Neonatal Emergencies Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010.
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Transcript of Neonatal Emergencies Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010.
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Neonatal Neonatal EmergenciesEmergencies
Lazaro Lezcano, MDDirector, Division of Neonatology
August 31, 2010
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Neonatal EmergenciesNeonatal Emergencies Neonates are a group of patients that
often present anxiety-provoking diagnostic challenges
They often present with non-specific 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
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The Misfits MovieThe Misfits Movie
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Neonatal EmergenciesNeonatal Emergencies“THE MISFITS”
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
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TraumaTrauma(accidental & non-(accidental & non-
accidental)accidental) 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
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TraumaTrauma(accidental & non-(accidental & non-
accidental) 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 Consider neuroimaging in any non-
accidental injury for other skeletal injuries regardless of physical examination of the head
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TraumaTrauma(accidental & non-(accidental & non-
accidental) 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 Pediatrics 6/2003
CHOP74% No retinal hemorrhages
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TraumaTrauma(accidental & non-(accidental & non-
accidental) accidental) Management:
Evaluation and stabilization of the ABC’s Bedside glucose evaluation Appropriate temperature regulation If bruising or known intracranial bleed:
CBC Platelet count PT/PTT Neuroimaging after stabilization
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TraumaTrauma(accidental & non-(accidental & non-
accidental) accidental)
Admit the patient Report injury to appropriate state
department for abuse Skeletal survey Ophthalmologic exam
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease Cyanosis requires immediate
attention and evaluation
Differential diagnosis: Respiratory causes Infectious causes CNS abnormalities Toxins Cyanotic heart disease
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease
Terrible T’s: Transposition of the great arteries (TGA) Tetralogy of Fallot (TOF) Tricuspid atresia (TA) Total anomalous pulmonary venous
return (TAPVR) Truncus arteriosus (TA)
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease May not be detected in the WBN Adequately oxygenated blood PDA
systemic circulation PDA functionallyfunctionally closes in the first 10-
14 hrs of life Several factors can delay its closure
Prematurity Respiratory distress Acidosis Hypoxia
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease PDA is anatomicallyanatomically closed by 2
weeks of age, contributing to a delayed detection of cyanotic heart disease
100% FiO2: Non-cardiac disease
At least 10% increase in O2 saturation Cyanotic heart disease
Minimal change in O2 saturation
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease Hyperoxia test:
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
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic 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 notnot
exclude a cardiac defect CXR & EKG should be included in the
evaluation ECHO is diagnostic
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Heart Disease and Heart Disease and HypoxiaHypoxia
Cyanotic Heart DiseaseCyanotic Heart Disease Management:
PGE1 Bolus of 0.05 mcg/Kg IV Drip of 0.05-0.1 mcg/Kg/min
Secure airway Profound apnea is a non-dose dependent
complication of PGE1
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Hypoplastic Left Heart Hypoplastic Left Heart SyndromeSyndrome
25% of cardiac deaths during first week of life
Occurs in both cyanotic and acyanotic forms In 15% of cases the FO is intact
preventing mixing at the atrial level Infants with mixing at the atrial level are
acyanotic
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Hypoplastic Left Heart Hypoplastic Left Heart SyndromeSyndrome
PE: Pallor Tachypnea Poor perfusion Poor to absent peripheral pulses Loud single S2 Gallop rhythm w/o murmur Hepatomegaly Metabolic acidosis
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Hypoplastic Left Heart Hypoplastic Left Heart SyndromeSyndrome
EKG: Small or absent (L) ventricular forces
CXR: Moderate cardiomegaly Large PA shadow
ECHO: Small or slit-like (L) ventricle Hypoplastic ascending aorta
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Hypoplastic Left Heart Hypoplastic Left Heart SyndromeSyndrome
Treatment: PGE1- systemic blood flow is ductal
dependent Surgical correction
Surgical correction 1st stage
Norwood procedure 2nd stage
Fontan procedure Neonatal cardiac transplantation Compassionate care may be appropriate
in some instances
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Acyanotic Heart DiseaseAcyanotic Heart DiseaseCongestive Heart FailureCongestive Heart Failure
Typically presents with symptoms of CHF Tachypnea Tachycardia Hepatomegaly History of poor or slow feeding Sweating or color change with feeding Poor weight gain
More gradual clinical decompensation when compared with CCHD
May not present until after the first 2-3 weeks of age
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Acyanotic Heart Disease Acyanotic Heart Disease Congestive Heart FailureCongestive Heart Failure
Causes of CHF in Neonates: Acyanotic heart disease (VSD, ASD, PDA,
CoA) Severe anemia Trauma Sepsis SVT Metabolic abnormalities SLE Thyrotoxicosis
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Acyanotic Heart DiseaseAcyanotic Heart Disease Congestive Heart FailureCongestive Heart Failure
Initial management: Stabilization of the ABC’s CXR EKG Labs:
CBC BMP ABG
ECHO- diagnostic of heart defect Furosemide
1 mg/Kg IV
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Acyanotic Heart DiseaseAcyanotic Heart Disease Congestive Heart FailureCongestive Heart Failure Pressors:
Dopamine 5-15 mcg/Kg/min IV
Dobutamine 2.5-15 mcg/Kg/min IV
Careful with fluid overloading Peds. Cardiology consult
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Acyanotic Heart DiseaseAcyanotic Heart DiseaseSupraventricular Supraventricular
TachycardiaTachycardia SVT is the most common neonatal
dysrhythmia (1/25,000 births) Signs/symptoms:
Tachycardia Poor feeding Irritability Heart Failure Shock
Heart rate sustained at >220 bpm with a QRS < 0.08 seconds
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Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular
TachycardiaTachycardia
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Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular
TachycardiaTachycardia Management:
Stable patient: Vagal maneuvers
Ice to face avoiding the nares If unsuccessful:
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
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Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular
TachycardiaTachycardia Unstable patient w/o IV access:
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 Amiodorone
5mg/Kg IV over 30-60 mins.
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Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular
TachycardiaTachycardia Procainamide- alternative to amiodorone
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 Final option for a wide QRS and should only be
used in consultation with a pediatric cardiologist
1mg/Kg IV
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Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular
TachycardiaTachycardia 12-lead EKG prior to and after
conversion from SVT to NSR Useful diagnostic tool for the
cardiologists to help determine further management
Consult pediatric cardiologist for further evaluation
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HypoxiaHypoxiaBronchiolitisBronchiolitis
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 In NY from October-April
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HypoxiaHypoxia BronchiolitisBronchiolitis
Signs/Symptoms: Rhinorrhea Cough Congestion Wheezing Significant respiratory distress Apnea may be the only initial symptom
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HypoxiaHypoxia BronchiolitisBronchiolitis
Management: Infants with severe, prolonged apnea with
bradycardia unresponsive to O2 therapy may need intubation
Nebulized racemic epinephrine or
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
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HypoxiaHypoxia BronchiolitisBronchiolitis
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
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HypoxiaHypoxia Apnea/ALTE Apnea/ALTE
Apnea cessation of respiration for 20 secs. or
more, associated with color change (cyanosis or pallor) or bradycardia
ALTE 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”
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HypoxiaHypoxiaApnea/ALTEApnea/ALTE
Management depends on history provided by observers and PE
Hospitalization for observation and monitoring
Common differential diagnosis: Sepsis Pneumonia RSV Hypothermia Anemia
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HypoxiaHypoxia Apnea/ALTEApnea/ALTE
Botulism Dysrhythmias Acid/base disturbances Intracranial hemorrhage Meningitis/encephalitis Pertussis Hypoglycemia Seizures GER Child abuse Inborn errors of metabolism Electrolyte abnormalities
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Endocrine EmergenciesEndocrine EmergenciesCongenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia
Most patients diagnosed by newborn screening
Occasionally diagnosis is missed because of inadequate blood sample, laboratory error, or inability to contact the family
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia Autosomal recessive Most common is 21-hydroxylase
deficiency- 95% of affected patients Inadequate cortisol levels Excessive ACTH stimulation Adrenal hyperplasia Excessive production of adrenal
androgens and testosterone virilization
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia Two forms
Virilizing form Relative aldosterone deficiency Mild salt loss Adrenal insufficiency tends not to occur unless
under stressful situations Salt-losing form
Absolute aldosterone deficiency Adrenal insufficiency under basal conditions Manifests in the neonatal period or soon after
as an adrenal crisis
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia 11- hydroxylase deficiency
Less common- 5-8% of cases Salt retention Volume expansion Hypertension
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia Management:
Labs: Blood glucose
Hypoglycemia Serum electrolytes
Hyponatremia Hyperkalemia
Hypotension unresponsive to fluids or inotropes heightens suspicion of CAH
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia Hydrocortisone
25-50mg/m2 IV Treat hypoglycemia Hyperkalemia usually responds to fluid
therapy If patient is symptomatic or with EKG
changes Calcium chloride NaHCO3 Insulin and glucose Polystyrene sulfonate (Kayexalate)
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Endocrine EmergenciesEndocrine Emergencies Congenital Adrenal Congenital Adrenal
HyperplasiaHyperplasia
Pediatric critical care management
Endocrinology consultation
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Endocrine EmergenciesEndocrine EmergenciesThyrotoxicosisThyrotoxicosis
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 Occurs in ~1/70 thyrotoxic pregnancies Incidence of maternal thyrotoxicosis in
pregnancy is 1-2/1000 pregnancies
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Endocrine EmergenciesEndocrine Emergencies ThyrotoxicosisThyrotoxicosis
Clinical presentation 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
Irritability Tachycardia Flushing Tremor Poor weight gain Trombocytopenia Arrhythmias
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Endocrine EmergenciesEndocrine Emergencies ThyrotoxicosisThyrotoxicosis
Initial diagnosis difficult w/o clear history of Graves’ disease from mother
Goiter usually present tracheal compression
Labs Increased T4, FT4 & T3 Suppressed levels of TSH
Treatment Mild
Close observation
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Endocrine EmergenciesEndocrine Emergencies ThyrotoxicosisThyrotoxicosis
Moderate Lugol’s solution (iodine)
1 drop PO Q8H Propylthiouracil
5-10mg/Kg/day in 3 divided doses Methimazole
0.5-1mg/Kg/day in 3 divided doses Severe
In addition to above meds Prednisone
2mg/Kg/day Propanolol – for tachycardia
1-2mg/Kg/day in 2-4 divided doses Digitalis may be used to prevent cardiovascular
collapse
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Inborn Errors of Inborn Errors of MetabolismMetabolism
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Urea cycle defects 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
HYPERAMMONEMMIA (-) ACIDOSIS
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Amino acid metabolism defects MSUD Nonketotic hyperglycinemia Hereditary tyrosinemia Pyroglutamic acidemia (5-oxoprolinuria) Hyperornithinemia-hyperammonemia-
homocitrulinemia syndrome Lysinuric protein intolerance Methylene tetrahydrofolate reductase deficiency Sulfite oxidase deficiency
(-) HYPERAMMONEMIA (-) ACIDOSIS
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Organic Acidemias 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
HYPERAMMONEMMIA ACIDOSIS INCREASED URINE KETONES
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Carbohydrate metabolism defects Galactosemia Fructose-1,6-biphosphatase deficiency Glycogen storage diseases (types IA. IB,
II, III and IV) Hereditary fructose intolerance
HYPERAMMONEMIA ACIDOSIS INCREASED URINE KETONES
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Fatty acid oxidation defects Short chain acyl-CoA dehydrogenase deficiency
(SCAD) Medium chain acyl-CoA dehydrogenase deficiency
(MCAD) Most common (incidence of 1/6,000-10,000)
Long chain acyl-CoA dehydrogenase deficiency (LCAD)
Acyl-CoA deficiency HYPERAMMONEMIA ACIDOSIS DECREASED URINE KETONES
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Metabolic EmergenciesMetabolic 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 Inborn Errors of MetabolismMetabolism
Metabolic EmergenciesMetabolic Emergencies
Nonspecific symptoms Poor feeding Vomiting FTT Tachycardia Tachypnea Irritability
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Metabolic EmergenciesMetabolic Emergencies
More apparent symptoms Seizures Lethargy Hypoglycemia Apnea Temperature instability Acidosis
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Metabolic EmergenciesMetabolic Emergencies Labs
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
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Inborn Errors of Inborn Errors of MetabolismMetabolism
Metabolic EmergenciesMetabolic Emergencies Management
Fluid resuscitation IV dextrose to prevent further catabolism Admission to hospital Genetics consultation
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SepsisSepsis
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)>100.4 F (38 C)
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SepsisSepsis Symptoms that should prompt the
consideration of a full sepsis evaluation Poor feeding Irritability Apnea Hypothermia Jaundice Rashes Increased sleeping Vomiting
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SepsisSepsis 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
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SepsisSepsis 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
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SepsisSepsis
The urinalysis may be unremarkable in infants with a culture (+) UTI
Approximately 14% of febrile neonates will be diagnosed with a UTI
Pediatrics 2000McKay Memorial Hospital in TaiwanCRP, ESR and U/A imperfect tools in discriminating for UTI
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SepsisSepsis Treatment
Broad spectrum antibiotics Ampicillin
50-100mg/Kg IV Gentamicin
2mg/Kg IV or Cefotaxime
50-100mg/Kg IV Acyclovir
20mg/Kg IV
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SepsisSepsis Neonatal herpes
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
High fever CSF lymphocytosis Numerous RBC’s in an atraumatic spinal tap Seizures Known maternal history of HSV infection
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SepsisSepsis CSF analysis
Herpes PCR Herpes culture
Elevated LFT’s Chest x-rays
Pneumonitis
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Formula MishapsFormula Mishaps Inappropriate mixing of water and
powder formula Overdilution of concentrated liquid or
premixed formula Life-threatening electrolyte disturbances
or FTT Hyponatremia
Seizures
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Intestinal CatastrophesIntestinal Catastrophes Consider pathologic process if vomiting
in newborn period Difficult to differentiate between a life-
threatening cause from a mild viral gastroenteritis or even severe gatroesophageal reflux
Initial symptoms may be nonspecific Bilious emesis is almost always an
ominous sign Initiate pediatric surgery consultation
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Intestinal CatastrophesIntestinal CatastrophesMalrotation with Midgut Malrotation with Midgut
VolvulusVolvulus
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 CatastrophesIntestinal Catastrophes Malrotation with Midgut Malrotation with Midgut
VolvulusVolvulus Symptoms
Bilious emesis Poor feeding Lethargy Shock in more advanced presentations
Management Fluid resuscitation NGT placement Pediatric surgical consultation
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Intestinal CatastrophesIntestinal Catastrophes Malrotation with Midgut Malrotation with Midgut
VolvulusVolvulus KUB’s
Normal Signs of small bowel obstruction
Upper GI series is the gold standard for diagnosis Transverse portion of the duodenum
leading to a fixed ligament of Treitz
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Intestinal CatastrophesIntestinal CatastrophesToxic MegacolonToxic 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 CatastrophesIntestinal Catastrophes Toxic MegacolonToxic Megacolon
Symptoms Poor feeding Vomiting Irritability Abdominal distention Hematochezia Shock as it progresses to enterocolitis
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Intestinal CatastrophesIntestinal Catastrophes Toxic MegacolonToxic Megacolon
Management Stabilization of ABC’s Fluid resuscitation Broad-spectrum antibiotics KUB
Enlarged or dilated section of colon Surgical consultation Pediatric critical care management in the
presence of enterocolitis
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Intestinal CatastrophesIntestinal CatastrophesNecrotizing EnterocolitisNecrotizing 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
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Intestinal CatastrophesIntestinal Catastrophes Necrotizing EnterocolitisNecrotizing Enterocolitis
Management Stabilization of ABC’s Fluid resuscitation NGT placement Broad-spectrum antibiotics Pediatric surgical consultation Critical care management
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Intestinal CatastrophesIntestinal CatastrophesHypertrophic Pyloric Hypertrophic Pyloric
StenosisStenosis 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
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Intestinal CatastrophesIntestinal CatastrophesHypertrophic Pyloric Hypertrophic Pyloric
StenosisStenosis 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”
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Intestinal CatastrophesIntestinal Catastrophes Hypertrophic Pyloric Hypertrophic Pyloric
StenosisStenosis 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
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ToxinsToxins 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
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ToxinsToxins Star anise tea
Relief of infantile colic Neurotoxicity Unexplained irritability Vomiting Seizures
Baking soda Used for intestinal gas Serious toxicity
Hospitalization for monitoring and observation
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SeizuresSeizures 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
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SeizuresSeizures
Common causes of neonatal seizures 1st day of life
Anoxia/hypoxia Trauma Intracranial hemorrhage Drugs Infection Hypoglycemia/hyperglycemia Pyridoxine deficiency
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SeizuresSeizures 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
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SeizuresSeizures 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
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SeizuresSeizures 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
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SeizuresSeizures
Because 5-10% of neonatal seizures are of infectious etiology, full sepsis work-up should be performed when patient is stable
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SeizuresSeizures 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 10-15 mins, additional 5mg/Kg doses up to 40mg/Kg
Maintenance of 3-4mg/Kg/dayday, 12-24 hours after loading dose
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SeizuresSeizures
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
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SeizuresSeizures
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
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SeizuresSeizures
Immediately start broad-spectrum antibiotics and acyclovir
Neuroimaging once patient is stabilized
Admit to hospital for completion of evaluation and monitoring
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ConclusionConclusion The mnemonic “THE MISFITS” “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