Transcript Neonatal Emergencies - St. Barnabas Hospital

Neonatal
Emergencies
Lazaro Lezcano, MD
Director, Division of Neonatology
August 18, 2009
Neonatal Emergencies
Neonates often present with nonspecific or a history of symptoms that
may or may not be benign
 In order to recognize which neonates
will require life-saving interventions,
clinicians need to remain current on
these life-threatening illnesses and
their management

The Misfits Movie
Neonatal Emergencies
“THE MISFITS”
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T- Trauma (accidental & nonaccidental)
H- Heart Disease/Hypovolemia/Hypoxia
E- Endocrine (congenital adrenal hyperplasia,
thyrotoxicosis)
M- Metabolic (electrolyte imbalance)
I- Inborn Errors of Metabolism: metabolic emergencies
S- Sepsis (meningitis, pneumonia, UTI)
F- Formula mishaps (under or overdilution)
I- Intestinal catastrophes (volvulus, intususception,
NEC)
T- Toxins/poisons
S- Seizures
Trauma
(accidental & non-accidental)
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May be a difficult process
Non-accidental subtle historical
findings and no physical exam findings
Presenting symptoms may be nonspecific
Early diagnosis of an occult head injury
may prevent significant long-term
morbidity
An ALTE is often an unrecognized
presenting symptom of abusive head
injuries
Trauma
(accidental & non-accidental)
Infants with ALTE w/o an immediate
obvious cause should be evaluated for
head trauma with neuroimaging
 CT scan, HUS or MRI
 Skull x-rays may not be helpful
significant head injury w/o skull fracture
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Consider neuroimaging in any nonaccidental injury for other skeletal
injuries regardless of physical
examination of the head
Trauma
(accidental & non-accidental)
37% of abused children < 2 y/o had
an occult traumatic injury
 In addition, the ophthalmologic
evaluation did not demonstrate
retinal hemorrhages in most of the
patients
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Pediatrics 6/2003
CHOP
74%  No retinal hemorrhages
Trauma
(accidental & non-accidental)
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Management:
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Evaluation and stabilization of the ABC’s
Bedside glucose evaluation
Appropriate temperature regulation
If bruising or known intracranial bleed:
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CBC
Platelet count
PT/PTT
Neuroimaging after stabilization
Trauma
(accidental & non-accidental)
Admit the patient
 Report injury to appropriate state
department for abuse
 Skeletal survey
 Ophthalmologic exam
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Heart Disease and Hypoxia
Cyanotic Heart Disease
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Cyanosis requires immediate
attention and evaluation
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Differential diagnosis:
 Respiratory
causes
 Infectious causes
 CNS abnormalities
 Toxins
 Cyanotic heart disease
Heart Disease and Hypoxia
Cyanotic Heart Disease
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Terrible T’s:
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Transposition of the great arteries (TGA)
Tetralogy of Fallot (TOF)
Tricuspid atresia (TA)
Total anomalous pulmonary venous return
(TAPVR)
Truncus arteriosus (TA)
Heart Disease and Hypoxia
Cyanotic Heart Disease
May not be detected in the WBN
 Adequately oxygenated blood  PDA
 systemic circulation
 PDA functionally closes in the first 1014 hrs of life
 Several factors can delay its closure
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Prematurity
Respiratory distress
Acidosis
Hypoxia
Heart Disease and Hypoxia
Cyanotic Heart Disease
PDA is anatomically closed by 2
weeks of age, contributing to a
delayed detection of cyanotic heart
disease
 100% FiO2:
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Non-cardiac disease
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At least 10% increase in O2 saturation
Cyanotic heart disease
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Minimal change in O2 saturation
Heart Disease and Hypoxia
Cyanotic Heart Disease
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Hyperoxia test:
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Initial ABG on R/A
Repeat ABG after 10-20 minutes of 100%
O2
Cyanotic heart disease PaO2 will not
increase significantly
If PaO2 rises above 150 mm Hg, cardiac
disease can generally be excluded
Failure of PaO2 to rise above 150 mm Hg
suggests a cyanotic cardiac malformation
Heart Disease and Hypoxia
Cyanotic Heart Disease
During stabilization the physical exam
should include B/P’s in all 4
extremities and careful cardiac exam
 A murmur may be audible
 Absence of a murmur does not
exclude a cardiac defect
 CXR & EKG should be included in the
evaluation
 ECHO is diagnostic
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Heart Disease and Hypoxia
Cyanotic Heart Disease
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Management:
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PGE1
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Bolus of 0.05 mcg/Kg IV
Drip of 0.05-0.1 mcg/Kg/min
Secure airway
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Profound apnea is a non-dose dependent
complication of PGE1
Hypoplastic Left Heart Syndrome
25% of cardiac deaths during first
week of life
 Occurs in both cyanotic and acyanotic
forms
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In 15% of cases the FO is intact
preventing mixing at the atrial level
Infants with mixing at the atrial level are
acyanotic
Hypoplastic Left Heart Syndrome
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PE:
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Pallor
Tachypnea
Poor perfusion
Poor to absent peripheral pulses
Loud single S2
Gallop rhythm w/o murmur
Hepatomegaly
Metabolic acidosis
Hypoplastic Left Heart Syndrome
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EKG:
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CXR:
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Small or absent (L) ventricular forces
Moderate cardiomegaly
Large PA shadow
ECHO:
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Small or slit-like (L) ventricle
Hypoplastic ascending aorta
Hypoplastic Left Heart Syndrome
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Treatment:
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PGE1- systemic blood flow is ductal
dependent
Surgical correction
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Surgical correction
 1st stage
 Norwood procedure
 2nd stage
 Fontan procedure
Neonatal cardiac transplantation
Compassionate care may be appropriate
in some instances
Acyanotic Heart Disease
Congestive Heart Failure
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Typically presents with symptoms of CHF
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Tachypnea
Tachycardia
Hepatomegaly
History of poor or slow feeding
Sweating or color change with feeding
Poor weight gain
More gradual clinical decompensation
May not present until after the first 2-3
weeks of age
Acyanotic Heart Disease
Congestive Heart Failure
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Causes of CHF in Neonates:
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Acyanotic heart disease (VSD, ASD, PDA,
CoA)
Severe anemia
Trauma
Sepsis
SVT
Metabolic abnormalities
SLE
Thyrotoxicosis
Acyanotic Heart Disease
Congestive Heart Failure
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Initial management:
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Stabilization of the ABC’s
CXR
EKG
Labs:
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CBC
BMP
ABG
ECHO- diagnostic of heart defect
Furosemide
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1 mg/Kg IV
Acyanotic Heart Disease
Congestive Heart Failure
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Pressors:
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Dopamine
 5-15 mcg/Kg/min IV
Dobutamine
 2.5-15 mcg/Kg/min IV
Careful with fluid overloading
Peds. Cardiology consult
Acyanotic Heart Disease
Supraventricular Tachycardia
SVT is the most common neonatal
dysrhythmia (1/25,000 births)
 Signs/symptoms:
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Tachycardia
Poor feeding
Irritability
Heart Failure
Shock
Heart rate sustained at >220 bpm
with a QRS < 0.08 seconds
Acyanotic Heart Disease
Supraventricular Tachycardia
Acyanotic Heart Disease
Supraventricular Tachycardia
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Management:
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Stable patient:
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Vagal maneuvers
 Ice to face avoiding the nares
If unsuccessful:
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Adenosine
 50 mcg/Kg rapid IVP (1-2 secs.), increase
dose in 50mcg/Kg increments Q2 mins. until
return of sinus rhythm, maximum dose 250
mcg/Kg
Acyanotic Heart Disease
Supraventricular Tachycardia
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Unstable patient w/o IV access:
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Synchronized cardioversion
 0.5-1 J/Kg
Initial cardioversion should be
attempted pharmacologically if IV
access is established and adenosine is
readily available
 If unresponsive to adenosine &
cardioversion
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Amiodorone
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5mg/Kg IV over 30-60 mins.
Acyanotic Heart Disease
Supraventricular Tachycardia
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Procainamide- alternative to amiodorone
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15 mg/Kg IV over 30-60 mins.
The administration of procainamide and
amiodorone together can lead to
hypotension and widening of the QRS
complex
Lidocaine
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1mg/Kg IV
Final option for a wide QRS and should only be
used in consultation with a pediatric
cardiologist
Acyanotic Heart Disease
Supraventricular Tachycardia
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12-lead EKG prior to and after
conversion from SVT to NSR
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Useful diagnostic tool for the cardiologists
to help determine further management
Consult pediatric cardiologist for
further evaluation
Heart Disease and Hypoxia
Bronchiolitis
Viral lower-airway disease caused by
RSV 80% of the time
 Other etiologies include adenovirus,
influenza, or parainfluenza
 RSV is responsible for 50-90% of
bronchiolitis hospital admissions
 More common in winter and spring
seasons, may present at any time
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In NY from October-April
Heart Disease and Hypoxia
Bronchiolitis
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Signs/Symptoms:
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Rhinorrhea
Cough
Congestion
Wheezing
Significant respiratory distress
Apnea may be the only initial symptom
Heart Disease and Hypoxia
Bronchiolitis
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Management:
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Infants with severe, prolonged apnea with
bradycardia unresponsive to O2 therapy
may need intubation
Nebulized racemic epinephrine
or
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Beta-agonist
The adjunct use of corticosteroids has not
been shown to improve symptoms
A fever or sepsis evaluation may be part of
the management
Heart Disease and Hypoxia
Bronchiolitis
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Controversy over the incidence of severe
bacterial infections in infants who have
RSV
The presence of a viral infection doesn’t
exclude the possibility of a concomitant
UTI
Consider hospitalization for all RSV(+)
neonates, especially preemies or all
neonates with other comorbidities
Heart Disease and Hypoxia
Apnea/ALTE
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Apnea
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cessation of respiration for 20 secs. or
more, associated with color change
(cyanosis or pallor) or bradycardia
ALTE
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poorly defined term used to describe any
event that is “frightening to the observer
and is characterized by some combination
of apnea, color change, marked change in
muscle tone, choking or gagging”
Heart Disease and Hypoxia
Apnea/ALTE
Management depends on history
provided by observers and PE
 Hospitalization for observation and
monitoring
 Common differential diagnosis:
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Sepsis
Pneumonia
RSV
Hypothermia
Anemia
Heart Disease and Hypoxia
Apnea/ALTE
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Botulism
Dysrhythmias
Acid/base disturbances
Intracranial hemorrhage
Meningitis/encephalitis
Pertussis
Hypoglycemia
Seizures
GER
Child abuse
Inborn errors of metabolism
Electrolyte abnormalities
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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Most patients diagnosed by newborn
screening
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Occasionally diagnosis is missed
because of inadequate blood sample,
laboratory error, or inability to
contact the family
Endocrine Emergencies
Congenital Adrenal Hyperplasia
Autosomal recessive
 Most common is 21-hydroxylase
deficiency- 95% of affected patients
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Inadequate cortisol levels
Excessive ACTH stimulation
Adrenal hyperplasia
Excessive production of adrenal
androgens and testosterone
 virilization
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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Two forms
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Virilizing form
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Relative aldosterone deficiency
Mild salt loss
Adrenal insufficiency tends not to occur unless
under stressful situations
Salt-losing form
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Absolute aldosterone deficiency
Adrenal insufficiency under basal conditions
Manifests in the neonatal period or soon after
as an adrenal crisis
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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11- hydroxylase deficiency
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Less common- 5-8% of cases
Salt retention
Volume expansion
Hypertension
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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Management:
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Labs:
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Blood glucose
 Hypoglycemia
Serum electrolytes
 Hyponatremia
 Hyperkalemia
Hypotension unresponsive to fluids or
inotropes heightens suspicion of CAH
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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Hydrocortisone
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25-50mg/m2 IV
Treat hypoglycemia
Hyperkalemia usually responds to fluid
therapy
If patient is symptomatic or with EKG
changes
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Calcium chloride
NaHCO3
Insulin and glucose
Polystyrene sulfonate (Kayexalate)
Endocrine Emergencies
Congenital Adrenal Hyperplasia
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Pediatric critical care management
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Endocrinology consultation
Endocrine Emergencies
Thyrotoxicosis
Hypermetabolic state resulting from
excessive thyroid hormone activity in
the newborn
 Usually results from transplacental
passage of thyroid-stimulating
immunoglobulin from a mother with
Graves’ disease
 Rare disorder
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Occurs in ~1/70 thyrotoxic pregnancies
Incidence of maternal thyrotoxicosis in
pregnancy is 1-2/1000 pregnancies
Endocrine Emergencies
Thyrotoxicosis
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Clinical presentation
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Fetal tachycardia in the 3rd trimester may be the
first manifestation
Signs usually apparent within hours from birth
If mother is on antithyroid medications
presentation may be delayed 2-10 days
Thyrotoxic signs
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Irritability
Tachycardia
Flushing
Tremor
Poor weight gain
Trombocytopenia
Arrhythmias
Endocrine Emergencies
Thyrotoxicosis
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Initial diagnosis difficult w/o clear
history of Graves’ disease from mother
Goiter usually present  tracheal
compression
Labs
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Increased T4, FT4 & T3
Suppressed levels of TSH
Treatment
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Mild
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Close observation
Endocrine Emergencies
Thyrotoxicosis
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Moderate
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Lugol’s solution (iodine)
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Propylthiouracil
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5-10mg/Kg/day in 3 divided doses
Methimazole
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1 drop PO Q8H
0.5-1mg/Kg/day in 3 divided doses
Severe
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In addition to above meds
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Prednisone
 2mg/Kg/day
Propanolol – for tachycardia
 1-2mg/Kg/day in 2-4 divided doses
Digitalis may be used to prevent cardiovascular
collapse
Inborn Errors of Metabolism
Inborn Errors of Metabolism
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Urea cycle defects
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Ornithine-transcarbamylase deficiency
Carbamyl phosphate synthetase
deficiency
Transient hyperammonemia of the
neonate (unclear cause)
Argininosuccinate synthetase deficiency
(citrulinemia)
Argininosuccinate lyase deficiency
Arginase deficiency
N-acetylglutamate synthetase deficiency
Inborn Errors of Metabolism
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Amino acid metabolism defects
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MSUD
Nonketotic hyperglycinemia
Hereditary tyrosinemia
Pyroglutamic acidemia (5-oxoprolinuria)
Hyperornithinemia-hyperammonemiahomocitrulinemia syndrome
Lysinuric protein intolerance
Methylene tetrahydrofolate reductase
deficiency
Sulfite oxidase deficiency
Inborn Errors of Metabolism
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Organic Acidemias
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Methylmalonic acidemia
Propionic acidemia
Isovaleric acidemia
Multiple carboxylase deficiency
Glutaric acidemia type II
HMG-CoA lyase deficiency
3-Memethylcrotonoyl-CoA carboxylase
deficiency
3-Hydroxyisobutyric acidemia
Inborn Errors of Metabolism
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Carbohydrate metabolism defects
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Galactosemia
Fructose-1,6-biphosphatase deficiency
Glycogen storage diseases (types IA. IB,
II, III and IV)
Hereditary fructose intolerance
Inborn Errors of Metabolism
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Fatty acid oxidation defects
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Short chain acyl-CoA dehydrogenase
deficiency (SCAD)
Medium chain acyl-CoA dehydrogenase
deficiency (MCAD)
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Most common (incidence of 1/6,000-10,000)
Long chain acyl-CoA dehydrogenase
deficiency (LCAD)
Acyl-CoA deficiency
Inborn Errors of Metabolism
Metabolic Emergencies
Often have a delayed diagnosis
 Symptoms may be unrecognized
because they are uncommon
 Require a high level of suspicion for
diagnosis
 Diagnosis should be considered in any
infant who does not have any other
obvious cause for symptoms
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Inborn Errors of Metabolism
Metabolic Emergencies
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Nonspecific symptoms
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Poor feeding
Vomiting
FTT
Tachycardia
Tachypnea
Irritability
Inborn Errors of Metabolism
Metabolic Emergencies
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More apparent symptoms
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Seizures
Lethargy
Hypoglycemia
Apnea
Temperature instability
Acidosis
Inborn Errors of Metabolism
Metabolic Emergencies
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Labs
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Bedside glucose
CBC
BMP
pH
Lactate and ammonia levels
LFT’s
Urine for reducing substances and
ketones
Blood and urine for organic and amino
acids
Inborn Errors of Metabolism
Metabolic Emergencies
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Management
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Fluid resuscitation
IV dextrose to prevent further catabolism
Admission to hospital
Genetics consultation
Sepsis

It is standard of care to complete a
full sepsis evaluation (CBC, blood
culture, urinalysis, urine culture, CSF
culture and analysis, CXR) in a
neonate with a rectal temperature of
>100.4 F (38 C)
Sepsis
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Symptoms that should prompt the
consideration of a full sepsis evaluation
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Poor feeding
Irritability
Apnea
Hypothermia
Jaundice
Rashes
Increased sleeping
Vomiting
Sepsis
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Thorough maternal history and physical
examination
One study evaluating the heart rate
characteristics of neonates found that
reduced heart rate variability was
present before clinical signs of sepsis*
Initial laboratory screening is not always
helpful
*
Pediatrics 2005
University of Virginia
Sepsis
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The use of peripheral WBC count is not
helpful to differentiate febrile neonates with
a more serious bacterial infection from
those w/o serious bacterial infection*
One study demonstrated that a low
peripheral WBC count increased the odds of
bacterial meningitis**
*Emergency Medicine Journal 2005
Loma Linda University Medical Center & Children’s Hospital
**Academic Emergency Medicine 6/08
Children’s Hospital of Columbus, OH
Sepsis
The urinalysis may be unremarkable
in infants with a culture (+) UTI
 Approximately 14% of febrile
neonates will be diagnosed with a UTI

Pediatrics 2000
McKay Memorial Hospital in Taiwan
CRP, ESR and U/A imperfect tools in discriminating for UTI
Sepsis
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Treatment
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Broad spectrum antibiotics
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Ampicillin
 50-100mg/Kg IV
Gentamicin
 2mg/Kg IV
or
Cefotaxime
 50-100mg/Kg IV
Acyclovir
 20mg/Kg IV
Sepsis
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Neonatal herpes
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Symptoms may be subtle
No maternal history in 60-80% of women with
unrecognized infection
Early recognition and treatment with acyclovir
may decrease mortality from 90%  31%
Initiate treatment in any infant with
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High fever
CSF lymphocytosis
Numerous RBC’s in an atraumatic spinal tap
Seizures
Known maternal history of HSV infection
Sepsis
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CSF analysis
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Herpes PCR
Herpes culture
Elevated LFT’s
Chest x-rays
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Pneumonitis
Formula Mishaps
Inappropriate mixing of water and
powder formula
 Overdilution of concentrated liquid or
premixed formula
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Life-threatening electrolyte disturbances
or FTT
Hyponatremia
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Seizures
Intestinal Catastrophes
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Consider pathologic process if vomiting
in newborn period
Difficult to differentiate between a lifethreatening cause from a mild viral
gastroenteritis or even severe
gatroesophageal reflux
Initial symptoms may be nonspecific
Bilious emesis is almost always an
ominous sign
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Initiate pediatric surgery consultation
Intestinal Catastrophes
Malrotation with Midgut Volvulus
Abnormal rotation of bowel in utero
resulting in an unfixed portion of
bowel that may later twist on itself 
bowel ischemia  death
 Incidence of 1/5,000 live births
 Usually diagnosed in the first month
of life
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Intestinal Catastrophes
Malrotation with Midgut Volvulus
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Symptoms
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Bilious emesis
Poor feeding
Lethargy
Shock in more advanced presentations
Management
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Fluid resuscitation
NGT placement
Pediatric surgical consultation
Intestinal Catastrophes
Malrotation with Midgut Volvulus
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KUB’s
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Normal
Signs of small bowel obstruction
Upper GI series is the gold standard
for diagnosis
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Transverse portion of the duodenum
leading to a fixed ligament of Treitz
Intestinal Catastrophes
Toxic Megacolon
Life-threatening presentation of a
patient with Hirschprung’s disease
 Hirschprung’s disease occurs in
1/5,000 live births
 May be unrecognized because
constipation is common and usually
benign
 History of constipation with failure to
pass meconium in the first 24 hours
of life is highly suspicious of
Hirschprung’s
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Intestinal Catastrophes
Toxic Megacolon
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Symptoms
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Poor feeding
Vomiting
Irritability
Abdominal distention
Hematochezia
Shock as it progresses to enterocolitis
Intestinal Catastrophes
Toxic Megacolon
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Management
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Stabilization of ABC’s
Fluid resuscitation
Broad-spectrum antibiotics
KUB
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Enlarged or dilated section of colon
Surgical consultation
Pediatric critical care management in the
presence of enterocolitis
Intestinal Catastrophes
Necrotizing Enterocolitis
Clasically a disease of premature
infants
 May occasionally occur in term
neonates after discharge from WBN
 Symptoms similar to those of
Hirschprung’s enterocolitis

Intestinal Catastrophes
Necrotizing Enterocolitis

Management






Stabilization of ABC’s
Fluid resuscitation
NGT placement
Broad-spectrum antibiotics
Pediatric surgical consultation
Critical care management
Intestinal Catastrophes
Hypertrophic Pyloric Stenosis
Common, incidence of 1/250 live
births
 Male:female ratio 4:1
 More common in firstborn male
 Classic metabolic abnormality of
hypochloremic, hypokalemic
metabolic alkalosis- now uncommon
 History of nonbilious projectile
emesis immediately after feeding

Intestinal Catastrophes
Hypertrophic Pyloric Stenosis
Increased incidence in infants with an
early exposure to oral erythromycin
 PE




Palpable “olive” structure in the RUQ
Visible peristaltic waves
Diagnosis

US


Thickened and lengthened pylorus
Upper GI

“String sign”
Intestinal Catastrophes
Hypertrophic Pyloric Stenosis

Management



*
Surgical is standard
IV atropine followed by oral atropine
shows satisfactory results*
Stabilization and IV access to replace
fluids and electrolytes
Osaka, Japan
Archives of Disease in Childhood 2002
89% resolution of projectile vomiting with reduced
pyloric muscle thickness
Toxins
Toxic ingestions are uncommon
 Occasionally the result of a maternal
ingestion in a breastfeeding mother,
homeopathic remedies, or overuse of
accepted medications
 Teething gels may be used for the
relief of colic


Benzocaine

Methemoglobinemia with overuse
Toxins

Star anise tea






Baking soda



Relief of infantile colic
Neurotoxicity
Unexplained irritability
Vomiting
Seizures
Used for intestinal gas
Serious toxicity
Hospitalization for monitoring and
observation
Seizures
May be difficult to diagnose
 “Not acting right”
 More somnolent than usual
 Immature cortical development



May not be tonic-clonic
Commonly




Lip-smacking
Abnormal eye or tongue movements
Pedaling
Apnea
Seizures

Common causes of neonatal seizures

1st day of life







Anoxia/hypoxia
Trauma
Intracranial hemorrhage
Drugs
Infection
Hypoglycemia/hyperglycemia
Pyridoxine deficiency
Seizures

2nd day of life










Sepsis
Trauma
Inborn errors of metabolism
Hypoglycemia
Hypocalcemia
Hyponatremia/hypernatremia
Hyperphosphatemia
Drug withdrawal
Congenital anomalies or developmental brain
disorders
Benign familial neonatal seizures
Seizures

Day 4 – 6 months of age









Hypocalcemia
Infection
Hyponatremia/hypernatremia
Drug withdrawal
Inborn errors of metabolism
Hyperphosphatemia
Congenital anomalies or developmental brain
disorders
Hypertension
Benign idiopathic neonatal seizures
Seizures

Management


Stabilization of ABC’s
Labs





Bedside glucose level
 Immediate correction of hypoglycemia
(<40mg/dL) with 2-4mL/Kg D10W may be
necessary
Serum electrolytes
CBC
Blood C&S
LFT’s
Seizures

Because 5-10% of neonatal seizures
are of infectious etiology, full sepsis
work-up should be performed when
patient is stable
Seizures

Management

Lorazepam



0.05-0.1mg/Kg slow IV
Repeat doses (2-3 times) based on clinical
response
Phenobarbital


Loading dose 20mg/Kg slow IV push over 1015 mins, additional 5mg/Kg doses up to
40mg/Kg
Maintenance of 3-4mg/Kg/day, 12-24 hours
after loading dose
Seizures

Phenytoin





Loading dose of 15-20mg/Kg IV over 30
minutes
Maintenance dose of 4-8mg/Kg IV slow push or
PO
Highly unstable in IV solutions
Avoid using in central lines because of risk of
precipitation
IM not an option- crystallizes in muscle
Seizures
Correct serum electrolyte
abnormalities
 More common


Hyponatremia (<125mg/Kg)


5-10mL/Kg IV 3% saline solution
Hypocalcemia (<7mg/dL)

100-300mg/Kg IV of calcium gluconate
Seizures
Immediately start broad-spectrum
antibiotics and acyclovir
 Neuroimaging once patient is
stabilized
 Admit to hospital for completion of
evaluation and monitoring

Conclusion

The mnemonic “THE MISFITS” is a
helpful tool that can be readily used
to formulate an approach to the most
common neonatal emergencies that
may present to general pediatricians
in their hospital or private offices as
well as ED clinicians in the ED
department