Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010

Name: Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010
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Description: Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010

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

Neonatal 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 Movie

Neonatal 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

Trauma (accidental & non-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

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

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 CHOP 74%  No retinal hemorrhages

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

Admit the patient Report injury to appropriate state department for abuse Skeletal survey Ophthalmologic exam

Heart Disease and Hypoxia Cyanotic Heart Disease
Cyanosis requires immediate attention and evaluation Differential diagnosis: Respiratory causes Infectious causes CNS abnormalities Toxins Cyanotic 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)

May not be detected in the WBN Adequately oxygenated blood  PDA  systemic circulation PDA functionally closes in the first hrs of life Several factors can delay its closure Prematurity Respiratory distress Acidosis Hypoxia

PDA is anatomically 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

Hyperoxia test: Initial ABG on R/A Repeat ABG after 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

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

Management: PGE1 Bolus of 0.05 mcg/Kg IV Drip of mcg/Kg/min Secure airway 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 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 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
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

Causes of CHF in Neonates: Acyanotic heart disease (VSD, ASD, PDA, CoA) Severe anemia Trauma Sepsis SVT Metabolic abnormalities SLE Thyrotoxicosis

Initial management: Stabilization of the ABC’s CXR EKG Labs: CBC BMP ABG ECHO- diagnostic of heart defect Furosemide 1 mg/Kg IV

Pressors: Dopamine 5-15 mcg/Kg/min IV Dobutamine 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: Tachycardia Poor feeding Irritability Heart Failure Shock Heart rate sustained at >220 bpm with a QRS < 0.08 seconds

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

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 mins.

Procainamide- alternative to amiodorone 15 mg/Kg IV over 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

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

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 In NY from October-April

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

Hypoxia Apnea/ALTE Apnea ALTE
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”

Hypoxia Apnea/ALTE Management depends on history provided by observers and PE Hospitalization for observation and monitoring Common differential diagnosis: Sepsis Pneumonia RSV Hypothermia Anemia

Hypoxia Apnea/ALTE 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
Most patients diagnosed by newborn screening Occasionally diagnosis is missed because of inadequate blood sample, laboratory error, or inability to contact the family

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

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

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

Management: Labs: Blood glucose Hypoglycemia Serum electrolytes Hyponatremia Hyperkalemia Hypotension unresponsive to fluids or inotropes heightens suspicion of CAH

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)

Pediatric critical care management 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 Occurs in ~1/70 thyrotoxic pregnancies Incidence of maternal thyrotoxicosis in pregnancy is 1-2/1000 pregnancies

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 Metabolism

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

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

Nonspecific symptoms Poor feeding Vomiting FTT Tachycardia Tachypnea Irritability

More apparent symptoms Seizures Lethargy Hypoglycemia Apnea Temperature instability Acidosis

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

Management 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 Symptoms that should prompt the consideration of a full sepsis evaluation Poor feeding Irritability Apnea Hypothermia Jaundice Rashes Increased sleeping Vomiting

Sepsis 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 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 Published in 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 Treatment Broad spectrum antibiotics Ampicillin 50-100mg/Kg IV
Gentamicin 2mg/Kg IV or Cefotaxime Acyclovir 20mg/Kg IV

Sepsis 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

Sepsis CSF analysis Elevated LFT’s Chest x-rays Herpes PCR
Herpes culture Elevated LFT’s Chest x-rays Pneumonitis

Formula Mishaps Inappropriate mixing of water and powder formula
Overdilution of concentrated liquid or premixed formula Life-threatening electrolyte disturbances or FTT Hyponatremia Seizures

Intestinal 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 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

Symptoms Bilious emesis Poor feeding Lethargy Shock in more advanced presentations Management Fluid resuscitation NGT placement Pediatric surgical consultation

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 KUB may be normal

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

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

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 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

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”

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 Baking soda 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 Phenobarbital 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 mins, additional 5mg/Kg doses up to 40mg/Kg Maintenance of 3-4mg/Kg/day, 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) mg/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

Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010

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Lazaro Lezcano, MD Director, Division of Neonatology August 31, 2010

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