Neonatal Emergencies Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010.

Neonatal Neonatal EmergenciesEmergencies

Lazaro Lezcano, MDDirector, Division of Neonatology

August 31, 2010

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

The Misfits MovieThe Misfits Movie

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

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


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


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


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


accidental) accidental)

Admit the patient Report injury to appropriate state

department for abuse Skeletal survey Ophthalmologic exam

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


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)


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


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


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


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


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

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


PE: Pallor Tachypnea Poor perfusion Poor to absent peripheral pulses Loud single S2 Gallop rhythm w/o murmur Hepatomegaly Metabolic acidosis


EKG: Small or absent (L) ventricular forces

CXR: Moderate cardiomegaly Large PA shadow

ECHO: Small or slit-like (L) ventricle Hypoplastic ascending aorta


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

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

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

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

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

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

Acyanotic Heart DiseaseAcyanotic Heart Disease Supraventricular Supraventricular

TachycardiaTachycardia


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


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.


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


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

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

HypoxiaHypoxia BronchiolitisBronchiolitis

Signs/Symptoms: Rhinorrhea Cough Congestion Wheezing Significant respiratory distress Apnea may be the only initial symptom


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


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

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”

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

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

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

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


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


HyperplasiaHyperplasia 11- hydroxylase deficiency

Less common- 5-8% of cases Salt retention Volume expansion Hypertension


HyperplasiaHyperplasia Management:

Labs: Blood glucose

Hypoglycemia Serum electrolytes

Hyponatremia Hyperkalemia

Hypotension unresponsive to fluids or inotropes heightens suspicion of CAH


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)


HyperplasiaHyperplasia

Pediatric critical care management

Endocrinology consultation

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

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


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


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

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


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


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


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


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


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


Metabolic EmergenciesMetabolic Emergencies

Nonspecific symptoms Poor feeding Vomiting FTT Tachycardia Tachypnea Irritability


Metabolic EmergenciesMetabolic Emergencies

More apparent symptoms Seizures Lethargy Hypoglycemia Apnea Temperature instability Acidosis


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


Metabolic EmergenciesMetabolic Emergencies Management

Fluid resuscitation IV dextrose to prevent further catabolism Admission to hospital Genetics consultation

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)

SepsisSepsis Symptoms that should prompt the

consideration of a full sepsis evaluation Poor feeding Irritability Apnea Hypothermia Jaundice Rashes Increased sleeping Vomiting

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

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

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

SepsisSepsis Treatment

Broad spectrum antibiotics Ampicillin

50-100mg/Kg IV Gentamicin

2mg/Kg IV or Cefotaxime

50-100mg/Kg IV Acyclovir

20mg/Kg IV

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

SepsisSepsis CSF analysis

Herpes PCR Herpes culture

Elevated LFT’s Chest x-rays

Pneumonitis

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

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

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

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

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

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

Intestinal CatastrophesIntestinal Catastrophes Toxic MegacolonToxic Megacolon

Symptoms Poor feeding Vomiting Irritability Abdominal distention Hematochezia Shock as it progresses to enterocolitis

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

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

Intestinal CatastrophesIntestinal Catastrophes Necrotizing EnterocolitisNecrotizing Enterocolitis

Management Stabilization of ABC’s Fluid resuscitation NGT placement Broad-spectrum antibiotics Pediatric surgical consultation Critical care management

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

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”

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

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

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

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

SeizuresSeizures

Common causes of neonatal seizures 1st day of life

Anoxia/hypoxia Trauma Intracranial hemorrhage Drugs Infection Hypoglycemia/hyperglycemia Pyridoxine deficiency

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

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

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

SeizuresSeizures

Because 5-10% of neonatal seizures are of infectious etiology, full sepsis work-up should be performed when patient is stable

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

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

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

SeizuresSeizures

Immediately start broad-spectrum antibiotics and acyclovir

Neuroimaging once patient is stabilized

Admit to hospital for completion of evaluation and monitoring

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

Neonatal Emergencies Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010.

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