3/27/2013
Disclosures
PROBLEMS of THE NEONATAL PERIOD ∗ “I have nothing to disclose” (financially) Susan Fisher-Owens, MD, MPH ∗ …except appreciation to Colin Partridge, MD, MPH Associate Clinical Professor of Clinical Pediatrics Associate Clinical Professor of Preventive and Restorative Dental Sciences for help with slides University of California, San Francisco San Francisco General Hospital
UCSF Family Medicine Board Review: Improving Clinical Care Across the Lifespan San Francisco March 27, 2013
Common Neonatal Problems Hypoglycemia Causes
∗ ∗ Hypoglycemia Inadequate glycogenolysis ∗ ∗ Respiratory conditions cold stress, asphyxia ∗ ∗ Infections Inadequate glycogen stores ∗ ∗ Polycythemia prematurity, postdates, intrauterine growth restriction, small for gestational age (SGA) ∗ Bilirubin metabolism: neonatal jaundice ∗ Increased glucose consumption ∗ Bowel obstruction ∗ asphyxia, sepsis ∗ Birth injuries ∗ ∗ Hyperinsulinism Rashes ∗ Infant of Diabetic Mother (IDM) ∗ Murmurs ∗ Feeding difficulties
1 3/27/2013
Hypoglycemia Treatment Respiratory Distress in the Neonate
∗ ∗ Early feeding when possible (breastfeeding, formula, Pulmonary causes ∗ oral glucose) Respiratory Distress Syndrome: surfactant deficiency ∗ ∗ Depending on severity of hypoglycemia and clinical Transient Tachypnea of the Newborn: retained fetal lung findings, may need to need to give intravenous glucose fluid bolus (D10 @ 2-3 ml/kg) ∗ Meconium Aspiration Syndrome ∗ Following bolus infusion, a continuous intravenous ∗ Congenital pneumonia infusion of D10 is often required to maintain normal ∗ Persistent pulmonary hypertension glucose levels ∗ Space occupying lesions: pneumothorax, chylothorax, pleural effusion, congenital diaphragmatic hernia, CCAM
Respiratory Distress Syndrome (RDS) Strategies for Prevention of RDS
∗ Surfactant insufficiency and ∗ Prevention of premature delivery pulmonary immaturity ∗ ∗ Decrease antenatal inflammation/infection 33% in infants between 28-34 wks ∗ ∗ <5% in infants > 34 wks Increased risk for preterm labor ∗ Incidence increased ∗ ∗ Antenatal glucocorticoids male infants ∗ ∗ ↑ Does not prevent all RDS or bronchopulmonary dysplasia 6-fold in infants of diabetic mom (IDM) ∗ ∗ multiple births, second-born twin No increased risk to mother of death, chorioamnionitis, or ∗ Severity of illness improved puerperal sepsis by antenatal steroids & surfactant
2 3/27/2013
Meconium Aspiration Syndrome RDS X-ray Findings
∗ Incidence of meconium staining Hypoexpanded lungs ∗ associated with fetal distress and increasing gestational age ∗ Reticulogranular opacification 20% of all deliveries ∗ 30% in infants > 42 weeks http://newborns.stanford.edu/PhotoGallery/MecStaining1.html ∗ Air bronchograms Hypoxia, acidosis lead to fetal gasping ( aspiration) ∗ Meconium Aspiration Syndrome (MAS) found in 2-20% of white-out lungs infants with meconium-stained fluid ∗ Most common cause of respiratory distress in term newborns, typically presenting in first few hours of life ∗ Disease range: mild to severe disease with air leaks, pulmonary hypertension, respiratory failure, and death (iNO, HFOV, and ECMO improve survival)
Meconium Aspiration Syndrome Complications of MAS
Air leaks pneumomediastinum pnemothorax pneumopericardium
Patchy, streaky infiltrates Hyperexpansion
pneumomediastinum pneumothorax
3 3/27/2013
Transient Tachypnea of Newborn (TTN) TTN X-ray Findings
Slightly hyperexpanded lungs ∗ Delayed clearance of fetal lung fluid “Sunburst” hilar streaks ∗ Term or near-term infants ∗ Delivered via c-section and/or no/little labor Fluid in minor fissure ∗ Chest Xrays: lung hyperaeration, prominent pulmonary Prominent pulmonary vascular markings vascular markings, interstitial fluid, pleural effusion CXR normalizes in 1st 24 hrs ∗ Transient respiratory symptoms (tachypnea, occasional hypoxia, rare dyspnea) resolve within 2-5 days
Extra-Pulmonary Causes of Respiratory Radiologic Finding Distress in the Neonate
∗ Hyperthermia, hypothermia ∗ Polycythemia ∗ Hypovolemia, shock, metabolic acidosis ∗ Cardiac disease ∗ Cyanotic congenital heart disease ∗ Left-sided obstructive lesions (coarctation) ∗ Congestive heart failure ∗ Myocardopathy ∗ Myocarditis ∗ Sepsis
http://www.medicine.cmu.ac.th/dept/radiology/pedrad/normal.html
4 3/27/2013
Perinatal Infections Risk Factors for Early-Onset Sepsis
∗ ∗ Bacterial infections TORCH infections: ∗ Prematurity < 37 weeks gestation ∗ Group B Streptococcus Incidence is 0.5-2.5%; ∗ ∗ many infants are Chorioamnionitis E. coli ∗ ∗ Listeria monocytogenes asymptomatic at delivery Prolonged ruptured membranes > 24 hours ∗ Toxoplasma gondii, ∗ ∗ Viral infections GBS positive mother ∗ treponema pallidum Herpes simplex ∗ ∗ Male infant ∗ “Other”: syphilis Hepatitis B and C ∗ Rubella ∗ Cytomegalovirus (most common) ∗ Herpes
Neonatal Group B Streptococcus Management of Neonatal Infections
∗ Septic work-up for infection Prevention of GBS neonatal sepsis ∗ CBC with differential including bands and platelets ∗ Routine antenatal cultures at 35-36 weeks ∗ Blood culture ∗ ∗ Treat women +/- C-reactive Protein ∗ ∗ +/- Lumbar Puncture with positive cultures with onset of labor ∗ ∗ Specific workup for viral infection with previously infected infants ∗ Treatment ∗ with GBS UTI ∗ Symptomatic: treat with ampicillin and gentamycin (or ampicillin and 2nd/3rd generation cephalosporin for bacterial meningitis). Acyclovir if concerned for herpes. Strategy misses women who deliver prematurely and ∗ Length of treatment depends on clinical findings, CBC, LP, and culture women with no prenatal care results. ∗ Asymptomatic infant at risk (e.g., a non-reassuring CBC): treat for 48 (-72 hrs) until bacterial cultures negative
5 3/27/2013
Prevention of Transmission of Perinatal Hepatitis C Perinatal Hepatitis B
∗ High-risk mothers screened during pregnancy Hepatitis B vaccine prior to hospital discharge for all ∗ Vertical transmission rate is 5-10% infants (<12 hr if Mom HBsAg positive) ∗ ∗ Hepatitis C antibody titers obtained on infant at 6 and 12 HBIG (hepatitis B immunoglobulin) plus vaccine for infants months (even 18 months), or Hepatitis C PCR at 4 mos born to HBsAg positive mother <12 hours of life ∗ All infants should receive routine Hepatitis B vaccine What about breastfeeding with Hepatitis C+ mother? during infancy (1 month and 6 months) ∗ Variable amounts of virus in milk ∗ Breastfeeding safe with HBsAg positive mother with ∗ Studies have not shown increase risk of transmission of vaccine plus HBIG treatment for the infant Hepatitis C with breastfeeding ∗ Recommend pump/dump if cracked/bleeding nipples
Perinatal TORCH Infections— Perinatal TORCH Infections— Non-Specific Findings More Specific Findings
∗ SGA, IUGR, postnatal growth failure ∗ Toxoplasmosis: hydrocephalus, chorioretinitis, ∗ Microcephaly, hydrocephalus, intracranial calcifications generalized intracranial calcifications (random ∗ Hepatosplenomegaly, hepatitis, jaundice (elevated direct component) distribution) ∗ ∗ Anemia (hemolytic), thrombocytopenia Syphilis: osteochondritis, periosteal new bone formation, ∗ Skin rashes, petechiae rash, snuffles ∗ Abnormalities of long bones ∗ Rubella: cataracts, “blueberry muffin” rash, patent ductus ∗ Chorioretinitis, cataracts, glaucoma arteriosus, pulmonary stenosis, deafness ∗ Nonimmune hydrops ∗ Cytomegalovirus: microcephaly, periventricular ∗ Developmental and learning disabilities calcifications, hydrocephalus, chorioretinitis, petechiae, thrombocytopenia, hearing loss (progressive)
6 3/27/2013
“Blueberry muffin” rash (cutaneous hematopoeisis) Ocular Findings
chorioretinitis
cataracts
Neonatal Herpes Simplex Herpes Simplex: Clinical Presentations
∗ HSV-1 (15 to 20%) and HSV-2 (80 to 85%) ∗ Disseminated (systemic) disease: ∗ st Neonatal infections with primary HSV is 35-50% ∗ Early onset (1 week of life), 25% of cases ∗ ∗ Neonatal infections with recurrent HSV is 0-5% Sepsis syndrome, liver dysfunction, pneumonia ∗ ∗ Increased risk of transmission with prolonged rupture of CNS disease: meningoencephalitis nd rd membranes, forceps or vacuum delivery, fetal scalp ∗ 2 -3 week of life, 35% of cases monitoring, preterm infants ∗ Fever, irritability, abnormal CSF, seizures ∗ 75% of cases have no history of maternal infection, nor ∗ Early treatment improves outcome, but 40-50% infants have evidence of skin lesions residual neurodevelopmental disability ∗ One may need to start treatment based on clinical presentation ∗ Localized disease: skin, eyes, mouth, 40% of cases and suspicion of infection
7 3/27/2013
Cutaneous HSV: clustered vesicular eruption ulceration Diagnosis of TORCH Infections
∗ Toxoplasmosis ∗ maternal antibody titer and neonatal IGM antibody ∗ Syphilis ∗ RPR or VDRL positive, obtain titers, order treponemal-specific test (FTA or MHA-TP) ∗ CMV ∗ urine culture ∗ Herpes simplex ∗ Surveillance: conjunctival, nasopharyngeal, and rectal swabs for Direct Fluorescent Antibody (DFA) 24-48 hours after birth if suspect exposure ∗ Culture of vesicle scrapings when lesions are present ∗ DFA of vesicle scrapings ∗ PCR: detect HSV-DNA in CSF
Polycythemia Polycythemia--Treatment
∗ Hematocrit > 65% on a spun, central venous blood sample ∗ ∗ Complications associated with hyperviscosity If symptomatic neonate with polycythemia, or an infant with ∗ Plethora, slow capillary fill time excessively high hematocrit (> 70%)--by dilutional exchange, ∗ Respiratory distress correcting Hct to approx 55% obs desired ∗ Hypoglycemia Volume of blood = Wt (kg) X 80 cc/kg X (Hct – Hct ) ∗ Hct obs Irritability, lethargy, poor feeding ∗ ∗ Cyanosis, heart murmur, and cardiomegaly Blood is removed through umbilical artery or umbilical ∗ Seizures and strokes venous catheter and normal saline is infused for blood ∗ Necrotizing enterocolitis volume replacement ∗ Renal vein thrombosis ∗ Hyperbilirubinemia
8 3/27/2013
Increased RBC Mass Hyperbilirubinemia
∗ Elevated hemoglobin level, RBC mass ∗ ∗ Types Polycythemia ∗ Physiologic vs Pathologic ∗ Increased rate of RBC degradation with shorter half-life of ∗ Conjugated/Direct vs Unconjugated/Indirect RBC ∗ Causes ∗ 70 days in preterm infants, 70-90 days in term infants, 120 days in ∗ Increased red cell mass adults ∗ ∗ Increased red cell breakdown Extravasated blood: cephalohematoma, caput/bruises, ∗ Delayed/abnormal conjugation swallowed blood, intracranial or intra-abdominal ∗ Abnormal excretion hemorrhage ∗ Increased enterohepatic circulation ∗ Effects of plasma albumin-bilirubin binding ∗ Newborns have lower albumin levels lower bilirubin-binding capacity
Increased Breakdown/Hemolysis Increased Bilirubin Impaired Conjugation
∗ ∗ Neonatal hepatitis Incompatibility: Rh, ABO, minor blood groups ∗ Sepsis (Kell, Duffy) ∗ Prematurity ∗ Enzyme defects: G6PD, pyruvate kinase ∗ Breast milk jaundice ∗ ∗ Sepsis Hypothyroidism ∗ ∗ Sepsis RBC membrane defects: hereditary ∗ Congenital enzyme deficiency eg Crigler-Najjar spherocytosis ∗ ∗ Metabolic diseases, e.g., galactosemia Extravascular blood
9 3/27/2013
Conjugated (Direct) Hyperbilirubinemia: Enterohepatic Circulation Impaired Excretion
∗ Obstruction to biliary flow: biliary atresia, ∗ Conjugated bilirubin is unconjugated and reabsorbed choledocal cyst, cystic fibrosis, stones ∗ ∗ Enterohepatic circulation and reabsorption is Dark urine (urine + for bilirubin), light colored enhanced by: stools, persistent jaundice (> 3weeks) ∗ Gut sterility (urobilinogen and stercobilinogen) ∗ ∗ Hepatic cell injury : syphilis, TORCH infections Bowel dysmotility (preterm infants, effects of magnesium or ∗ morphine) Hepatic dysfunction: E. coli (UTI) ∗ ∗ Ileus Toxic effects: hyperalimentation cholestasis ∗ Obstruction: atresia, pyloric stenosis, meconium plugs, cystic ∗ fibrosis Metabolic errors: galactosemia ∗ ∗ Delayed feeding (“breast-feeding jaundice”) Chronic “overload”: erythroblastosis fetalis, G6PD, spherocytosis
Causes Suggested by Clinical Findings Management of Indirect Hyperbilirubinemia
∗ Hemolysis ∗ st Increased susceptibility to neurotoxicity seen with ∗ Onset of jaundice in 1 24 hours ∗ asphyxia, sepsis, acidosis, prematurity, and hemolysis Rapid rate of rise of bili (>0.5mg/dL per hour) ∗ ∗ Consider treatment at lower levels of unconjugated bilirubin Hepatosplenomegaly, pallor in these cases ∗ Family history (G6PD, spherocytosis) ∗ When to worry ∗ “Set-up” with incompatibility, Coombs (+DAT), elevated ∗ Visible jaundice in the first 24 hours of life reticulocytes, abnormal hemolytic smear ∗ Serum bilirubin rising rapidly > 5 mg/dl/24 hrs ∗ Prolonged hyperbilirubinemia > 1 week term infant and > 2 ∗ weeks in the preterm Sepsis or inborn error ∗ ∗ Emesis, lethargy, poor feeding Direct bilirubin > 2mg/dl ∗ Hepatosplenomegaly, tachypnea, temperature instability
10 3/27/2013
Treatment Guidelines (AAP Nomograms) Clinical Presentations of Bowel Obstruction in the Neonate
∗ Decision to treat depends on clinical risk status (well vs ill ∗ infant), unconjugated bilirubin Emesis: Bilious emesis suggests a lesion distal to ampulla of level, chronologic age (hours Vater; sporadic emesis suggests partial obstruction, of life), and gestational age malrotation, duplications, or annular pancreas ∗ ∗ More conservative treatment Failure to pass meconium (although some infants with of preterm infants (< 37 wks “high” lesions will pass meconium) **NOT at birth ∗ with more immature blood- Symptoms start soon after birth with high lesions or with brain barrier), or infants with complete obstruction, delayed in lower lesions of partial sepsis or acidosis obstruction ∗ Fetal diagnosis: polyhydramnios and fetal u/s
Obstruction in the Newborn Causes of Obstruction in the Newborn
∗ Atresia: complete obstruction of the lumen ∗ 30% occur in duodenum (distal to ampulla) Intrinsic: Functional: ∗ Stenosis: narrowing of the lumen Atresia Hirschsprung ∗ intrinsic cause or compression by extrinsic lesions (annular Stenosis Meconium plug pancreas, peritoneal bands) Meconium ileus Ileus ∗ plain films not diagnostic Anorectal malformations ∗ emesis (amount and onset) depends on degree of Volvulus obstruction Annular pancreas Peritoneal bands
11 3/27/2013
Duodenal Atresia Malrotation with Volvulus
∗ 70% of neonates have other th th anomalies: Down syndrome, ∗ Malrotation (8 -10 week) can lead annular pancreas, cardiac to volvulus malformation, multiple atresias ∗ Complete obstruction ∗ Clinical findings: dehydration with ∗ Vascular compromise: metabolic alkalosis ∗ gangrene of the gut, peritonitis, sepsis, ∗ and shock. Xray findings: “double-bubble” ∗ (dilated stomach and dilated Infants present with emesis, bowel proximal duodenum) distention. Intermittent emesis with ∗ incomplete obstruction Management: NG tube, correct ∗ electrolytes and surgical Xrays: dilated stomach and consultation duodenum, little air in distal bowel, diagnosis by UGI (barium enema) ∗ Surgical emergency
Hirschprung’s Disease Meconium Ileus (inspissated meconium)
∗ Lower bowel obstruction: agenesis ∗ of ganglion cells (Auerbach and Meissner 90% of patients have cystic fibrosis, 10- plexuses) 15% of CF patients have meconium ileus ∗ Rectal lesion extending in varying ∗ Family history may be helpful degree; in 80-90% patients no extension ∗ Abdominal distention and emesis within beyond sigmoid colon ∗ 48 hrs Associated w/ Downs (15%), ∗ Waardenburg syndrome Delayed meconium passage ∗ Delayed meconium passage (>24-48 ∗ 1/3 of patients have volvulus, atresia, hrs) in 90% of patients meconium peritonitis, pseudocyst, and ∗ Clinical findings: Abdominal distention, present earlier emesis, obstipation ∗ Xrays: dilated bowel loops, intra- ∗ Barium enema: narrowing segment, “corkscrew” appearance of colon, abdominal calcification (peritonitis), no delayed clearing of barium air-fluid levels seen ∗ Diagnosis: rectal suction biopsy
12 3/27/2013
Meconium Plug Syndrome Birth Injuries
∗ ∗ Etiology: colonic dysmotility Cephalhematoma ∗ ∗ Hirschsprung’s disease in 50% of these Caput succedaneum ∗ patients Subgaleal hematoma ∗ ∗ Clinical findings: Erb’s palsy ∗ ∗ Delayed meconium passage: (24-48 hrs) Klumpke’s palsy ∗ Abdominal distention, emesis ∗ Clavicular fracture ∗ and Barium enema diagnostic ∗ Phrenic nerve injury with diaphragmatic paralysis therapeutic
Injuries to the Head
Caput: vaguely demarcated, pitting edema on presenting part of scalp, w/ ecchymosis. Hemorrhagic edema is superficial to the periosteum, often crossing sutures. Cephalohematoma: subperiosteal bleeding from rupture of vessels that traverse from the skull to periosteum. Bleeding limited by periosteal attachments, thus swelling does not cross sutures (tight water balloon to palpation) . Subgaleal hemorrhage: superficial bleed into loose connective tissue. Bleeding not limited enlarging, mobile hematoma can lead to shock (loose water balloon with fluid wave to palpation). Cephalohematoma and subgaleal can be associated with skull fracture and hyperbilirubinemia http://nursingcrib.com/wp-content/uploads/caput-and-cephal.jpg?9d7bd4
13 3/27/2013
Subgaleal Abnormal Arm Position in a Newborn
∗ Erb’s palsy C-5 and C-6 ∗ Decreased spontaneous movement and absent biceps reflex on affected side, abnormal Moro, "waiter's tip" appearance ∗ Klumpke's paralysis C-7, C-8, T-1 ∗ Hand paralysis, absent grasp reflex, Horner syndrome usually seen (ipsilateral ptosis, miosis, anhidrosis) ∗ Fractured clavicle ∗ Crepitus felt, decreased spontaneous movements, pseudoparalysis, asymmetric Moro, biceps reflex normal ∗ Fractured humerus
http://www.pediatriconcall.com/fordoctor/casereports/subgaleal_hematoma.asp
Brachial Plexus Injury: Erb’s Palsy Common Neonatal Skin Conditions
∗ Incidence of brachial plexus injuries: 1.6 - 2.9 per 1,000 live births ∗ ∗ Erythema toxicum neonatorum (“E tox”) 45% of brachial nerve injuries associated ∗ with shoulder dystocia. Benign pustular melanosis (“BPN”) ∗ The arm is adducted, extended, and ∗ Hemangiomata internally rotated. Absent biceps and ∗ Nevus flammeus Moro reflexes on affected side. Sensory ∗ function usually preserved. Capillary ∗ ∗ Recovery is often spontaneous and may Cavernous occur within 48 hours or up to six months ∗ ∗ Mixed Nerve laceration may result in a ∗ Port wine stain permanent palsy
14 3/27/2013
Benign Pustular Melanosis Erythema Toxicum
∗ Yellow papules w/ erythematous macular base, ∗ Seen in 4.4% of African-American infants, 0.2% in evanescent and found over white infants entire body ∗ ∗ Common in term infants Lesion: superficial pustular lesions that easily rupture then leave a scaley “collar” around ∗ Most seen 24-48 hours after delivery; can be seen up to 2 hyperpigmented macules. These fade within weeks wks of age to months. ∗ ∗ Eosinophil-filled papules Lesions most in clusters under chin, nape of neck, ∗ Unknown etiology, benign, forehead, and may be on trunk and extremities ∗ resolves spontaneously Lesions are sterile and transient. Not associated with systemic disease.
Pustules with scaling “collar” Pustules
15 3/27/2013
Post-inflammatory hyperpigmentation Hemangiomata
∗ Strawberry hemangioma ∗ 2.6% of infants (higher incidence in preterm infants) ∗ May be seen at birth, but typically develop during first few weeks of life and 90% seen by 1 mo of life ∗ Start as small, discrete, well demarcated lesions. These grow rapidly during infancy, and eventually involute. ∗ Infants with large lesions, lesions on the face, eyelids, airway, mouth, or cavernous lesions should be referred. ∗ Nevus flammeus ∗ Very common, up to 40% of infants ∗ “Salmon patch” on nape of neck, on eyelids, between eyebrows ∗ Do not grow during infancy and do not completely disappear. Lesions fade and are less noticeable except during crying or exertion
Hemangiomata Hemangiomas
Nevus flammeus Refer for : Eyes (upper lid) Nasal tip Mouth/midline (respiratory) Elbows/knees/heels Spine Diaper area
Hemangioma Port-wine stain (Sturge-Weber) Gary Larson
16 3/27/2013
Cardiac/Murmurs Cardiac/Murmurs , cont’d
∗ What you hear when ∗ ∗ st What else to see? Day of birth/1 DOL—outflow stenoses ∗ st Congestive heart failure—sweating, poor feeding, ∗ After 1 day—coarctation st failure to grow, HSM ∗ 1 week—left-to-right shunts (PDA, VSD, etc) ∗ What else to do? Standard to check post-ductal ∗ “Tachycardia”/bradycardia of newborn (DOL ~3) ∗ saturation after 24 HOL How? Training ear to VSD vs patent ductus ∗ Post-ductal <95%, or gradient >3% ∗ Stanford’s newborn nursery site: http://newborns.stanford.edu/PhotoGallery/Heart.html
Breastfeeding Ankyloglossia
∗ Benefits ∗ Challenges ∗ Who is your patient? ∗ Resources ∗ Lactation ∗ Public health nurses ∗ Local groups/stores/insurance
http://newborns.stanford.edu/PhotoGallery/Ankyloglossia1.html http://www.ghorayeb.com/TongueTie.htm l
17 3/27/2013
Frenulectomy Common Neonatal Problems
∗ Hypoglycemia ∗ Respiratory conditions ∗ Infections ∗ Polycythemia ∗ Bilirubin metabolism: neonatal jaundice ∗ Bowel obstruction ∗ Birth injuries ∗ Rashes ∗ Murmurs ∗ http://www.tongue-o-rama.com/2010/05/ankyloglossia.html Feeding difficulties
Questions?
Thank you!
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