystalline penicillin 100,000iu/kg /day in two
divided doses and
– Gentamicin 5 mg/kg/day in two divided doses
– Change crystalline penicillin with Ampicillin if
Listeria monocytogens is incriminated as the
causative agent
12/23/2013

19
Management
In meningitis the dose of Ampicillin and
Crystalline penciline are doubled.
 Second line drugs
– Ceftriaxone 50mg/kg/dose BID +
– Aminoglycoside dose which is also 50mg/kg
BID.
• Dose of ceftriaxone is doubled in cases of
meningitis
• Supportive therapy to correct metabolic
complications
12/23/2013

20
Management cont.
Duration of therapy
-suspected sepsis( blood culture –ve)= 7

days
-proven sepsis(blood culture +ve)=14 days
-Gram positive meningitis=14 days
-Gram negative meningitis=21 days
-Septic arthritis/osteomyelitis=4-6 weeks
12/23/2013

21
Prevention strategies of Neonatal
infections

Universal precautions
-Hand washing before entering labor ward and
before and after examining each infant
-wear Gowns and slippers when entering NICUs
-Health care providers with acute infections(
fever,ARI,skin lesions and Viral exanthemas)
should be restricted from providing care to the
Neonates
12/23/2013

22
Prevention Cotd…
-keep clean both the NICU and labor ward by
Cleaning and Fumigating at regular interval
-Proper skin and cord care
-Keep all Equipments used in NICU and labor
ward clean so there will be no infection source.

12/23/2013

23
Hypothermia
• Skin temperature of <36.5 and core
temperature of <35.5
• Neonates have high surface area to volume
ratio ,so heat loss is so much higher.
• After birth , the skin and core temperature of
the baby fall by 0.1 and 0.3/min respectively
.Which is equivalent to heat loss of 200kcal/kg
body weight/minute.
Mechanisms of heat loss/production
Mechanisms of heat loss:
1 Convection
2 Conduction
3 Radiation
4 Evaporation(common source of heat loss)
Mechanism of heat production
1 muscular activity
2 metabolic thermogenesis(most important
source of heat production in the new born)
Thermo Regulation

Thermo neutral environment :This is the ideal
temperature at which the baby can maintain
normal body temperature.
The optimal function of heat generating system
is dependent up on the integrity of
-CNS thermo regulation system
-adequacy of brown fat
-availability of glucose and oxygen
-NBW and term gestational age.
Stages of hypothermia
 36-36.4 c (96.8-97.5f)
-mild hypothermia (cold stress)
 32-35.9 c (89.6-96.6f)
-moderate hypothermia
 <32 c (89.6f)
-severe hypothermia (neonatal cold injury)
Warm chain system
• System of keeping the baby warm immediately after
birth,in delivery room,post partum ward
,transportation and while nursing the baby at home.
components:
-immediate drying
-warm resuscitation
-skin to skin contact with the mother
-immediate initiation of breast feeding
-bathing and weighing post pond
-appropriate clothing and bedding
-warm transportation.
Causes of hypothermia
External factors
cold environment,wet or naked baby ,blood
sampling,IV sampling
Poor ability to conserve heat
large surface area,poor insulation,paucity of fat,
Poor metabolic heat production
-deficiency of brown fat(preterm ,SFD)
-CNS problems
-hypoxia
-hypoglycemia
Sign and symptoms of hypothermia
1 peripheral vasoconstriction
Acrocyanosis
cold extrimity
decreased peripheral perfusion
2 CNS depression
Lethargy
Poor feeding
Apnea and bradycardia
3 Increased metabolism
hypoglycemia
hypoxia
metabolic acidosis
4 Increased pulmonary arterial pressure
tachypenia
respiratory distress
Management of hypothermia
There are 3 methods:
1.Kangaroo mother care
2.Warming in an open care using a radiant
heater
3.Warming in an incubator
Hazard’s of temperature control:
hyperthermia
undetected infection
volume depletion.
RESPIRATORY DISTRESS and APNEA
IN THE NEWBORN
PREPARED BY KIBRA.S

12/23/2013

32
RESPIRATORY DISTRESS
Definition
• The presence of any one of the following four
clinical features :
– RR > 60/min ( counted two times for full one
minute)
– Significant lower chest indrawing
– Grunting
– Central cyanosis

12/23/2013

33
ETIOLOGY
1.Pulmonary cause
Lung parenchyma disease

Congenital airway
obstruction

Intrathoracic
malformation

Hyaline membrane disease

Choanal atresia, nasal
edema

Pulmonary hypoplasia or
agenesis

Meconium aspiration
syndrome

Maroglossia, micrognathia,
retrognathia

Diaphragmatic hernia

Congenital pneumonia

Congenital goiter, cystic
hygroma

Intra thoracic cyst

Transient tachypnea of the Subglottic stenosis ,
newborn
laryngomalacia
Bronchopulmonary
dysplasia

Congenital lobar
emphysema

Tracheomalacia, congenital
tracheal stenosis

Pulmonary hemorrhage,
air leak
12/23/2013

34
2.Extrapulmonary cause
Cardiac

Metabolic

Neurological

Hematological

Congenital heart
disease

Hypoglycemia

Neonatal meningitis Anemia

Congestive heart
failure

Hypocalcaemia

Neonatal seizure

Cardiac arrhythmia

Hypothermia

Hypoxic ischemic
encephalopathy

Metabolic acidosis

Extreme immaturity

Polycythemia

Intracranial bieed

12/23/2013

35
APPROACH
 History
•
•
•
•
•
•
•

12/23/2013

Gestational age
Previous preterm baby
Antenatal steroid prophylaxis
Maternal DM
Ante partum hemorrhage
PROM
Prolonged duration of labor

36
CONT’D
•
•
•
•
•
•
•

12/23/2013

Maternal fever
Unclean vaginal examination
Foul smelling, meconium stained liquor
Hx of intrapartum or post partum suctioning
Excessive salivation
Difficulty of feeding
Hx of traumatic delivery

37
CONT’D
Physical Examination
Vital sign, capillary refill time and SO2
Meconium staining of the cord or nail
Hyperinflated chest or with bowel sound
Cyanosis, tachycardia, murmur
Scaphoid abdomen, hepatomegally
Evidences of intracranial bleed
Unable to pass nasal catheter

12/23/2013

38
CONT’D
Investigation
•
•
•
•
•
•

12/23/2013

Blood group of mother and baby
CBC , CXR
Septic screening & complete septic work up
Serum electrolytes and blood sugar
gastric aspirate (shake test, PMN cells)
Cord pH, arterial blood gas

39
MANAGMENT
General MX
– Give vit.k if not given
– Basic support care
• Keep in thermo neutral zone
• Breast feeding or assist feeding
• Maintain adequate oxygenation & circulation

Specific TX for specific problems
– Chest tube, decongestive measures, volume expanders,
antibiotics, surgical correction

12/23/2013

40
Hyaline Membrane Disease
 Incidence
– Primarily in premature infants; inversely
proportional to GA & birth weight

 Risk factor
–
–
–
–
–
–

Prematurity
Maternal DM
Male sex
2nd born twins
C/S delivery
Perinatal asphyxia

 Protective factor
12/23/2013

41
Pathogenesis

12/23/2013

42
CONT’D
Clinical Feature
-Signs occur with in minutes or hours of
birth, reach peak with in 3 days
-Characteristically
•
•
•
•
•
12/23/2013

Tachypnea
Nasal flaring
SC or IC retraction
Cyanosis
Expiratory grunting
43
CONT’D
Diagnosis
─based on clinical picture in conjunction with
characteristic chest radiograph
─The CXR abnormalities:
Low lung volume
Diffuse reticulogranular ground glass appearance
with air bronchogram

12/23/2013

44
CXR findings in Classic RDS
* Bell-shaped thorax

* ↓lung volume
* Air bronchogram
extended beyond cardiac
border
* Absolutely opaque lung
(whiteout lung)

12/23/2013

45
CONT’D
 Management
Basic supportive care
Specific measures
Prevent hypoxia & acidosis
 Warm humified o2 administration
 CPAP(indication, procedure & complication)
 Assisted ventilation

Surfactant replacement therapy
(poractant,calfactant,beractant)

 Prevention
Prenatal testing & appropriate prophylaxis
12/23/2013

46
Congenital pneumonia
• Is acquired transplacentally or perinatally
• Accounts for >50% of cases of RD in the new born
 Risk factor
–PROM
–Prolonged labour (> 24 hrs)
–Unclean vaginal examinations.
–Foul smelling liquor
–Maternal fever
12/23/2013

47
CONT’D
 Causative organisms:
-Group B streptococcus
-Gram negative organisms : E.coli, klebsiela, pseudomonas
-Staph aureus and Listeria monocytogens

 Clinical manifestations
Respiratory distress soon after birth
Recurrent apneic attack
They are often asphyxiated and sick at birth
 Prolonged capillary filling time
 Hypothermia
Cough is rare

12/23/2013

48
Investigations
– CBC, esp. ANC
– Gastric aspirate for PMN
– Blood culture
– CXR(infiltrates, lobar consolidation, interstitial
reticular opacities)

12/23/2013

49
Management
– Basic supportive therapy
– Specific
• Emperical broad spectrum antibiotics
– Penicillin/Ampicillin 100mg/kg in 2 divided doses +
Gentamicin 4mg/kg q24hr or 2.5 mg/kg q12hr

12/23/2013

50
Meconium Aspiration Syndrome
Definition
• Respiratory distress in newborn infants
born through meconium stained
amniotic fluid whose symptom cannot
be otherwise explained

Incidence
─10-15% of births-meconium stained amniotic fluid
– 5% -meconium aspiration pneumonia
• 30% require mechanical ventilation
• 3-5% expire
12/23/2013

51
CONT’D
 Risk factors
• Placental dysfunction
• Fetal hypoxia
• Ante partum haemorrhage
• Post maturity or SGA
• Listeriosis
• Breech delivery
12/23/2013

52
CONT’D
Pathophysiology
─Fetal hypoxia
– Peristalsis & IU passage of meconium
– Meconium stained amniotic fluid
– Meconium aspiration
– Peripheral & proximal air way
obstruction, inflammatory &chemical pneumonitis

12/23/2013

53
CONT’D
Clinical feature
– Respiratory distress- onset soon after birth in a
baby born to mother with meconium stained
liquor .
– Hyper inflated chest
– Meconium stained skin and cord
– Urine may appear dark and brown

12/23/2013

54
CONT’D
Investigation
– CXR
• Hyperinflation
• Bilateral fluffy shadows
• Evidence of air leak

12/23/2013

55
12/23/2013

56
CONT’D
 Management
─Prevention of meconium aspiration
• Prevention of IU hypoxia
• Intrapartum suctioning

– Postnatal suctioning
• Thick meconium
–
–
–
–
–

Direct laryngoscopy & tracheal suction
Stabilize the baby
Stomach wash
Work up for sepsis
Antibiotics can be started

• Thin meconium
– Depressed baby-do all like thick meconium
– Active baby-no tracheal suctioning and needs close observation
12/23/2013

57
APNEA
Definition
– Cessation of respiratory airflow
– Absence of respiratory movement

• Apnea vs periodic breathing
Incidence
– Increases with decreasing GA

12/23/2013

58
Classification
• Based on the cause
– Primary(apnea of
prematurity)
– Secondary

• Based on presence of
continued inspiratory
effort and upper airway
obstruction
– Central
– Obstructive
– Mixed

12/23/2013

59
CONT’D
Pathogenesis
unable to react to hypercapnia
•
•
•
•
•
•
•

12/23/2013

Impaired respiratory response(hypercapnia)
Apnea
↓HR, Pao2
Hypoperfusion and hypoxia
Hypercapnia
Recurrent apnea(≥3 attacks in one hour)
Brain damage & multiorgan damage

60
CONT’D
 Management
General management
–
–
–
–
–

ABC of resuscitation
Avoid vigorous suctioning
Keep NPO for 24 hrs put them on maintenance IVF
Keep in thermoneutral environment
Treat the underlying cause of apnea

Specific therapy
• Drug─theophylline
─aminophylline
─ caffeine
• Positive pressure ventilation
12/23/2013

61
prepared by kiflom seyoum
12/23/2013

62
Layout
•
•
•
•
•
•
•
•

Definition
epidemiology
Pathophysiology
Risk factors
Clinical features
Management
Prevention
Neonatal seizure

12/23/2013

63
Perinatal Asphyxia
Definition:


PNA is an insult to the fetus or newborn due to lack of oxygen (
hypoxia ) and /or a lack of perfusion ( ischemia ) to various organs.



Failure to establish efficient breathing at one minute of age(APGAR
score 0 - 6) with hypo/hypertonia and/or seizure.


This definition using APGAR score is not applicable in



Babies with birth trauma



12/23/2013

Preterm babies

Congenital neurologic abnormalities

64
Epidemology
•
•
•
•
•

Ranges 1-1.5% in gneral
9% in babes born <36 weeks of gastion
0.3% in babies born >36 weeks of gastion
Accounts 23% of perinatal death
23-30% of survivors have permanent damage
like CP

12/23/2013

65
Timing of ingury
• Asphyxia can occur in the,
 Antepartem

Intrapartem
 Postnatal priod

12/23/2013

66
Risk factors
1 .Antepartem condition
 Abnormal maternal oxygenation ( sever
animia, cardiopulmonary disease)
Inadequate placental perfusion( sever HTN,
maternal vascular disease)
Congenital infection or anomalies

12/23/2013

67
Conti…
2. intrapartem events
Interruption of umblical circulation (true
knote, cord prolaps)
inadequate placental perfusion ( abrabtio
placenta, utrine rupture, abnormal utrin
contraction )
Abnormal maternal oxygenation
Vasa previa
12/23/2013

68
Conti…
• 3, post natal disorders
Persistent plumnary hypertention of the new
born
Sever circulatory insuficency ( acut blood loss,
septic shock )

12/23/2013

69
Eitology and pathphysiology
90% of insult occur due to placental
insufficiency
Decrease oxygen supply &
Decrease carbon dioxide and hydrogen
removal
<10% are post natal insult due to pulmonary,
CVS or neurologic insufficiency

12/23/2013

70
Cont…
• When the new born is depraved of O2 an
initial period of rapid breathing occur
• This is followed by primary apnea
• Which responds to O2 administration and
physical stimulation

12/23/2013

71
Cont…
If asphyxia contnues the new born devoleps
Gasping respiration
Decreased puls rate
Blood pressure fail
And the new born develops secondary apnea
which will respond only to advanced life
support including CPAP

12/23/2013

72
Con…
• If asphyxia is not reversed on time there will
be hypoxic damage that leads to ischemic
challenge
• A diving reflex will be initiated that causes
shunting of blood to vital organs

12/23/2013

73
Clinical feature
• Depends on the organ affected
• Target organs of prenatal asphyxia
 Kidney in 50% of cases

CNS in 28% of cases

CVS in 25% of cases
 Pulmonary 23% of cases

12/23/2013

74
Renal dysfunction
• Often accompanies prenatal asphyxia
• renal damage ranges from reversible cloudy swelling &
hydropic digeneration of tubles to infarction of the
entire nephron.
• Decrease in UO(<0.5ml/kg/hr which may last 2 day to 2
weeks
• Protein & cast may present in the urin
• Gross hematuria may present
• Elevation of BUN& creatinine may occur
• Poly urea may flow oliguric phase or they may develop
anuria
12/23/2013

75
CVS dysfunction
• May cause myocardial ischemia which usually
is transient
• Patients show tachypnea,tachycardea &
hepatomegally consistent with heart fealur
• Rarely causes cardiogenic shock and death

12/23/2013

76
Pulmonary dysfunction
1.Plumonary edema
Due to myocardial dysfunction
May have sign of respiratory distress
2.Acute respiratory distress syndrome
Increased plumnary capilary permebility to
plasma protien which leads to inactivation of
surfactant

12/23/2013

77
Hypoxic ischemic encephalopathy
• The most serous complication of perenatal asphyxia
• The neuralgic squale often persists
• Hypoxia impairs cerebral oxidative mechanism and
leads to myocardial depression this leads to fail in
cerebral blood flaw
• And then ischemia of the brain tissue occur
• Persistance of hypoxia increase anarobic glycolysis
which leads to lactic acidosis
• Worsening of lactic acidosis if not corrected on time
cuases loss of cerebral vascular auto regulation
12/23/2013

78
Conti…
• Most of the time prolonged partial episode of
aspheyxia is because of abruptio placenta
• And usually it causes diffuse cerebral necrosis
• Clinically this may be present in the form of seizure
and paresis.
• Acute total asphysia which is mainly due to cord
plolapse primerly affects brain stem,thalamus, &
basal ganglia.
• This may manifest in the form disturbance of
respiration,heart rate & blood pressure
12/23/2013

79
Investstigations
• EEG-to determine severity presence of seizure
• Cranial u/s- to determine presence ICH &
brain edeama
• CT scan –early (2-4 days) brain edema
-late(2-4weeks) for encephalomalesia

12/23/2013

80
Sarnat staging of hypoxic-ischemic encephalopathy.
Grade 1
(mild)

Grade2
(moderate)

Level of
consciousness

Irritable/hyperalert

Lethargy

Coma

Muscle tone

Normal or
hypertonia

Hypotonia

Flaccid

Tendon reflexes

Increased

Increased

Depressed or absent

Seizures

Absent

Frequent

Frequent

Complex reflexes

Normal

weak

Absent

Prognosis

Good
(100%) Normal

12/23/2013

Grade 3 (severe)

Variable
High mortality and
(80% ) Normal neurological disability
(50% Death 50%
major sequelae)
81
Management of perinatal asphyxia
• Anticipate need for neonatal resuscitation
from maternal obstetric & labor history
• Avoid blood pressure fluctuation
• Intravenous fluid 2/3 of maintenance
• Appropriate ventilation support
• Correct metabolic abnormalities
• Prophylactic anti convulsant (phenobarbital)..?
12/23/2013

82
Therapeutic hypothermia
• It improves out come after perinatal asphyxia
• The only effective neuro protective therapy
currently available for Tx of neonatal
encephalopathy
• Safe and easy to administer
• Selective head cooling & whole body
cooling…?

12/23/2013

83
Prevention of prenatal asphyxia
 The minimum preventive measure which is
provided during perinatal period is much better
than a sophisticated care provided to an
asphyxiated new born.
 Prenatal assessment of changing fetal and
placental condition by clinical assessment and
altrasonography
 Fetal BPP
 Monitor progress of labor
 Effective neonatal resuscitation
12/23/2013

84
Neonatal seizure
The most important & common indicator of
significant neurologic dysfunction in the
neonatal period
The immature brain is more likely to develop
seizure
Not similar to adult b/c of ariboraisation of
axons dendrites & myelin sheath

12/23/2013

85
Cont…
• They are five clinical types of NS
1.subtle
2.clonic
3.Tonic
4.spasem
5.Myoclonic

12/23/2013

86
Con…
• Based on EEG NZ classified into three
Electroclinical seizure
Electrical seizure
Clinical seizure

12/23/2013

87
causes
1.Age 1-4 days
HIE
IVH
Drug toxicity,(lidocain,pencilin)
Acute metabolic disorder

12/23/2013

88
Conti…
Age (4-14 days)
Infection
Metabolic disorder
Benign neonatal convelsion
kernicterus

12/23/2013

89
Cont…
Age (2-8wks)
Infection
Head injury
Inherited disorder of cortical development

12/23/2013

90
Diagnosis
Post natal & prenatal history
Blood should be obtaine
Lumbar puncture
EEG(show paroxysmal activity, sharp wave )

12/23/2013

91
Management of NS
Treatment of the underlying etiology
Complete control of clinical as well as
electrographic seizure vs clinical seizure
control…?
Neonates required assisted ventilation after
receiving IV or PO loading doses of AED

12/23/2013

92
CONT…
1.Phenobarbitol
 The drug of first choice in the neonatal seizure
 20mg/kg loading dose, if not effective an additional
dose of 5-10mg/kg until a maximam dose of 40mg/kg,
 the mentenance doses is 3-6mg/kg
2.Phenytoin
 If no response phenytoin loading dose of 15-40mg/kg
can be given
 Rate must note exced 0 .5-1mg/kg/min to pereven
cardiac toxicty
12/23/2013

93
Cont…
3.Lorazepam;
the initial drug used to control acute seizure
Can be used as first line or second line Tx in
the new born who didn’t respond to
phenobarbitol or phenytone
4.diazepam;
It is highly lipophilic so cleared very quickly
out carring the risk of recurrence of seizure
12/23/2013

94
When to discontinu…..?
• At the time of discharge
• two wks or three month after discharge if the
neonate had sever PNA

12/23/2013

95
prognosis
• Mortality from neonatal seizure has decreased
from 40% to 20%.
• The correlation b/n EEG & prognosis is very clear
• Prolonged electrographic seizure >10min/hr,
multifocal periodic electrographic discharge,&
spread of electrogrophic seizure to contralateral
hemospher has poor prognosis
• Seizure due to HIE 50% of them have normal out
come
12/23/2013

96
97

NEONATAL JAUNDICE

12/23/2013
JAUNDICE
98



Visible form of bilirubinemia
 Adult

sclera >2mg / dl
 Newborn skin >5 mg / dl





Occurs in 60% of term and 80% of preterm
neonates
Is common problem and is mostly benign.
However, significant jaundice occurs in 6 % of
term babies
12/23/2013
99



The conjugated bilirubin will go to bowel with bile.



In adults E.coli and C.perfirngens present but absent in

neonets.


β-glucourinidase enzyme present in newborns.

Conjugation and enterohepatic resorption.
12/23/2013
100



Direct Vs Indirect?
 Van

den Bergh reaction



Indirect billirubin acts as an anti-oxidant



It is only the indirect billirubin which crosses the
BBB and results in billirubin encephalopathy

12/23/2013
Physiologic Jaundice
101



Jaundice becomes evident as physiologic in
neonates B/c :
A. Short life span of RBCs(70-90days)
B. RBC mass is increased
C. Immature ligandine
D. Less UDPGT
E. High activity β-glucuronidase (gut)
F. Decreased flora in the gut

12/23/2013
Physiologic jaundice ( Icterus
neonatorum)
102

Preterm

Term

Peak time

4th -7th days

2nd – 4th day

Peak level

8 – 12 mg/dl

5 -6 mg/dl

Resolution time Before 10th day

5th – 7th day
12/23/2013
Physiologic Vs pathologic
103

Signs

PhysiologicJx

Pathologic Jx

Clinical Jx

Visible in2-3day

With in 24hrs

TSB rise

<5mg/dl/day

>5mg/dl/day

TSB

Term<12mg/dl
Preterm<15mg/dl

Term>12g/dl
Preterm>15mg/dl

Conj BBn

<1.5mg/dl

>1.5(2)mg/dl

Jaundice
persisting

Term <1 week
Preterm <2weeks

Term >1week Preterm
>2weeks
12/23/2013
Jaundice associated with breast feeding
104

Breast milk

Breast feeding

Cause

?glucouronidase in ↓ intake
BM

Time of
onset
Max level

After 1st week

In the 1st week

10 – 30 mg/dl

Any

Treatment

Discontinuation for Continuing
2 – 3 days
breast feeding
12/23/2013
ETIOLOGY OF JAUNDICE
105

1. Jaundice appearing in the 1st 24 hr
Rh incompatability(erythroblastosis fetalis)
 ABO incompatibility
 Mild BG incompatibility (Kelly, Duffy Ags)
 Defect (G6PD def. and spherocytosis
 TORCHS
 Criggler Najar syndrome
 Transient familial neonatal jaundice


12/23/2013
Cont…
106

2.Jaundice appearing with in 24-72hr of age



Physiological jaundice
Conditions w/c aggravate physiologic Jx.

Cephalhematoma

Hypothermia

Prematurity

Hypoglycemia

Multiple bruises

hypoxia
12/23/2013
Cont…
107

3. prolonged jaundice( after 72 hrs.)
TORCHS
 Sepsis
 Hypothyroidism
 Biliary Artesia
 Breast milk jaundice
 Drugs (vit. K, oxytocin,diazepam)
 Metabolic disease eg. galactosemia


12/23/2013
108

Hemolytic disease of the
newborn


Rh incompatibility
 Less

common but sever than ABO incompatibility
 90% due to D antigen
 Black vs white
 Severity from mild hemolysis to sever anemia
 Dx by blood group incompatiblity
 Reduce risk of sensitization with 300μg of human
anti- D globulin during ANC ff up

12/23/2013
Cont…
109



ABO incompatibility
 Most

common cause of HDN but mild
 0.3-2.2% only manifest the disease.
 Type O mother with type A or B infant.
 Jaundice the only clinical manifestation.
 Hemoglobin level usually normal.
 Dx by ABO incompatibility (weak to moderate
positive direct coombs test)

12/23/2013
Clinical assessment of jaundice
110



Jaundice in the newborn progresses in cephalocaudal
direction


Face =5-7mg/dl



Chest =10mg/dl



lower abdomen /thigh= 12mg/dl



Sole/palms≥15mg/dl

12/23/2013
Work up neonates with Jx
111

History


Age of onset



Family history of Jaundice,pallor,splenectomy



Previous sibling with Jaundice



Maternal illness during pregnancy



Maternal drug intake



Delivery history e.g. PROM ,sepsis, prolonged
labor
12/23/2013
Cont’d
112

P/E
 Proper

classification of the newborn according to

GA, & wgt.
 Pallor,

petechea

 Bruises
 Dark

and cephalhematoma

urine and clay colored stool

 Examination

geared to specific cause
12/23/2013
Investigations
113








TSB with conjugated fraction
Hct with RBC morphology and reticulocyte
count
Bg of the baby with direct coomb’s test
Bg of the mother with indirect coomb’s test.
Specific investigations for suspected specific
problems

12/23/2013
Management
114

Aim













lower serum billirubin
decrease neurtoxicity

Principles of treatment
Avoid drugs w/c interfere with BBn
metabolism
Treat factors w/c↑ neurotoxicity
Give adequate feeding
Specific therapy
Decrease serum billirubin
12/23/2013
115



Lower serum Billirubin
Phototherapy
 Exchange transfusion




Phototherapy
 Indicated when TSB rises more than normal
but not exchange transfusion level
 May be therapeutic or prophylactic
12/23/2013
Prophylactic phototherapy
116

INDICATIONS
 RH

isoimmunization with sever hemolysis
 Birth weight<1000gm(EVLBW)
 Sever multiple bruises

SIDE EFFECTS
 Erythematous

skin rash
 Retinal damage
 Increased insensible water loss
 Bronze baby syndrome
 Loose stool
 Low calcium
12/23/2013
Exchange transfusion( ET)
117





Most effective way of treating Jaundice and
anemia
Could be partial or double exchange transfusion

INDICATIONS
 Rh isoimmunization with hydrops fetalis
 History of previous sibling required ET with pallor
 Cord blood Billirubin >5mg/dl
 Rise in Billirubin >0.5mg/dl/hr despite
phototherapy
 Hemoglobin <11gm/dl
 TSB >20mg/dl
 VLBW, preterm, sepsis
12/23/2013
Choice of blood for exchange BT
118



ABO incompatibility
 Use



O blood of same Rh type

Rh isoimmunization
 Emergency

0 -ve blood
 Ideal 0 -ve suspended in AB plasma
 or baby's blood group but Rh –ve


Other situations
 Baby's

blood group
12/23/2013
Exchange transfusion
119

COMPLICATIONS
 Portal

vein thrombosis
 Umbilical vein perforation/bleeding
 Necrotizing enterocolitis
 Cardiac arrest/arrhythmia
 Hypoglycemia, hypocalcemia, hypomagnisemia,
hyperkalemia
 Increased risk of infection
 Respiratory and metabolic acidosis
12/23/2013
KERNICTERS (Billirubin encephalopathy)
120



Definition: neurologic syndrome resulting from
deposition of unconjugated billirubin in brain cells .



Sites of billirubin staining and necrosis include
-Basal ganglia , Hippocampal cortex, Sub thalamic
nucleus & cerebellum
Cerebral cortex is spared





Half of the neonates with kernicters at autopsy have
extra neuronal lesions

12/23/2013
Pathophysiologic mechanism
121





Unconjugated BBn is nonpolar ,lipid soluble and can
traverse BBB.
Factors that ↑ billirubin toxicity
 Hypoxia

(asphyxia)
 Hypothermia & hypoglycemia
 sepsis
 Prematurity
 Acidosis
 Hypoalbuminemia

12/23/2013
Clinical staging of KI
122

Stage-1

Poor Moro reflex, decreased tone, lethargy,
poor
feeding, vomiting, high pitched cry

Stage-2

Opisthotonus, fever, seizure, rigidity,
oculogyric
crises,
paralysis of upward gaze

Stage-3

Stage-4
-

Spasticity is decreased

Late sequale including spasticity,athetosis,
deafness,MR,paralysis of the upward gaze
12/23/2013
Clinical progression of encephalopathy
123

12/23/2013
Thank you!

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

neonatal sepsis
neonatal sepsisneonatal sepsis
neonatal sepsis
 
Neonatal Sepsis
Neonatal SepsisNeonatal Sepsis
Neonatal Sepsis
 
Newborn Care: Care of high-risk and sick infants
Newborn Care: Care of high-risk and sick infantsNewborn Care: Care of high-risk and sick infants
Newborn Care: Care of high-risk and sick infants
 
Newborn adaptation
Newborn adaptationNewborn adaptation
Newborn adaptation
 
Low birth weight
Low birth weightLow birth weight
Low birth weight
 
Meconium aspiration syndrome
Meconium aspiration syndromeMeconium aspiration syndrome
Meconium aspiration syndrome
 
Prematurity
PrematurityPrematurity
Prematurity
 
Breastfeeding
BreastfeedingBreastfeeding
Breastfeeding
 
Neonatal Sepsis
Neonatal SepsisNeonatal Sepsis
Neonatal Sepsis
 
NEONATAL SEPSIS
NEONATAL SEPSISNEONATAL SEPSIS
NEONATAL SEPSIS
 
Neonatal hypoglycemia
Neonatal hypoglycemia Neonatal hypoglycemia
Neonatal hypoglycemia
 
Common neonatal disorders
Common neonatal disordersCommon neonatal disorders
Common neonatal disorders
 
Management of neonatal hypoglycemia ppt
Management of neonatal hypoglycemia pptManagement of neonatal hypoglycemia ppt
Management of neonatal hypoglycemia ppt
 
LOW BIRTH WEIGHT BABY
LOW BIRTH WEIGHT BABYLOW BIRTH WEIGHT BABY
LOW BIRTH WEIGHT BABY
 
Intensive care in neonates
Intensive care in neonatesIntensive care in neonates
Intensive care in neonates
 
Neonatal resuscitation
Neonatal resuscitation Neonatal resuscitation
Neonatal resuscitation
 
Low birth weight
Low birth weightLow birth weight
Low birth weight
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsis
 
Neonatal Hypothermia
Neonatal HypothermiaNeonatal Hypothermia
Neonatal Hypothermia
 
Respiratory distress of newborn
Respiratory distress of newbornRespiratory distress of newborn
Respiratory distress of newborn
 

Destacado

Common neonatal problems
Common  neonatal    problemsCommon  neonatal    problems
Common neonatal problemsAbdul Ghaffar
 
Minor disorders of newborn
Minor disorders of newbornMinor disorders of newborn
Minor disorders of newbornP V GREESHMA
 
Minor disorders of newborn
Minor disorders of newbornMinor disorders of newborn
Minor disorders of newbornPriya Dharshini
 
Nursing management of low birth weight(lbw) babies
Nursing management of low birth weight(lbw) babiesNursing management of low birth weight(lbw) babies
Nursing management of low birth weight(lbw) babiesRose Vadakkut
 
Common neonatal problems
Common neonatal problemsCommon neonatal problems
Common neonatal problemsVarsha Shah
 

Destacado (7)

Common neonatal problems
Common  neonatal    problemsCommon  neonatal    problems
Common neonatal problems
 
Minor disorders of newborn
Minor disorders of newbornMinor disorders of newborn
Minor disorders of newborn
 
Minor disorders of newborn
Minor disorders of newbornMinor disorders of newborn
Minor disorders of newborn
 
Nursing management of low birth weight(lbw) babies
Nursing management of low birth weight(lbw) babiesNursing management of low birth weight(lbw) babies
Nursing management of low birth weight(lbw) babies
 
Common neonatal problems
Common neonatal problemsCommon neonatal problems
Common neonatal problems
 
Neonatal Problems
Neonatal ProblemsNeonatal Problems
Neonatal Problems
 
Low birth weight
Low birth weightLow birth weight
Low birth weight
 

Similar a Managment of common neonatal problems

Managmentofcommonneonatalproblems 140201143840-phpapp01(1)
Managmentofcommonneonatalproblems 140201143840-phpapp01(1)Managmentofcommonneonatalproblems 140201143840-phpapp01(1)
Managmentofcommonneonatalproblems 140201143840-phpapp01(1)Ranbir Kaur
 
atypical neonatal infection
atypical neonatal infectionatypical neonatal infection
atypical neonatal infectionmandar haval
 
Perinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxPerinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxAmirAhmedGeza
 
Perinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxPerinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxAmirAhmedGeza
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsisdrskverma2
 
Neonatal Sepsis and Necrotizing Enterocolitis
Neonatal Sepsis and Necrotizing EnterocolitisNeonatal Sepsis and Necrotizing Enterocolitis
Neonatal Sepsis and Necrotizing EnterocolitisThe Medical Post
 
Newborn infection
Newborn infectionNewborn infection
Newborn infectionAbu Takele
 
Dengue in pregnancy
Dengue in pregnancy Dengue in pregnancy
Dengue in pregnancy annith123
 
Neonatal sepsis kinara
Neonatal sepsis kinaraNeonatal sepsis kinara
Neonatal sepsis kinaraKinara Kenyoru
 
2 diseases of the newborn
2 diseases of the newborn2 diseases of the newborn
2 diseases of the newbornNyl Oineza
 
Session 37_Neonatal Pneumonia.pptx
Session 37_Neonatal Pneumonia.pptxSession 37_Neonatal Pneumonia.pptx
Session 37_Neonatal Pneumonia.pptxAugustusCaesar7
 
Neonatal sepsis...ppt
Neonatal sepsis...pptNeonatal sepsis...ppt
Neonatal sepsis...pptRahul Dhaker
 

Similar a Managment of common neonatal problems (20)

Managmentofcommonneonatalproblems 140201143840-phpapp01(1)
Managmentofcommonneonatalproblems 140201143840-phpapp01(1)Managmentofcommonneonatalproblems 140201143840-phpapp01(1)
Managmentofcommonneonatalproblems 140201143840-phpapp01(1)
 
atypical neonatal infection
atypical neonatal infectionatypical neonatal infection
atypical neonatal infection
 
Perinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxPerinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptx
 
Perinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptxPerinatal asphyxia.lecture.pptx
Perinatal asphyxia.lecture.pptx
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsis
 
Neonatal Sepsis and Necrotizing Enterocolitis
Neonatal Sepsis and Necrotizing EnterocolitisNeonatal Sepsis and Necrotizing Enterocolitis
Neonatal Sepsis and Necrotizing Enterocolitis
 
Newborn infection
Newborn infectionNewborn infection
Newborn infection
 
Dengue in pregnancy
Dengue in pregnancy Dengue in pregnancy
Dengue in pregnancy
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsis
 
NEONATAL SEPSIS
NEONATAL SEPSISNEONATAL SEPSIS
NEONATAL SEPSIS
 
C r p
C r pC r p
C r p
 
Neonatal sepsis kinara
Neonatal sepsis kinaraNeonatal sepsis kinara
Neonatal sepsis kinara
 
Neonatal sepsis ppp
Neonatal sepsis pppNeonatal sepsis ppp
Neonatal sepsis ppp
 
2 diseases of the newborn
2 diseases of the newborn2 diseases of the newborn
2 diseases of the newborn
 
Neonatal Sepsis3
Neonatal Sepsis3Neonatal Sepsis3
Neonatal Sepsis3
 
PROTOCOLS FOR NEONATES
PROTOCOLS FOR NEONATESPROTOCOLS FOR NEONATES
PROTOCOLS FOR NEONATES
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsis
 
Neonatal sepsis
Neonatal sepsisNeonatal sepsis
Neonatal sepsis
 
Session 37_Neonatal Pneumonia.pptx
Session 37_Neonatal Pneumonia.pptxSession 37_Neonatal Pneumonia.pptx
Session 37_Neonatal Pneumonia.pptx
 
Neonatal sepsis...ppt
Neonatal sepsis...pptNeonatal sepsis...ppt
Neonatal sepsis...ppt
 

Último

Unit I herbs as raw materials, biodynamic agriculture.ppt
Unit I herbs as raw materials, biodynamic agriculture.pptUnit I herbs as raw materials, biodynamic agriculture.ppt
Unit I herbs as raw materials, biodynamic agriculture.pptPradnya Wadekar
 
Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Peter Embi
 
Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024EwoutSteyerberg1
 
BENIGN BREAST DISEASE
BENIGN BREAST DISEASE BENIGN BREAST DISEASE
BENIGN BREAST DISEASE Mamatha Lakka
 
Using Data Visualization in Public Health Communications
Using Data Visualization in Public Health CommunicationsUsing Data Visualization in Public Health Communications
Using Data Visualization in Public Health Communicationskatiequigley33
 
Red Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfRed Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfMedicoseAcademics
 
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfPAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfDolisha Warbi
 
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfSGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfHongBiThi1
 
Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.kishan singh tomar
 
SGK ĐIỆN GIẬT ĐHYHN RẤT LÀ HAY TUYỆT VỜI.pdf
SGK ĐIỆN GIẬT ĐHYHN        RẤT LÀ HAY TUYỆT VỜI.pdfSGK ĐIỆN GIẬT ĐHYHN        RẤT LÀ HAY TUYỆT VỜI.pdf
SGK ĐIỆN GIẬT ĐHYHN RẤT LÀ HAY TUYỆT VỜI.pdfHongBiThi1
 
High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)kishan singh tomar
 
AORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectionAORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectiondrhanifmohdali
 
AUTONOMIC NERVOUS SYSTEM organization and functions
AUTONOMIC NERVOUS SYSTEM organization and functionsAUTONOMIC NERVOUS SYSTEM organization and functions
AUTONOMIC NERVOUS SYSTEM organization and functionsMedicoseAcademics
 
ORAL HYPOGLYCAEMIC AGENTS - PART 2.pptx
ORAL HYPOGLYCAEMIC AGENTS  - PART 2.pptxORAL HYPOGLYCAEMIC AGENTS  - PART 2.pptx
ORAL HYPOGLYCAEMIC AGENTS - PART 2.pptxNIKITA BHUTE
 
Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Vaikunthan Rajaratnam
 
ANATOMICAL FAETURES OF BONES FOR NURSING STUDENTS .pptx
ANATOMICAL FAETURES OF BONES  FOR NURSING STUDENTS .pptxANATOMICAL FAETURES OF BONES  FOR NURSING STUDENTS .pptx
ANATOMICAL FAETURES OF BONES FOR NURSING STUDENTS .pptxWINCY THIRUMURUGAN
 
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdf
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdfSGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdf
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdfHongBiThi1
 

Último (20)

Unit I herbs as raw materials, biodynamic agriculture.ppt
Unit I herbs as raw materials, biodynamic agriculture.pptUnit I herbs as raw materials, biodynamic agriculture.ppt
Unit I herbs as raw materials, biodynamic agriculture.ppt
 
Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024
 
Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024
 
BENIGN BREAST DISEASE
BENIGN BREAST DISEASE BENIGN BREAST DISEASE
BENIGN BREAST DISEASE
 
Using Data Visualization in Public Health Communications
Using Data Visualization in Public Health CommunicationsUsing Data Visualization in Public Health Communications
Using Data Visualization in Public Health Communications
 
Red Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfRed Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdf
 
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfPAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
 
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
 
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfSGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
 
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
 
Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.
 
SGK ĐIỆN GIẬT ĐHYHN RẤT LÀ HAY TUYỆT VỜI.pdf
SGK ĐIỆN GIẬT ĐHYHN        RẤT LÀ HAY TUYỆT VỜI.pdfSGK ĐIỆN GIẬT ĐHYHN        RẤT LÀ HAY TUYỆT VỜI.pdf
SGK ĐIỆN GIẬT ĐHYHN RẤT LÀ HAY TUYỆT VỜI.pdf
 
High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)
 
AORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectionAORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissection
 
AUTONOMIC NERVOUS SYSTEM organization and functions
AUTONOMIC NERVOUS SYSTEM organization and functionsAUTONOMIC NERVOUS SYSTEM organization and functions
AUTONOMIC NERVOUS SYSTEM organization and functions
 
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
 
ORAL HYPOGLYCAEMIC AGENTS - PART 2.pptx
ORAL HYPOGLYCAEMIC AGENTS  - PART 2.pptxORAL HYPOGLYCAEMIC AGENTS  - PART 2.pptx
ORAL HYPOGLYCAEMIC AGENTS - PART 2.pptx
 
Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.
 
ANATOMICAL FAETURES OF BONES FOR NURSING STUDENTS .pptx
ANATOMICAL FAETURES OF BONES  FOR NURSING STUDENTS .pptxANATOMICAL FAETURES OF BONES  FOR NURSING STUDENTS .pptx
ANATOMICAL FAETURES OF BONES FOR NURSING STUDENTS .pptx
 
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdf
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdfSGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdf
SGK RỐI LOẠN TOAN KIỀM ĐHYHN RẤT HAY VÀ ĐẶC SẮC.pdf
 

Managment of common neonatal problems

  • 1. MEKELLE UNIVERSITY CHS DEPARTMENT OF PEDIATRICS & CHILD HEALTH SEMINAR ON MANAGEMENT OF COMMON NEONATAL PROBLEMS By: KIROS W/GERIMA KIBRA SEBUH KIFLOM SEYOUM KESATEA G/WAHD WORKU ASFAW 12/23/2013 1
  • 2. Seminar outline Neonatal Sepsis Hypothermia Respiratory distress syndrome Perinatal Asphyxia Neonatal Seizure Neonatal Jaundice Rh and ABO incompatibility New born Anemia Hypoglycemia References and Sources  12/23/2013 2
  • 3. NEONATAL SEPSIS by Kiros Weldegerima 12/23/2013 3
  • 4. Sepsis Outline of presentation • • • • • • • • Classifications Risk factors Clinical Manifestations Meningitis and Pneumonia Diagnostic work up Management principles Prevention Strategies of Sepsis Hypothermia and its management 12/23/2013 4
  • 5. Neonatal Sepsis Infection or sepsis is a problem faced to all new borns But the risk and severity is high in small and premature infants It is the cause of 30-50 % of Neonatal mortality in developing countries Sepsis in the Neonate includes meningitis, septicemias, pneumonia, Arthritis, o steomyelitis, and UTI or combinations of those. 12/23/2013 5
  • 6. • Neonatal Sepsis can be divided as early and late onset depending on the time of occurrence • Early-onset neonatal sepsis occurs with in the first 72 hrs of life in 90% of cases – Is caused by organisms prevalent in the maternal genital tract – Or in the labor room or operation theatre where the neonate exposes initially to the Environment 12/23/2013 6
  • 7. Early onset Causative Agents – Majority are caused by Group B streprococcus, E-coli, klebsiela and enterobacter – Majority manifest with respiratory distress due to an early intrauterine pneumonia – The manifestation of illness is earlier than the time limit of 1 week (24hr=85%, 2448hr=5%, 2-6 days=10) 12/23/2013 7
  • 8. RISK FACTORS Neonatal sepsis is associated with certain high risk obstetric factors; -Birth asphyxia -Unclean vaginal examination -foul smelling liquor -prolonged labor(>24 hours) -preterm and low birth weight Neonates -prolonged rupture of membranes(>18 hours) -maternal pyrexia 12/23/2013 8
  • 9. Late onset causative Agents • Late onset neonatal sepsis occurs after 7 days most of which is after the first week of life up to 90 days. • Most are caused by gram negative bacteria – Klebsiela, enterobacter, E-coli, pseudomonas and salmonella – Gram positives like staphylococcus aureus also contribute as causes of late onset sepsis. 12/23/2013 9
  • 10. Infection Acquiring areas Late onset infections are acquired as nosocomial after delivery in: -the normal newborn nursery -Neonatal Intensive care Unit or -the Community. 12/23/2013 10
  • 11. Sources of infection in late onset The usual sources of late onset neonatal sepsis: -Incubators -Resustation Equipment -Feeding bottles -Catheters -Infusion sets and sites 12/23/2013 11
  • 12. Clinical features • It may be subtle especially in those who are very small and premature • This is mostly due to depressed immunity of the premature neonates • Early manifestations could be change in behavior or feeding patterns • But Gradually/sometimes suddenly they develop signs and symptoms 12/23/2013 12
  • 13. Clinical features of sepsis Common clinical Features are -Lethargic/Unconscious -Inactive/Unresponsive -failure to suck -Hyperthermia/Hypothermia -Respiratory Distress/Apnea -failure to gain weight/weight loss -Anemic/pale conjunctiva, palms 12/23/2013 13
  • 14. Bacterial meningitis • About a third of babies with neonatal sepsis can have coexisting meningitis • It is more common with late onset neonatal sepsis • Clinical evidence of meningial irritation are usually absent in the new born period • So to diagnose meningitis in New born we should see other Clinical clues 12/23/2013 14
  • 15. Meningitis cont.… In a baby with sepsis the findings of -convulsion/twitching -staring look/fixed eye -Bulged anterior fontanel -abnormal excessive high pitched cry Should arouse the suspicion of meningitis and proceed with lumbar puncture. 12/23/2013 15
  • 16. Lumbar puncture result that Indicates meningitis 12/23/2013 > 30 cells/ml in Neonates , other than Neonate >5 cells/ml of CSF >60% polymorphs cells –CSF glucose /blood glucose ratio <50% –Protein>150 mg/dl in Terms and >175 in preterm –Presence of microorganisms –If the CSF not clear may also suggest abnormality. 16
  • 17. Pneumonia in the newborn • Is more common in early onset neonatal sepsis • Some peculiarities of pneumonia in the NB – Minimal clinical signs – Generalized signs of sepsis predominate esp in premature NBs – Some neonates can have apnea rather than tachypnea. – Clinical signs of pneumonic consolidation may not be evident in the neonatal period 12/23/2013 17
  • 18. Diagnostic work up of sepsis • Clinical features + presence of high risk obstetric factors • Blood culture and sensitivity • CSF analysis when indicated • Chest X-ray • Urine analysis and /or urine culture • Head to Toe physical examination to identify focus of infection (bone, joint, skin, GI) 12/23/2013 18
  • 19. Management • Depending on the etiologic agent but Till etiologic agent is identified:– Good broad spectrum coverage i.e. for gram +ve and gram –ve organisms is essential • First line drugs – Crystalline penicillin 100,000iu/kg /day in two divided doses and – Gentamicin 5 mg/kg/day in two divided doses – Change crystalline penicillin with Ampicillin if Listeria monocytogens is incriminated as the causative agent 12/23/2013 19
  • 20. Management In meningitis the dose of Ampicillin and Crystalline penciline are doubled.  Second line drugs – Ceftriaxone 50mg/kg/dose BID + – Aminoglycoside dose which is also 50mg/kg BID. • Dose of ceftriaxone is doubled in cases of meningitis • Supportive therapy to correct metabolic complications 12/23/2013 20
  • 21. Management cont. Duration of therapy -suspected sepsis( blood culture –ve)= 7 days -proven sepsis(blood culture +ve)=14 days -Gram positive meningitis=14 days -Gram negative meningitis=21 days -Septic arthritis/osteomyelitis=4-6 weeks 12/23/2013 21
  • 22. Prevention strategies of Neonatal infections Universal precautions -Hand washing before entering labor ward and before and after examining each infant -wear Gowns and slippers when entering NICUs -Health care providers with acute infections( fever,ARI,skin lesions and Viral exanthemas) should be restricted from providing care to the Neonates 12/23/2013 22
  • 23. Prevention Cotd… -keep clean both the NICU and labor ward by Cleaning and Fumigating at regular interval -Proper skin and cord care -Keep all Equipments used in NICU and labor ward clean so there will be no infection source. 12/23/2013 23
  • 24. Hypothermia • Skin temperature of <36.5 and core temperature of <35.5 • Neonates have high surface area to volume ratio ,so heat loss is so much higher. • After birth , the skin and core temperature of the baby fall by 0.1 and 0.3/min respectively .Which is equivalent to heat loss of 200kcal/kg body weight/minute.
  • 25. Mechanisms of heat loss/production Mechanisms of heat loss: 1 Convection 2 Conduction 3 Radiation 4 Evaporation(common source of heat loss) Mechanism of heat production 1 muscular activity 2 metabolic thermogenesis(most important source of heat production in the new born)
  • 26. Thermo Regulation Thermo neutral environment :This is the ideal temperature at which the baby can maintain normal body temperature. The optimal function of heat generating system is dependent up on the integrity of -CNS thermo regulation system -adequacy of brown fat -availability of glucose and oxygen -NBW and term gestational age.
  • 27. Stages of hypothermia  36-36.4 c (96.8-97.5f) -mild hypothermia (cold stress)  32-35.9 c (89.6-96.6f) -moderate hypothermia  <32 c (89.6f) -severe hypothermia (neonatal cold injury)
  • 28. Warm chain system • System of keeping the baby warm immediately after birth,in delivery room,post partum ward ,transportation and while nursing the baby at home. components: -immediate drying -warm resuscitation -skin to skin contact with the mother -immediate initiation of breast feeding -bathing and weighing post pond -appropriate clothing and bedding -warm transportation.
  • 29. Causes of hypothermia External factors cold environment,wet or naked baby ,blood sampling,IV sampling Poor ability to conserve heat large surface area,poor insulation,paucity of fat, Poor metabolic heat production -deficiency of brown fat(preterm ,SFD) -CNS problems -hypoxia -hypoglycemia
  • 30. Sign and symptoms of hypothermia 1 peripheral vasoconstriction Acrocyanosis cold extrimity decreased peripheral perfusion 2 CNS depression Lethargy Poor feeding Apnea and bradycardia 3 Increased metabolism hypoglycemia hypoxia metabolic acidosis 4 Increased pulmonary arterial pressure tachypenia respiratory distress
  • 31. Management of hypothermia There are 3 methods: 1.Kangaroo mother care 2.Warming in an open care using a radiant heater 3.Warming in an incubator Hazard’s of temperature control: hyperthermia undetected infection volume depletion.
  • 32. RESPIRATORY DISTRESS and APNEA IN THE NEWBORN PREPARED BY KIBRA.S 12/23/2013 32
  • 33. RESPIRATORY DISTRESS Definition • The presence of any one of the following four clinical features : – RR > 60/min ( counted two times for full one minute) – Significant lower chest indrawing – Grunting – Central cyanosis 12/23/2013 33
  • 34. ETIOLOGY 1.Pulmonary cause Lung parenchyma disease Congenital airway obstruction Intrathoracic malformation Hyaline membrane disease Choanal atresia, nasal edema Pulmonary hypoplasia or agenesis Meconium aspiration syndrome Maroglossia, micrognathia, retrognathia Diaphragmatic hernia Congenital pneumonia Congenital goiter, cystic hygroma Intra thoracic cyst Transient tachypnea of the Subglottic stenosis , newborn laryngomalacia Bronchopulmonary dysplasia Congenital lobar emphysema Tracheomalacia, congenital tracheal stenosis Pulmonary hemorrhage, air leak 12/23/2013 34
  • 35. 2.Extrapulmonary cause Cardiac Metabolic Neurological Hematological Congenital heart disease Hypoglycemia Neonatal meningitis Anemia Congestive heart failure Hypocalcaemia Neonatal seizure Cardiac arrhythmia Hypothermia Hypoxic ischemic encephalopathy Metabolic acidosis Extreme immaturity Polycythemia Intracranial bieed 12/23/2013 35
  • 36. APPROACH  History • • • • • • • 12/23/2013 Gestational age Previous preterm baby Antenatal steroid prophylaxis Maternal DM Ante partum hemorrhage PROM Prolonged duration of labor 36
  • 37. CONT’D • • • • • • • 12/23/2013 Maternal fever Unclean vaginal examination Foul smelling, meconium stained liquor Hx of intrapartum or post partum suctioning Excessive salivation Difficulty of feeding Hx of traumatic delivery 37
  • 38. CONT’D Physical Examination Vital sign, capillary refill time and SO2 Meconium staining of the cord or nail Hyperinflated chest or with bowel sound Cyanosis, tachycardia, murmur Scaphoid abdomen, hepatomegally Evidences of intracranial bleed Unable to pass nasal catheter 12/23/2013 38
  • 39. CONT’D Investigation • • • • • • 12/23/2013 Blood group of mother and baby CBC , CXR Septic screening & complete septic work up Serum electrolytes and blood sugar gastric aspirate (shake test, PMN cells) Cord pH, arterial blood gas 39
  • 40. MANAGMENT General MX – Give vit.k if not given – Basic support care • Keep in thermo neutral zone • Breast feeding or assist feeding • Maintain adequate oxygenation & circulation Specific TX for specific problems – Chest tube, decongestive measures, volume expanders, antibiotics, surgical correction 12/23/2013 40
  • 41. Hyaline Membrane Disease  Incidence – Primarily in premature infants; inversely proportional to GA & birth weight  Risk factor – – – – – – Prematurity Maternal DM Male sex 2nd born twins C/S delivery Perinatal asphyxia  Protective factor 12/23/2013 41
  • 43. CONT’D Clinical Feature -Signs occur with in minutes or hours of birth, reach peak with in 3 days -Characteristically • • • • • 12/23/2013 Tachypnea Nasal flaring SC or IC retraction Cyanosis Expiratory grunting 43
  • 44. CONT’D Diagnosis ─based on clinical picture in conjunction with characteristic chest radiograph ─The CXR abnormalities: Low lung volume Diffuse reticulogranular ground glass appearance with air bronchogram 12/23/2013 44
  • 45. CXR findings in Classic RDS * Bell-shaped thorax * ↓lung volume * Air bronchogram extended beyond cardiac border * Absolutely opaque lung (whiteout lung) 12/23/2013 45
  • 46. CONT’D  Management Basic supportive care Specific measures Prevent hypoxia & acidosis  Warm humified o2 administration  CPAP(indication, procedure & complication)  Assisted ventilation Surfactant replacement therapy (poractant,calfactant,beractant)  Prevention Prenatal testing & appropriate prophylaxis 12/23/2013 46
  • 47. Congenital pneumonia • Is acquired transplacentally or perinatally • Accounts for >50% of cases of RD in the new born  Risk factor –PROM –Prolonged labour (> 24 hrs) –Unclean vaginal examinations. –Foul smelling liquor –Maternal fever 12/23/2013 47
  • 48. CONT’D  Causative organisms: -Group B streptococcus -Gram negative organisms : E.coli, klebsiela, pseudomonas -Staph aureus and Listeria monocytogens  Clinical manifestations Respiratory distress soon after birth Recurrent apneic attack They are often asphyxiated and sick at birth  Prolonged capillary filling time  Hypothermia Cough is rare 12/23/2013 48
  • 49. Investigations – CBC, esp. ANC – Gastric aspirate for PMN – Blood culture – CXR(infiltrates, lobar consolidation, interstitial reticular opacities) 12/23/2013 49
  • 50. Management – Basic supportive therapy – Specific • Emperical broad spectrum antibiotics – Penicillin/Ampicillin 100mg/kg in 2 divided doses + Gentamicin 4mg/kg q24hr or 2.5 mg/kg q12hr 12/23/2013 50
  • 51. Meconium Aspiration Syndrome Definition • Respiratory distress in newborn infants born through meconium stained amniotic fluid whose symptom cannot be otherwise explained Incidence ─10-15% of births-meconium stained amniotic fluid – 5% -meconium aspiration pneumonia • 30% require mechanical ventilation • 3-5% expire 12/23/2013 51
  • 52. CONT’D  Risk factors • Placental dysfunction • Fetal hypoxia • Ante partum haemorrhage • Post maturity or SGA • Listeriosis • Breech delivery 12/23/2013 52
  • 53. CONT’D Pathophysiology ─Fetal hypoxia – Peristalsis & IU passage of meconium – Meconium stained amniotic fluid – Meconium aspiration – Peripheral & proximal air way obstruction, inflammatory &chemical pneumonitis 12/23/2013 53
  • 54. CONT’D Clinical feature – Respiratory distress- onset soon after birth in a baby born to mother with meconium stained liquor . – Hyper inflated chest – Meconium stained skin and cord – Urine may appear dark and brown 12/23/2013 54
  • 55. CONT’D Investigation – CXR • Hyperinflation • Bilateral fluffy shadows • Evidence of air leak 12/23/2013 55
  • 57. CONT’D  Management ─Prevention of meconium aspiration • Prevention of IU hypoxia • Intrapartum suctioning – Postnatal suctioning • Thick meconium – – – – – Direct laryngoscopy & tracheal suction Stabilize the baby Stomach wash Work up for sepsis Antibiotics can be started • Thin meconium – Depressed baby-do all like thick meconium – Active baby-no tracheal suctioning and needs close observation 12/23/2013 57
  • 58. APNEA Definition – Cessation of respiratory airflow – Absence of respiratory movement • Apnea vs periodic breathing Incidence – Increases with decreasing GA 12/23/2013 58
  • 59. Classification • Based on the cause – Primary(apnea of prematurity) – Secondary • Based on presence of continued inspiratory effort and upper airway obstruction – Central – Obstructive – Mixed 12/23/2013 59
  • 60. CONT’D Pathogenesis unable to react to hypercapnia • • • • • • • 12/23/2013 Impaired respiratory response(hypercapnia) Apnea ↓HR, Pao2 Hypoperfusion and hypoxia Hypercapnia Recurrent apnea(≥3 attacks in one hour) Brain damage & multiorgan damage 60
  • 61. CONT’D  Management General management – – – – – ABC of resuscitation Avoid vigorous suctioning Keep NPO for 24 hrs put them on maintenance IVF Keep in thermoneutral environment Treat the underlying cause of apnea Specific therapy • Drug─theophylline ─aminophylline ─ caffeine • Positive pressure ventilation 12/23/2013 61
  • 62. prepared by kiflom seyoum 12/23/2013 62
  • 64. Perinatal Asphyxia Definition:  PNA is an insult to the fetus or newborn due to lack of oxygen ( hypoxia ) and /or a lack of perfusion ( ischemia ) to various organs.  Failure to establish efficient breathing at one minute of age(APGAR score 0 - 6) with hypo/hypertonia and/or seizure.  This definition using APGAR score is not applicable in   Babies with birth trauma  12/23/2013 Preterm babies Congenital neurologic abnormalities 64
  • 65. Epidemology • • • • • Ranges 1-1.5% in gneral 9% in babes born <36 weeks of gastion 0.3% in babies born >36 weeks of gastion Accounts 23% of perinatal death 23-30% of survivors have permanent damage like CP 12/23/2013 65
  • 66. Timing of ingury • Asphyxia can occur in the,  Antepartem  Intrapartem  Postnatal priod 12/23/2013 66
  • 67. Risk factors 1 .Antepartem condition  Abnormal maternal oxygenation ( sever animia, cardiopulmonary disease) Inadequate placental perfusion( sever HTN, maternal vascular disease) Congenital infection or anomalies 12/23/2013 67
  • 68. Conti… 2. intrapartem events Interruption of umblical circulation (true knote, cord prolaps) inadequate placental perfusion ( abrabtio placenta, utrine rupture, abnormal utrin contraction ) Abnormal maternal oxygenation Vasa previa 12/23/2013 68
  • 69. Conti… • 3, post natal disorders Persistent plumnary hypertention of the new born Sever circulatory insuficency ( acut blood loss, septic shock ) 12/23/2013 69
  • 70. Eitology and pathphysiology 90% of insult occur due to placental insufficiency Decrease oxygen supply & Decrease carbon dioxide and hydrogen removal <10% are post natal insult due to pulmonary, CVS or neurologic insufficiency 12/23/2013 70
  • 71. Cont… • When the new born is depraved of O2 an initial period of rapid breathing occur • This is followed by primary apnea • Which responds to O2 administration and physical stimulation 12/23/2013 71
  • 72. Cont… If asphyxia contnues the new born devoleps Gasping respiration Decreased puls rate Blood pressure fail And the new born develops secondary apnea which will respond only to advanced life support including CPAP 12/23/2013 72
  • 73. Con… • If asphyxia is not reversed on time there will be hypoxic damage that leads to ischemic challenge • A diving reflex will be initiated that causes shunting of blood to vital organs 12/23/2013 73
  • 74. Clinical feature • Depends on the organ affected • Target organs of prenatal asphyxia  Kidney in 50% of cases  CNS in 28% of cases  CVS in 25% of cases  Pulmonary 23% of cases 12/23/2013 74
  • 75. Renal dysfunction • Often accompanies prenatal asphyxia • renal damage ranges from reversible cloudy swelling & hydropic digeneration of tubles to infarction of the entire nephron. • Decrease in UO(<0.5ml/kg/hr which may last 2 day to 2 weeks • Protein & cast may present in the urin • Gross hematuria may present • Elevation of BUN& creatinine may occur • Poly urea may flow oliguric phase or they may develop anuria 12/23/2013 75
  • 76. CVS dysfunction • May cause myocardial ischemia which usually is transient • Patients show tachypnea,tachycardea & hepatomegally consistent with heart fealur • Rarely causes cardiogenic shock and death 12/23/2013 76
  • 77. Pulmonary dysfunction 1.Plumonary edema Due to myocardial dysfunction May have sign of respiratory distress 2.Acute respiratory distress syndrome Increased plumnary capilary permebility to plasma protien which leads to inactivation of surfactant 12/23/2013 77
  • 78. Hypoxic ischemic encephalopathy • The most serous complication of perenatal asphyxia • The neuralgic squale often persists • Hypoxia impairs cerebral oxidative mechanism and leads to myocardial depression this leads to fail in cerebral blood flaw • And then ischemia of the brain tissue occur • Persistance of hypoxia increase anarobic glycolysis which leads to lactic acidosis • Worsening of lactic acidosis if not corrected on time cuases loss of cerebral vascular auto regulation 12/23/2013 78
  • 79. Conti… • Most of the time prolonged partial episode of aspheyxia is because of abruptio placenta • And usually it causes diffuse cerebral necrosis • Clinically this may be present in the form of seizure and paresis. • Acute total asphysia which is mainly due to cord plolapse primerly affects brain stem,thalamus, & basal ganglia. • This may manifest in the form disturbance of respiration,heart rate & blood pressure 12/23/2013 79
  • 80. Investstigations • EEG-to determine severity presence of seizure • Cranial u/s- to determine presence ICH & brain edeama • CT scan –early (2-4 days) brain edema -late(2-4weeks) for encephalomalesia 12/23/2013 80
  • 81. Sarnat staging of hypoxic-ischemic encephalopathy. Grade 1 (mild) Grade2 (moderate) Level of consciousness Irritable/hyperalert Lethargy Coma Muscle tone Normal or hypertonia Hypotonia Flaccid Tendon reflexes Increased Increased Depressed or absent Seizures Absent Frequent Frequent Complex reflexes Normal weak Absent Prognosis Good (100%) Normal 12/23/2013 Grade 3 (severe) Variable High mortality and (80% ) Normal neurological disability (50% Death 50% major sequelae) 81
  • 82. Management of perinatal asphyxia • Anticipate need for neonatal resuscitation from maternal obstetric & labor history • Avoid blood pressure fluctuation • Intravenous fluid 2/3 of maintenance • Appropriate ventilation support • Correct metabolic abnormalities • Prophylactic anti convulsant (phenobarbital)..? 12/23/2013 82
  • 83. Therapeutic hypothermia • It improves out come after perinatal asphyxia • The only effective neuro protective therapy currently available for Tx of neonatal encephalopathy • Safe and easy to administer • Selective head cooling & whole body cooling…? 12/23/2013 83
  • 84. Prevention of prenatal asphyxia  The minimum preventive measure which is provided during perinatal period is much better than a sophisticated care provided to an asphyxiated new born.  Prenatal assessment of changing fetal and placental condition by clinical assessment and altrasonography  Fetal BPP  Monitor progress of labor  Effective neonatal resuscitation 12/23/2013 84
  • 85. Neonatal seizure The most important & common indicator of significant neurologic dysfunction in the neonatal period The immature brain is more likely to develop seizure Not similar to adult b/c of ariboraisation of axons dendrites & myelin sheath 12/23/2013 85
  • 86. Cont… • They are five clinical types of NS 1.subtle 2.clonic 3.Tonic 4.spasem 5.Myoclonic 12/23/2013 86
  • 87. Con… • Based on EEG NZ classified into three Electroclinical seizure Electrical seizure Clinical seizure 12/23/2013 87
  • 88. causes 1.Age 1-4 days HIE IVH Drug toxicity,(lidocain,pencilin) Acute metabolic disorder 12/23/2013 88
  • 89. Conti… Age (4-14 days) Infection Metabolic disorder Benign neonatal convelsion kernicterus 12/23/2013 89
  • 90. Cont… Age (2-8wks) Infection Head injury Inherited disorder of cortical development 12/23/2013 90
  • 91. Diagnosis Post natal & prenatal history Blood should be obtaine Lumbar puncture EEG(show paroxysmal activity, sharp wave ) 12/23/2013 91
  • 92. Management of NS Treatment of the underlying etiology Complete control of clinical as well as electrographic seizure vs clinical seizure control…? Neonates required assisted ventilation after receiving IV or PO loading doses of AED 12/23/2013 92
  • 93. CONT… 1.Phenobarbitol  The drug of first choice in the neonatal seizure  20mg/kg loading dose, if not effective an additional dose of 5-10mg/kg until a maximam dose of 40mg/kg,  the mentenance doses is 3-6mg/kg 2.Phenytoin  If no response phenytoin loading dose of 15-40mg/kg can be given  Rate must note exced 0 .5-1mg/kg/min to pereven cardiac toxicty 12/23/2013 93
  • 94. Cont… 3.Lorazepam; the initial drug used to control acute seizure Can be used as first line or second line Tx in the new born who didn’t respond to phenobarbitol or phenytone 4.diazepam; It is highly lipophilic so cleared very quickly out carring the risk of recurrence of seizure 12/23/2013 94
  • 95. When to discontinu…..? • At the time of discharge • two wks or three month after discharge if the neonate had sever PNA 12/23/2013 95
  • 96. prognosis • Mortality from neonatal seizure has decreased from 40% to 20%. • The correlation b/n EEG & prognosis is very clear • Prolonged electrographic seizure >10min/hr, multifocal periodic electrographic discharge,& spread of electrogrophic seizure to contralateral hemospher has poor prognosis • Seizure due to HIE 50% of them have normal out come 12/23/2013 96
  • 98. JAUNDICE 98  Visible form of bilirubinemia  Adult sclera >2mg / dl  Newborn skin >5 mg / dl    Occurs in 60% of term and 80% of preterm neonates Is common problem and is mostly benign. However, significant jaundice occurs in 6 % of term babies 12/23/2013
  • 99. 99  The conjugated bilirubin will go to bowel with bile.  In adults E.coli and C.perfirngens present but absent in neonets.  β-glucourinidase enzyme present in newborns. Conjugation and enterohepatic resorption. 12/23/2013
  • 100. 100  Direct Vs Indirect?  Van den Bergh reaction  Indirect billirubin acts as an anti-oxidant  It is only the indirect billirubin which crosses the BBB and results in billirubin encephalopathy 12/23/2013
  • 101. Physiologic Jaundice 101  Jaundice becomes evident as physiologic in neonates B/c : A. Short life span of RBCs(70-90days) B. RBC mass is increased C. Immature ligandine D. Less UDPGT E. High activity β-glucuronidase (gut) F. Decreased flora in the gut 12/23/2013
  • 102. Physiologic jaundice ( Icterus neonatorum) 102 Preterm Term Peak time 4th -7th days 2nd – 4th day Peak level 8 – 12 mg/dl 5 -6 mg/dl Resolution time Before 10th day 5th – 7th day 12/23/2013
  • 103. Physiologic Vs pathologic 103 Signs PhysiologicJx Pathologic Jx Clinical Jx Visible in2-3day With in 24hrs TSB rise <5mg/dl/day >5mg/dl/day TSB Term<12mg/dl Preterm<15mg/dl Term>12g/dl Preterm>15mg/dl Conj BBn <1.5mg/dl >1.5(2)mg/dl Jaundice persisting Term <1 week Preterm <2weeks Term >1week Preterm >2weeks 12/23/2013
  • 104. Jaundice associated with breast feeding 104 Breast milk Breast feeding Cause ?glucouronidase in ↓ intake BM Time of onset Max level After 1st week In the 1st week 10 – 30 mg/dl Any Treatment Discontinuation for Continuing 2 – 3 days breast feeding 12/23/2013
  • 105. ETIOLOGY OF JAUNDICE 105 1. Jaundice appearing in the 1st 24 hr Rh incompatability(erythroblastosis fetalis)  ABO incompatibility  Mild BG incompatibility (Kelly, Duffy Ags)  Defect (G6PD def. and spherocytosis  TORCHS  Criggler Najar syndrome  Transient familial neonatal jaundice  12/23/2013
  • 106. Cont… 106 2.Jaundice appearing with in 24-72hr of age   Physiological jaundice Conditions w/c aggravate physiologic Jx.  Cephalhematoma  Hypothermia  Prematurity  Hypoglycemia  Multiple bruises  hypoxia 12/23/2013
  • 107. Cont… 107 3. prolonged jaundice( after 72 hrs.) TORCHS  Sepsis  Hypothyroidism  Biliary Artesia  Breast milk jaundice  Drugs (vit. K, oxytocin,diazepam)  Metabolic disease eg. galactosemia  12/23/2013
  • 108. 108 Hemolytic disease of the newborn  Rh incompatibility  Less common but sever than ABO incompatibility  90% due to D antigen  Black vs white  Severity from mild hemolysis to sever anemia  Dx by blood group incompatiblity  Reduce risk of sensitization with 300μg of human anti- D globulin during ANC ff up 12/23/2013
  • 109. Cont… 109  ABO incompatibility  Most common cause of HDN but mild  0.3-2.2% only manifest the disease.  Type O mother with type A or B infant.  Jaundice the only clinical manifestation.  Hemoglobin level usually normal.  Dx by ABO incompatibility (weak to moderate positive direct coombs test) 12/23/2013
  • 110. Clinical assessment of jaundice 110  Jaundice in the newborn progresses in cephalocaudal direction  Face =5-7mg/dl  Chest =10mg/dl  lower abdomen /thigh= 12mg/dl  Sole/palms≥15mg/dl 12/23/2013
  • 111. Work up neonates with Jx 111 History  Age of onset  Family history of Jaundice,pallor,splenectomy  Previous sibling with Jaundice  Maternal illness during pregnancy  Maternal drug intake  Delivery history e.g. PROM ,sepsis, prolonged labor 12/23/2013
  • 112. Cont’d 112 P/E  Proper classification of the newborn according to GA, & wgt.  Pallor, petechea  Bruises  Dark and cephalhematoma urine and clay colored stool  Examination geared to specific cause 12/23/2013
  • 113. Investigations 113      TSB with conjugated fraction Hct with RBC morphology and reticulocyte count Bg of the baby with direct coomb’s test Bg of the mother with indirect coomb’s test. Specific investigations for suspected specific problems 12/23/2013
  • 114. Management 114 Aim          lower serum billirubin decrease neurtoxicity Principles of treatment Avoid drugs w/c interfere with BBn metabolism Treat factors w/c↑ neurotoxicity Give adequate feeding Specific therapy Decrease serum billirubin 12/23/2013
  • 115. 115  Lower serum Billirubin Phototherapy  Exchange transfusion   Phototherapy  Indicated when TSB rises more than normal but not exchange transfusion level  May be therapeutic or prophylactic 12/23/2013
  • 116. Prophylactic phototherapy 116 INDICATIONS  RH isoimmunization with sever hemolysis  Birth weight<1000gm(EVLBW)  Sever multiple bruises SIDE EFFECTS  Erythematous skin rash  Retinal damage  Increased insensible water loss  Bronze baby syndrome  Loose stool  Low calcium 12/23/2013
  • 117. Exchange transfusion( ET) 117   Most effective way of treating Jaundice and anemia Could be partial or double exchange transfusion INDICATIONS  Rh isoimmunization with hydrops fetalis  History of previous sibling required ET with pallor  Cord blood Billirubin >5mg/dl  Rise in Billirubin >0.5mg/dl/hr despite phototherapy  Hemoglobin <11gm/dl  TSB >20mg/dl  VLBW, preterm, sepsis 12/23/2013
  • 118. Choice of blood for exchange BT 118  ABO incompatibility  Use  O blood of same Rh type Rh isoimmunization  Emergency 0 -ve blood  Ideal 0 -ve suspended in AB plasma  or baby's blood group but Rh –ve  Other situations  Baby's blood group 12/23/2013
  • 119. Exchange transfusion 119 COMPLICATIONS  Portal vein thrombosis  Umbilical vein perforation/bleeding  Necrotizing enterocolitis  Cardiac arrest/arrhythmia  Hypoglycemia, hypocalcemia, hypomagnisemia, hyperkalemia  Increased risk of infection  Respiratory and metabolic acidosis 12/23/2013
  • 120. KERNICTERS (Billirubin encephalopathy) 120  Definition: neurologic syndrome resulting from deposition of unconjugated billirubin in brain cells .  Sites of billirubin staining and necrosis include -Basal ganglia , Hippocampal cortex, Sub thalamic nucleus & cerebellum Cerebral cortex is spared   Half of the neonates with kernicters at autopsy have extra neuronal lesions 12/23/2013
  • 121. Pathophysiologic mechanism 121   Unconjugated BBn is nonpolar ,lipid soluble and can traverse BBB. Factors that ↑ billirubin toxicity  Hypoxia (asphyxia)  Hypothermia & hypoglycemia  sepsis  Prematurity  Acidosis  Hypoalbuminemia 12/23/2013
  • 122. Clinical staging of KI 122 Stage-1 Poor Moro reflex, decreased tone, lethargy, poor feeding, vomiting, high pitched cry Stage-2 Opisthotonus, fever, seizure, rigidity, oculogyric crises, paralysis of upward gaze Stage-3 Stage-4 - Spasticity is decreased Late sequale including spasticity,athetosis, deafness,MR,paralysis of the upward gaze 12/23/2013
  • 123. Clinical progression of encephalopathy 123 12/23/2013

Notas del editor

  1. .