2. OBJECTIVES
Define the neonatal period and a helpful
mnemonic for neonatal emergencies
Review case-based emergencies associated
with the neonate
Discuss common infections in the neonate
Differentiate between
infectious, cardiac, GI, metabolic, and endocrine
emergencies
Gain confidence in dealing with neonatal
patients
3. CASE PRESENTATION
7 day old M presents to the ED with a 1 day
history of poor feeding, lethargy, and
increased work of breathing.
Pre and postnatal history are unremarkable
What is your next step?
5. SO REALLY…. WHAT’S SHOULD I BE THINKING?
“THE MISFITTS”
Trauma/Abuse (NAT)
Heart and Lung
Endocrine
Metabolic disturbances
Inborn errors of metabolism
Sepsis
Formula issues
Intestinal
Toxins
Trisomies
Seizures
6. CASE PRESENTATION #1
7 day old M presents to the ED with a 1 day
history of poor feeding, lethargy, and
increased work of breathing. At PMD today, a
temperature of 101.5 noted rectally.
Pre and postnatal history are unremarkable
What is your next step?
8. RULE OUT SEPSIS WORK UP
Blood culture
CBC
CMP
Urinalysis
Urine culture
CSF studies
CSF culture
HSV PCR
CXR (+/-)
RVP (+/-)
NS bolus (+/-)
Antibiotics- Ampicillin and Gentamicin or 3rd generation
cephalosporin (0-28 days)
9. FEVER IN THE NEONATE
Neonate: 0-28 days
Fever: 38 C or 100.4 F
Also consider hypothermia
Difficult to evaluate clinically
Increased susceptibility to infection
>10% of infants with fever will
have a serious bacterial infection
UTI- 30%
Meningitis- 20%
Bacteremia/septicemia- 15%
10. NEONATAL FEVER
Peripheral WBC alone not an accurate
screen for SBI
Consider concomitant viral illness with SBI
All febrile neonates should have a full sepsis
evaluation and be admitted for IV antibiotics
11. STUDY ON NEONATAL FEVER IN THE PEDS ED
2253 neonates ( 0-28 days old)
16% discharged, 84% admitted
Jain et al, Pediatrics, 2014
12. INFECTIONS IN THE NEONATE
Group B Streptococcus
E. coli
Listeria
S. aureus
H. influenza
S. pneumonia
N. meningitis
Viral
RSV
HSV
Enterovirus
13. GROUP B STREPTOCOCCUS
Gram positive cocci
Most common infection of the newborn
Cause of neonatal
pneumonia, bacteremia, and meningitis
Up to 1/3 of women are colonized
Early and late-onset infections
Tx: Ampicillin
Fatality rates 2-15%
14. EARLY AND LATE ONSET
Early onset:
1 hour to 7 days
Bacteremia 45%
Pneumonia 40%
Meningitis <10%
Higher fatality rate
Late onset:
7 days to 3 months (27 day median)
Bacteremia 45%
Meningitis 40%
15.
16. ESCHERICHIA COLI
Gram negative rod
Most frequent cause of infection in the first 7
days of life
Most common cause of meningitis in
neonates
Significant cause of UTI’s and urosepsis
Tx: Gentamicin or 3rd generation
cephalosporin
17. LISTERIA MONOCYTOGENES
Gram positive rod
Can mimic diphtheroids on gm stain
Highest incidence in patients < 1 month old
Infected from colonized mothers
Meconium staining, PROM,
transplacentally
Tx: Ampicillin
Resistant to cephalosporins
Fatality rate 15%
18.
19. CASE PRESENTATION #2
7 day old M presents to the ED with a 1 day history of
poor feeding, lethargy, increased work of breathing
and poor color. No history of fever and afebrile on
presentation. Cap refill 4 seconds on exam and no
palpable femoral pulses.
Pre and postnatal history are unremarkable
What diagnosis is
concerning for this
patient?
20. CONGENITAL HEART DISEASE
1/125 births
Usually ductal dependent
Closes by 72 hours
Symptoms include:
Tachypnea
Cyanosis
Pallor
Lethargy
FTT
Sweating with feeds
Hypoxia and cyanosis usually unresponsive to oxygen
Left and right sided heart lesions
21. CONGENITAL HEART DISEASE
Left sided: systemic blood flow is dependent on
ductal patency
Coarctation of the aorta
Hypoplastic left heart
Right sided: pulmonary blood flow is dependent
on ductal patency (Cyanotic Lesions)
Truncus Arteriosus
Transposition of the great vessels
Tricuspid atresia
Tetralogy of Fallot
TAPVR
23. CASE PRESENTATION #2
7 day old M presents to the ED with a 1 day
history of poor feeding, lethargy, increased
work of breathing and poor color. No history
of fever and afebrile on presentation. Poor
perfusion on exam.
Pre and postnatal history are unremarkable
What medication do you want to give?
24. WHAT TO DO?
Prostaglandin E1!!!!!
0.05mcg/kg/min
Response within 15 minutes
Watch for:
Hypotension, flushing, APNEA!
Pressure support
Fluids
Echo
Cardiology consult
30. TRANSPOSITION OF THE GREAT ARTERIES
Most common cyanotic lesion presenting in
the first week of life
To be compatible with life, mixing must occur
via an ASD, VSD, or PDA
33. TOTAL ANOMALOUS PULMONARY VENOUS RETURN
All four pulmonary veins fail to make their
normal connection to the left atrium
34.
35. CASE PRESENTATION #3
7 day old M presents to the ED with a 1 day
history of poor feeding, irritability, very
jittery, and mild respiratory distress. No
fevers but clammy/ wet skin. PE reveals a
tachycardic infant with microcephaly and
triangular faces.
What do you want
to know about Mom?
37. GRAVES DISEASE AND THE NEONATE
1-5% of infants from moms with Graves
Results from the transplacental passage of
maternal stimulatory TSHR-Ab
Can be seen in mom’s with active Graves or
ones previously treated with thyroidectomy or
radioactive iodine
38. GRAVES DISEASE AND THE NEONATE
At birth, infants can be
Hypothyroid with a goiter
Euthyroid due to maternal PTU
Hyperthyroid due to maternal TSHR-Ab
Neonatal screening
Self- limiting
Resolution by 12 weeks
40. NEONATAL THYROTOXICOSIS
Treatment includes:
Beta-blockade
Propanolol 0.1mg/kg IV
Blocking thyroxine production
PTU 5-10mg/kg PO
Blocking thyroxine release
Potassium-iodide 1-4 drop PO
Decreasing T4 T3 conversion
Dexamethasone 0.1mg/kg IV
41.
42. CASE PRESENTATION #4
7 day old F presents to the ED with a 1 day
history of poor feeding, vomiting, poor
tone, and lethargy. No history of fever.
BP 50/32 with a cap refill of 4 seconds
It was a home birth and neonatal screening
wasn’t performed
44. CONGENITAL ADRENAL HYPERPLASIA
Autosomal recessive, variable penetrance
Involve a defect in the adrenal production of
cortisol, mineralocorticoid, or both
Salt-wasting or non-salt-wasting
21-hydroxylase deficiency: >90% of all cases
Functioning 21-hydroxylase
Converts 17-hydroxyprogesterone into cortisol
Converts progesterone to aldosterone
46. CAH PRESENTATION
Cortisol deficiency
hypoglycemia, hypotension, and shock
Aldosterone deficiency
hyponatremia, hyperkalemia, and dehydration
Androgen excess virilization of female
genitalia, less common in males
Males will have normal genitalia at birth and will
present in salt-losing adrenal crisis
47. WORK UP
Blood work:
CMP
Accucheck
17-hydroxyprogesterone levels
Cortisol levels
Aldosterone and renin levels
48. CAH TREATMENT
NS bolus
Treat any electrolyte abnormalities
If hypoglycemia given dextrose
Na+
K+
Stress dose hydrocortisone 50-100mg/m2 IV
Glucocorticoid and mineralocorticoid activity
49.
50. CASE PRESENTATION #5
7 day old F presents to the ED with a 1 day
history of poor feeding, vomiting green
material, poor tone, and lethargy. No history
of fever.
BP 57/42 with a cap refill of 4 seconds
What intestinal emergency are you
concerned for?
51. MALROTATION AND VOLVULUS
Congenital anomaly during intestinal
development
Small bowel predominantly on the right side
Cecum is displaced into the epigastrium
Ladd’s bands course over the horizontal part of
the duodenum
Small intestine mesentery has an unusually
narrow base
Midgut is prone to volvulus
53. DIAGNOSIS
Abd xray
May show duodenal obstruction
“Double bubble sign”
Upper GI- gold standard
Concern for malrotation if the duodenal C-
loop doesn’t cross midline and the
duodenojejunal junction isn’t the left of the
spine
56. PUTTING IT ALL TOGETHER
History is key! (prenatal, birth, maternal)
ABC’s
IV access with appropriate blood work
Fluids
Antibiotics
Imaging?
Remember the differential
THE MISFITTS
RESPECT THE NEONATE
57. THE MISFITTS
Trauma/Abuse (NAT)
Heart and Lung
Endocrine
Metabolic disturbances
Inborn errors of metabolism
Sepsis
Formula issues
Intestinal
Toxins
Trisomies
Seizures
58.
59. REFERENCES
Jain S, Cheng J, Alpern E, et al. Management of febrile neonates
in US pediatric emergency departments. Pediatrics.
2014;133:187-195.
Menrke DP, Nieman LK, Martin KA, et al. Diagnosis of classic
congential adrenal hyperplasia due to 21-hydroxylase deficiency.
In: UpToDate. March 2014.
Menrke DP, Nieman LK, Martin KA, et al. Genetics and clinical
presentation of classic congenital adrenal hyperplasia due to 21-
hydroxylase deficiency. In: UpToDate. April 2013.
Batra CM. Fetal and neonatal thyrotoxicosis. Indian Journal of
Endocrinology and Metabolism.2013.17:50-54.
