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.

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 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.

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

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

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

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.

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

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

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

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

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

cuases loss of cerebral vascular auto regulation12/23/2013 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

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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

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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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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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

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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…

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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…

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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

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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…

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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

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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

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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

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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

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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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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)

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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

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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)

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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

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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

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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!