Pediatrics Lecture 2 (Neonatology) (15!3!2011) Dr.M.hesham

7/29/2019 Pediatrics Lecture 2 (Neonatology) (15!3!2011) Dr.M.hesham

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Neonatology

Neonatology is an exciting and relatively young subspecialty. Newborns are both fragile and

surprisingly resilient. Providing the right intervention for the right diagnosis can dramatically

improve long-term outcome, making care of the sick newborn a particularly rewardingexperience

Neonatal Jaundice

General considerations

Sixty-five percent of newborns develop visible jaundice with a total serum bilirubin (TSB)

level higher than 6 mg/dL during the first week of life.

Extremely high and potentially dangerous TSB levels can cause kernicterus, characterized

by injury to the basal ganglia and brainstem.

Bilirubin metabolism

Bilirubin is produced by the breakdown of heme (iron protoporphyrin) in the

reticuloendothelial system and bone marrow. Heme is cleaved by heme oxygenase to iron,

which is conserved; and biliverdin, which is converted to bilirubin by bilirubin reductase.

This unconjugated bilirubin is bound to albumin and carried to the liver, where it is taken up

by hepatocytes. In the presence of glucuronyl transferase, bilirubin is conjugated.

Conjugated bilirubin is then excreted through the bile to the intestine. In the presence of gut

flora, conjugated bilirubin is metabolized to stercobilins and excreted in the stool.

Physiologic Jaundice

Visible jaundice appearing after 24 hours of age.

Peak bilirubin occurs at 35 days of age, with a total bilirubin of no more than 15 mg/dL.

Visible jaundice resolves by 1 week in the full-term infant and by 2 weeks in the preterm

infant.

Pathologic Unconjugated Hyperbilirubinemia

Pathologic unconjugated hyperbilirubinemia can be grouped into two main categories:

overproduction of bilirubin or decreased conjugation of bilirubin. The TSB is a reflection of the

balance between these two processes. Visible jaundice with a TSB greater than 5 mg/dL before

24 hours of age is most commonly a result of significant hemolysis.

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Etiology

A. Overproduction of bilirubin

1. Hemolytic causes of increased bilirubin production

a. Immune-mediated: ABO blood group incompatibility, Rh incompatibility

b. Nonimmune : spherocytosis and glucose-6-phosphate dehydrogenase deficiency

c. Patients with bacterial or viral sepsis

2. Nonhemolytic causes of increased bilirubin production

a. Cephalohematoma, extensive bruising, intracranial hemorrhage

b. Breast feedingassociated jaundice (inadequate intake of breast milk)

B. Decreased rate of conjugation

1. Prematurity.

2. Crigler-Najjar syndrome (rare, glucuronyl transferase deficiency)

3. Hypothyroidism

C. Decreased binding of bilirubin to albumin due to medications (e.g., ceftriaxone, aspirin,

sulfonamides).

ABO Blood Group Incompatibility

It occurs in blood group O mothers having group A or B babies. Hemolysis is usually mild.

RH-Isoimmunization

- This hemolytic process is less common and more severe than ABO incompatibility. - Rh

incompatibility is almost completely preventable. Rh-negative mothers should be followed

closely by their obstetricians during pregnancy. Special immune globulins, called RhoGAM, are

now used to prevent RH incompatibility.

If the father of the infant is Rh-positive or if his blood type cannot be confirmed, the mother is

given a mid-term injection of RhoGAM and a second injection within a few days of delivery.

These injections prevent the development of antibodies against Rh-positive blood. However,

women with Rh-negative blood type must receive this injection:

During every pregnancy

If they have a miscarriage or abortion

After prenatal tests such as amniocentesis and chorionic villous biopsy.

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Treatment of Indirect Hyperbilirubinemia

Phototherapy

Phototherapy is the most common treatment for indirect hyperbilirubinemia.

It is relatively noninvasive and safe. Light of wavelength 425475 nm (blue-green

spectrum) is absorbed by unconjugated bilirubin in the skin converting it to a water-

soluble stereoisomer that can be excreted in bile without conjugation.

The infant's eyes should be shielded to prevent retinal damage.

Exchange Transfusion

As TSB nears the potentially toxic range, serum albumin should be determined. Albumin

(1 g/kg) will aid in binding and removal of bilirubin during exchange transfusion, as well

as afford some neuroprotection while preparing for the procedure.

Double-volume exchange transfusion (approximately 160 mL/kg body weight) is most

often required in infants with extreme hyperbilirubinemia.

Exchange transfusion is also indicated in any infant with TSB above 30 mg/dL, or when

intensive phototherapy has not lowered TSB to safe levels.

Immunoglobulins

In infants with isoimmune hemolytic disease and TSB level rising despite intensive

phototherapy administer immunoglobulin (IVIG) 0.5 to 1 g/kg over 2 hours and repeat in

12 hours if necessary.

Protoporphyrins

Metalloprotoporphyrins are inhibitors of heme oxygenase, the enzyme that initiates the

catabolism of heme (iron protoporphyrin).

Studies are underway involving a single injection of these substances shortly after birth to

prevent the formation of bilirubin. These drugs are not yet approved for use in the USA.

Drug therapy for neonatal jaundice

Phenobarbital (Increase bilirubin conjugation) Oral agar (Decrease enterohepatic circulation)

Metalloprotoporphyrins (Inhibit heme oxygenase)

High dose IV immunoglobulins (Inhibit hemolysis)

IV albumin (Increase binding of bilirubin)

Respiratory Distress in the Term Newborn Infant3


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Essentials of diagnosis and typical features

Tachypnea, respiratory rate > 60 breaths/min

Intercostal and sternal retractions

Expiratory grunting

Cyanosis in room air


Respiratory distress is one of the most common symptoms of the newborn.

It may result from cardiopulmonary and noncardiopulmonary causes.

Chest radiography, arterial blood gases, and pulse oximetry are useful in assessing the cause

and severity of the distress.

Causes of respiratory distress in the newborn

A. Pulmonary

- Transient tachypnea of newborn- Meconium aspiration

- Clear fluid aspiration

- Pneumonia

- Hyaline membrane disease

B. Cardiovascular

- Left-sided outflow tract obstruction e.g. coarctation of the aorta

- Cyanotic lesions e.g. transposition of the great vessels

C. Non-cardiopulmonary

- Hypothermia - Hypoglycemia

- Metabolic acidosis

- Drug intoxications or withdrawal

- Insult to the central nervous system e.g. asphyxia, hemorrhage

A) Transient Tachypnea of Newborn

Respiratory distress is typically present at birth, usually associated with a mild-to-

moderate oxygen requirement (2550% O2).

The infant is usually full term born following a cesarean section without labor. Pathogenesis: delayed clearance of fetal lung fluid via lymphatics.

Chest radiograph: perihilar streaking and fluid in interlobar fissures.

Resolution usually occurs within 1224 hours.

B) Aspiration Syndromes

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The infant is typically full term or late preterm with fetal distress prior to delivery.

Blood or meconium is often present in the amniotic fluid.

Respiratory distress is present from birth, which needs an increasing O2 need and may

require intubation and ventilation.

Chest radiograph: coarse irregular infiltrates and hyperexpansion.

The Preterm Infant

Preterm infant faces a variety of physiologic handicaps:

1. The ability to coordinate sucking, swallowing, and breathing is not achieved until 3436

weeks' gestation. Therefore, enteral feedings must be provided by gavage. Further,

preterm infants often have an immature gag reflex, which increases the risk of aspiration

of feedings.

2. Lack of body fat stores causes decreased ability to maintain body temperature.

3. Pulmonary immaturitysurfactant deficiency. This condition is exacerbated by thecombination of noncompliant lungs and an extremely compliant chest wall, causing

inefficient respiratory mechanics.

4. Immature respiratory control leads to apnea and bradycardia.

5. Persistent patency of the ductus arteriosus compromises pulmonary gas exchange because

of overperfusion and edema of the lungs.

6. Immature cerebral vasculature and structure predisposes to subependymal and

intraventricular hemorrhage, and periventricular leukomalacia.

7. Impaired substrate absorption by the GI tract compromises nutritional management.

8. Immature renal function (including both filtration and tubular functions) complicates

fluid and electrolyte management.

9. Increased susceptibility to infection.

10. Immaturity of metabolic processes predisposes to hypoglycemia and hypocalcemia.

Care in the Nursery

A)Thermoregulation

Thermal environment of the preterm neonate must be regulated carefully.

The infant can be kept warm in an incubator, in which the air is heated and convective

heat loss is minimized.

The infant can also be kept warm on an open bed with a radiant heat source.

Generally, when infants reach 17001800 g, they are able to maintain temperature while

bundled in an open crib.

B) Monitoring

Equipment to monitor heart rate, respirations, and blood pressure should be available.

Oxygen saturation can be assessed continuously using pulse oximetry.

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C) Fluid and electrolyte therapy

Fluid requirements in preterm infants are a function of:

(1) insensible losses (skin and respiratory tract), (2) urine output,

(3) stool output (< 5% of total), and (4) others, such as nasogastric losses.

The major contribution to insensible water loss is evaporative skin loss. The rate of water

loss is a function of gestational age (body weight, skin thickness, and maturity),

environment (losses are greater under a radiant warmer than in an isolette), and the use of

phototherapy. Respiratory losses are minimal when humidified oxygen is used.

Electrolyte requirements are minimal for the first 2448 hours until there is significant

urinary excretion.

Basal requirements thereafter are as follows: sodium, 3 mEq/kg/d; potassium, 2

mEq/kg/d; chloride, 23 mEq/kg/d; and bicarbonate, 23 mEq/kg/d.

In the infant younger than 30 weeks' gestation, sodium and bicarbonate losses in the

urine are often elevated, thereby increasing the infant's requirements.

Initial fluid management after birth varies with the infant's size and gestation. Infants of more than 1200 g should start at 80100 mL/kg/d of D10W.

Those weighing less should start at 100120 mL/kg/d of either D10W or D5W (infants

< 800 g and born before 26 weeks' gestation often become hyperglycemic on D10W).

Fluid requirements (mL/kg/day):

Birth weight (g) Day 1 Day 2 Day 3

1,500 6080 80120 120160

The most critical issue in fluid management is monitoring. Monitoring body weight, urineoutput, fluid and electrolyte intake, serum and urine electrolytes, and glucose allows

fairly precise determination of the infant's water, glucose, and electrolyte needs.

Parenteral nutrition should be started early, preferably on the first day, and continued

until an adequate enteral intake is achieved

D)Nutritional support

The average caloric requirement for the growing premature infant is 120 kcal/kg/d.

Infants initially require IV glucose infusion to maintain blood glucose concentration in

the range of 60100 mg/dl. Infusions of 57 mg/kg/min (approximately 80100 ml/kg/d

of D10W) are usually needed.

Aggressive nutritional support in the very low-birth-weight infant should be started as

soon as possible after birth, with parenteral alimentation solutions containing 3 g/kg/d of

amino acids, given either peripherally or centrally via an umbilical vein line or

percutaneous catheter.

Small-volume trophic feeds with breast milk or 20 kcal/oz premature formula should be

started by gavage at 10% or less of the infant's nutritional needs (< 10 mL/kg/d) as soon

as possible, generally within the first few days after birth.

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After several days of trophic feeds the infant can be slowly advanced to full caloric needs

over 57 days. Even extremely small feedings can enhance intestinal readiness to accept

larger feeding volumes.

Intermittent bolus feedings are preferred because these appear to stimulate the release of

gut-related hormones and may accelerate maturation of the GI tract.

A more rapid advancement schedule is used for infants weighing more than 1500 g, and

the slowest schedule for those weighing less than 1000 g.

Use of parenteral alimentation solutions.

Volume

(mL/kg/d)

Carbohydrate

(g/dL)

Protein

(g/kg)

Lipid

(g/kg)

Calories

(kcal/kg)

Peripheral: Short-term (710 d)

Starting

solution

100150 D10W 3 1 5684

Target

solution

150 D12.5W

33.5 3 108

Central: Long-term (> 10 d)

Starting

solution

100150 D10W 3 1 5684

Target

solution

130 D15D18W

34 3 118130

Notes

1. Advance dextrose in central hyperalimentation as tolerated per day as long as bloodglucose remains normal.

2. Advance lipids by 0.51.0 g/kg/d as long as triglycerides are normal. Use 20%

concentration.

3. Total water should be 100150 mL/kg/d, depending on the child's fluid needs.

Monitoring

1. Blood glucose two or three times a day when changing dextrose concentration, then

daily.

2. Electrolytes daily, then twice a week when the child is receiving a stable solution.

3. Every 12 weeks: blood urea nitrogen and serum creatinine; total protein and serum

albumin; serum calcium, phosphate, magnesium, direct bilirubin, and CBC with plateletcounts.

4. Triglyceride level after 24 h at 2 g/kg/d and 24 h at 3 g/kg/d, then every other week.

Long-term nutritional support for infants of very low birth weight consists either of:

Breast milk supplemented to increase protein, caloric density, and mineral content, or

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Infant formulas modified for preterm infants. In these formulas, protein concentrations

(approximately 2 g/dL) and caloric concentrations (approximately 24 kcal/oz) are

relatively high. In addition, premature formulas contain some medium-chain

triglycerideswhich do not require bile for absorptionas an energy source. Increased

calcium and phosphorus are provided to enhance bone mineralization.

Formulas for both full-term and premature infants are enriched with long-chain

polyunsaturated fatty acids in the hope of enhancing brain and retinal development.

Additional iron supplementation (24 mg/kg/d) is recommended for premature infants,

beginning at 2 weeks to 2 months of age, depending on gestational age and number of

previous transfusions.

Neonatal Apnea

is defined as the cessation of breathing. It is considered pathological when the duration is longer

than 20 seconds. It can cause bradycardia, cyanosis, pallor, hypotonia, and metabolic acidosis

with symptoms progressing as apnea is sustained. Periodic breathing, which is common in full-

term and preterm infants, is defined as regularly recurring ventilatory cycles interrupted by short

pauses not associated with bradycardia or color change.

Etiology of apnea can be broadly divided into central and obstructive.

Central apnea

Developmental immaturity of central respiratory drive causes apnea in the preterm infant. Apnea

of prematurity(AOP) generally begins at 1 to 2 days of age and may continue until the infant is

approximately 35 weeks PMA, or longer in infants born profoundly premature.

Respiratory center depression can result from hypoglycemia, electrolyte abnormalities (including

hypocalcemia), sepsis, intracranial disorders, medications, and drugs of abuse.

Obstructive apnea

Apnea due to airway obstruction can result from supine positioning or neck flexion. Ill infants

can also develop obstruction due to tenacious secretions and mucous plugs.

Evaluation and diagnosis

All infants younger than 35 weeks GA should be observed on CVR monitors. When a monitor

alarm sounds, check for cyanosis, bradycardia, and airway obstruction.

AOP is a diagnosis of exclusion. A first apneic episode, apnea in the first 24 hours, or apnea in

infants older than 35 weeks gestation should prompt an evaluation for other etiologies.

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Treatment

1. The main goal of treatment is to reduce the number and severity of apneic attacks without

having to resort to assisted ventilation. Pharmacologic intervention is necessary for infants with

severe or frequent episodes:

Methylxanthines. Start a stimulant in the setting of moderate to severe and/or frequent AOP. It

may also be started prophylactically in anticipation of AOP that may be clinically manifested as

ventilator support is reduced. Caffeine is gaining popularity over aminophylline because its wide

therapeutic window reduces the need to measure levels.

Caffeine citrate. Loading dose of 20 mg/kg (10 mg/kg caffeine base) PO or IV over 30 minutes,

followed by maintenance dose of 5 to 8 mg/kg (2.5 to 4 mg/kg caffeine base) daily, starting 24

hours after the loading dose.

If significant apnea spells continue, give an additional dose of up to 10 mg/kg caffeine citrate

and increase the maintenance dose by up to 20%.

Because of the wide therapeutic index and lack of established dose-response relationship, only

obtain serum levels if there are signs of toxicity or hepatic dysfunction. In the rare instance that

levels are measured, serum levels of 5 to 20 g/mL caffeine are considered to be therapeutic.

Aminophylline. Loading dose of 5 to 7 mg/kg of aminophylline IV (over 30 minutes) or

theophyline PO/PG, followed by a maintenance dose of 1.5 to 2 mg/kg every 6 to 8 hours. Side

effects include tachycardia, gastrointestinal (GI) dysfunction, feeding intolerance, jitteriness,

irritability and seizures. Doxapram is occasionally given as an adjunct to both a methylxanthine

and CPAP, to avoid putting the baby on a ventilator.

Most clinician stops giving respiratory stimulants when the baby is around 34 weeks gestation,

at which time most babies will have achieved and adequate degree of cardiorespiratory stability.

2. If monitoring and drug therapy fails, mechanical ventilation or nasal continuous positive

airway pressure (nCPAP) is required until the infant's respiratory control matures.

Hyaline Membrane Disease (Respiratory Distress Syndrome)


The most common cause of respiratory distress in the preterm infant.

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This condition is caused by a deficiency of surfactant production. The absence or

inactivation of surfactant results in poor lung compliance and atelectasis. The infant must

expend a great deal of effort to expand the lungs with each breath.

The condition is rare in term babies and becomes increasingly likely the more preterm

birth takes place. The natural history is that RDs becomes worse over first 2 days, reaches

a plateau and then gradually improves.

The use of antenatal steroid therapy to the mother and surfactant therapy for the infant

has changed dramatically the clinical course and greatly decreased mortality. Optimum

treatment to the mother is four oral doses of 6 mg betamethasone, each given 12-hourly,

or two doses of 12 mg intramuscularly 24 hours apart.

Clinical findings

Infants with hyaline membrane disease show all the clinical signs of respiratory distress

(Tachypnea, cyanosis, and expiratory grunting).

On auscultation, air movement is diminished despite vigorous respiratory effort.

Chest radiograph: diffuse bilateral atelectasis, causing a ground-glass appearance.

Treatment

Supplemental oxygen, early intubation for surfactant administration and ventilation, and

placement of umbilical artery and vein lines are the initial interventions required.

Mechanical ventilation is usually needed for more premature or more severely affected

babies. Paralyzing agents such as pancuronium are often given to ventilated babies to

prevent them from fighting the ventilator, but they are not sedatives. Morphine iscommonly given either as intermittent dose or as an infusion to provide narcosis and

analgesia to reduce the distress of neonatal intensive care.

High-frequency ventilators are available for rescue of infants doing poorly on

conventional ventilation or who have air leak problems.

Surfactant replacement

Surfactant therapy is used both in the delivery room as prophylaxis for infants born

before 27 weeks' gestation and with established hyaline membrane disease as rescue,

preferably within 24 hours of birth.

Therapy decreases both the mortality rate in preterm infants and air leak complicationsof the disease.

During the acute course, ventilator settings and oxygen requirements are significantly

lower in surfactant-treated infants than in controls.

The dose of the bovine-derived beractant (Survanta) is 4 mL/kg, the calf lung surfactant

extract (Infasurf) is 3 mL/kg, and the porcine-derived poractant (Curosurf) is 1.252.5

mL/kg, given intratracheally.

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Repeat dosing is indicated in infants who remain on the ventilator in > 3040% oxygen.

A total of two to three doses given 812 hours apart may be administered.

Trade Name

(generic)Source Dose

Survanta

(beractant)

Bovine lung extract 4 mL/kg at 6-hour intervals; up to four doses

Infasurf

(calfactant)

Calf lung extract 3 mL/kg at 12-hour intervals; up to four doses

Curosurf

(poractant alpha)

Porcine lung extract 2.5 mL/kg (first dose) followed by subsequent doses

of 1.25 mL/kg at 12-hour intervals; up to three doses

Exosurf

(colfosceril)

Proteinfree synthetic,

pulmonary surfactant

5 mL/kg at 12-hour intervals; up to three doses

Chronic Lung Disease in the Premature Infant


Chronic lung disease (CLD), defined as respiratory symptoms, oxygen requirement, and

chest radiograph abnormalities at 36 weeks postconception.

The factors predisposing to CLD are the degree of prematurity, the severity of RDS,

infection, and exposure to high oxygen concentrations and ventilator volutrauma.

Surfactant-replacement therapy or early nasal CPAP has diminished the severity of CLD.

Treatment

Long-term supplemental oxygen, mechanical ventilation, and nasal CPAP are the primary

therapies for chronic lung disease of the premature.

Diuretics (furosemide, 12 mg/kg/d, or hydrochlorothiazide-spironolactone, 12

mg/kg/d), inhaled 2-adrenergics, inhaled corticosteroids (fluticasone or budesonide),

and systemic corticosteroids (dexamethasone, 0.20.5 mg/kg/d, or hydrocortisone, 15

mg/kg/d) are used as adjunctive therapy.

Patent Ductus Arteriosus


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Patent ductus arteriosus (PDA) can be a problem in the recovery phase of RDS, and

usually shows itself as a secondary increase in respiratory distress and/or increase in

oxygen requirement.

Clinical signs include a hyperdynamic precordium, increased peripheral pulses, and a

widened pulse pressure with or without a systolic heart murmur.

The presence of patent ductus arteriosus is confirmed by echocardiography.

Treatment

Treatment options are either medical with indomethacin or surgical ligation.

A clinically significant ductus can be closed with indomethacin (0.2 mg/kg IV q12h for

three doses) in about two-thirds of cases. If the ductus reopens or fails to close

completely, a second course of drug may be used.

If indomethacin fails to close the ductus or if a ductus reopens a second time, or if

indomethacin is contraindicated, surgical ligation can be considered.

In the extremely low-birth-weight infant (2 mg/dL, or

the platelet count is


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Treatment

Medical treatment

Stop enteral feedings.

Place a nasogastric tube to continuous suction.

Obtain appropriate cultures and start broad-spectrum systemic antibiotics, such as

ampicillin and gentamicin. Add anaerobic coverage (e.g., clindamycin or metronidazole).

Treat shock, acidosis, hyponatremia, thrombocytopenia, and DIC.

Provide intravenous feeding for a period of time.

Continue bowel rest and antibiotics generally for 14 days.

Surgical treatment

Early surgical consultation is recommended. GI perforation is a clear indication for surgery.

Intraventricular Hemorrhage


Periventricularintraventricular hemorrhage occurs almost exclusively in premature

infants. The highest incidence occurs in infants of the lowest gestational age

Bleeding most commonly occurs in the subependymal germinal matrix. Bleeding can

extend into the ventricular cavity.

Clinical findings

Up to 50% of hemorrhages occur before 24 hours of age, and virtually all occur by the

fourth day.

Clinical syndrome ranges from rapid deterioration (coma, hypoventilation, decerebrateposturing, fixed pupils, bulging anterior fontanelle, hypotension, acidosis, or acute drop

in hematocrit) to a more gradual deterioration with more subtle neurologic changes, to

absence of any specific physiologic or neurologic signs.

Diagnosis can be confirmed by real-time ultrasound scan.

Treatment

During acute hemorrhage, supportive treatment (restoration of volume and hematocrit,

oxygenation, and ventilation) should be provided to avoid further cerebral ischemia.

Strategies to decrease the risk of intracranial bleeding: Maternal antenatal corticosteroids appear to decrease the risk, and phenobarbital may

have a role in the mother who has not been prepared with steroids and is delivering

before 28 weeks' gestation.

The route of delivery may be important as infants delivered by cesarean section have a

decreased rate of intracranial bleed.

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Infections in the Newborn Infant

There are three major routes of perinatal infection:

(1) Blood-borne transplacental infection (eg, cytomegalovirus [CMV], rubella, and syphilis);

(2) Ascending infection with disruption of the barrier provided by the amniotic membranes, and

(3) Infection on passage through an infected birth canal or exposure to infected blood at delivery

(eg, herpes simplex, hepatitis B, HIV, and bacterial infections).

Susceptibility of the newborn infant to infection is related to immaturity of both the natural and

acquired immune systems at birth. This feature is particularly evident in the preterm neonate.

Passive protection against some organisms is provided by transfer of IgG across the placenta,

particularly during the third trimester of pregnancy. Preterm infants, especially those born before

30 weeks' gestation, do not have the full amount of passively acquired antibody.

Bacterial Sepsis


Early-onset infection is most often caused by group B -hemolytic streptococci (GBS) and

gram-negative enteric pathogens (most commonly E coli). Other organisms to consider

are Haemophilus influenzae, Enterococcus, Staphylococcus aureus, other streptococci

andListeria monocytogenes.

Late-onset sepsis is caused by coagulase-negative staphylococci (most common in infants

with indwelling central venous lines), S aureus, GBS, Enterococcus, and gram-negative

organisms.

Clinical findings

Early-onset bacterial infections appear most commonly on day 1 of life, and the majority

appears at less than 12 hours. Respiratory distress due to pneumonia is the most common

presenting sign. Late-onset bacterial infection (> 7 days of age) presents in a more subtle

manner, with poor feeding, lethargy, hypotonia, temperature instability, altered perfusion,

new or increased oxygen requirement, and apnea. Late-onset bacterial sepsis is more

often associated with meningitis or other localized infections.

Low total white count, absolute neutropenia (


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Treatment can be stopped after 48 hours if cultures prove negative.

Early-onset sepsis is usually caused by GBS or gram-negative enteric organisms; broad-

spectrum coverage, therefore, should include ampicillin plus an aminoglycoside or third-

generation cephalosporinfor example, ampicillin, and gentamicin, or cefotaxime.

Cephalosporins such as cefotaxime and ceftazidime have been advocated for use in the

blind treatment of neonatal infection due to their lower toxicity when compared to

aminoglycosides, their wide therapeutic index and the absence of any need to monitor

plasma concentrations.

Late-onset infections; coverage may need to be expanded to include staphylococci. In

particular, the preterm infant with an indwelling line is at risk for infection with

coagulase-negative staphylococci, for which vancomycin is the drug of choice. Initial

broad-spectrum coverage should also include a third-generation cephalosporin

(cefotaxime or ceftazidime, ifPseudomonas aeruginosa is strongly suspected.

The duration of treatment for proven sepsis is 1014 days of IV antibiotics.

Other therapy includes IVIG (500750 mg/kg) in infants with overwhelming infection.

Seizures

Newborns rarely have well-organized tonic-clonic seizures because of their incomplete

cortical organization. The most common type of seizure is characterized by subtle

findings, including horizontal deviation of the eyes with or without jerking; eyelid

blinking; sucking, smacking, and other oral-buccal movements; swimming, or paddling

movements; and apneic spells. Strictly tonic or multifocal clonic episodes are also seen.

Most common causes of seizures include hypoxic-ischemic encephalopathy,

hypoglycemia, hypocalcemia, intracranial bleeds, and infection.

Clinical Findings

Most neonatal seizures occur between 12 and 48 hours of age.

Screening workup should include blood glucose, calcium, and electrolytes in all cases.

Further workup depends on diagnoses suggested by the history and physical examination.

Treatment

Adequate ventilation and perfusion should be ensured.

Hypoglycemia should be treated immediately with a 2-mL/kg infusion of D10W

followed by 6 mg/kg/min of D10W.

Treatment of the cause e.g. for hypocalcemia; IV administration of 10% Ca gluconate is

given slowly as a 100200 mg/kg (12 mL/kg) over approximately 1020 minutes.

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Phenobarbital (20 mg/kg IV); supplemental doses of 5 mg/kg can be used if seizures

persist, up to a total of 40 mg/kg. In most cases, phenobarbital controls seizures. If

seizures controlled, maintenance dose is initiated as 5 mg/kg /day, divided as two doses.

If seizures continue, therapy with fosphenytoin or lorazepam may be indicated.

Hemorrhagic disease of the Newborn

(Vitamin K-dependent Bleeding)

Vitamin K deficiency bleeding is caused by the deficiency of the vitamin Kdependent clotting

factors (II, VII, IX, and X). Bleeding occurs in some newborns who do not receive vitamin K

prophylaxis after birth, generally in the first 5 days to 2 weeks in an otherwise well infant.

Sites of bleeding include the GI tract, umbilical cord, circumcision site, and nose, althoughdevastating intracranial hemorrhage can occur. Bleeding from vitamin K deficiency is more

likely to occur in exclusively breast-fed infants because of very low amounts of vitamin K in

breast milk, with slower and more restricted intestinal colonization.

Prevention is by IM injection of 1 mg (0.5 mL) vitamin K to every newborn in the delivery

room. Treatment consists of 5 -10 mg of vitamin K SC or IV. IM injections should be avoided in

infants who are actively bleeding. Such infants may also require factor replacement in addition to

vitamin K administration. Fresh blood or plasma may be needed in severe bleeding.

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Documents

Pediatrics Lecture 2 (Neonatology) (15!3!2011) Dr.M.hesham