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Neonates in the Emergency Department


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1
The First Month
Neonates in the Emergency Department
Maureen McCollough MD, MPH, FACEP
Associate Professor of Clinical Emergency Medicine and Pediatrics
USC School of Medicine
Director of Pediatric Emergency Medicine Department
LAC-USC Medical Center

The First Month
2
NEWBORN DELIVERY and
RESUSCITATION IN THE ED
PREPARATION PRIOR TO DELIVERY
• Have neonatal resuscitation kit or cart available - to include both airway and vascular access equipment; include small
charts with drug dosages inside
• Warming bed
• Hotline to nearby NICU
• Non-sterile gloves in your back pocket (in case you discover yourself delivering a newborn in the parking lot)
• Quickie questions for Mom:
- due date – are you dealing with a premature birth?
- only one fetus inside uterus – are you dealing with multiple births?
- gestational diabetes - are you dealing with a potentially large newborn that will be more difficult to deliver?
• Take a look at Mom’s underwear – might be able to tell about meconium – yes or no, thick or thin?
DELIVERY OF NEWBORN
• Fortunately, usually not a problem !
• If possible, suction nose then mouth before newborn is completely delivered
- too vigorous stimulation of posterior pharynx can cause bradycardia
- if meconium is present, attempt suction with 10F or larger suction (usually not possible because newborn delivers too
quickly)
• Prevent newborn from hitting the ground!
MECONIUM – WHAT IS IT?
• Meconium is the newborn’s first bowel movement while still in-utero; usually a sign of distress!
• Meconium aspirated into the newborn’s lungs can cause a pneumonitis with prolonged sequelae
• Whether or not ALL meconium, watery or thick, needs to be suction out of the TRACHEA remains somewhat
controversial
• All newborns, with watery or thick meconium, do need their nose then mouth suctioned at the perineum when the head is
delivered
• Newest guidelines from AHA say if newborn is “depressed” (non-responsive), is apneic or has a heart rate < 80, and there is
thick meconium present, DO NOT STIMULATE THE NEWBORN AFTER DELIVERY!
• Thick meconium with a depressed newborn, or apneic or bradycardic (<80) then trachea needs to be suctioned with an ET
tube attached to a meconium aspirator attached to wall suction (wall suction should be set to
< 100 mm Hg)
• The ET tube is the SUCTION CATHETER! Do not attempt to pass a small suction catheter through the ET tube; the size
of any suction catheter through the ET tube will be too small for removal of meconium
- alternative to the ET tube is to use a large (size 12 F) suction catheter directly into the trachea
• How long to suction trachea? Generally, not longer than 3-5 seconds at a time.
• If newborn is severely depressed and heart rate is dropping, then positive-pressure ventilation may need to be applied even
if some meconium still exists in the airway
• Can use the same ET tube, if necessary, to deliver positive-pressure ventilation
RESUSCITATION BASICS – in order !
• Suction nose then mouth
• Dry ‘em off then piss ‘em off !! (i.e. stimulate the newborn after meconium suctioning, if necessary)
• Blow-by O2
• Bag-and-mask ventilation (positive-pressure)
• Intubate
• Chest compressions
• Epinephrine
• Intervention, then re-evaluate!
• KEEP NEWBORN WARM!

The First Month
3
WHO TO RESUSCITATE ?
• Sometimes when a baby is delivered in the ED, the true gestational age of the child may not be know, i.e. mom does not
know her LMP or her due date
• A good estimate of the viability of a newborn is the infant’s foot should be at least 3cm long; less than that is considered a
non-viable fetus
NORMAL FETAL CARDIOPULMONARY PHYSIOLOGY TRANSITION
• During fetal life, lungs/alveoli are fluid-filled sacs and blood flow through the lungs is markedly diminished
• Majority of blood flow during fetal life is diverted away from the lungs via the ductus arteriosus (connects pulmonary
artery to the aorta)
• When newborn takes first breath at birth, the lungs expand with air and fetal lung fluid gradually leaves the alveoli (process
of labor may only facilitate the process of removal of lung fluid; majority of the fluid is absorbed through the lymphatics and
blood vessels within the lungs)
• Arterioles open and allow more blood flow to the lungs
• Ductus arteriosus begins to close soon after the first breath; functionally closed usually by 24 hours but can take up to
several days to close
• First several breaths a newborn takes may require two to three times the negative pressure required for any succeeding
breaths, i.e. IT TAKES EFFORT! Anything that inhibits the newborn’s ability to generate this pressure can result in
respiratory depression!
REASONS FOR HYPOXEMIA AT BIRTH
• Problems clearing fetal lung fluid – fluid in alveoli is not cleared quickly; usually due to newborn not making adequate
respiratory efforts; if newborn has not taken an initial breath, assume that no expansion of alveoli has occurred and the alveoli
remain filled with fluid
• Persistent fetal circulation – arteriolar vasoconstriction in the lungs persists after birth process
REASONS FOR INADEQUATE RESPIRATORY EFFORTS (LEADING TO DECREASED
CLEARANCE OF LUNG FLUID)
• Mom’s age > 35 or < 16yo
• Maternal diabetes or hypertension
• Maternal hemorrhage
• Prematurity or multiple fetuses
• Drugs given to mom or taken by mom prior to birth
• Congenital neuromuscular diseases
• Congenital malformations
• Abnormal presentation causing hypoxia e.g. nuchal cord, breech presentation
• Meconium-stained amniotic fluid
PHYSIOLOGY OF APNEA
• Neonate deprived of oxygen will have a brief period of rapid breathing ‹ respiratory movements soon stop, heart rate
falls, tone becomes floppy, and neonate soon develops primary apnea
• During primary apnea, stimulation and oxygen will usually induce spontaneous respirations
• If apnea continues, neonate soon develops deep gasping respirations ‹ heart rate continues to fall, blood pressure falls,
and neonate is now flaccid ‹ gasping soon stops and neonate develops secondary apnea
• During secondary apnea, blood pressure and heart rate continue to fall until neonate develops cardiac arrest
• During secondary apnea, neonate is unresponsive to stimulation and will not resume spontaneous respiratory efforts ‹
resuscitation must now include assisted ventilation, oxygen, and potentially cardiac compressions or medications
• Neonate born apneic may already be in primary or secondary apnea; these two conditions are virtually indistinguishable
from each other; infant is not breathing and the heart rate < 100 bpm
• A newborn in primary apnea will usually respond to simple stimulation and oxygen; CAUTION – respiratory effort that
does resume may be irregular or may be ineffective!
• A newborn in secondary apnea will not resume spontaneous breathing on his or her own; assisted ventilation with positivepressure
ventilation with oxygen usually necessary
• ASSUME NEWBORN IS IN SECONDARY APNEA UNTIL PROVEN OTHERWISE!
• DELAY IN INITIATING ASSISTED VENTILATION CAN RESULT IN LONG DELAY IN ESTABLISHING
SPONTANEOUS RESPIRATIONS !

The First Month
4
PERSISTENT FETAL CIRCULATION or PERSISTENT PULMONARY HYPERTENSION
• Pulmonary vessels remain constricted in the newborn, leading to hypoxemia and acidosis.
• In the presence of hypoxemia and acidosis, the newborn’s pulmonary vessels remain even more constricted ‹ persistent
fetal circulation ‹ right to left shunting of blood ‹ deoxygentated blood to systemic circulation through ductus and foramen
ovale
• Can occur as a result of birth asphyxia, meconium aspiration, pulmonary hypoplasia due to diaphragmatic hernia, group B
streptococcus, or hyaline membrane disease of prematurity
• Presents with tachypnea and respiratory distress; 2nd heart sound is not split due to early closure of pulmonary valve
• Confirm by obtaining right brachial artery ABG and ABG from more distal area (umbilical, femoral, post tibial artery); will
see a 15mm Hg difference; or O2 sats from right hand and one foot will have 10-15% sat difference
• Persistent fetal circulation may be improved by calming patient, increasing oxygenation (ventilating with 100% oxygen) and
if severe, may require correction of acidosis with bicarbonate (controversial)
BAGGING OF NEONATES
• Initiated in newborns who are apneic or whose heart rate is < 100bpm
- measure newborns heart rate at cardiac apex or brachial artery or umbilical stump
• Occiput is large so place towel under the shoulders, approximately 1 inch
• Avoid hyperextension of the neck as this may actually close off the newborn’s airway
• Choose a mask that fits – bridge of the nose to cleft of the chin, without pushing on the eyes
• Squeeze/Release/Release at a rate of 40 – 60 breaths per minute
• Less compliant lungs means higher pressures needed to generate air movement into the lungs
• If self-inflating bag has a pop-off valve, may need to depress it while ventilating infant
• Aim for chest rise only – entire tidal volume is only 25cc
• If pressure gauge available,
- initial few breaths after delivery (requiring more pressure) 30-40 cm H2O
- normal lungs soon after delivery 15-20 cm H2O
• Nasal airways are avoided due to large adenoids and size of nares
• Oral airways work well - measure level of gums to angle of the jaw
INTUBATING NEONATES
• Size 3.5 – 4.0 ETT, uncuffed tube for term babies > 3000g or > 38 wks
- size 3.5 for neonate 2000 – 3000 g or 34-38 wks
- size 3.0 for neonate 1000 – 2000 g or 28-34 wks
- size 2.5 for a premature neonate < 1000 g
- tapered ET tubes may be more difficult to place correctly into trachea since view is obstructed by the wide part of the
tube
• Size 0 or 1 straight laryngoscope blade
• Don’t need paralytics generally when intubating neonates
• Watch for reflex bradycardia associated with the laryngoscope
• Finesse is the name of the game !!!
• Tongues are larger, epiglottis is longer, cords are more anterior
• Place towel under the shoulders to align airway
• Breath sounds normally heard over the stomach because of transmission of sounds; listen for gurgling which would indicate
an esophageal intubation
• Don’t pull a good tube!!
• Pediatric CO2 detectors now available
• Cut off any extra tube extending beyond 4 cm from neonate’s lips – this will reduce the amount of dead space
• NG tube may be necessary to decompress an overinflated stomach that is preventing adequate ventilations
CARDIAC COMPRESSIONS
• Newest recommendation from AHA says to start chest compressions for any newborn whose heart rate is < 60 bpm
• Two-hand wrap method - wrap two hands around the newborn’s chest, use thumbs to do compressions; this method has
been found to be superior to the two-finger chest compression method; AHA now recommends the two-hand wrap method
• Rate: 120 per minute, interposed with ventilations (3:1)
INTRAVENOUS ACCESS
• Umbilical line - use a 3.5 or 5F umbilical catheter or feeding tube and insert into vein

The First Month
5
- normal umbilicus has 2 arteries and 1 vein (like Mr.Bill from Saturday Night Live)
- insert saline-filled catheter just below skin level and free blood flow is present (use pickups or small clamp to pull
umbilical cord straight for easier catheter insertion)
- if a young neonate ( < 7days) returns to ED in extremis, can still attempt umbilical line if crusted scab is still present;
more difficult if mom’s using alcohol religiously and cord is very dry
• Jugulars are hard since neonates have no neck; can hold neonates head gently off edge of gurney and neck veins should
stand out; careful not to extend head too far as this position will occlude airway
• Prep groin well if attempting femoral vein catheter; avoids infection in the joint
• Intraosseous lines are perfectly acceptable in the any newborn who needs significant resuscitation; found to be much faster
access in a study with medical students using IO’s vs umbilical line placement.
MEDICATIONS
• Epinephrine
- indicated in the resuscitation when adequate ventilation and cardiac compressions fails to increase heart rate > 60 - 80
- 1:10,000 concentration used in neonates
- dose is 0.01 – 0.03 mg / kg ( 0.1 – 0.3 ml / kg ) via IV, umbilical line, ET tube or IO
- in order to deliver small amounts of epinephrine down the ET tube, may need to dilute with normal saline to deliver at
least 2 ml of volume
• Volume expanders
- indicated in the resuscitation when there is evidence or suspicion of acute blood loss with signs of hypovolemia
- neonate can lose 10-15% blood volume and only show mild decrease in blood pressure
- > 20% loss can result in pallor, weak pulses but good heart rate, poor response to resuscitation, decreased blood
pressure
- whole blood (O-negative crossmatched with mother’s blood)
- 5% albumin-saline solution
- normal saline
- Ringer’s lactate
- dose for all volume expanders = 10 ml / kg IV, umbilical or IO given over 5 minutes
• Sodium bicarbonate
- indicated in the resuscitation when there is prolonged arrest that does not respond to other therapy
- 0.5 mEq / ml = 4.2% solution is the concentration used in neonates
- dose = 2 mEq / kg IV, umbilical or IO given slowly over 2 minutes
• Naloxone (Narcan)
- indicated in the resuscitation when there is severe respiratory depression and a history of maternal narcotic
administration within the past 4 hours
- 0.4 mg / ml or 1.0 mg / ml solution is the concentration used in neonates
- dose = 0.1 mg / kg IV, umbilical, ET, or IO
- CAUTION – if mom is narcotic-addicted, naloxone may induce withdrawal seizures in the newborn!
• Glucose
- indicated for evidence of hypoglycemia – acceptable glucose in neonates > 40; some references state
> 30 acceptable
- D 10W concentration used in neonates
- dose = 0.3 – 1.0 g / kg (3 – 10 ml / kg) IV, umbilical, or IO
LAB TESTS
• Heel sticks are great for a glucose and hct
- Check glucose early in neonates; hypoglycemia can be end result of many different processes
- Normal hct is 55%; low 30’s nadir by 2 months of age
- WBC 7 - 28,000 during first month of life
• IV’s and labs: In general, prep a neonate for a blood culture every time you stick him for blood
- 85% of IV or blood draw attempts are successful the first time on young infants
- collect extra tube (“didja” tube) for neonatologists – especially for neonates with potential inborn errors, adrenal
hyperplasia, etc
• 24 or 26 gauge catheters
• Use antecubital area, hands, scalp veins

The First Month
6
• Difficult to get an arterial stick in neonates
- Capillary blood gas can give the pH and the CO2 ‹ if normal, great !!
NOT YOUR TYPICAL NEWBORN
• Transient tachypnea of the newborn - tachypneic and may have retractions or grunting
- usually not cyanotic
- caused by retained fluid in lung alveoli
- chest x-ray will show prominent pulmonary vascular markings, fluid lines in fissures, overinflation, and flattened
diaphragms
- supportive care usually all that is necessary
• Choanal atresia – congenital blockage of one or both of the posterior nares by a membrane or bone
- newborns are obligate nose breathers except when crying
- newborn will be pink and oxygenated when crying and then become apneic and cyanotic when quiet – will usually be
apparent during the first few minutes of life
- cannot pass a 5F feeding tube down either nares
- an oral airway or ET tube must be inserted and left in place until surgery to correct defect
• Pierre-Robin Syndrome – congenital abnormality that results in an abnormally small mandible
- can be very difficult to bag-and-mask ventilate and requires an oral airway
- will usually have a cleft palate
• Diaphragmatic hernia – suspected if newborn has scaphoid abdomen, difficulty breathing, and bowel sounds over chest
- rarely may present clinically a few days or weeks after birth; may not have a scaphoid abdomen then
- newborn may also have asymmetry of contour or movement of the chest
- tachypneic, apnea, potential respiratory distress
- may have shift of apical impulse
- Chest xray will show loops of bowel in the chest cavity
- NG tube may deviate up into chest cavity
- intubate early since bag-and-mask ventilation will only allow more air to enter the bowel and compromise lung
expansion
- pulmonary hypertension may develop
• Premature – if < 1000 grams, majority will require endotracheal intubation
NORMAL NEONATAL ANATOMY AND PHYSIOLOGY
WEIGHTS AND GROWTHS
• most term infants will lose weight (10%) during first few days but level off by 5 - 7 days old
• most term infants will regain their birth weight by 10 - 14 days and then gain 20 - 30 grams (~1oz)/day for
first few months
NORMAL PULMONARY FUNCTION
• normal respiratory rate is 30 - 40 per minute
• neonates are obligate nose-breathers ‹ watch that nasal cannulas don’t cause respiratory distress !
• infant’s ribs are aligned horizontally, so in order to increase thoracic diameter to inhale, infant must lower his diaphragm (if
stomach is distended with air, diaphragm will not function properly and child will not be able to ventilate well ‹ use an
NG or OG tube when trying to ventilate a critically ill infant)
PERIODIC BREATHING PATTERN
• occurs in normal full term infants during first few months of life
• apneic-like pauses of 5 - 10 secs followed by a burst 50 - 60 resp/minute for 10 - 15 secs
• not associated with heart rate or color change
• infants should have respiratory rate recorded for 30 second intervals x 2 to avoid falsely high or low counts
NORMAL CARDIAC FUNCTION
• normal heart rate in a neonate ranges from 90 – 180; average is 120-150
• varying degrees of acrocyanosis is common
• newborns have a relatively thick right ventricular wall and elevated pulmonary vascular resistance (PVR)

The First Month
7
- right axis deviation (RAD) of the QRS on EKG is normal and can range from +125 to +180 degrees
- QRS and T waves show small voltages
- RV dominance results in tall R waves in V1, V2, and rV4
- this PVR gradually decreases by 6 - 8 weeks and resembles that of an adult
• normal PMI is at the left lower sternal border
• early systolic murmur caused by a normal persistent patency of the ductus arteriosus may be heard in the first few days of
life
• innocent pulmonary flow murmur can be heard radiating to sides and back, usually < or = II/VI
• peripheral pulses should be palpable in all normal neonates, including pulses in the feet
• normal cardiothoracic ratio (CT ratio) on CXR is greater than 0.50 (inspiration and thymus affect CT ratio)
NORMAL ABDOMINAL ANATOMY
• liver is palpable 1 - 2 cm below the right costal margin
• spleen tip may be palpable
NORMAL FEEDING PATTERNS
• FORMULA FED INFANTS - will consume 3 - 4 ounces every 3 - 4 hours by the end of the first week of life
• BREAST FED INFANTS - will generally empty a breast within 7 - 8 minutes, so it’s preferable to switch the infant
to the other breast at that point and let him finish nursing on the side that still contains a supply of milk
• some infants will stop middle-of-the-night feeds by 3 - 6 weeks old, while others continue until 4 - 8 mo old
• infants may want to continue to suckle after feeding, try a pacifier !
MAKE SURE CHILD IS ACHIEVING ADEQUATE WEIGHT GAIN !!
NORMAL STOOLING PATTERNS
• first meconium stool should be passed within 24 hours of birth; if stool is not passed, possible Herschsprung’s or
hypothyroidism
• after milk feedings start, transitional stools start on the 3rd - 4th day and are greenish-brown with milk curds
• typical milk stools follow after an interval of 3 - 4 days
- breast fed stools will be stringy, loose, yellow and sweet smelling
- formula fed stools will be pasty, homogenous, yellow-brown; can be foul smelling
• frequency of stools closely relate to the frequency and amount of feeds, usually 3 - 5/day
- breast fed infants may stool after every feeding
• No two infants are alike !!!
NORMAL GENITOURINARY ANATOMY
• infants born in the breech position may have significant bruising to the genital area
NORMAL VITAL SIGNS
AGE HR BP RR
Systolic Diastolic
Newborn 60 +/- 1 37 +/- 8 40
1 - 2 days ( 91) 123 (159) < 40
3 - 6 days ( 91) 129 (166)
1 - 3 weeks (107) 148 (182)
1 - 2 mo (121) 149 (179) 80+/- 16 46 +/- 16 24 - 35
NORMAL HEMATOLOLOGY VALUES
AGE HGB gm% HCT% MCV RETIC% WBC
newborn 13.7 - 20.1
1 - 3 days 18.5 (14.5) 56 (45) 108 (95) 1.8 - 4.6 18.9 (9.4 - 34)
2 weeks 16.6 (13.4) 53 (41) 105 (88) 11.4 (5 - 20)
1 mo 13.9 (10.7) 44 (33) 101 (91) 0.1 - 1.7 10.8 (4 - 19.5)
2 mo (nadir!) 11.2 (9.4) 35 (28) 95 (84)
6 mo 12.6 (11.1) 36 (31) 76 (68) 0.7 - 2.3 11.9 (6 - 17.5)
• Normal term newborn hemoglobin = 13.7 - 20.1 gm/dl

The First Month
8
• Physiologic nadir occurs at 8 - 12 weeks old; hemoglobin = 11.4 +/- 0.9 gm/dl; then erythropoiesis resumes
• Percentage that is fetal varies from infant to infant; fetal hemoglobin gone by 7 months old
NORMAL CSF VALUES
CELL COUNT term 0 - 28 days 0 - 22WBC/mm3 (mean 8.2) predominant lymphs
> 1mo old 0 - 7 WBC/mm3 0% PMN
GLUCOSE term infant 34 - 119mg/dl (mean 52)
child 40 - 80mg/dl
PROTEIN term infant 20 - 170mg/dl (mean 90)
child (lumbar) 5 - 40mg/dl
• VS, Hematology, CSF values modified from The Harriet Lane Handbook 13th Edition
NEWBORN SCREENS and TREATMENT
AAP GUIDELINES STATE ANY NEWBORN DISCHARGED PRIOR TO 48 HOURS OLD BE RE-EVALUATED WITHIN 2 - 3 DAYS !!!
• Phenylketonuria (PKU)
• Congenital Hypothyroidism
• Beta Thalassemia
• Galactosemia
• +/- other inborn errors, sickle cell, congenital toxoplasmosis, congenital adrenal hyperplasia,
cystic fibrosis
• Coomb’s test for infants of Rh (-) and “O” mothers
• Vitamin K 1mg IM
• Erythromycin ointment, Silver nitrate, (or diluted Betadine) to the eyes
NEONATAL RESUSCITATION EQUIPMENT
• ETT TUBE 3.5 – 4.0 for term infant, > 38 weeks, > 3000g
• ETT BLADE 0 for newborn resuscitation; 1 straight blade for beyond newborn period
• CHEST TUBE 10 - 12 F
• NG TUBE 6 - 8 F
• FOLEY TUBE 5.0 feeding tube, or 6 - 8 F Foley
• UMBILICAL VEIN CATHETER 5 F catheter or 5 F feeding tube
• CENTRAL LINE 4.0 F
• INTRAOSSEOUS with T-connector / 3 way stopcock
• EPINEPHRINE
IV, SL, IO, or umbilical 0.01mg/kg (0.1cc/kg) 1:10,000 1st dose
ETT 0.1mg/kg (0.1cc/kg) 1:1,000
** High dose epi no longer recommended for children by AHA
BIRTH INJURIES
• injuries sustained during labor and delivery by natural, sometimes iatrogenic means
• on average 6 - 8 injuries/1000 live births; more often in large infants, breech births, or precipitous deliveries
PETECHIAE OF THE HEAD AND NECK AREAS
• petechiae or bluish suffusion are probably the result of venous obstruction caused by nuchal cord or sudden increase in
intrathoracic pressure during delivery
• may take 2 - 3 weeks for suffusion to disappear
SUBCONJUNCTIVAL AND RETINAL HEMORRHAGES
• resulting from increased pressure in the head and neck region during birth
• generally disappear within 4 weeks
• to induce an infant to open its eyes, gently rock him from an upright to a horizontal position; feed the baby; turn lights off
and on

The First Month
9
CAPUT SUCCEDANEUM
• diffuse, edematous swelling of the scalp involving the presenting portion of the head during a vertex delivery
• appears in the delivery room
• extends across midline, across suture lines
• can be ecchymotic
• if extensive, can cause anemia and hyperbilirubinemia
• should not be routinely aspirated , as this predisposes to infection
SUBGALEAL HEMORRHAGE
• hemorrhage underneath the galea resulting in a ballotable collection of blood on the head (can feel like a bag of liquid)
• may take several hours to appear
• can extend across midline, across suture lines
• if extensive, can cause anemia and hyperbilirubinemia
• slowly resorbs; may begin to calcify
• should not be routinely aspirated, as this predisposes to infection
CEPHALOHEMATOMA
• subperiosteal hemorrhage, hence limited to one cranial bone, usually parietal
• does not cross suture lines
• may take several hours to appear
• no discoloration of overlying scalp
• may have underlying linear, non-depressed, skull fracture that requires no intervention
• may also cause anemia and jaundice
• may begin to calcify, and then slowly resorb over 2wk - 3mo (or longer)
• central depression results as organized rim develops
• should not be routinely aspirated, as this predisposes to infection
CRANIAL MENINGOCELE
• not a birth injury
• defect in skull closure with resultant bulging of dura filled with CSF only
- (cranial encephalocele also contains cerebral cortex, cerebellum or brain stem)
• most common in occiput area or below inion
• pulsates, increases with crying, and Xray will show a bony defect
• management - referral to a pediatric neurologist or neurosurgeon
SCALP ELECTRODES
• can appear in the first few days as a localized infection on the scalp where the fetal electrodes were placed
• NEONATE WITH LOCALIZED INFECTION SHOULD BE ADMITTED !!
SUBCUTANEOUS FAT NECROSIS
• discovered within the 5th - 10th day of life, but as early as day 2 or as late as day 24
• lesions are sharply circumscribed nodules or plaques, hard, and of a dusky reddish-purple hue; surface may be uneven and a
sharp margin delineates it from the surrounding normal skin
• found in the cheeks, buttocks, back, arms, and thighs; mostly over bony prominences
• benign; usually asymptomatic, not hot or tender
• occasionally will extensively calcify or drain a liquid material
• versus sclerema neonatorum - wax-like diffuse hardening of skin in infants with underlying systemic disease (sepsis,
congenital heart disease, dehydration); usually seen in premature or debilitated infants
• treatment - avoid warm or hot packs to the area
- should be followed by a pediatrician for signs of extensive calcification or drainage
- process is usually self-limited and resolves over a few weeks
STERNOCLEIDOMASTOID MUSCLE INJURY
• result of muscle or fascial sheath injury during hyperextension
• associated with breech or forceps births, congenital dislocated hips, and female sex
• clinical signs present at birth or in first month - usually right sided , nontender 1 - 2 cm, firm palpable mass in the muscle
bed, with shortening or contracture of the muscle, with obligatory head tilt toward affected side, chin away from affected side
• treatment - resolves spontaneously in most infants
- gentle passive stretching exercises is controversial as to utility

The First Month
10
- referral to pediatrician to follow
CLAVICLE
• fractured secondary to large infant with shoulder distocia, or difficult arm delivery of a breech
• infant may not move arm and may lose Moro refex on affected side
• callus develops within one week and may be first sign of fracture
• Treatment - no treatment necessary; will heal well on its own
BRACHIAL PLEXUS INJURY
• caused by lateral traction on head/neck during vertex delivery, arms over head in breech delivery, or excessive traction on
shoulders
• can affect entire arm, or upper arm with or without paralysis of forearm or hand
• C5-C6 most common - lack of shoulder motion with extremity lying adducted, prone, and internally rotated; hand muscle
intact; no sensory deficit
• exam can show loss of Moro reflex on affected side
• prognosis depends on if paralysis is due to edema or hemorrhage, or due to laceration of the nerve
• treatment - referral to pediatric orthopedist for splinting and exercises, or possible surgery
HEPATIC OR SPLENIC HEMATOMA
-- caused by increased abdominal pressure during breech birth
-- neonate appears normal for 1 - 3 days (up to 1 week), and then may present with nonspecific signs of blood loss such as poor
feeding, listlessness, pallor, jaundice, tachypnea, tachycardia
-- shock and death may result if hematoma ruptures and allows fresh bleeding
-- exam may show a palpable RUQ mass or “blue” abdomen
-- ultrasound should diagnosis hematoma
DERMATOLOGY
ACROCYANOSIS
• cyanosis of the distal extremities resulting from vasoconstriction and decreased perfusion
• can occur in cool temperature rooms
• does not necessarily indicate true desaturation
• central cyanosis (lips and tongue) indicates true oxygen desaturation
• if neonate is ill-appearing, do not assume cyanosis of the hands and feet are simply acrocyanosis; must check for true
hypoxia
CUTIS MARMORATA “MOTTLING”
• occurs when child is exposed to colder temperatures
• lacy, reticulated red or blue vascular cutaneous pattern occurs over most of the body
• represents an accentuated physiologic response that disappears as child gets older but sometimes can be seen even in older
children
• can also be a sign of sepsis, or dehydration
HARLEQUIN COLOR CHANGE
• seen usually in immediate newborn period, but up to 2 - 3 weeks old
• seen in up to 10% of newborns
• probably reflects an autonomic vascular imbalance
• when the infant is placed on its side, the body is bisected with a pale upper half and deep red dependent half lasting only
several minutes
MILIARA RUBRA “PRICKLY HEAT or HEAT RASH”
• common in hot and humid climates
• lesions reflect blocked sweat duct openings that lead to tiny vesicular papules that itch and burn
• usually located on the face, in the diaper area or axilla areas
• treatment key is prevention!
- allow areas to cool and air dry if possible
- instruct parents not to evaluate their neonates need for more layers of clothes based on temperature of his hands/feet;
feel his chest or neck for better temperature gauge

The First Month
11
ACNE NEONATORUM
• caused by maternal hormones still circulating within neonate
• lesions appear at birth or several weeks later
• appear in crops on the cheeks, nose, chin and forehead; affects males more often
• lesions appear as comedos, pustules, and inflammatory papules
• Treatment - lesions are self-limited, and face should be washed with plain soap and water
- black skin may become hyper/hypopigmented with aggresive medicated treatments
MILIA
• 1-2mm, firm, pearly white papules scattered over the face and gingiva, especially the forehead, nose, ears, chin and
periorbital areas
• on the midline of the oral palate, called Epstein’s Pearls
• represents a defect in pilosebaceous formation in which invagination of epidermal layer forms a keratin-producing pocket; • •
• material expressed from cysts resemble tiny white pearls and exfoliate spontaneously in most infants
SEBACEOUS HYPERPLASIA
• minute yellow/white papules on the forehead, nose, upper lip and cheeks representing sebaceous glands
• smaller than milia, more yellow with sebaceous material expressed
• gradually diminish in size and disappear within a few weeks
ERYTHEMA TOXICUM NEONATORUM “NEWBORN RASH”
• benign, self-limited skin disorder that occurs in 50% of full term infants
• 1-3mm, firm, yellow/ white papules or pustules with a surrounding erythematous flare (sometimes only splotchy erythema
is seen)
• can be migratory on body
• pustules form at stratum corneum or deep in the epidermis, and also have eosinophils that accumulate around the
pilosebaceous follicles
• lesions are not related to infection
• lesions can be clustered or scattered widespread over the body, frequently involving the chest and back; palms and soles are
usually spared
• lesions usually appear on day 2 - 3 of life but can occur up to one week
• neonate has no other evidence of systemic disease, other than eosinophilia on CBC
• Diagnosis - Wright or Giemsa-stain for eosinophils (rash usually diagnosed clinically)
• Treatment - lesions are self-limited lasting a few hours to 3 - 6 days; no treatment is necessary
NEONATAL PUSTULAR MELANOSIS
• transient, benign, occuring more often in black infants
• Three characteristic lesions:
1) evanescent superficial pustules
2) ruptured pustules surrounded by fine scales
3) hyperpigmented macules
• pustules contain PMN's, debris, and occasional eosinophil
• usually present at birth or within 24 hours
• common sites are anterior neck, forehead, and lower back, although scalp, trunk, limbs, palms and soles can be affected
• pustular phase should not last more than 3 days; hyperpigmented maculas may last for 3 months
SEBORRHEIC DERMATITIS/ECZEMA
• appears during the first two weeks as “cradle cap” or “milk crust” on the scalp, and then again at 4 - 12 weeks involving the
scalp, ears, forehead, neck, flexor areas, and perineum
• lesions are greasy, yellow, flaky scales on erythematous base ---> scales may coalesce to form patches that may erode and
bleed
• most infants appear perfectly well except for the dermatitis, and other systemic signs like fever, listlessness, or mouth sores •
• may be signs of serious illnesses like histiocytosis
• dermatitis usually lasts 3 - 6 weeks, or may reappear as atopic dermatitis
• treatment -
- cradle cap treated with frequent shampooing with mild anti-seborrheic shampoo used 2 -3 times per week; mom can
gently comb out the flaky scales

The First Month
12
- for flexor or diaper areas, bathe in tepid water with Alpha Keri oil and any mild soap (advise mom to expect a slippery
infant); use cotton clothing; change diapers frequently; use zinc oxide on perineum area, then remove with mineral oil
CANDIDA DIAPER RASH
• well defined, erythematous macular papular rash with satellite lesions and small pustules
• treatment - Nystatin cream applied with each diaper change
- for severe cases, can mix Hydrocortisone 1% cream to the Nystatin; Lotrisone cream (combo steroid and antifungal)
generally not recommended for neonates; too strong)
SUCKING BLISTERS
• Solitary or scattered superficial bullae on the upper limbs at birth caused by the infant sucking on the affected part in utero
• common areas include the forearms, thumb, and index finger
• resolve rapidly on their own
• sucking pads (calluses) found on the lips during the first few months are a combination of intracellular edema and
hyperkeratosis
HEMANGIOMAS
SALMON PATCH (NEVUS SIMPLEX)
• small, pale pink, ill-defined, flat vascular lesions
• occurs mostly on the forehead (flame nevus), nape of the neck (stork bite), glabella, eyelids, upper lip and nuchal areas
• occurs in 30 - 50% of normal newborns
• represent localized plaques of vascular ectasia that will persist for several months and increase intensity when child cries
or has changes in temperature
• facial lesions eventually fade, but neck lesions may persist
PORT WINE STAIN
• red to purple color, variable size and shape and location, and not elevated
• do not blanch and do not disappear spontaneously
STRAWBERRY MARK
• dilated capillaries associated with connective tissue hypertrophy
• lesions are raised, sharply demarcated, dark red, and rough surfaced; 75% occuring in head region
• present at birth but more commonly appear in first month or two
• after period of variable growth, the lesion will begin to regress in size
• lesions around the neck can increase in size and COMPROMISE THE AIRWAY !!
CAVERNOUS HEMANGIOMA
• interconnected venules, located in the subcutaneous tissue; overlying skin usually not involved
• lesion is poorly circumscribed, deep, soft compressible swelling with may give a bluish elevation to the skin
• usually enlarge before they regress
• can bleed or cause anemia/thrombocytopenia due to sequestration of blood in the lesion
MONGOLIAN SPOTS
• blue or slate-gray macules, with variably defined margins, occurring in the presacral area, posterior thighs, legs, back, and
shoulders
• 80% of black, Asian, East Indian infants affected; < 10% of caucasion infants affected
• caused by melanocytes presumed to be arrested in their migration from neural crest to epidermis
• usually fade within a few years, but widespread, unusual location lesions may not disappear
• many times are mistaken for child abuse
BREAST ENLARGEMENT and MASTITIS NEONATORUM
• breast enlargement and, on occasion, expression of white discharge from the nipples during the first few days of life is
caused by maternal hormonal stimulation (see Genitourinary “Vaginal bleed”)
• infection can be started with undue manipulation of the breasts causing redness, heat, swelling, pain and possibly fever
• Staph aureus and E. coli are usual causative microbes
• prophylaxis consists of avoiding manipulation/trauma of the engorged breasts
• if infected, treatment includes systemic antibiotics and warm compresses
• abscesses need drainage
• scar formation can affect future secretory power of the female breast

The First Month
13
UMBILICAL CARE
• cord contains 2 arteries, one vein, rudimentary allantois, remnant of omphalomesenteric duct and wharton jelly
• cord usually dries and seperates within 6 - 8 days after birth ‹ raw surface becomes covered by thin layer of skin ‹ scar
tissue forms and wound is healed within 12 - 15 days
• Treatment: fold the top edge of the diaper down, away from the umbilicus, so the stump stays dry
- clean the area with a cotton ball and alcohol two times per day and for several days after the stump falls off
- parent must avoid soaking the umbilical area in alcohol; case reports of toxicity exist !!!
- do not submerse the umbilical area in a bath until after stump has fallen off and healed over
UMBILICAL CORD PROBLEMS
• DELAYED SEPARATION of the cord greater than one month is associated with an immune disorder and/or overwhelming
bacterial infection
• PERSISTANT URACHUS/ URACHAL CYST: failure of closure of the allantoic duct and is associated with bladder outlet
obstruction; results in clear urine-like discharge from the umbilicus ‹ surgical consult needed
• GRANULATION TISSUE: tissue is a persistant, soft, vascular, granular and dull red or pink with seropurulent discharge ‹
cauterize with silver nitrate every several days until base is dry
• MUCOID DISCHARGE: results from inadequate air drying or cleaning of the cord area ‹ cleanse the base several times a
day with alcohol and allow air drying
• OMPHILITIS: infection can result in hematogenous spread or extension to the liver or peritoneum
- can have minimal signs such as mild erythema on abdomen, usually circumferential around umbilicus
** “redness” at the umbilicus may appear as a result of a normal cord stump bent over pressing onto neonate’s abdomen held
down by a diaper; remove diaper; lift cord off abdomen; redness should go away in a few minutes; if not, may be early
infection
- ANY ERYTHEMA EXTENDING ONTO ABDOMEN IS OMPHILITIS UNTIL PROVEN OTHERWISE !!
- Treatment - MEDICAL EMERGENCY !!!
- IV Oxacillin and Gentamicin and admission to observation area -
- surgery usually necessary for abscesses
OPHTHALMOLOGY
• tears rarely appear with crying until the 3rd - 4th week of life
• to encourage a neonate to open its eyes for examination, feed him or gently rock him from an upright to a horizontal position
CONJUNCTIVITIS “OPHTHALMIA NEONATORUM”
• SILVER NITRATE - occurs usually within 6 - 12 hours after birth, with clearing by 24 - 48 hour
- used prophylactically against gonorrhea
- 10% of infants treated with silver nitrate develop conjunctivitis
• GONORRHEA -
- incubation period usually 2 - 5 days (can be present at birth or be delayed beyond 5 days because of the ocular
prophylaxis given)
- begins with mild inflammation and serosanguineous discharge, but within 24 hours, becomes thick, purulent with tense
edema of eyelids and marked chemosis
- complications include corneal ulcers and anterior synechiae
- diagnosis made by gram stain of intracellular gram negative diplococci
- Treatment - culture and gram stain eye (use Thayer-Martin plates); culture nasopharynx for chlamydia
- until proven otherwise, admit for IV antibiotics (PCN G 50,000 units/kg/24hr or Ceftriaxone or Cefotaxime)
- irrigate eyes every hour initially
• CHLAMYDIA (INCLUSION BLENNORRHEA) - incubation period usually 5 - 14 days
- usually mild inflammation and discharge, but can progress to severe eyelid swelling and copious discharge
- usually only the tarsal conjunctiva involved, not the corneas
- cause of 20 - 40% of neonatal conjunctivits

The First Month
14
- diagnosis can be made by Giemsa-stained epithelial cells scraped from the tarsal conjunctiva containing
intracytoplasmic inclusions; chlamydia cultures are preferred
- since eye infection usually precedes the respiratory infection, if the infant is well with no clinical evidence of
pulmonary infection, a chest xray is not necessary
- Treatment - culture and gram stain the eye
- culture nasopharynx for chlamydia
- until cultures return, admit for IV antibiotics then oral erythromycin for 2 weeks to cure the eye infection and prevent
pulmonary pneumonia
ALL EYE DISCHARGES APPEARING AFTER INFANT IS 48 HOURS OLD NEEDS CULTURE AND GRAM STAIN!!
DACRYOSTENOSIS
• congenital lacrimal duct stenosis
• Clinical signs include tearing of the eye, aggravated by an upper respiratory infection or exposure to wind or cold, often
accompanied by mucoid discharge “matting” and crusting
• reflux of fluid can be elicited by massaging the nasolacrimal sac, proving obstruction
• exam of the eye itself shows clear cornea, red retinal reflex, and no erythema of conjunctiva
• can lead to dacryocystitis (sac), pericystitis (surrounding tissue) or periorbital cellulitis
• Treatment - massaging of the area three times per day
- cleanse lids with warm water
- antibiotic eye drops used PRN for infection
- most resolve spontaneously with conservative management by one year
- for persistant stenosis, referral to an opthalmologist for dilation of duct
DACRYOCYSTITIS
• infection of the obstructed nasolacrimal sac
• etiology is usually Staph, Strep, or H. flu
• clinical signs include swelling, redness, tenderness of the sac area, with or without signs of systemic infection such as fever or
irritability
• usually will have a yellow/green eye discharge
• Treatment - neonates with dacrocystitis require admission to the hospital for IV antibiotics
- older infants traditionally treated with antibiotic eye drops
- warm compress to the area
- referral to opthalmology for possible surgical intervention
ORAL/DENTAL
MUCOCELE/ MUCOUS RETENTION CYST
• small, circumscribed, elevated, translucent, compressible, and bluish lesion
• probably results from trauma which ruptures the minor salivary gland ducts and accumulates saliva in
the tissues
• occurs on lips and tongue, but can occur anywhere in oral cavity except anterior half of hard palate
(has no salivary glands)
• when ruptured, discharges a sticky mucoid material and collapses, only to recur
• may persisit for months but usually subsides earlier
EPSTEIN’S PEARLS/ BOHN’S NODULES
• similar to milia of the face; occur in 85% of newborns
• lesions are usually multiple, firm, and opaque white, occuring at the junction of the hard and soft palate on either side of the
median raphe
• on the alveolar mucosa, can appear like “rice”; can be mistaken for teeth
• self limited but may take months to resolve
NATAL AND NEONATAL TEETH
• Natal teeth - present at birth • Neonatal teeth - appear in the first month of life
• 20% have family history of natal teeth or early eruption
• usually two at the mandibular incisor area
• attachment can be limited to gingiva, with little root or bony support

The First Month
15
• can result in pain and refusal to eat, secondary to looseness, and can cause discomfort to the breast-feeding mom
• tooth is usually an extra tooth that is structurally defective and nearly always loose
(rarely, tooth is an early primary tooth ‹ some OMFS’ will recommend xray to differentiate)
• if tooth is loose, neonate is at risk for aspiration of the tooth !!
• Treatment - referral to oral surgeon/dentist for tooth removal
- if tooth is very loose, remove by ED physician ? or consult by OMFS in ED
ORAL THRUSH
• caused by Candida fungal infection
• characterized by painless white, slightly elevated plaques resembling curdled milk
• occur on the buccal mucosa, lips, tongue, and pharynx
• can be differentiated from milk by scraping the lesion ‹ mild bleeding occurs when scraping thrush lesions
• occurs in children who are still in diapers; if no longer in diapers, consider immune deficiency
• think about immune deficiency in infants with chronic candida
• Treatment: scrape off the excess plaques, then place 1cc oral Nystatin liquid on each side of the buccal mucosa; use for
1 - 2 days beyond the lesions being gone
- need to treat the Candida diaper rash at the same time
PULMONARY
NOISY BREATHING
• “STUFFY NOSE SYNDROME”
- turbinate hypertrophy may be secondary to suctioning or inflammation from meconium or other materials
- resolves within several days to weeks
• SIMPLE CONGENITAL LARYNGEAL STRIDOR “laryngomalacia”
- most common cause of stridor in the newborn period
- no serious laryngeal or extralaryngeal lesions are suspected or found on examination
- larynx is softer than normal and collapses with inspiration, epiglottis is overlong, or arytenoids may be loose or flabby
- onset occurs usually in first month, occasionally as late as four months
- usually lower pitched, vibratory or fluttering
- usually confined to inspiration
- tracheal pathology usually causes expiratory stridor; such as vascular rings or tracheomalacia
- phonation is unimpaired; voice and cry remain strong
- commonly intermittent; increasing with excitement, physical activity, feeding and viral URI’s; diminishing or
disappearing when child is at rest
- intensified when child is supine with possible retractions; lessened when prone
- infant does not appear bothered by the stridor; color and appetite remain good
- usually disappears between 6 - 18 months
- differential includes laryngeal webs, cysts, laryngoceles, and hemangiomas
- Recommend referral to head/neck specialist for possible endoscopy if diagnosis uncertain or any other symptomatology
exist e.g. change in cry, difficulty feeding
UPPER RESPIRATORY TRACT INFECTION
• obligate nose breathers until approximately 4 months old; URI can interrupt feeding / sleep pattern because infant can’t
breathe
• if temperature > 38.0 (100.4) present, recommend septic workup and err on the side of admission; higher the temp and
younger the neonate, err on side of admission
• history and physical exam to evaluate signs of sepsis, hydration status, and signs of lower respiratory tract involvement (see
below for neonatal pneumonia)
• Treatment - if no fever present, ensure parent is using a bulb syringe to clear nasal passages before eating and sleeping
- can use saline drops if nasal passages are crusted (or home-made warm water and salt mixture)
- avoid decongestants in neonates
CONGENITAL LOBAR EMPHYSEMA
• cause and exact incidence is unknown, but neonate may present to the ED in respiratory distress and be misdiagnosed as a
pneumothorax
• can present at birth, but more likely clinical symptoms at 1 - 4 weeks old

The First Month
16
• most commonly involves the left upper lobe, then right upper or middle lobes
• believed to result from deficiency of bronchial cartilage causing collapse during expiration and air-trapping in the lobe
• can rupture and result in true pneumothorax
• symptoms can be triggered by viral infection or just progress over time after birth
• Clinical signs include poor feeding, respiratory distress, cyanosis, decreased breath sounds on one side with hyperresonance
** Symptoms may develop slowly over time; pneumothorax much more rapidly
• Differential includes pneumothorax, pulmonary sling (compression of right main bronchus by aberrant left pulmonary
artery), congenital adenomatoid malformation
• Chest Xray -
Pneumothorax - no interstitial or reticular markings seen in the lucent area
- compressed lung is seen around hilum in tension pneumothorax
- air will layer out along higher side in a decubitus film
Congenital Lobar Emphysema - reticular markings in the lucent area may be seen
- compressed lower lobe in the phrenicovertebral angle
• Treatment -
- AIRWAY, BREATHING, CIRCULATION !!
- congenital lobar emphysema needs a surgical consult
- Avoid chest tube, if possible, for pure lobar emphysema
NEONATAL PNEUMONIA
• acquired transplacentally as part of a generalized intrauterine infection (CMV, rubella, Toxoplasma, Listeria, Treponema
pallidum)
• acquired by infected amniotic fluids or birth canal secretions with onset in first few days of life (Group B strep, Gram-negative
enteric bacilli, Chlamydia, herpes simplex)
• acquired nosocomially or community-acquired (Staph aureus, Pseudomonas aeruginosa, Klebsiella, Serratia, B.pertussis, viruses
- RSV, CMV)
• poor feeding, lethargy, irritability, poor color, rise or fall in body temperature, abdominal distension, sudden loss or gain of
weight,"not doing well"
• cyanosis, tachypnea, nasal flaring, grunting, tachycardia, apnea, accentuation of periodic breathing, retractions
• auscultate chest when infant is quiet as well as crying, because rales may only be heard at end of deep inspiration
• treatment - ERR ON THE SIDE OF ADMITTING ALL NEONATES WITH PNEUMONIA !!
• Blood cultures
• nasalpharynx culture for Chlamydia
• nasal secretions for fluorescent antibody techniques of Chlamydia, Herpes simplex, and RSV as indicated
• Chest Xray usually shows hyperinflation, and interstitial or alveolar infiltrates
• Antibiotics - (same empiric regimen as for sepsis)
- if presumed Chlamydia, Erythromycin 40mg/kg/day IV
• neonates with RSV and Pertussis are at risk for apnea ‹ admit to monitored bed!
AFEBRILE PNEUMONIA SYNDROME
• present at 4 - 8 weeks old
• 50% will have a history of a conjunctivitis
• Clinical signs - "staccato" cough, respiratory distress, hypoxia, rales, apneic spells without fever
- may have mild respiratory symptoms with very gradual onset
• Chest Xray shows focal or diffuse interstitial pneumonitis
• Labs may show an eosinophilia
• etiology usually Chlamydia trachomatis; less often Pneumocystis carinii, CMV, RSV, genital mycoplasma
ü If neonate appears well and has good follow-up, may consider discharge home on Erythromycin if > 4 weeks old
APNEA, SIDS and ACUTE LIFE-THREATENING EVENT
• SIDS is the most common cause of death between the ages of 1 week and 1 year, affecting 1.5 out of 1000 live births
(NICHD Epidemiological Cooperative Study)
• peaks between 2 - 4 months old; usually more in the winter months, at night, in males and with a history of a recent URI or
gastrointestinal infection
• up to 5% thought to be homicides ! (DiMaio 1988)
• Apnea is defined as the cessation of breathing for greater than 20 seconds; or the cessation of breathing accompanied by a
decrease in heart rate , presence of cyanosis, or altered mental status

The First Month
17
• premature and, to a lesser extent, term infants have a paradoxical response to a fall in pO2 ‹ initially the neonate increases
his respiratory effort in response to hypoxia, followed by a decrease in respiratory effort with resultant apnea and further
hypoxia
• this paradoxical response can last up to 25 days post-birth
• ALTE (acute life-threatening event) is defined as an episode of sudden color change (cyanotic or pallor), tone changes
(limpness, rarely stiffness) and apnea, which required significant intervention (vigorous shaking, mouth-to-mouth
breathing, or full CPR) to revive the infant
* ANY INFANT WITH A DIAGNOSIS OF APNEA or ALTE SHOULD BE ADMITTED TO A MONITORED BED !
• Good history and physical exam indicated - what was infant doing at the time, how long apneic, color changes, muscle tone
changes, what did parent do to revive infant ??
• MONITOR INFANT WHILE IN ED, in case apnea or ALTE reoccurs !!
• Labs- hematocrit, electrolytes, glucose, calcium, magnesium, ABG, and cultures, including CSF
• Pulse oximeter
• CXR- unlikely to be helpful without clinical symptoms, but may show cardiomegaly resulting from recurrent hypoxia, or
infiltrates from chronic aspiration
• Other tests may include an ammonia, thryoid functions, EEG, barium swallow, esophageal probes, EKG, or head CT
DIFFERENTIAL DIAGNOSIS FOR APNEA
Acute illnesses
Sepsis
Meningitis
Metabolic disorders (hypoglycemia, hyponatremia, hypomagnesemia,
hypocalcemia)
Cardiorespiratory disorders (congenital hearts, pneumonia ex
Pertussis, RSV,
airway obstruction)
Seizures
CNS hemorrhage
Maternal narcotic use
Anemia
Temperature instability / hypothermia
Botulism
Non-acute conditions
Gastroesophageal reflux
Congenital head/neck anomalies (migrognathia, macroglossia)
Congenital myopathies
Immature CNS
Hypoxic encephalopathy/ birth injury

The First Month
18
GASTROINTESTINAL
SPITTING UP / GASTROESOPHAGEAL REFLUX
• Need to differentiate between vomiting and spitting up:
• spitting up usually occurs during feeds and should only cover mouth and chin areas; child will continue to increase in weight
- considered the ultimate gastroesophageal reflux !
• vomiting usually occurs after feeds, will cover more extensive area and may be projectile
• many time spitting up caused by over-zealous feeding by parent; make sure intake not too much at one time (3-4 oz at one time)
• reflux may be improved by slowing feeds, burping during feeds, thickening formula with rice cereal, and sitting infant up to 30
degrees after feeds
VOMITING
DIFFERENTIAL DIAGNOSIS OF NEONATAL VOMITING
Diseases of the CNS
Increased ICP
Meningitis, Encephalitis
Intracranial Mass
Intracerebral Hemorrhage
Head Trauma/ Abuse
Metabolic Diseases
Acidosis or Hyperammonemia, Inborn Errors of Metabolism
Drug Toxicity
Salicylates
GI/ Hepatic Diseases
Gastroenteritis
Pyloric Stenosis (see below)
Malrotation/Volvulus (see below)
Appendicitis
Gastroesophageal Reflux
Hepatitis
Hepatic Failure
Pancreatitis
Intussusception
Infections
Otitis Media
Pneumonia
Urinary Tract Infection
Milk Allergy
• PYLORIC STENOSIS
- occurs in 1 - 3/1000 livebirths; males three times as affected; definite genetic predisposition
- Clinical signs include vomiting, constipation, gastric peristaltic waves, and a pyloric palpable mass
- symptoms usually start in 3rd - 5th week of life; usually starts intermittently but soon vomiting soon becomes projectile and
with every feed; vomitus never contains bile
- peristaltic waves move from LUQ toward the midline (can be accentuated by feeding child one ounce of formula and then
flicking the epigastrium with a fingernail)
- pyloric mass can be felt at the umbilicus, or well to the right, at the umbilical level, above or below (use left hand to push
right flank upward, and right hand presses downward ‹ catch the olive-like mass in between the hands)
- Diagnosis - ultrasound will show a thickened pyloric wall
- upper GI will show a “string sign” as thin streak of barium flows through the pylorus
- Treatment - Restore fluid and electrolyte losses and provide glucose
- NPO, place NG tube
- surgical consult for a pyloromyotomy
- in Japan, has been treated with IV and oral atropine; no surgery; infant outgrows “pyloric spasm”

The First Month
19
• MALROTATION with MIDGUT VOLVULUS:
- see NIGHTMARE NEONATE – Intestinal Disasters
CONSTIPATION
DIFFERENTIAL DIAGNOSIS OF NEONATAL CONSTIPATION
General
Sepsis
Respiratory Distress Syndrome
Mom’s drugs - Opiates, MagSO4
Hypothyroidism
Breast fed
Stomach/Duodenum
Antral Web
Pyloric stenosis
Duodenal atresia
Anular pancreas
Small Intestine
Meconeum ileus/plug
Volvulus
Large Intestine
Hirschsprung’s disease (anal exam - “sleeve”)
Anus
Anteriorly displaced anus (anal exam - “shelf”)
Anal fissure - (anal exam - insert bottom of small glass test tube into
rectum to examine fissure)
Perianal dermatitis
• a complaint of “constipation” in a neonate is usually just a change in the stool pattern noticed by the parents
• stooling is a new behavior; newborn begins to recognize physical symptoms associated with stooling; consider how difficult it
would be to stool lying on your back
• breast fed infants will usually pass stools more liquidy and more frequently, but can go up to one week without stooling
especially when converting to formula (e.g. mom goes back to work)
• iron in formula does not cause constipation
• breast fed neonates may present with no stool output for 4 -5 days and no other symptomatology
• constipation diagnosed in older infants when stools are hard, dry and pellet-like; neonates usually do not manifest this
• can lead to anorexia, abdominal distension, and vomiting
• very infrequent stools, ie only once per week in a 3 week old, may be a sign of partial Hirschsprung’s or hypothyroidism
• Botulism - history of Karo syrup or honey with constipation, lethargy, feeding problems, progressive muscle weakness,
hypotonia, and decreased movements
• Ensure the child is taking feeds well, gaining weight, and not vomiting
• look for signs of abdominal distension, anal fissures, or other pathology
• Treatment
- many times the rectal thermometer or abdominal exam will induce a stooling
- try flexing and extending neonates legs while she is on her back to mimic walking
- increase fluids (1 oz/day) if summertime
- DO NOT USE KAROSYRUP or HONEY WHICH CAN LEAD TO BOTULISM !
- DO NOT USE ENEMAS and DIGITAL MANIPULATION OF THE RECTUM if these can be avoided; again, neonate is
learning to recognize need to stool
- suppositories or Vaseline can be used for infants with anal fissures
- Time usually heals all “constipation” in an asymptomatic neonate !

The First Month
20
COLIC
• colic is a diagnosis of exclusion and other etiologies for uncontrolled crying must be ruled out
COMMON CAUSES OF NEONATAL AND EARLY INFANCY CRYING
ID - sepsis, otitis media
CNS - meningitis, child abuse
Cardio - SVT, aberrant coronary artery, myocarditis
GI - incarcerated hernia, intussusception, colic, anal fissure, AGE
Musculoskeletal - fractures, digital tourniquet, osteo/pyarthrosis, syphilitic periostitis
Genitourinary - testicular torsion, UTI, penile tourniquet
Metabolic - hyponatremia, hypocalcemia, hypoglycemia
Sensory - corneal abrasion, ocular foreign body, glaucoma
Miscellaneous - drug withdrawl, DPT reaction, open diaper pin, improper feeding, colic
(Singer: A Fatal Case of Colic 1992)
• chronic pattern of daily paroxysms of irritability and crying
• Wessel et al definition - > 3 hours/day, > 3 days/week, for at least 3 weeks
• usually occurs at the same time every day
• infant is otherwise healthy and thriving
• onset is in 2nd - 3rd week of life, may last several hours usually in late afternoon or evening
• “piercing scream, as if the child were in pain”; infant may draw his legs up, abdomen may appear distended, and flatus may be
passed
• underlying cause of colic still has not been determined
• ED PHYSICIAN’S JOB IS TO RULE OUT PATHOLOGY !!
• 15% of cases of “crying” found to have a treatable cause
• Treatment - assure parents that colic will eventually resolve, usually by 12 weeks
- temporary treatments include wrapping the infant with his arms to his side, and use of pacifiers
- placing child in car seat on the dryer (don’t leave child alone), taking child for a car ride, placing infant in an infant swing
have all been suggested
- ?? trial of hydrolyzed casein formulas for milk allergies, simethicone for relief of gas, fiber for relief of hardened stools ---
all questionable solutions
- AVOID ANTICHOLINERGIC + ANTISPASMODIC PREPARATIONS !
- Look for the parent that just is not coping with a colicky child; infants have died as a result of abuse due to colic
HEMATEMESIS and HEMATOCHEZIA
NEONATAL UPPER GI BLEED NEONATAL LOWER GI BLEED
Swallowed maternal blood Swallowed maternal blood
Stress ulcer Anal fissures
Gastritis/Esophagitis Infectious colitis
Bleeding disorder Milk allergy (from infant or mom intake)
Foreign body irritation Bleeding disorder
Vascular malformation Meckel’s
Bowel duplication Midgut volvulus
Idiopathic Intussusception
Bowel duplication
• SWALLOWED MATERNAL BLOOD SYNDROME-
- presents usually on 2nd or 3rd day of life
- maternal blood swallowed from birth canal should be resolved by 24 hours old
- fissure in the mother’s cracked nipples usually occurs in first week
• Clinical signs - look for other evidence of bleeding, ie oropharynx, nasal passages, bruising
- Confirm infant had Vitamin K at birth (see HEMORRHAGIC DISEASE OF THE NEWBORN)

The First Month
21
- physical exam for signs of sepsis, or bowel obstruction
• Treatment
- if maternal blood, check for cracked nipples
- if positive for infant blood, and not due to anal fissure, ADMIT FOR OBSERVATION !!
- other treatment dependent upon diagnosis ?? trial of d/cing whole milk from mom’s diet
HERNIAS
• UMBILICAL HERNIAS - common in low birth weight infants and blacks
- protrudes during crying or straining and sizes can vary from 1 - 5cm
- most will disappear by one year of age (large ones can take several years).
- strangulation is extremely rare
- use of abdominal binders is discouraged
• INGUINAL HERNIA
- embryology - testis descends with processes vaginalis (part of peritoneum) into scrotum ‹ portion attached to testis is called
tunica vaginalis; the remainder fuses together, obliterating the entrance of the peritoneal cavity into the scrotum;
- failure of obliteration can result in inguinal hernia or hydrocele
- incidence between 10 - 20/1000 live births
- indirect more common; affecting boys > girls; right > left sides
- Clinical signs include a intermittent scrotal mass, that appears with crying or straining, and withdraws with sleeping
- testis can be palpable at bottom of mass, hernia generally reducible, and does not transilluminate (see below for
hydrocoeles)
* EXAM TIP !! to identify hernia, lie infant supine on table with legs stretched and arms over head ‹ infant will cry and
increase intra-abdominal pressure
- neonate may be extremely irritable for 2 - 3 weeks before hernia becomes apparent
- anorexia, inordinate crying, vomiting, distension and blood or mucus in stools are signs of incarceration; irreducible mass
may indicate strangulation
- management - if incarcerated, admit for emergent surgery
- if reducable, needs elective surgery sooner rather than later
APT Test
- now used to differentiate between maternal or fetal blood in the stool or vomitus
- fetal hgb (infant) is alkaline-resistant
- adult hgb (mom) will change to alkaline hematin upon the addition of alkali
1. Rinse the bloody diaper or stool with water to obtain a pink supernatant hemoglobin solution
- fresh red blood must be used; melena or coffee-ground blood will falsely appear as “adult” hgb
2. Centrifuge the mixture or strain through filter paper.
(Supernate should be pink due to presence of blood)
3. To 5 parts supernate, add 1 part of 1% sodium hydoxide
4. Within 2 min, a yellow-brown color indicates the hgb is swallowed maternal blood (hgb A) ; persistant
pink color indicates the hgb is fetal (F)
* (A control test with known infant or mom's blood is advisable)
Modified APT Test
1. apply 10 - 20% NaOH solution directly to the stain in the diaper until a margin of solution was absorbed
into the diaper past the stain
2. Read color change off the diaper
Mcrury’s study showed if blood was > 30 minutes old, test was unreliable ‹ blood was oxidized by the air and changed
color from red to brown - could be mistaken for maternal
** NaOH found in hospital nursery or the laboratory - usually found as 1.0 N, can be diluted with NS

The First Month
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GENITOURINARY
HYPOSPADIAS
• male infant with hypospadias should not be circumcised as this redundant skin may be used for surgical repair
SCROTAL HYDROCOELE
• commonly found in the newborn, up to 50% of 1year old male children
• see “ GI - Inguinal Hernia” for anatomical development of hydocoeles
• processus may be patent only just below the inguinal ring so only the cord appears thickened, or patency may include the tunica
vaginalis so there appears to be testicular enlargement
• hydrocoeles can be communicating or noncommunicating
• hydroceles have fluctuant, cystic feel and transilluminate; testis generally not palpable, but the dark oval/round shadow of the
testis stands out sharply within it
- external inguinal ring is usually narrow
• hydroceles size remains relatively constant, whereas hernias vary in size or disappear
(communicating hydroceles may be slightly larger at night than in the morning)
• treatment - Noncommunicating hydoceles seldom require treatment and will resolve usually by one year
- Communicating ones are watched for signs of herniation and usually resolve
CIRCUMCISION CARE
• persistant bleeding may be a sign of hemophilia or hemorrhagic disease of the newborn
• urinary retention is a well known complication after circumcision
• case reports of lower extremity cyanosis after circumcision secondary to compression of iliac vein by a distended bladder
• Treatment - genital area should be cleansed with soap and water with each diaper change for the first several days
- applying ointment or vaseline to the area will prevent the diaper from sticking to the glans
- OK to catheterize if infant has urinary retention
- stuck glans can be freed from the diaper by using warm water
VAGINAL BLEEDING and BREAST DISCHARGE
• whitish vaginal discharge, withdrawal vaginal bleeding, or breast discharge (“witches’ milk”) can occur during the first few days,
and last for 1 - 2 weeks
• caused by circulating maternal hormones in the neonate
• hymenal tags may be noted but should not be removed because they will involute with time
MUSCULOSKELETAL
DEVELOPMENTAL HIP DISLOCATION (formerly known as congenital hip dislocation)
• risk factors include “5 F’s” family history, first baby, female, fluid decreased in-utero, frank breech
• most common presenting finding in the dislocated hip is limitation of abduction after the 2nd or 3rd month of life
• goal is to find these infants at birth (or soon after) looking for stability of the joint, not just range of motion
• examination will distinguish those hips that are unstable and can be displaced from their acetabulum to a dislocated positon
and then reduced back into the socket
• Barlow maneuver: dislocates the hip out of the socket
- hold pelvis with one hand, while the other hand holds the hip and knee flexed ‹ the thumb is on the knee,
while the middle finger is on the greater trochanter
- the hip is brought into slight adduction, while gently pressure downward is applied to the knee
- an abnormal hip will move very smoothly and subtly out of the socket
• Ortolani test: reduces the dislocated hip back into the socket
- hip is abducted and the dislocated femoral head is lifted over the rim of the socket with pressure of the middle finger
on the greater trochanter
- examiner will feel a “clunk” as femoral head is reduced back into the socket

The First Month
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• Pelvis Xray -
- line drawn vertically through anterior superior iliac spine
- line drawn horizontally on top of
- femoral head ossification center should be positioned in the medial inferior quadrant if hip is normal
- Shenton’s line will also be discontinuous
- acetablular line (index) is elevated
• Treatment - if positive Barlow or Ortolani, or positive pelvic xray, refer to pediatric orthopedist
FUNNY TURNED FEET
• intrauterine positioning may cause temporary distortion of the feet
• exam shows feet that are easily manipulated into normal position
• congenital club feet “talipes equinovarus” usually cannot be manipulated into a normal position without force
• Treatment - resolves spontaneously
• if in doubt, referral to pediatric orthopedist
JAUNDICE
* Newborn period is the only time in life when clinical jaundice is very common, and yet elevated bilirubin can cause significant
morbidity !!
BACKGROUND
• Over 60% of newborns will develop jaundice
• Seidman et al studied 6700 discharged newborns and found 0.36% developed severe hyperbilirubinemia in the first week of life
• Conrad and Seidman studies showed that 10 - 15% of moms instructed to return within 3 days after early discharge failed to
return for follow-up !
• Conrad study showed despite screening exams, hospital readmission rate for early-discharged newborns was 2.3% and for 48
hour-discharged newborns was 0.89%
• Number one reason newborns are readmitted to the hospital is for hyperbilirubinemia !!
PATHOPHYSIOLOGY
• hemoglobin is broken down to bilirubin (unconjugated) ‹ bilirubin is then conjugated in the liver by the enzyme glucuronyl
transferase and excreted in bile ‹ intestinal bacteria convert bilirubin to urobilinogen which is evacuated in the stool
• in utero, fetal unconjugated bilirubin excretion is handled by the placenta, and at birth, the sudden loss of the placenta route,
immaturity of newborn hepatic conjugation, immaturity of conversion to urobilinogen in the intestine, and a sometimes increased
RBC load leads to increased unconjugated bilirubin levels after birth
UNCONJUGATED VS CONJUGATED
• considered unconjugated hyperbili when direct (conjugated) < 15% of total
- unconjugated form is neurotoxic at certain concentrations
- kernicterus - CNS changes due to deposits of unconj bilirubin in nuclei of the brain
- depending upon gestational age, neonates at risk with bilirubin > 10 - 20 mg/dl (now being re- investigated)
- usually due to hemolytic hyperbilirubinemia; extremely rare for physiologic (Maisels et al: 6 cases in 18 years litigated in
the U.S.)
• considered conjugated hyperbili when direct (conjugated) > 30 - 40% of total
- conjugated form is not toxic, but indicates a potentially serious pathological disorder

The First Month
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APPEARANCE OF JAUNDICE
• within first 24 hours of birth (ALWAYS PATHOLOGIC): Rh disease, concealed hemorrhage, sepsis, rubella, or congenital
toxoplasmosis
• first appearing on the 2nd or 3rd day: "physiologic", Crigler-Najjar
• first appearing after 3rd day and within 1st week: breast feeding jaundice, sepsis, syphilis, TORCH, infections
• first appearing after day 7: breast milk jaundice, sepsis, congenital biliary atresia, hepatitis, syphilis, TORCH infections,
galactosemia, congential hemolytic anemias (ex spherocytosis or G6PD deficiency)
• first appearing after day 14: NOT PHYSIOLOGIC OR BREAST MILK RELATED !! PATHOLOGICAL UNTIL PROVEN
OTHERWISE !!
PHYSIOLOGIC JAUNDICE (ICTERUS NEONATORUM)
• occurs in > 60% of term newborns and 80% of premature newborns
• result of breakdown of fetal RBC's combined with transient limitation in the conjugation of bilirubin by the liver
• newborn intestine is sterile so conversion in the gut to urobilinogen does not take place, and conjugated bilirubin can be
hydrolyzed back to unconjugated form and reabsorbed if bowel contents are not evacuated
• bilirubin level rises < 5mg/dL/24hr so jaundice visible by the 2nd-3rd day of life, peaking between 3rd - 4th days, decreasing to
below 2mg/dL between 5th - 7th day of life
• level usually < 13 mg/dl with direct < 10% of total
• direct bilirubin > 1.5 - 2.0 mg/dl ( or > 15% of total) is NEVER physiologic !!
• neonate appears well (except he/she is yellow), is eating well, has no hepatosplenomegally
• risk factors for higher unconjugated levels include prematurity, Asian race, American Indian, male sex, trisomy-21, maternal
diabetes, polycythemia, cephalohematomas or skin bruises, oxytocin induction, vitamin K, dehydration, weight loss, delayed
stooling, and sibling with physiologic jaundice, and breast feeding/milk
- example: 37 week gestation infant 4 times more likely to have levels >13 mg/dl, compared to a 40 week gest infant
- higher levels decreased by 10 - 14 days old
ETIOLOGY OF JAUNDICE IN THE NEONATE
INCREASED RBC LOAD - increased unconjugated bili, normal reticulocyte
Extravasation of blood (hematoma, bruising)
Polycythemia
Swallowed maternal blood
DECREASED RATE OF CONJUGATION - increased unconjugated, normal reticulocyte
Immaturity of bili conjugation “physiological jaundice” (see below)
Congenital familial nonhemolytic jaundice - inborn errors affecting glucuronyl
transferase and bili transport (ex Crigler-Najjar syndrome)
Breast milk jaundice ???? (see below)
Bowel obstruction - increased deconjugation in the intestine followed by reabsorption
INCREASED RATE OF HEMOLYSIS - increased unconjugated, increased reticulocyte
Positive Coomb’s test - ABO incompatiblity, Rh disease
Negative Coomb’s test
- Abnormal RBC shape (sphero, eliptocytosis, etc)
- Abnormal RBC enzyme (G6PD deficiency, pyruvate kinase deficiency)
Sepsis - toxins from E. coli, Staph, Strep produce hemolysis
ABNORMAL LIVER FUNCTION - increased conjugated and unconjugated bili,
Coombs negative, normal reticulocyte
Sepsis / Hepatitis - viral, bacterial, parasite, toxic
Metabolic abnormalities - galactosemia, glycogen storage, diabetic mom, cystic fibrosis
hypothyroidism
Biliary atresia
Choledochal cyst
Obstructed ampulla of Vater

The First Month
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BREAST FEEDING JAUNDICE “EXAGGERATED PHYSIOLOGIC” or “EARLY” JAUNDICE
• breast fed infants especially at risk for higher unconjugated levels thought secondary to mild dehydration or calorie deficiency
sometimes found in breast fed neonates
• occurs in first week of life
BREAST-MILK JAUNDICE ”LATE” (different than breast-feeding jaundice!)
• occurs in 1 - 2% of breast-milk fed babies; usually family history of same
• breast milk may contain a glucuronidase that may inhibit glucuronyl tranferase activity
• bilirubin increases between 4th - 7th day of life, (classically appears during 2nd week of life) peaks during the 3rd week of life;
gradually decreases then plateaus to persist for 3 - 10 weeks
- infant usually will be resolving his physiological jaundice then suddenly start to turn yellow again
• levels = 10 - 30mg/dL
• If breast feeding is stopped for 2-4 days, then levels rapidly decline and breast feeding can be resumed without a return of
bilirubin to its previously high levels
CLINICAL SIGNS of JAUNDICE
• jaundice intensity bears no reliable relation to the degree of hyperbilirubinemia, however, typically starts at the head/neck area
and spreads to chest and extremities
• more difficult to diagnose jaundice in a neonate than in the adult (bilirubin level 4 - 6mg/dl before clinically visible)
- if unsure, press a clean glass slide onto skin to view yellow color
• unconjugated form tends to be bright yellow or orange
• conjugated/direct form tends to be greenish or muddy yellow
ED WORKUP
• Bilimeters - can be useful in the ED for following bili levels; potentially avoids future needle sticks
- bilimeter level usually greater (? 1-2mg/dl) than a venous blood sample, but difference is not reliable at higher levels
• History and physical focused on signs of hematomas, hemorrhage, dehydration, sepsis, bowel obstruction, constipation
- hepatomegally +/- splenomegally seen in severe hemolysis, sepsis, CHF, TORCH infections
• Potential labs - blood type and Rh of mom and infant, and/or Coomb’s test, (find Popras or call the hospital), fractionated
bilirubin, CBC, reticulocyte, platelets, peripheral blood smear, PT/PTT, APT test, sepsis workup, thyroid screen (call hospital),
liver function tests
* ** Red flag:
- jaundice in the first 24 hours of life
- total serum bili rising > 5mg/dl/24hrs
- conjugated bili > 1.5 mg/dl
- premature or small-birth weight infants
- infants at risk for perinatal infections
ED TREATMENT
* TREATMENT WILL DEPEND UPON AGE OF INFANT (? PREMATURE ) ETIOLOGY OF HYPERBILIRUBINEMIA,
AND THE BILIRUBIN LEVEL !!
CONSULTATION AND FOLLOW-UP SHOULD BE INSTITUTED WITH A PEDIATRICIAN IN THE AREA !!
GUIDELINES FOR TREATMENT OF PHYSIOLOGICAL JAUNDICE
(AAP: Practice parameter: management of hyperbilirubinemia in the healthy term newborn 1994)
**full term infant with negative history and exam for pathology:
• unconjugated level < 12 mg/dl, just follow
- increase frequency of feedings
- take infant out into sun - cover eyes
- avoid added glucose water, suppositories (DeCarvalho, Herrera, and Nicoll studies show water supplemented infants had
higher levels)
• unconjugated level > 15 - 17 mg/dl, ?? consider stopping breast feeding temporarily
- CAUTION: many mom’s will never go back to breast feeding when told to stop temporarily !

The First Month
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- If breast feeding temporarily terminated, need to explain to mom that her breast milk is not toxic and she needs to
pump until she resumes breast feeding
• unconjugated level > 17 consider phototherapy
• unconjugated level > 20 admit for phototherapy
- forms photoisomers of bilirubin that are water-soluble and bile excreted
• unconjugated level >25 if phototherapy fails - exchange transfusion
- removes bilirubin from blood
- rarely needed in physiological jaundice
4 DAY OLD INFANT WITH ONE DAY OF JAUNDICE
• physiological juandice with additive breast feeding jaundice ???
• history and physical exam directed as signs of prematurity, sepsis, constipation, bowel obstruction, hematomas, or risk factors for
higher levels of physiological hyperbili, like breastfeeding
• check birth history for mom’s blood type, thyroid screen
• labs - total and direct bili to start
- CBC and reticulocyte for higher levels (? >12)
10 DAY OLD INFANT WITH ONE DAY OF JAUNDICE
• breast milk related ???, pathologic ???
• history and physical exam directed at signs of sepsis, hemolysis
• check birth history for mom’s blood type, thyroid screen
• labs - CBC, reticulocyte, total and direct bili, peripheral smear
4 WEEK OLD INFANT WITH ONE DAY OF JAUNDICE
• sign of pathology !!!
• history and physical exam directed at signs of sepsis, pathological liver, hemolysis
• check birth history for mom’s blood type, thyroid screen
- ask if ABO incompatible neonate who has required repeated blood transfusions in the past
- G6PD deficiency may present itself at this time
• labs - CBC, reticulocyte, total and direct bili, peripheral smear
- other labs may include liver function tests or septic workup depending on diagnosis

The First Month
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HEMATOLOGY
ANEMIA OF THE NEWBORN
• secondary to decreased production, increased destruction, or blood loss
COMMON CAUSES OF NEONATAL ANEMIA
Hemolytic disease of the newborn - ABO or Rh incompatiblility, G6PD deficiency,
spherocytosis, or infections (like TORCH or E.coli) (see below)
Hemorrhagic disease of the newborn (see below)
Bleeding from or early clamping of umbilical cord
Large cephalohematoma
Intracranial hemorrhage
Subcapsular hematoma of the liver, spleen, or kidney
• pallor, tachycardia, prolonged capillary refill (hypotension is a late finding)
• jaundice
• hepatomegaly can be seen with severe hemolysis, viral infections, congestive heart failure, or extramedullary
hematopoiesis
• elevated reticulocyte count suggests increased destruction or blood loss
• abnormal blood smear suggests red cell dyscrasia
• jaundice within first 24 hrs of life suggests red cell destruction
• positive Coombs’ test is highly sensitive for Rh disease but 50% reliable for ABO hemolysis
HEMOLYTIC DISEASE OF THE NEWBORN
• Rh Disease: Rh negative mother forms antibodies to Rh positive fetus’ RBCs
- more serious of the hemolytic diseases
- Coomb’s test positive
- Three forms:
- Hydrops fetalis - usually stillborn, with edema, ascites, anemia
- Erythroblastosis Fetalis / Jaundice - during first few hours of life
- above two are the most common presentations
- Anemia - gradual onset of anemia during first few weeks of life with only mild jaundice
- will have a history of blood transfusions during first few days of life for incompatibility
• ABO incompatible: group O mother has anti-A or anti-B hemolysins that act against a group A or B fetus
- many ABO incompatibles only mildly clinically affected
- may be Coomb’s test negative
- usually develop jaundice in first 24 hours
- usually not anemic
- Treatment - usually phototherapy is all that is required
• G6PD deficiency or Spherocytosis: due to abnormal RBC enzyme or shape
-- Coomb’s test negative
-- presents when breast fed infant is exposed to certain “toxins” like sulfa medications or fava beans in the breast
milk
-- Clinical signs include anemia and jaundice

The First Month
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HEMORRHAGIC DISEASE OF THE NEWBORN
• decrease in factors II, VII, IX, and X occurs at 48 - 72 hours after birth, with gradual return to normal
by 7 - 10 days old
• probably due to lack of free Vitamin K in the mom and abscence of bacterial intestinal flora in the newborn normally
responsible for synthesis of Vitamin K
• infants receive 1mg of Vitamin K IM at the time of birth to prevent this fall in coagulation factors
• infants born at home may not receive regular newborn care, or hospital nursery may fail to give Vitamin K as an
oversight
• breast milk has minimal Vit K 15mcg/ml; infant formulas are fortified 50 - 100mcg/ml
• breast fed infants intestine colonized with lactobacilli, incapable of synthesizing Vit K; formula fed infants intestine
colonized with E.coli, producers of Vit K
• Early presentation - < 24 hrs old - associated with maternal drugs that interfere with Vit K metabolism (phenobarb,
dilantin, rifampin, INH, coumadin)
- presents as umbilicial or circumcision site bleeding
• Classic presentation - 2nd - 5th day of life - found in breast fed infants who did not get Vit K at birth
- presents as spontaneous bruising, GI, nasal, subgaleal, intracranial or cirumcision site bleeding
• Late presentation - develops after 2 weeks in breast fed infants who did not get Vit K at birth
- can present as late as 1 - 2 months old
- presents as pallor, intracranial hemorrhage, deep ecchymosis, nodular purpura
- has been mistaken for child abuse
• CHECK MID-THIGH AREA FOR EVIDENCE OF VITAMIN K NEEDLE STICK !!!
• labs include normal platelet count, prolonged PTT, and prolonged PT
• TREATMENT - resuscitate neonate !!
- PRBC (type O, Rh negative) replacement 10 - 20 cc/kg over 20 - 30 min for neonates who are unstable or have
respiratory compromise
- For severe bleeds, correct coagulopathy with FFP 10cc/kg
- Administer Vitamin K 1mg
- Admit for observation
CONGENITAL METHEMOGLOBINEMIA
• Iron must be ferrous (3+) state to bind reversibly with oxygen; in methemoglobinemia, iron is in ferric (2+) state
making it useless for oxygen transport
• usually, enzymes keep methemoglobin level to < 1%, but inherited conditions involving abnormal hemoglobins or
enzymes can lead to higher levels
• also toxins and drugs can cause an acquired form
• at levels > 10% , chocolate brown blood and slate gray cyanosis is apparent
• neonates born with congenital form usually present cyanotic at birth, but can present cyanotic in the first few months
of life; usually there is a family history of the same
• infants less than 6 months old have 70% of adult activity of methemoglobin reductase activity
• fetal hemoglobin also is more easily oxidized to ferric (2+) state
• NOTE: infants with diarrhea and acidosis:
- can present with methemoglobinemia
- body can produce an ?? oxidant in association with the diarrhea
- also acidosis stresses the infants enzyme system
• toxins include IV and local anesthetics (circumcision !!) and OTC teething medications
• Test - chocolate brown blood does not turn red on exposure to room air
• Labs - ABG - pO2 and O2 sat are normal (O2 sat calculated off pH and PO2)
• pulse oximeter - low O2 sat (reads deoxygenated and oxygentated hgb wavelengths seperately)
• co-oximeter - will differentiate hemoglobin versus methemoglobin
• Treatment - find inducing toxin or limit exposure
- methylene blue 1 - 2 mg/kg IV

The First Month
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NIGHTMARE NEONATE
• term infant, with usually normal Apgars, who suddenly deteriorates in the first 1 - 2 weeks of life after a well interval
at home ----> presents to the ED in extremis !!
COMMON CAUSES OF A CRASHING NEONATE
S – Sepsis
Viral (Herpes, Enterovirus)
Bacterial (E.coli, Strep, Listeria)
S - Seizures
I - Inborn Errors of Metabolism or other metabolic derangements
C - Congenital cardiac disease
Ductus-dependent left-outflow obstruction lesions
Large left-to-right shunts
Cardiomyopathies
Dysrhythmias, e.g. SVT
C - Congenital Adrenal Hyperplasia (CAH)
C - CNS hemorrhages
AV malformation
Child abuse
Vitamin K deficiency (Hemorrhagic Disease of the Newborn)
F - Formulas mix-ups
I - Intestinal disasters
Volvulus
Necrotizing enterocolitis
Incarcerated hernias
T - Toxins and other home remedies
• modified, in part, from Michael Simmons MD - Harbor/UCLA
NEONATAL SEPSIS
BACKGROUND
• “Early onset” - seen in first few days of life, associated with maternal or perinatal risk factors, such as maternal fever,
PROM, and fetal distress; septic shock and neutropenia more common presentation
• “Late onset” - usually occurs after 1 week of age, develops more gradually, less associated with above risk factors;
meningitis more common presentation
CAUSES OF NEONATAL SEPSIS
• common viral causes are the most common causes overall
• Group B streptococcus (most common bacterial cause in US)
• Listeria monocytogenes, E. coli, Klebsiella, enterococcus, nongroup D alpha hemolytic strep, and nontypable Haemophilus
influenzae
• viral causes include herpes simplex, enterovirus (coxsackie, ECHO), and adenovirus (hepatic and CNS usually involved)
** Group B strep and Listeria can present early (<72 hrs) with sepsis, or late (4 - 14 days) with meningitis

The First Month
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CLINICAL SIGNS OF NEONATAL SEPSIS
“Not doing well”
Lethargy, irritability, seizures
Poor feeding, vomiting, diarrhea
Temperature instability (high or low)
Abdominal distension (ileus)
Apnea, tachypnea, cyanosis, respiratory distress
Hypoglycemia, hyperglycemia
Jaundice, pallor, petechiae
Tachycardia, bradycardia
Low blood pressure, poor perfusion
Hepatosplenomegally
Congestive heart failure
ABDOMINAL DISTENSION and ILEUS MAY BE THE FIRST SIGN OF A SEPTIC NEONATE !!
ED WORKUP
• ask mom about maternal viral symptoms - check for asymptomatic herpes in mother
• Herpes Simplex -
- usually presents as
(1) disseminated infection involving multiple organs presenting as irritability,
seizures, respiratory distress, jaundice, coagulopathy and shock
- 20% will not have a vesicular rash
(2) encephalitis with or without the skin lesions
- CSF will show pleocytosis and elevated protein
(3) disease localized to skin, eyes, or mouth
- least frequent of all forms of disease
- neonatal infection usually associated with primary herpes in the mother
- examine neonate for herpetic lesions - usually occurs at the birth “presenting” portion of the body
- check scalp electrode sites for herpetic lesions
• culture all body fluids, including CSF
- less likely to make the child hypoxic if LP done in sitting position or lateral nonflexed
- place infant on a pulse oximeter while LP is being performed
- obtain blood glucose (prior to lumbar puncture) to compare with CSF glucose and to rule out hypoglycemia
• send urine culture even if dipstick, micro negative
- if circumcised male, some advocate preping area and bagging; Betadine can be stimulant so watch for urination
- if female or uncircumcised male, then urethral catheterize with 5 or 8F feeding tube
• chest Xray only if symptomatic ??
• RSV and Pertussis in the first month of life can result in apnea so ADMIT to monitored bed !
LAB RESULTS
• Neutropenia (< 2,000 PMN/mm3), neutrophilia (> 16,000 PMN/mm3) or elevated immature-to-total
neutrophil ratio (> 0.2) can be useful in predicting sepsis
• platelet count may be low in infants with sepsis
• CSF showing WBC’s or high protein, but no organisms ---> think HERPES !
ED TREATMENT
* ALL NEONATES WHO ARE WORKED UP FOR SEPSIS SHOULD BE ADMITTED !!
• IV Ampicillin 100 - 200 mg/kg/24hr (Gram positives, Listeria, enterococcus ) and Gentamicin 5 mg/kg/24hr (synergism plus
broad gram negative coverage)
OR Ampicillin and Cefotaxime (100mg/kg/day)
• If patient has positive CSF, use IV Cefotaxime for better CNS penetration

The First Month
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• Consider Acyclovir 10mg/kg per dose q 8 hours IV if WBC’s or high protein but no organisms on CSF, pleocytosis, vesicular
rash on infant, focal neurological signs, pneumonitis or hepatitis are present, or if there is a positive maternal history for
herpes
CONGENITAL INFECTIONS
• Usually acquired transplacentally and symptoms undetectable in early newborn period
• ETIOLOGY:
- TORCH - toxoplasma gondii, rubella, cytomegalovirus, herpes simplex
- syphilis (Treponema pallidum)
- HIV
- parvovirus (“Fifth disease”), Ebstein-Barr, hepatitis B
• signs - IUGR, hepatosplenomegaly, jaundice, retinopathy, cataracts, corneal clouding, encephalitis, hearing defects,
adeonopathy, hemorrhagic rhinitis, “snuffles”, dermal erythropoiesis (“blueberry muffin”), pneumonia
• CMV: 5 - 10% of cases diagnosed in neonatal period yet leading cause of childhood deafness
• Herpes: incubation period of 2 - 40 days (mean 6 days) see SEPSIS for more details
• CONSIDER THESE INFANTS POTENTIALLY CONTAGIOUS !!
• Labs - serology for Toxoplasma, rubella, CMV, herpes simplex, Treponema pallidum, and HIV
- (tiger top tube, 7 ml blood)
- test mom and baby
• CMV cultures from urine
• Herpes simplex culture from skin lesions, CSF and nasopharynx
• Giemsa stain shows multinucleated cells with viral particles in skin lesions
• immunofluorescence test can detect herpes virus in skin lesion
• treatment - if ill appearing, ADMIT
• if herpes is suspected, culture all fluids, admit to ICU and start Acyclovir 30mg/kg/24hr divided into 3 doses IV
• syphilis, toxoplasmosis, and ?CMV infections treatment can be delayed for specific diagnositic test results
- Syphilis (+) - Benzathine penicillin G 50,000 units/kg IM x one
- for (+) CSF - aqueous crystalline penicillin G 50,000 units/kg/24hours q 12 hours IV or IM x 10days
CARDIOLOGY
A BRIEF INTRODUCTION TO CONGENITAL HEART DISEASE PRESENTING IN THE NEONATAL PERIOD !!
• congenital heart disease (CHD) occurs in 8/1000 live births
* Most cardiac emergencies presenting in the neonatal period will present as cyanosis, cardiovascular collapse, congestive
heart failure, or as an arrhythmia !!
CLUES TO CONGENITAL HEART DISEASE
BLUE ‹ cyanotic heart disease with right to left shunting
MOTTLED or GRAY ‹ outflow obstruction with systemic hypoperfusion and shock
PINK ‹ congestive heart failure with left to right shunting
AGE OF PRESENTATION
Ductus-dependent lesions - cyanotic or shock-producing cardiac lesions- usually have sudden onset and usually present in first
week of life
CHF lesions - usually have slower onset and present in late neonatal or early infancy period
• modified from Tintinalli 4th Edition
CYANOTIC HEART DISEASE
Cyanosis implies 5 gm/dl of deoxygenated (reduced) blood or abnormal pigment like methemoglobin
• becomes deoxygenated due to decreased arterial saturation or increased extraction of oxygen by sluggish blood (shock,
hypovolemia, or vasoconstriction)

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0xygen-Hemoglobin Dissociation Curve -
• low pO2 leads to large drops in hgb saturation (affinity) so O2 can
be delivered more effectively to the tissues
• shift to right (incr temp, incr pCO2, decr pH, incr 2,3 DPG)
for a given pO2, better delivery to the tissues
• shift to left (fetal hgb)
• for a given pO2, have higher O2 sats and less delivery to tissues Saturation %
• curve shifts to right like adult hemoglobin at approx 3 mo of age
Cyanosis is based on amount of deoxygentated blood and not the percentage,
• normally deoxygenated hgb = 2 g/dl in the venules; need another 3 g/dl to appear cyanotic pO2
• polycythemic infants (neonates) may be cyanotic but still delivering O2 to the tissues
ex: hgb 20 g/dl ---> if deoxy 3 g/dl ---> oxygenated hgb 17/20 = 85% oxygenated
• anemic infants may not appear cyanotic yet still hypoxic, and not delivering O2 to the tissues
ex: hgb 6 g/dl ---> deoxy 3 ---> oxygenated hgb 3/6 = 50% oxygenated
• may not appear cyanotic until the 02 sats drop to 50%
If hemoglobin and cardiac output are normal, a right-to-left shunt must be present to produce cyanosis; this can be either
intracardiac, intrapulmonary or both !!
CONGENITAL HEART DISEASE causing CYANOSIS
Tetralogy of Fallot (TOF) - may be overlooked in nursery
Tricuspid atresia
Transposition of the Great Arteries (TGA)
Total Anomalous Pulmonary Venous Return (TAPVR)
Truncus Arteriosus - may be overlooked in the nursery
Pulmonary atresia or stenosis
other less common lesions
• modified from Donn Neonatal Emergencies
** These congenital heart defects produce cyanosic (hypoxemia) because of right-to-left intracardiac shunting
** Many of these lesions may be dependent upon the ductus arteriosus to remain patent and maintain blood flow to the lungs ‹
when the ductus finally closes, the child may suddenly become noticeably cyanotic !!
DIFFERENTIAL DIAGNOSIS FOR NEONATAL CYANOSIS
Cyanotic congenital heart disease
Parenchymal pulmonary disease
Diaphragmatic hernia
Persistant pulmonary hypertension of the newborn
Polycythemia
Hypoglycemia
Shock and sepsis
Central Nervous System Disease
Hemoglobinopathy
Congenital Methemoglobinemia

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CLINICAL SIGNS
• previously healthy neonate suddenly presents with lethargy, pallor or central cyanosis
• usually presents in the 1st week of life (up to 3 weeks old)
• history reveals difficulty feeding, poor weight gain, tachypnea, and diaphoresis
- feeding times are the neonate’s cardiac stress test !!
• differentiate central vs peripheral cyanosis -
- peripheral cyanosis will still have pink tongue, mucous membranes (hard to evaluate lips)
- can be difficult to evaluate in presence of acrocyanosis, darker skin, and artificial light
• neonate may appear quite comfortable with only mild tachypnea and cyanosis and no respiratory distress
- infant is often described as “happily tachypneic”
- cyanosis due to pulmonary pathology will usually present with retractions, nasal flaring, and grunting
• cardiac cyanosis will worsen with crying, improve with rest
- pulmonary cyanosis will improve with crying due to increased ventilation
DON’T ASSUME THAT ACROCYANOSIS IS NORMAL IN A LETHARGIC NEONATE !!!
• cardiac exam - pulses typically normal and equal; precordium is quiet; may not have a murmur
- pulmonary stenosis - right ventricular lift and thrill
- Tetralogy of Fallot, truncus arteriosus - murmur usually
• ABG - will show decreased PaO2
- Hyperoxitest - 100% O2 will not alter the ABG (allow at 10 min for O2 effect)
- a rise of > 30 torr or pO2 > 100 - 150 is highly suggestive of lung disease, and not cardiac disease but must be
interpreted in light of clinical situation
- CO2 retention suggests pulmonary or central nervous system disease
- low pH suggests sepsis, shock or severe hypoxemia
• EKG - usually non-diagnostic because of normal neonatal RAD and dominant R wave in right chest leads
- Tricuspid atresia will show LAD and LVH since right heart not well developed
- T wave also upright in V1 for first 4 days; beyond 4 days consider pathology
• CHEST XRAY - should include heart size and position, liver shape and position, and increased or decreased vascularity
- Cardiothoracic ratio can be hard to evaluate due to thymus size and depth of inspiration
- CT ratio usually greater than 0.5 in normal neonate without CHD
- cardiomegaly due to cong heart disease may not manifest yet in the newborn period
- if unequivocal cardiomegaly, common causes include:
- cong heart disease - VSD, PDA, TGA, Hypoplastic left heart, Ebstein’s anomaly
- myocarditis, cardiomyopathy
- pericardial effusion
- metabolic disturbances like hypoglycemia or acidosis
- overhydration or overtransfusion
- abnormal cardiac silhouette-
- “boot shaped” - TOF or tricuspid atresia
- “egg shaped” - TGA
- large globular heart - Ebstein’s anomaly
- dextrocardia or mesocardia can be a sign for congenital heart disease
- location of stomach bubble, shape and location of liver can also be a marker for CHD
- pulmonary vascular markings -
- cyanotic with decreased vessels - TOF, Pulmonary atresia, Tricuspid atresia
- cyanotic with increased vessels - TGA, Truncus arteriosus, Single ventricle, TAPVR
- acyanotic with increased vessels - VSD, PDA, endocardial cushion defect

The First Month
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ALGORITHM FOR EVALUATION OF CYANOTIC NEONATE (Flynn 1992)
CYANOSIS
PERIPHERAL CENTRAL
Tongue, conjunctiva pink Cyanotic, including tongue, conjunctiva
Extremities cool, cap refill poor
Cyanotic but PaO2 saturation low
Warm and well perfused Diagnosis- sepsis, cold or shock
Treat cause
CARDIAC PULMONARY
Worsens with crying May improve with crying
Comfortable at rest Respiratory distress
+/-abnormal EKG Normal EKG
+/-cardiomegaly or other Normal cardiac silhouette
Normal pCO2 CO2 retention
No response to 100% O2 + responsive to 100% O2
+/- Murmur, +/- hyperdynamic Rx: O2, treat cause
Rx: PGE1, cardiac consult
INCREASED PULMONARY FLOW DECREASED PULMONARY FLOW
Transposition of Great Arteries Tetralogy of Fallot
Total Anomalous Venous Return Pulmonary Atresia
Truncus Arteriosus Tricuspid Atresia
Single Ventricle
ED TREATMENT
• AIRWAY, BREATHING, CIRCULATION !!
• Oxygen and ventilatory support as needed
- even a small rise in p02 may be of benefit
• If ductal-dependent cardiac lesion is suspected,
Prostaglandin E1 (PGE1) 0.05 - 0.1 mcg/kg/min IV
- 500 mcg/100 ml NS = 5 mcg/ml ---> start infusing 0.1 mcg/kg/min = 0.02 ml/kg/min
- potent vasodilator --> ductal tissue very sensitive to its action
- O2 sats usually rise to 80 - 90%, sometimes up to 100%
- neonate now at risk for apnea (12%), so consider intubation, especially if inter-hospital transport is necessary
- other side effects include hypotension, seizures, fever, jitteriness
- results usually within 15 minutes
- can increase rate up to 0.4 mcg/kg/min if needed for effect
- after cyanosis is relieved (or BP improved) , lower PGE1 rate down slowly by small increments to 0.01 mcg/kg/min
• Any neonate this ill deserves a septic workup and antibiotics until sure of diagnosis !!
• Admit to Neonatal or Pediatric ICU
• Echocardiogram
CONSULT A PEDIATRIC CARDIOLOGIST OR THE NEONATAL ICU IN YOUR AREA!! (
CARDIOVASCULAR COLLAPSE
• usually occurs in the first 2 weeks of life; neonate had been discharged prior to ductus constriction, without obvious signs:
- perfusion and pulses were maintained by the patent ductus
- ductus was so wide, a murmur wasn’t audible at birth

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CONGENITAL HEART DISEASE causing CARDIOVASCULAR COLLAPSE
Coarctation of the Aorta or Interrupted Aortic Arch
Hypoplastic Left Heart
Critical Aortic Stenosis
* Patent ductus had allowed adequate right to left blood flow to the systemic circulation prior to its closure ‹ after ductus
closure, greatly diminished systemic blood flow results !
* Can also result in congestive heart failure with pulmonary edema
CLINICAL SIGNS
• upon ductus closing, neonate presents in shock with a history of poor feeding, tachypnea and poor color
• pale, clammy, hypotension, diminished/absent pulses, mottling, poor perfusion, lethargy
• can be mistaken for an overall septic picture
• aortic stenosis, hypoplastic left heart ‹ poor pulses throughout
- aortic stenosis ‹ thrill, murmur
- hypoplastic left heart - cardiomegaly
• coarctation - ductus usually positioned right at the area of coarctation and adds to aortic lumen size
- closure of ductus allows even less blood flow through the aortic coarctation
- absent or delay in pulses to the lower extremities is most common presentation
- rarely, upper body may be pink (precoarc) and lower body may be blue (postcoarc)
- check blood pressures/O2 sats/pulses in the right arm and leg
- a difference in p02 of 10 - 15 mmHg is significant
- left subclavian artery can be variably pre or post-ductal so don’t use left arm
- difference in peripheral blood pressures may not be apparent until after inotropes administered
- may have an associated VSD which may cause mixing of oxygenated and deoxygenated blood
• interrupted aortic arch ‹ incr pulses in right upper extremity; poor pulses in the left upper and both lower extremities
• pulmonary exam usually positive for dyspnea and pulmonary congestion (usually wheezing, not true rales)
• CXR will usually show cardiomegaly and pulmonary edema
- coarctation may have a “3” sign on plain Xray or “E” on barium swallow
• EKG typically shows RVH or RBBB (older infants will show LBBB)
ED TREATMENT
• see treatment for “Cyanotic Congenital Heart”
• anticongestive agents like inotropic agents (dopamine, dobutamine) and diuretics should be started
CONGESTIVE HEART FAILURE
DIFFERENTIAL DIAGNOSIS FOR NEONATAL HEART FAILURE
Congenital heart disease
Myocarditis
Arrhythmia (SVT or complete heart block)
Arteriovenous fistula (intracerebral, intrahepatic)
Asphyxia
Hypoglycemia; Hypocalcemia
Anemia
Sepsis

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CONGENITAL HEART DISEASE causing CONGESTIVE HEART FAILURE
Large left-to-right intracardiac shunt - excessive pulmonary circulation (more common)
Ventricular septal defect, large
Arterio-venous malformations
Complete AV canal
Patent ductus arteriosus, large
Diminished left ventricular function (less common)
Myocarditis
Dilated cardiomyopathy
Anomalous origin of left coronary artery from the pulmonary artery
• modified from Donn Neonatal Emergencies
* Normal transitional circulation after birth includes a gradual decline in pulmonary vascular resistance ‹ this allows a
pre-existing left-to-right shunt to progressively increase its flow
• neonate usually presents after 2 weeks of age, as late as several months
• symptoms present more gradually, often insidiously; murmur may not present until 2 weeks - 2months old
CLINICAL SIGNS
• CHF signs are due to pulmonary overcirculation and sympathetic stimulation, or due to left ventricular failure !
• poor feeding, diaphoresis (especially while eating), tachypnea, tachycardia, hepatomegaly, cardiomegaly and finally, pallor,
mottling, hypotension, and oliguria
• difficulty feeding is a fairly constant feature, with the neonate tiring and diaphoretic
• heart rates above 180 - 200 when the neonate is at rest suggest increased autonomic activity to compensate for a failing
myocardium
• respiratory rates above 50 - 60/ minute, usually without increased depth, is an early sign
• grunting, flaring of the nose, and retractions are unusual unless there is pulmonary disease or frank pulmonary edema
- often an intercurrent illness is what tips the infant over the edge
• neck veins are usually not discernible in a neonate
- other peripheral edema signs and ascites are unusual in the neonate, sometimes sacral edema present
- “hepatomegaly” usually due to depressed diaphragm due to pulmonary hyperinflation
• wheezing may be heard; rales are unusual
• cardiac exam - usually has an hyperactive precordium
- significant left-to-right shunts ---> diastolic flow rumble at the apex
- large PDA - classic continuous “machinery” murmur, with wide pulse pressure
• AV malformation may be heard over anterior fontanelle or liver
• CXR usually shows cardiomegaly, increased vessels, and fluid in the minor fissure
ED TREATMENT
• AIRWAY, BREATHING, CIRCULATION !!
• Oxygen and ventilatory support as needed
• Lasix 1mg/kg IV
• Dopamine or Dobutamine for systemic hypotension
• Echocardiogram
• Any neonate this ill deserves a septic workup and antibiotics until sure of diagnosis !!
• Admit child to a Neonatal or Pediatric ICU
CONSULT A PEDIATRIC CARDIOLOGIST OR THE NEONATAL ICU IN THE AREA !! (

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INBORN ERRORS OF METABOLISM
PATHOPHYSIOLOGY
• Inborn errors refer to the hundreds of hereditary biochemical disorders resulting in the alteration of a
protein structure or amount being synthesized
• usually the result is a deficiency of an enzyme needed in the conversion of one metabolite to another ‹
results in the accumulation in body fluids of a metabolic intermediate that normally is present in low concentration
- normally these metabolic intermediates are not toxic but high levels can cause serious effects
- usual target organ affected is the central nervous system
• some of these biochemical disorders are clinically inconsequential, and others range from mild to lethal
• most inborn errors manifest themselves in the newborn period or soon after
CLINICAL SIGNS
• lethargy, coma, failure to thrive, or just persistent vomiting as the only symptom !
• seizures
• hepatomegaly with or without icterus or coagulopathy
• metabolic acidosis with or without ketosis or ketonuria, often with hyperpnea
- acidosis present only in the organic acidemias, unless other causes exist like dehydration, or cardiac arrest
• elevated blood or urine levels of a particular metabolite, like an amino acid or ammonia
• a peculiar odor
• sepsis with or without bone marrow suppression
• intraventricular or pulmonary hemorrhages are frequent agonal events
- look for signs of increased intracranial pressure
• ask about previous siblings, especially males, who died in infancy !!
* A HISTORY OF CLINICAL DETERIORATION IN A PREVIOUSLY NORMAL NEONATE SHOULD SUGGEST SEPSIS
and / or AN INBORN ERROR OF METABOLISM !!
ALGORITHM FOR INBORN ERRORS OF METABOLISM
Initial findings include:
• poor feeding
• vomiting (may be the only symptom !!)
• lethargy
• convulsion- not responsive to IV glucose or calcium
• coma- not responsive to IV glucose or calcium
Metabolic Disorder Infection
Obtain plasma AMMONIA
High Normal
Obtain blood pH, CO2 Obtain blood pH, CO2
Normal Acidosis Normal
UREA CYCLE DEFECT ORGANIC ACIDEMIAS AMINOACIDOPATHIES
OR GALACTOSEMIA
• Nelson’s TEXTBOOK OF PEDIATRICS 14th Edition

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ED TREATMENT
• Admit to an observation unit or ICU
• goal is to limit production of more toxic metabolite and encourage elimination via hydration and adequate glucose
• rehydrate the infant with adequate boluses of normal saline 20cc/kg IV
• maintenance fluid then at one and a half to two times normal maintenance rate
• follow glucoses and bolus as needed with 0.3 - 1g / kg = D10 3-10 cc / kg IV
• D10 as constant infusion will stimulate insulin production and protein synthesis
• Labs include electrolytes, glucose, calcium, ketones, ABG, urinalysis
• ammonia level (best if arterial, green top/heparin tube, on ice)
• lactic acid if metabolic acidosis is found (7 ml green top, on ice)
• urine may show spindle shape orotic acid crystals if urea cycle defect exists
• save urine and plasma in freezer for further studies (red and green top blood tubes)
• treat seizures with benzodiazepines
• consider HCO3 for pH < 7.1 (but alkalinization can increase ammonia passage into CNS )
• any neonate presenting this ill should also have a sepsis workup and appropriate antibiotics
• contact the NICU/PICU in your area to discuss “antidote therapy” like sodium benzoate for ammonia
and transport
GLUCOSE and CALCIUM DISORDERS
NEONATAL HYPOGLYCEMIA
• Defined as plasma glucose level < 35 mg/dl for a term newborn during the first three days of life and then plasma
glucose level < 45 mg/dl after the fourth day of life
• blood glucose levels are maintained by a balance between hepatic glucose production (glycogenolysis,
gluconeogenesis) and peripheral glucose utilization
• following an abrupt cessation of the constant glucose supply from the mother when the infant is born, the newborn is
susceptible to hypoglycemia during the first 24 - 48 hours after birth (?? longer):
• glucose production is limited by a subnormal glycogenolytic response to glucagons
• complete maturation of the hepatic pathway for gluconeogenesis may be delayed
• glucose utilization is much higher in infants than in adults
CAUSES OF NEONATAL HYPOGLYCEMIA
Decreased glycogen storage
Prematurity
Small for gestational age infant
Metabolic
Galactosemia
Glycogen Storage Disease
Hyperinsulinism
Diabetic mother
Insulin-secreting tumor
Other
SEPSIS !!!
Asphyxia
Cold stress
• signs - irritability, jitteriness, myoclonic jerks, poor feeding, hypotonia, lethargy, apnea, cyanosis, hypothermia,
seizures and coma
• accounts for up to 6% of neonatal seizures
• differential includes sepsis, congenital cardiac lesions, and poisonings

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• treatment - 0.3 - 1.0 grams/kg of glucose = 3 - 10 cc/kg D10) IV over 1 - 2 min
• then IV infusion D 10% at 4 ml/kg/hr
• monitor glucose levels ---> treat further hypoglycemia with repeat bolus D 25 and then increase IV infusion by 1
ml/hr
• if neonate asymptomatic and has a good suck, may consider oral feeding of formula or glucose water
• if no IV available (and no umbilical vein or intraosseous line available), may use glucagon 0.1 mg/kg/24 hr IM until
IV established
• septic workup usually indicated
NEONATAL HYPOCALCEMIA
• Defined as plasma calcium < 7 mg/dl
• Early onset - occurs in first 72 hrs - low birth weight infants, maternal hyperparathyroidism, maternal diabetes,
DiGeorge syndrome, ?? birth asphyxia
• Late onset - occurs late in first week - formulas high in phosphates, maternal hyperparathyroidism, congenital
hypoparathyroidism, immature renal function, hypomagnesemia, maternal Vit D deficiency
• signs - jitteriness, and poor feeding
• tetany ‹ increased muscle activity, twitching, vomiting, carpal pedal spasm, clonus, laryngospasm/ stridor (most
classically, the neonate presents only with a weak cry, like a baby lamb!)
• doesn’t have the classic hypocalcemic tetany signs as in adults
• can present as CLONIC SEIZURES !! Accounts for up to 34% of neonatal seizures
- usually alert between seizures, and seizures are multifocal and migratory
• EKG - QTc interval > 0.19 seconds supports hypocalcemia
• draw serum calcium, magnesium, and ionized calcium levels
• document hypocalcemia before treatment IF POSSIBLE
• Calcium gluconate 10% 100 - 300 mg/kg IV (1 - 3 ml/kg at 1 ml/min) for hypocalcemic seizures (slow infusion to
prevent bradycardia); can be repeated as needed
• after seizures controlled, add calcium gluconate 3 - 5 grams per 1 liter IV fluid
• Hypomagnesemia (<1meq/L) treated with 0.1 - 0.3 ml/kg of 50% Magnesium sulfate IM
CONGENITAL ADRENAL HYPERPLASIA
• occurs in 1/10,000 - 1/15,000 live births; much higher in Alaskan Yupik Eskimos (1/300)
PATHOPHYSIOLOGY
• Adrenal insufficiency resulting from deficient activity of one of the five enzymes required to produce cortisol
• most common enzyme deficient is 21-hydroxylase enzyme
• results in decreased conversion of 17-OH progesterone ‹ 11-desoxycortisol in the glucocorticoid pathway
- this leads to a deficiency in cortisol synthesis, and subsequent hyperplasia of the adrenal gland as a result of overstimulation
by ACTH (has no negative feedback by cortisol)
- cortisol deficiency results in cardiovascular collapse
• most also have decreased conversion of progesterone ‹ 11-desoxycorticosterone in the mineralcorticoid pathway
-this leads to a deficiency of aldosterone synthesis, leading to urinary salt wasting
- aldosterone deficiency results in classical electrolyte findings and contributes to cardiovascular collapse
• as a result of elevated ACTH stimulation, adrenal steroid precursors accumulate and are metabolized to androgens ‹ resulting
in the virilization of the external genitalia in female infants
- since male infants genitalia usually are not affected, may go unrecognized at birth !!
CLINICAL SIGNS
• total body salt depletion, vomiting, dehydration that may lead to circulatory collapse and death during the initial
2 - 3 weeks of life (commonly at the end of the first week of life)
• females may have enlarged clitoris and fusion of labial folds; males may have small phallus

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LAB RESULTS
• hyponatremia, hyperkalemia, azotemia, and metabolic acidosis
• can also cause hypoglycemia
ED TREATMENT
• Admit to an PICU or NICU
• labs - 17 hydroxyprogesterone, dehydroepiandrosterone, androstenedione, testosterone if possible before giving hydrocortisone
(red top tube, 5 - 6 ml total)
• volume repletion with 0.9% normal saline (20cc/kg boluses) then D5 0.9% NS at 100 - 125 ml/kg/24hr
• cortisol replacement with hydrocortisone 25 mg IV bolus, then 25 - 50 mg/m2/day divided q 6 - 8 hrs
• extreme hyperkalemia usually well tolerated and saline is usually only measure needed to lower K+, but may use IV 10%
calcium gluconate for arrhythmias
• Remember to monitor temperature and glucose also !!
SEIZURES
NEONATAL SEIZURES
• Generalized tonic/clonic, jacksonian march and absence seizures are rarely seen in neonates
• Electrical discharges are incompletely spread and tend to remain localized due to anatomic and physiologic CNS immaturity
• Many neonatal seizures involve subtle motor automatisms (see below)
• “Electroclinical dissociation” is common - clinical seizure but no EEG correlation
• Few idiopathic seizures in neonates; SEARCH FOR ETIOLOGY IS MANDATORY !
• Focal seizures can be caused by metabolic disorders, and do not necessarily imply a focal CNS lesion
• Evidence to suggest that the seizures themselves may be damaging to the developing neonatal brain
• Occurs in 0.2 - 1.4% of all newborns; mortality ranges from 15 - 40%

The First Month
41
DIFFERENTIAL DIAGNOSIS OF NEONATAL SEIZURES
Central Nervous System
Hemorrhage - subdural, intracortical, intraventricular (15 - 20%) *
- rule out hemorrhagic disease, ABUSE !!
Hypoxic encephalopathy/ birth trauma (30 - 65% of cases) *
Congenital anomalies or developmental brain disorder *
Cerebral necrosis/ infarcts
Cortical vein thrombosis
Metabolic and Systemic
Hypertension
Hypocalcemia *
Hypoglycemia *
Hypomagnesemia
Electrolyte imbalance (hyper or hyponatremia) *
Inborn Errors of Metabolism *
Hyperthermia
Pyridoxine (B6) deficiency/dependency *
- maternal use of INH
Infections (10 - 15%)
Bacterial Meningitis *
Cerebral Abscess
Herpes Encephalitis *
Coxsackie meningoencephalitis
Congenital (Cytomegalovirus, Toxoplasmosis, Syphilis) *
Drug Withdrawal *
Methadone
Heroin
Barbiturates * = unique or of concern in neonatal period
Propoxyphene
Toxins
Local anesthetic
Bilirubin *
Familial seizures
Benign familial neonatal seizures *
Benign idiopathic neonatal (“5th day fits”) seizures *
CLINICAL SIGNS
• seizures may be subtle in the neonate i.e. staring spells, prolonged eye deviation, nystagmus, lip smacking, tongue thrusting,
bicycling, brief altered muscle tone, apnea, or autonomic changes (BP fluctuation, tachycardia, pupil dilation)
• clonic seizure may be focal and migratory (first one leg, then opposite arm); consciousness usually maintained
- clonic movement is slower and more rhythmic than an older child’s clonic movements
• tonic seizure with hyperextension of trunk, neck or limbs is another variant
• convulsive apnea, unlike non-convulsive paroxysms, thought not associated with bradycardia (Fenichel 1983; although Watanabe
1982 did not confirm this)
• neonatal jitteriness (non-seizure) will involve fast movements of all extremities, stimulation will induce movements, movements
will stop with restraint or passive flexion, eye movement and gaze are normal, and rarely has autonomic signs or symptoms
CLUES TO NEONATAL SEIZURES BASED ON AGE AT PRESENTATION
First 48 hours - trauma, pyridoxine dependency, hypoxic encephalopathy, hypoglycemia
- benign familial neonatal seizures - usually begin on 2nd - 3rd day, resolve by 1 - 6 months
4 - 7 days old - hypocalcemia due to high phosphate load from formulas
- benign idiopathic “fifth day fits” - start on 5th day and cease by day 15
> 7 days old - infection

The First Month
42
ED WORKUP
• History - prenatal and labor history regarding infection risks, prenatal TORCH studies, substance abuse, perinatal asphyxia, or
family history of seizures
- opiate withdrawal seizures can present up to several weeks post-birth
- if bottle fed, how does mom mix formula; has mom supplemented or replaced infants diet with free water or tea or other
home remedies ex baking soda for colic
• Physical Exam - blood pressure check for hypertension
- unusual odor of sweat or urine for inborn errors
- cranial bruits for AVMs
- skin for jaundice, cafe-au-lait spots, herpes vesicles (look at scalp electrode sites)
- neuro exam for cranial nerves, motor exam, neonatal reflexes
• Potential labs - glucose, hematocrit, electrolytes, BUN, calcium, magnesium, phosphate, serum ammonia, ABG, blood cultures
(bact and viral), TORCH titers
(send calcium and magnesium even if seizures ceased by anticonvulsants)
- urine for urinalysis and toxicology screen
- urine for 2,4-dinitrophenilhydrazine and reducing substances
- blood for amino and organic acids, lactate and pyruvate (green top tube in freezer)
- urine for amino and organic acids, lactate and pyruvate (save in freezer)
- CSF for glucose, protein, cell count, diff, gram stain, bacterial and viral cultures, latex agglutination for viral antigens,
lactate and pyruvate, glycine
• Ultrasound of cranium plus CT or MRI scan
TREATMENT
• AIRWAY, BREATHING, CIRCULATION !
• bedside glucose check
- administer a glucose bolus 0.3 - 1.0 grams/kg = 3-10 cc/kg D 10
• standard anticonvulsant therapy such as benzodiazepines, phenobarbital or dilantin indicated
- most NICUs will recommend benzodiazepines or phenobarbital as first line drug
- Phenobarbital 18 - 20 mg/kg IV (infuse no faster than 1 mg/kg/min); may repeat 5 mg/kg/dose q 5 - 10 minutes, up to total
dose of 40 - 60 mg/kg
- Lorazepam (Ativan) 0.1 mg/kg IV or rectally over 2 minutes, may repeat 0.05 mg/kg IV x one
- Diazepam (Valium) 0.5 mg/kg IV or rectally q 15 - 30 min x 2 - 3 doses
- ? sodium benzoate theoretically can displace bilirubin from albumin --> at risk for kernicterus
- Dilantin 15 - 20 mg/kg IV (infuse no faster than 1mg/kg/min)
- ?? Paraldehyde 0.3ml/kg diluted 1:2 in mineral oil given rectally
• consider infusing calcium gluconate 10% 100 - 300 mg/kg IV (1 - 3 ml/kg at 1 ml/min) if still seizing after standard therapy, or
has a weak cry (like a bleating lamb)
• consider infusing magnesium sulfate 50% 0.1 - 0.3 ml/kg IV or IM
• consider infusing pyridoxine (B6) 50 - 100 mg IV if still seizing after standard anticonvulsant therapy, glucose, and calcium
infusion
- pyridoxine is a cofactor for the synthesis of inhibitory neurotransmitter GABA
- need EEG monitoring; will see clinical response within minutes
• treat hypertension induced seizures with antihypertensive meds
• antibiotics (i.e. Cefotaxime and Ampicillin) to the septic patient
• consider Acyclovir 10mg/kg per dose q 8 hours IV if WBC’s or high protein but no organisms on CSF, pleocytosis, vesicular
rash on infant, focal neurological signs, pneumonitis or hepatitis present, or maternal history of herpes
• ADMIT TO A MONITORED BED !!!

The First Month
43
SUBSTANCE WITHDRAWAL
• most commonly described with heroin, methadone, and morphine
• can also be seen with demerol, codeine, propoxyphene, and pentazocin even if not chronically abused
• onset of symptoms is usually between 24 - 48 hrs old, but as late as 2 weeks if newborn is exposed to methadone; up to 34 days for
heroine (classically day 10)
• classical symptoms include excessive irritability, decreased sleep time (can be wrongly diagnosed as colic), fever, vomiting, diarrhea,
SEIZURES !!
SIGNS and SYMPTOMS OF NEONATAL DRUG WITHDRAWAL
W = wakefulness
I = irritability
T = tremulousness, temperature variation, and tachypnea
H = hyperactivity, high-pitched persistent cry, hyperacusis, hyperreflexia, hypertonus
D = diarrhea, diaphoresis, disorganized suck
R = rub marks, respiratory distress, rhinorrhea
A = apneic attacks, autonomic dysfunction, alkalosis
W = weight loss or failure to gain weight
L = lacrimation (AAP Committee on Drugs 1983)
ED TREATMENT
• ADMIT TO A MONITORED BED
• if history is unreliable, consider sepsis, hypoglycemia, and hypocalcemia
• increase infants comfort (swaddling, pacifier, decrease environmental stimuli)
• phenobarbital used as needed
FORMULA MIXUPS and TOXINS
FORMULAS
* IF YOU DON’T ASK HOW THEY ARE MIXING UP THE FORMULA, PARENTS WON’T ALWAYS TELL YOU!!
• Formula varieties:
- Ready-made – just poor in bottle
- Concentrated liquid – 1:1 mix with water
- Powder forms – 1 part powder to 2 parts water
TOXINS and other home remedies
* IF YOU DON’T ASK ABOUT ADDITIONAL LIQUIDS, POWDERS, HERBS, or OTHER SUBSTANCES GIVEN TO THE
NEONATE, PARENTS WON’T ALWAYS TELL YOU !!
• examples: baking soda for colic, herbal teas for constipation or colic

The First Month
44
INTESTINAL DISASTERS
VOLVULUS
• Congenital malrotation of the midgut portion of the intestine - during the 5 - 8th week in embryonic life, the intestine
projects out of the abdominal cavity, rotates 270 degrees and returns into the abdomen; if the rotation is not right, the intestine
will not be “fixed down” correctly at the mesentery ‹ at risk for malrotation
• Volvulus is the twisting of a loop of bowel about its mesenteric base attachment
• True medical emergency because necrotic bowel can occur within hours of onset of the twisting
CLINICAL SIGNS
• Generally peak occurrence in the first month of life but can present anytime in childhood; male to female 2:1 ratio; rarely
familial
• Presents one of three ways:
- sudden onset of bilious vomiting and abdominal pain
- history of “feeding problems” with bilious vomiting that now appears like a bowel obstruction
- failure to thrive with severe feeding intolerance (least common)
• BILIOUS (green) VOMITING IN NEONATES IS ALWAYS WORRISOME AND IS A TRUE EMERGENCY !!
• if bowel is already ischemic or necrotic, neonate may present pale and grunting
• abdomen may or may not be distended depending upon location of the volvulus; if obstruction is high, abdomen may not be
distended; abdomen may be “blue” if bowel is already ischemic / necrotic
• pain is a constant pain, not intermittent
• neonate may be jaundiced
• hematochezia is a late, BAD sign !
• neonates present ill !!
• Differential:
- Gastroenteritis - ill contacts ??; volvulus can appear like AGE early on; CAUTION
- Pyloric stenosis - longer history; child acts well and hungry
ED WORKUP
• labs - nothing classic except dehydration and acidosis
• Abdominal plain film
- classic “double bubble sign” - paucity of gas (airless abdomen) with two air bubbles - one in the stomach and one in the
duodenum
- plain film can also be entirely normal
• Upper GI - considered the gold standard
- small intestine is rotated to right side of the abdomen; contrast narrows at site of obstruction “cork-screwing”; spiraling
of small bowel about the superior mesenteric artery
• Ultrasound
- may show a distended fluid-filled duodenum, increased peritoneal fluid and dilated small bowels loops to the right of the
spine
- Radiology 1996 - Shmianuki - Japan - Clockwise whirlpool sign of color Doppler - Japan - 236 children with suspicion
for volvulus (day 0 to 14yo); whirlpool sign = wrapping of sup mes vein and mesentary around the sup mes artery; was
clockwise in 12 / 13 kids with surgically confirmed volvulus; was counterclockwise in 3 without volvulus; sensitivity
92%, specificity 100%, PPV 100%
- American Journal of Roentgenology October 1992 - 337 infants had utz for r/o HPS. Normally sup mes vein should be
on right side of artery on transverse utz; in 74%, the anatomy could be seen; Nine were abnormal - 5 had vein on left
side and all had malrotation; 4 had vein ventral to the artery and one had malrotation
ED TREATMENT
• Need to diagnose this life threatening process EMERGENTLY !!!
• Re-hydrate the infant aggressively; place an NG tube
• Antibiotics: Ampicillin, Clindamycin and Gentamicin
• When the diagnosis is being considered, contact the Pediatric Surgeon on-call immediately; the sooner the infant gets to the
OR, the lower the morbidity and mortality
- some peds surgeons will take an ill appearing neonate with BILIOUS vomiting to the OR directly without any additional
diagnostic tests
- Journal of Formosan Medical Association April 1995 - Taiwan - 15 year retro review - bilious vomiting and bloody
stools were more common in neonatal period; recurrent abdominal pain and FTT more common after newborn period;
obscure symptoms and longer duration of symptoms were more common in the older child, leading to delayed diagnosis

The First Month
45
NECROTIZING ENTEROCOLITIS
• Usually seen in premature infants but can be seen in term infants, usually in first 10 days of life
• usually have a history of an anoxic event or stress at birth
• present quite ill, with lethargy, irritability, anorexia, distended abdomen, and bloody stools
• abdominal xray usually shows pneumotosis cystoids intestinalis caused by gas in the intestinal wall
• antibiotics, admission to the ICU and consultation with a pediatric surgeon are imperative
INCARCERATED HERNIA
• More common in premature infants
• Mom may notice swelling at time of diaper change
• Included in differential for inconsolable crying infant
• Gentle reduction can be attempted in the ED; use morphine (0.1 mg/kg) for pain
• if non-reducable or ischemic / necrotic bowel is suspected, consultation with a pediatric surgeon is required
SAFETY
• As recommended by the American Academy of Pediatrics infants should be placed on their sides or back while sleeping to decrease
the risk of SIDS “BACK TO SLEEP!!”
- smoking in the house increases risk of SIDS
• Infant should sleep in a regulated infant crib
- slats should be no greater than “two adult sized fingers” apart
- infant should not sleep on an adult bed - risk of falling off the bed, between the slats and asphyxiation, or risk being smothered by
the mother
- no pillows or plastics in the infants crib
- infant should never be placed on a bean bag, water bed, sheep skin, or other soft beds
• Infant should never be left alone on a changing table or bed
• Infant should never, never, never be left alone in a bathtub; have a portable phone, install a phone in the bathroom or just let the
phone ring
• When infant becomes mobile, never leave buckets of water unattended or toilets open
• Never leave a baby alone with a pet, even a well-behaved pet may accidently hurt a young infant
• Never leave a baby alone in a room with a sibling who is < 5 years old
- a game of peekaboo could turn into tragic suffocation
- an enthusiastic bearhug could break a rib
• Never leave the infant home alone
- “I just stepped out for a second” can lead to tragedy
• In the car, infant must be placed in an appropriate car seat, and not held on parent’s lap
• Never leave a child in a car alone
- cars can overheat or someone can steal the car or the infant
• Never take eyes off the child when in public, and be cautious when strangers offer to hold the child
• Never jiggle or shake the baby vigorously or throw him up in the air
• Infants less than 12 months old should not be allowed to eat grapes (fruits with skin), hard vegetables, hot dogs, popcorn, raisins,
nuts, hard candies, lollipops, peanut butter, hard crusty bread, or hard meat
- foods should easily dissolve if caught in the airway
- children should be taught not to play or run while eating

The First Month
46
• Infants should not be allowed to “bite” an inflated balloon ‹ when the balloon explodes, the balloon pieces fly backwards into the
infant’s airway and occludes it
• Avoid using any kind of chain or string on the baby or on any of the toys or belongings
- no necklaces, no chains, no string on pacifiers, no ribbon longer than five inches near crib
• Parent should know how to use and read a thermometer and be instructed to bring a neonate to the doctor for a temp > 100.4 degrees
• Modified from “WHAT TO EXPECT THE FIRST YEAR”
REFERENCES
GENERAL
• NEONATAL EMERGENCIES Donn S., Faix R., Futura Publishing Company, 1991
• PRIMARY CARE OF THE NEWBORN Coen R., Koffler H., Little, Brown and Company 1987
• CARE OF THE NEWBORN 2nd Edition Schreiner R., Bradburn N., Raven Press 1988
• SCHAFFER’S DISEASES OF THE NEWBORN 5th Edition Avery M., Taeusch H.,
W.B.Saunders Company 1984
• WHAT TO EXPECT THE FIRST YEAR Eisenberg A., Murkoff H., Hathaway S.,
Workman Publishing 1989
• THE NEWBORN CHILD 6th Edition Vulliamy DG., Johnston PGB Churchill Livingson 1987
• TEXTBOOK OF PEDIATRIC EMERGENCY MEDICINE 3rd Edition Williams &Wilkins 1993
• PEDIATRIC EMERGENCY MEDICINE CONCEPTS AND CLINICAL PRACTICE
Barkin R., et al Mosby Year Book 1992
• EMERGENCY MEDICINE: A COMPREHENSIVE STUDY GUIDE 4th Edition
Tintinalli J, et al McGraw Hill 1995
GASTROINTESTINAL
• Mcrury JM, Barry RC, A Modified APT Test: A New Look at an Old Test Pediatric Emergency Care June 1994 10(3)
189 - 191
• Apt L, Downey M, “Melena” neonatorum: The Swallowed Blood Syndrome. A Simple Test for the
Differentiation of Adult and Fetal Hemoglobin in Bloody Stools J Pediatrics 1955; 47: 6 - 12
• Nichols M et al, Baking Soda: A Potentially Fatal Home Remedy Pediatric Emergency Care 1995 11(2) 109
• Swischuk L, Acute Onset Vomiting in a 15 day old Infant Pediatric Emergency Care 1992 8(6) 359 - 360
• Swischuk L Vomiting in a nine-day-old Infant Pediatric Emergency Care 1995 11(2) 131 - 132
JAUNDICE
• Rosenthal P., Sinatra F., Jaundice in Infancy Pediatrics in Review Sept 1989, 11(3): 79 - 86
• Chrisopher N., Hyperbilirubinemia in the Newborn Pediatric Emergency Medicine Notes 2(11): 1 -5 1992
• Seidman D. et al, Hospital Readmission Due to Neonatal Hyperbilirubinemia Pediatrics 96(4): 727 - 729 Oct 1995
• Conrad PD. et al, Safety of Newborn Discharge in Less than 36 Hours in an Indigent Population
American J Disease Childhood 1989; 143: 98 - 101
• Maisels MJ et al, Kernicterus in Otherwise Healthy, Breast-Fed Term Newborns Pediatrics Oct 1995 96(4) 730 - 733
• Catz C. et al, Summary of Workshop: Early Discharge and Neonatal Hyperbilirubinemia
Pediatrics October 1995 96(4): 743 - 745
• DeCarvalho M et al, Effect of Water Supplementation on Physiological Jaundice in Breast Fed Babies
Archives Disease Childhood 1981; 56: 568 - 569
• Herrar AJ, Supplemented vs Unsupplemented Breastfeeding Perinatology-Neonatology 1984; 70 - 71
• Nicoll A et al, Supplementary Feeding in Jaundiced Newborns Acta Paed Scand 1982; 71: 759 - 761
SEPSIS
• Poland R., Watterberg K, Sepsis in the Newborn Pediatrics in Review July 1993 14(7) 262 - 263
• Stamos J et al Timely Diagnosis of Congenital Infections
The Pediatric Clinics of North America October 1994 41(5) 1017 - 1033
• Alpert G et al A Practical Guide to the Diagnosis of Congenital Infections in the Newborn Infant
The Pediatric Clinics of North America June 1986 33(3) 465 - 479
• Rosenber N Congenital Syphilis: An Emerging Emergency Pediatric Emergency Care 1991 7(3) 171 - 173
• Baraff L., et al Practice Guideline for the Management fo Infants and Children 0 - 36 Months of Age

The First Month
47
with Fever Without a Source Pediatrics July 1993 92 (1) 57 - 67
CARDIOLOGY
• Pediatric Cardiology for Practioners 3rd Edition Park MK., Mosby 1996
• Essentials of the Pediatric Intensive Care Levin D., Morriss F., Quality Medical Publishing Inc. 1990
• Burton D., Cabalka A., Cardiac Evaluation of Infants: The First Year of Life
The Pediatric Clinics of North America October 1994 41(5): 991 - 1011
• Flynn P. et al, Cardiac Issues in the Pediatric Emergency Room The Pediatric Clinics of North America
October 1992 39(5): 955 - 983
• Lees M, King D, Cyanosis in the Newborn Pediatrics in Review August 1987 9(2) 36 - 42
• DiMaio A et al The Infant with Cyanosis in the Emergency Department
The Pediatric Clinics of North America October 1992 39(5) 987 - 1006
PULMONARY
• Keens T., Davidson Ward S., Apnea Spells, Sudden Death, and the Role of the Apnea Monitor
The Pediatric Clinics of North America October 1993 40(5): 897 - 909
• Sudden Infant Death Syndrome: Medical Aspects and Psychological Management The Johns Hopkins Univ
Press 1988
• Swischuk L, Acute Respiratory Distress in a Young Infant Pediatric Emergency Care Aug 1991 7(4) 255 - 257
• DiMaio V, SIDS or Murder? (letter) Pediatrics 81: 747, 1988
• Spitzer A et al Infant Apnea The Pediatric Clinics of North America June 1986 33(3) 561 - 581
NEUROLOGY
• Bernes S., Kaplan A., Evolution of Neonatal Seizures The Pediatric Clinics of North America
October 1994 41(5): 1069 - 1104
• Fenichel G., et al, Heart Rate Changes in Convulsive and Nonconvulsive Apnea Ann Neurology 1983 7:577-586
• Sfafstrom C, Neonatal Seizures Pediatrics in Review July 1995 16(7) 248 - 256
• Watanabe, K et al Apneic seizures in the newborn Am J. Dis Child 136: 980, 1982
A special thanks to the pediatric and neonatology staff at Harbor/UCLA and Children’s of Orange County for answering my unending
questions !!



This Web page is referenced from another page containing related information about Miscellaneous Newborn Care

 




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