The gentlebirth.org website is provided courtesy of
Ronnie Falcao, LM MS,
a homebirth midwife in Mountain View, CA
The gentlebirth.org website is provided courtesy of
Ronnie Falcao, LM MS,
a homebirth midwife in Mountain View, CA
|
An interactive resource for moms on easy steps they can take to reduce exposure to chemical toxins during pregnancy. Other excellent resources about avoiding toxins during pregnancy These are easy to read and understand and are beautifully presented. |
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 Moms 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 newborns first bowel movement while still in-utero;
usually a sign of distress!
Meconium aspirated into the newborns 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 infants 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 newborns
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)
Moms 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 newborns 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
newborns 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
Dont 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
Dont pull a good tube!!
Pediatric CO2 detectors now available
Cut off any extra tube extending beyond 4 cm from neonates 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 newborns 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 moms 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 IOs 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 mothers blood)
- 5% albumin-saline solution
- normal saline
- Ringers 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 30s nadir by 2 months of age
- WBC 7 - 28,000 during first month of life
IVs 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
dont cause respiratory distress !
infants 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 its 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 Herschsprungs 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
Coombs 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 Epsteins 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 neonates 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
EPSTEINS PEARLS/ BOHNS 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 URIs; 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 cant
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
Moms drugs - Opiates, MagSO4
Hypothyroidism
Breast fed
Stomach/Duodenum
Antral Web
Pyloric stenosis
Duodenal atresia
Anular pancreas
Small Intestine
Meconeum ileus/plug
Volvulus
Large Intestine
Hirschsprungs 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 Hirschsprungs 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 PHYSICIANS 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 (dont 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 Meckels
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 mothers 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 moms 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
Mcrurys 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
22
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 Fs 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
23
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
- Shentons 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
24
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 Coombs test - ABO incompatiblity, Rh disease
Negative Coombs 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
25
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 Coombs
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 moms will never go back to breast feeding when told
to stop temporarily !
The First Month
26
- 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 moms 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 moms 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 moms 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
27
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
- Coombs 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 Coombs 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
-- Coombs 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
28
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
29
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
30
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 WBCs 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
31
Consider Acyclovir 10mg/kg per dose q 8 hours IV if WBCs 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)
The First Month
32
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
The First Month
33
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 neonates 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
DONT 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, Ebsteins
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 - Ebsteins 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
34
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 wasnt audible at birth
The First Month
35
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 dont
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
The First Month
36
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 !!
(
The First Month
37
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
Nelsons TEXTBOOK OF PEDIATRICS 14th Edition
The First Month
38
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
The First Month
39
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!)
doesnt 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
The First Month
40
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 childs
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 WBCs 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 DONT ASK HOW THEY ARE MIXING UP THE FORMULA, PARENTS WONT
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 DONT ASK ABOUT ADDITIONAL LIQUIDS, POWDERS, HERBS, or OTHER
SUBSTANCES GIVEN TO THE
NEONATE, PARENTS WONT 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 parents 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
infants 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
SCHAFFERS 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 Childrens of Orange County for answering my unending
questions !!
| About the Midwife Archives / Midwife Archives Disclaimer |