managment of common neonatal problems
DESCRIPTION
NeonatologyTRANSCRIPT
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MEKELLE UNIVERSITY CHS
DEPARTMENT OF
PEDIATRICS & CHILD HEALTH
SEMINAR ON MANAGEMENT OF COMMON NEONATAL PROBLEMS By: KIROS W/GERIMAKIBRA SEBUHKIFLOM SEYOUMKESATEA G/WAHDWORKU ASFAW12/23/2013 1
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Seminar outline Neonatal Sepsis HypothermiaRespiratory distress syndromePerinatal AsphyxiaNeonatal SeizureNeonatal JaundiceRh and ABO incompatibilityNew born AnemiaHypoglycemia References and Sources
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NEONATAL SEPSIS
by Kiros Weldegerima
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Sepsis Outline of presentation
• Classifications • Risk factors • Clinical Manifestations • Meningitis and Pneumonia• Diagnostic work up • Management principles • Prevention Strategies of Sepsis • Hypothermia and its management12/23/2013
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Neonatal SepsisInfection or sepsis is a problem faced to all new
bornsBut the risk and severity is high in small and
premature infantsIt is the cause of 30-50 % of Neonatal mortality
in developing countriesSepsis in the Neonate includes meningitis,
septicemias, pneumonia, Arthritis, osteomyelitis, and UTI or combinations of those.
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• 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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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%, 24-48hr=5%, 2-6 days=10)
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RISK FACTORSNeonatal 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 pyrexia12/23/2013
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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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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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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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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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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
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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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Meningitis cont.…
In a baby with sepsis the findings of -convulsion/twitching-staring look/fixed eye-Bulged anterior fontanel-abnormal excessive high pitched cryShould arouse the suspicion of meningitis and proceed with lumbar puncture.
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Lumbar puncture result that Indicates meningitis
> 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.12/23/2013
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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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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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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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ManagementIn meningitis the dose of Ampicillin andCrystalline 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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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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Prevention strategies of Neonatal infectionsUniversal 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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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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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.
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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)
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Thermo RegulationThermo 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.
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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)
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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.
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Causes of hypothermia
External factors cold environment,wet or naked baby ,blood sampling,IV
samplingPoor ability to conserve heatlarge surface area,poor insulation,paucity of fat,Poor metabolic heat production -deficiency of brown fat(preterm ,SFD) -CNS problems -hypoxia -hypoglycemia
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Sign and symptoms of hypothermia1 peripheral vasoconstriction Acrocyanosis cold extrimity decreased peripheral perfusion2 CNS depression Lethargy Poor feeding Apnea and bradycardia3 Increased metabolism hypoglycemia hypoxia metabolic acidosis4 Increased pulmonary arterial pressure tachypenia respiratory distress
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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 incubatorHazard’s of temperature control: hyperthermia undetected infection volume depletion.
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RESPIRATORY DISTRESS and APNEAIN THE NEWBORN
PREPARED BY KIBRA.S
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RESPIRATORY DISTRESSDefinition• 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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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 newborn
Subglottic stenosis , laryngomalacia
Congenital lobar emphysema
Bronchopulmonary dysplasia
Tracheomalacia, congenital tracheal stenosis
Pulmonary hemorrhage, air leak
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2.Extrapulmonary causeCardiac Metabolic Neurological Hematological
Congenital heart disease
Hypoglycemia Neonatal meningitis Anemia
Congestive heart failure
Hypocalcaemia Neonatal seizure Polycythemia
Cardiac arrhythmia Hypothermia Hypoxic ischemic encephalopathy
Metabolic acidosis Extreme immaturity
Intracranial bieed
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APPROACH
History• Gestational age• Previous preterm baby• Antenatal steroid prophylaxis• Maternal DM• Ante partum hemorrhage• PROM• Prolonged duration of labor
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CONT’D
• 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
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CONT’D
Physical ExaminationVital sign, capillary refill time and SO2 Meconium staining of the cord or nailHyperinflated chest or with bowel soundCyanosis, tachycardia, murmurScaphoid abdomen, hepatomegallyEvidences of intracranial bleedUnable to pass nasal catheter
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CONT’D
Investigation• 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
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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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Hyaline Membrane Disease
Incidence– Primarily in premature infants; inversely proportional to GA
& birth weightRisk factor– Prematurity– Maternal DM– Male sex– 2nd born twins– C/S delivery– Perinatal asphyxia
Protective factor12/23/2013 41
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Pathogenesis
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CONT’D
Clinical Feature -Signs occur with in minutes or hours of birth, reach peak with in 3 days -Characteristically• Tachypnea • Nasal flaring• SC or IC retraction• Cyanosis • Expiratory grunting
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CONT’D
Diagnosis─based on clinical picture in conjunction with
characteristic chest radiograph
─The CXR abnormalities:Low lung volumeDiffuse reticulogranular ground glass appearance
with air bronchogram
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CXR findings in Classic RDS * Bell-shaped thorax * ↓lung volume
* Air bronchogram extended beyond cardiac border
* Absolutely opaque lung (whiteout lung)
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CONT’D
Management Basic supportive careSpecific measures
Prevent hypoxia & acidosisWarm humified o2 administrationCPAP(indication, procedure & complication)Assisted ventilation
Surfactant replacement therapy(poractant,calfactant,beractant)
PreventionPrenatal testing & appropriate prophylaxis
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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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CONT’D
Causative organisms:-Group B streptococcus-Gram negative organisms : E.coli, klebsiela, pseudomonas-Staph aureus and Listeria monocytogens
Clinical manifestationsRespiratory distress soon after birthRecurrent apneic attackThey are often asphyxiated and sick at birth Prolonged capillary filling time HypothermiaCough is rare
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Investigations
– CBC, esp. ANC– Gastric aspirate for PMN– Blood culture– CXR(infiltrates, lobar consolidation, interstitial
reticular opacities)
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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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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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CONT’D
Risk factors• Placental dysfunction
• Fetal hypoxia
• Ante partum haemorrhage
• Post maturity or SGA
• Listeriosis
• Breech delivery
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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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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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CONT’D
Investigation– CXR• Hyperinflation• Bilateral fluffy shadows• Evidence of air leak
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CONT’DManagement
─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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APNEA
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Definition– Cessation of respiratory airflow– Absence of respiratory movement
• Apnea vs periodic breathingIncidence– Increases with decreasing GA
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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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CONT’D
Pathogenesisunable to react to hypercapnia• Impaired respiratory response(hypercapnia)• Apnea• ↓HR, Pao2
• Hypoperfusion and hypoxia• Hypercapnia• Recurrent apnea(≥3 attacks in one hour)• Brain damage & multiorgan damage
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CONT’D
ManagementGeneral 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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prepared by kiflom seyoum
Perinatal Asphyxia &
Neonatal seizure
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Layout
• Definition• epidemiology• Pathophysiology• Risk factors• Clinical features• Management• Prevention• Neonatal seizure12/23/2013 63
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Perinatal AsphyxiaDefinition:
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
Preterm babies
Babies with birth trauma
Congenital neurologic abnormalities
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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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Timing of ingury
• Asphyxia can occur in the, Antepartem Intrapartem Postnatal priod
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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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Conti…
2. intrapartem eventsInterruption of umblical circulation (true
knote, cord prolaps) inadequate placental perfusion ( abrabtio
placenta, utrine rupture, abnormal utrin contraction )
Abnormal maternal oxygenationVasa previa
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Conti…
• 3, post natal disordersPersistent plumnary hypertention of the new
bornSever circulatory insuficency ( acut blood loss,
septic shock )
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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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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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Cont…
If asphyxia contnues the new born devolepsGasping respirationDecreased puls rateBlood pressure fail
And the new born develops secondary apnea which will respond only to advanced life support including CPAP
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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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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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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
anuria12/23/2013 75
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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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Pulmonary dysfunction
1.Plumonary edemaDue to myocardial dysfunctionMay have sign of respiratory distress
2.Acute respiratory distress syndromeIncreased plumnary capilary permebility to
plasma protien which leads to inactivation of surfactant
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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
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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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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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Sarnat staging of hypoxic-ischemic encephalopathy.Grade 3 (severe) Grade2
(moderate)Grade 1 (mild)
Coma Lethargy Irritable/hyperalert Level of consciousness
Flaccid Hypotonia Normal or hypertonia
Muscle tone
Depressed or absent Increased Increased Tendon reflexes
Frequent Frequent Absent Seizures
Absent weak Normal Complex reflexes
High mortality and neurological disability
(50% Death 50% major sequelae)
Variable(80% ) Normal
Good
(100%) Normal
Prognosis
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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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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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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 BPPMonitor progress of laborEffective neonatal resuscitation12/23/2013 84
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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
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Cont…
• They are five clinical types of NS1.subtle2.clonic3.Tonic4.spasem5.Myoclonic
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Con…
• Based on EEG NZ classified into threeElectroclinical seizureElectrical seizureClinical seizure
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causes
1.Age 1-4 daysHIEIVHDrug toxicity,(lidocain,pencilin)Acute metabolic disorder
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Conti…
Age (4-14 days)InfectionMetabolic disorderBenign neonatal convelsionkernicterus
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Cont…
Age (2-8wks)InfectionHead injuryInherited disorder of cortical development
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Diagnosis
Post natal & prenatal historyBlood should be obtaine Lumbar punctureEEG(show paroxysmal activity, sharp wave )
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Management of NS
Treatment of the underlying etiologyComplete 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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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/kg2.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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Cont…
3.Lorazepam; the initial drug used to control acute seizureCan 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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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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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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NEONATAL JAUNDICE
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JAUNDICE
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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
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12/23/2013
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.
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12/23/2013
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
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Physiologic Jaundice
12/23/2013
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
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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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Physiologic jaundice ( Icterus neonatorum)
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Physiologic Vs pathologic
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
Jaundicepersisting
Term <1 week Preterm <2weeks
Term >1week Preterm >2weeks
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Jaundice associated with breast feeding
Breast milk Breast feeding
Cause ?glucouronidase in BM
↓ intake
Time of onset
After 1st week In the 1st week
Max level 10 – 30 mg/dl Any
Treatment Discontinuation for 2 – 3 days
Continuing breast feeding12/23/2013
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ETIOLOGY OF JAUNDICE
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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
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Cont…
12/23/2013
2.Jaundice appearing with in 24-72hr of age
Physiological jaundice Conditions w/c aggravate physiologic Jx.
Cephalhematoma Hypothermia Prematurity Hypoglycemia Multiple bruises hypoxia
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Cont…
12/23/2013
3. prolonged jaundice( after 72 hrs.)
TORCHS Sepsis Hypothyroidism Biliary Artesia Breast milk jaundice Drugs (vit. K, oxytocin,diazepam) Metabolic disease eg. galactosemia
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Hemolytic disease of the newborn
12/23/2013
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
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Cont…
12/23/2013
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)
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Clinical assessment of jaundice
12/23/2013
Jaundice in the newborn progresses in cephalocaudal direction
Face =5-7mg/dl
Chest =10mg/dl
lower abdomen /thigh= 12mg/dl
Sole/palms≥15mg/dl
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Work up neonates with Jx
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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
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Cont’d
12/23/2013
P/E
Proper classification of the newborn according
to GA, & wgt.
Pallor, petechea
Bruises and cephalhematoma
Dark urine and clay colored stool
Examination geared to specific cause
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Investigations
12/23/2013
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
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Management
12/23/2013
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
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12/23/2013
Lower serum Billirubin Phototherapy Exchange transfusion
PhototherapyIndicated when TSB rises more than
normal but not exchange transfusion level
May be therapeutic or prophylactic
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Prophylactic phototherapy
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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
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Exchange transfusion( ET)
12/23/2013
Most effective way of treating Jaundice and anemia
Could be partial or double exchange transfusion
INDICATIONSRh isoimmunization with hydrops fetalisHistory of previous sibling required ET with
pallorCord blood Billirubin >5mg/dlRise in Billirubin >0.5mg/dl/hr despite
phototherapyHemoglobin <11gm/dlTSB >20mg/dlVLBW, preterm, sepsis
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Choice of blood for exchange BT
12/23/2013
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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Exchange transfusion
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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
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KERNICTERS (Billirubin encephalopathy)
12/23/2013
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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Pathophysiologic mechanism
12/23/2013
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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Clinical staging of KI
12/23/2013
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 Spasticity is decreased
Stage-4 Late sequale including spasticity,athetosis, - deafness,MR,paralysis of the upward gaze
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Clinical progression of encephalopathy
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Thank you!