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NEONATAL EMERGENCIES
Rebecca Starr, D.O.Pediatric Emergency Medicine FellowMarch 20, 2014
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
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?
FREAK OUT!!!!
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
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?
RULE OUT SEPSIS WORK UP?
What do you want to order?
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)
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%
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
STUDY ON NEONATAL FEVER IN THE PEDS ED
2253 neonates ( 0-28 days old) 16% discharged, 84% admitted
Jain et al, Pediatrics, 2014
INFECTIONS IN THE NEONATE
Group B Streptococcus E. coli Listeria S. aureus H. influenza S. pneumonia N. meningitis Viral
RSV HSV Enterovirus
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%
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%
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
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%
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?
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
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
CLINICAL
Shock Poor/absent distal pulses Poor perfusion/color Cap refill >3 sec Tachypnea
Cardiac Failure Hepatomegaly Large heart Gallop Harsh murmur
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?
WHAT TO DO?
Prostaglandin E1!!!!! 0.05mcg/kg/min Response within 15 minutes Watch for:
Hypotension, flushing, APNEA!
Pressure support Fluids Echo Cardiology consult
TETRALOGY OF FALLOT
Boot-shaped heart
TETRALOGY OF FALLOT
Four criteria1. Pulmonary atresia/stenosis2. RV hypertrophy3. VSD4. Over-riding aorta
NAME THAT CARDIAC ABNORMALITY
TRANSPOSITION OF THE GREAT ARTERIES Egg on a string
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
TOTAL ANOMALOUS PULMONARY VENOUS RETURN
Snowman sign
TOTAL ANOMALOUS PULMONARY VENOUS RETURN
All four pulmonary veins fail to make their normal connection to the left atrium
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?
Maternal History of Grave’s Disease!
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
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
NEONATAL THYROTOXICOSIS
Essentially “thyroid storm” picture Irritability Respiratory distress Tachycardic Hyperthermic Shock Cardiac Failure
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
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
CASE PRESENTATION #4
Physical exams reveals
What is the diagnosis?
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
CONGENITAL ADRENAL HYPERPLASIA Lack of 21-hydroxylase causes:
Build-up of 17-hydroxyprogesterone Converted into androgens
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
WORK UP
Blood work: CMP Accucheck 17-hydroxyprogesterone levels Cortisol levels Aldosterone and renin levels
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
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?
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
MALROTATION AND VOLVULUS
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
MALROTATION ON UPPER GI
“Whirlpool sign” indicates volvulus
TREATMENT
ABC’s Fluid resuscitation NPO NG tube to suction Pediatric Surgery consult!
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
THE MISFITTS
Trauma/Abuse (NAT) Heart and Lung Endocrine Metabolic disturbances Inborn errors of metabolism Sepsis Formula issues Intestinal Toxins Trisomies Seizures
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.
Questions?