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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” 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 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 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 Pediatrics 6/2003 CHOP 74% No retinal hemorrhages Trauma (accidental & non-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 Trauma (accidental & non-accidental) 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 Heart Disease and Hypoxia 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) 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 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: Non-cardiac disease At least 10% increase in O2 saturation Cyanotic heart disease Minimal change in O2 saturation Heart Disease and Hypoxia Cyanotic 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 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 Heart Disease and Hypoxia Cyanotic 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 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 Hypoplastic Left Heart Syndrome PE: Pallor Tachypnea Poor perfusion Poor to absent peripheral pulses Loud single S2 Gallop rhythm w/o murmur Hepatomegaly Metabolic acidosis Hypoplastic Left Heart Syndrome EKG: CXR: Small or absent (L) ventricular forces Moderate cardiomegaly Large PA shadow ECHO: Small or slit-like (L) ventricle Hypoplastic ascending aorta Hypoplastic Left Heart Syndrome 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 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 May not present until after the first 2-3 weeks of age Acyanotic Heart Disease Congestive 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 Disease Congestive 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 Disease Congestive 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 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 Acyanotic Heart Disease Supraventricular Tachycardia Acyanotic Heart Disease Supraventricular Tachycardia 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 Acyanotic Heart Disease Supraventricular Tachycardia 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. Acyanotic Heart Disease Supraventricular Tachycardia 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 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 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 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 In NY from October-April Heart Disease and Hypoxia Bronchiolitis Signs/Symptoms: Rhinorrhea Cough Congestion Wheezing Significant respiratory distress Apnea may be the only initial symptom Heart Disease and Hypoxia Bronchiolitis 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 Heart Disease and Hypoxia Bronchiolitis 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 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” Heart Disease and 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 Heart Disease and 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 Endocrine Emergencies Congenital Adrenal Hyperplasia 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 Endocrine Emergencies Congenital Adrenal Hyperplasia 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 Endocrine Emergencies Congenital Adrenal Hyperplasia 11- hydroxylase deficiency Less common- 5-8% of cases Salt retention Volume expansion Hypertension Endocrine Emergencies Congenital Adrenal Hyperplasia Management: Labs: Blood glucose Hypoglycemia Serum electrolytes Hyponatremia Hyperkalemia Hypotension unresponsive to fluids or inotropes heightens suspicion of CAH Endocrine Emergencies Congenital Adrenal Hyperplasia 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) Endocrine Emergencies Congenital Adrenal Hyperplasia 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 Endocrine Emergencies Thyrotoxicosis 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 Endocrine Emergencies Thyrotoxicosis 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 Endocrine Emergencies Thyrotoxicosis Moderate Lugol’s solution (iodine) Propylthiouracil 5-10mg/Kg/day in 3 divided doses Methimazole 1 drop PO Q8H 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 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 Inborn Errors of Metabolism Amino acid metabolism defects 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 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 Inborn Errors of Metabolism Carbohydrate metabolism defects Galactosemia Fructose-1,6-biphosphatase deficiency Glycogen storage diseases (types IA. IB, II, III and IV) Hereditary fructose intolerance Inborn Errors of Metabolism 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 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 Inborn Errors of Metabolism Metabolic Emergencies Nonspecific symptoms Poor feeding Vomiting FTT Tachycardia Tachypnea Irritability Inborn Errors of Metabolism Metabolic Emergencies More apparent symptoms Seizures Lethargy Hypoglycemia Apnea Temperature instability Acidosis Inborn Errors of Metabolism Metabolic 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 Inborn Errors of Metabolism Metabolic Emergencies 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 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 50-100mg/Kg IV 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 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 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 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 Intestinal Catastrophes Malrotation with Midgut Volvulus Symptoms Bilious emesis Poor feeding Lethargy Shock in more advanced presentations Management Fluid resuscitation NGT placement Pediatric surgical consultation Intestinal Catastrophes Malrotation with Midgut Volvulus 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 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 Intestinal Catastrophes Toxic Megacolon Symptoms Poor feeding Vomiting Irritability Abdominal distention Hematochezia Shock as it progresses to enterocolitis Intestinal Catastrophes Toxic 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 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
