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
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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.
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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
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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)
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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
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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.
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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.
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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
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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
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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
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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
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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.
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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
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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)
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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
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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
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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
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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
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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.
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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
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.
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
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33
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
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38
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
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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
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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
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44
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
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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
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48
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
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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
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51
52. CONT’D
Risk factors
• Placental dysfunction
• Fetal hypoxia
• Ante partum haemorrhage
• Post maturity or SGA
• Listeriosis
• Breech delivery
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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
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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
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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
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58. APNEA
Definition
– Cessation of respiratory airflow
– Absence of respiratory movement
• Apnea vs periodic breathing
Incidence
– Increases with decreasing GA
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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
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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
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61
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
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65
66. Timing of ingury
• Asphyxia can occur in the,
Antepartem
Intrapartem
Postnatal priod
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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
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67
69. Conti…
• 3, post natal disorders
Persistent plumnary hypertention of the new
born
Sever circulatory insuficency ( acut blood loss,
septic shock )
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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)..?
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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…?
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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
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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
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86
87. Con…
• Based on EEG NZ classified into three
Electroclinical seizure
Electrical seizure
Clinical seizure
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87
91. Diagnosis
Post natal & prenatal history
Blood should be obtaine
Lumbar puncture
EEG(show paroxysmal activity, sharp wave )
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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
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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
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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
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94
95. When to discontinu…..?
• At the time of discharge
• two wks or three month after discharge if the
neonate had sever PNA
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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
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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
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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
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
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
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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
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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
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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
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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
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