Managmentofcommonneonatalproblems 140201143840-phpapp01(1)

MEKELLE UNIVERSITYCHS

DEPARTMENT OF

PEDIATRICS & CHILD HEALTH

SEMINAR ON MANAGEMENT OF COMMON NEONATAL PROBLEMS By: KIROS W/GERIMAKIBRA SEBUHKIFLOM SEYOUMKESATEA G/WAHDWORKU ASFAW

12/23/2013 1

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 management

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Neonatal SepsisInfection 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, 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 8

Late onset causative Agents

• Late onset neonatal sepsis occurs after 7 days most of which is after the first week of life up to 90 days.

• Most are caused by gram negative bacteria

– Klebsiela, enterobacter, E-coli, pseudomonas and salmonella

– Gram positives like staphylococcus aureus also contribute as causes of late onset sepsis.

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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

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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 cry

Should 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.

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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 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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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 factorscold environment,wet or naked baby ,blood sampling,IV sampling

Poor 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 hypothermia

1 peripheral vasoconstrictionAcrocyanosiscold extrimity

decreased peripheral perfusion2 CNS depression

LethargyPoor feedingApnea and bradycardia

3 Increased metabolismhypoglycemiahypoxiametabolic acidosis

4 Increased pulmonary arterial pressuretachypeniarespiratory distress

Management of hypothermia

There are 3 methods:

1.Kangaroo mother care

2.Warming in an open care using a radiant heater

3.Warming in an incubator

Hazard’s of temperature control:

hyperthermia

undetected infection

volume depletion.

RESPIRATORY DISTRESS and APNEAIN THE NEWBORN

PREPARED BY KIBRA.S

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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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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 lobaremphysema

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 heartfailure

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 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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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 weight

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

Protective factor

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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 volume

Diffuse 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 care

Specific measuresPrevent hypoxia & acidosis

Warm humified o2 administration

CPAP(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 breathing

Incidence

– 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

Pathogenesis

unable 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

12/23/2013 62

Layout

• Definition

• epidemiology

• Pathophysiology

• Risk factors

• Clinical features

• Management

• Prevention

• Neonatal seizure

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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

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

12/23/2013 66

Risk factors

1 .Antepartem condition

Abnormal maternal oxygenation ( sever animia, cardiopulmonary disease)

Inadequate placental perfusion( sever HTN, maternal vascular disease)

Congenital infection or anomalies

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Conti…

2. intrapartem events

Interruption of umblical circulation (true knote, cord prolaps)

inadequate placental perfusion ( abrabtioplacenta, utrine rupture, abnormal utrincontraction )

Abnormal maternal oxygenation

Vasa previa

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Conti…

• 3, post natal disorders

Persistent plumnary hypertention of the new born

Sever 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 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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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

anuria

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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 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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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 glycolysiswhich leads to lactic acidosis

• Worsening of lactic acidosis if not corrected on time cuases loss of cerebral vascular auto regulation

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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)

ComaLethargyIrritable/hyperalertLevel of

consciousness

FlaccidHypotoniaNormal or

hypertonia

Muscle tone

Depressed or absentIncreasedIncreasedTendon reflexes

FrequentFrequentAbsentSeizures

AbsentweakNormalComplex 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 resuscitation

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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 NS

1.subtle

2.clonic

3.Tonic

4.spasem

5.Myoclonic

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Con…

• Based on EEG NZ classified into three

Electroclinical seizure

Electrical seizure

Clinical seizure

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causes

1.Age 1-4 days

HIE

IVH

Drug toxicity,(lidocain,pencilin)

Acute metabolic disorder

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Conti…

Age (4-14 days)

Infection

Metabolic disorder

Benign neonatal convelsion

kernicterus

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Cont…

Age (2-8wks)

Infection

Head injury

Inherited disorder of cortical development

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Diagnosis

Post natal & prenatal history

Blood should be obtaine

Lumbar puncture

EEG(show paroxysmal activity, sharp wave )

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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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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 perevencardiac toxicty

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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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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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97

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

98

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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.

99

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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

100

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

101

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) 102

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

Jaundice

persisting

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

104

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

105

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

106

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

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

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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

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

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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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12/23/2013

Lower serum Billirubin

Phototherapy

Exchange transfusion

Phototherapy

Indicated 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

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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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

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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123

Thank you!