Rosen & Barkin's 5-Minute Emergency Medicine Consult (478 page)

FOLLOW-UP

Admission not necessary

Manage as outpatients with appropriate follow-up in occupational medicine clinic

• Beltrami EM, Williams IT, Shapiro CN, et al. Risk and management of blood-borne infections in health care workers.
  Clin Microbiol Rev
  . 2000;13:385–407.
  
• Panlilio AL, Cardo DM, U.S. Public Health Service, et al. Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis.
  MMWR Recomm Rep
  . 2005;54(RR-9):1–17.
  
• U.S. Public Health Service. Updated U.S. Public Health Service Guidelines for the management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for Postexposure Prophylaxis.
  MMWR Recomm Rep
  . 2001;50(RR-11):1–52.
  
• National Clinicians’ Post-Exposure Prophylaxis Hotline: Phone (888) 448-4911; Available at
  Http://www.nccc.ucsf.edu
  . Accessed on January 29, 2013.
  
• Centers for Disease Control and Prevention (CDC). Update: Influenza activity–United States, September 30-December 1, 2007.
  MMWR Morb Mortal Wkly Rep
  . 2007;56(49):1287–1291.
  

CODES

• V01.79 Contact with or exposure to other viral diseases
  
• V07.8 Other specified prophylactic or treatment measure
  
• V15.85 Personal history of contact with and (suspected) exposure to potentially hazardous body fluids
  

BASICS

Produced by an imbalance between rates of bilirubin production and bilirubin elimination:

• Newborns have higher rate of bilirubin production than adults because of increased RBC mass and shorter RBC life span.
  
• Newborns, especially preterm infants, have rate limitations in hepatic conjugation and biliary excretion of bilirubin, increased enterohepatic circulation, and diminished bilirubin binding to albumin- and bilirubin-binding protein.
  

• In most newborns, this represents
  physiologic jaundice
  and is not pathologic:
  
  • Bilirubin normally increases from 1.5 mg/dL in cord blood to a mean of 6.5 mg/dL on day 3, followed by a gradual decline to levels of <1.5 mg/dL by day 10 or 12 of life.
    
• Serum bilirubin may rise to levels exceeding neuroprotective defenses, causing bilirubin tissue binding in basal ganglia, hippocampus, brainstem nuclei, and cerebellum:
  
  • Bilirubin-induced neurologic dysfunction (BIND)
    caused by increasingly severe hyperbilirubinemia from mild dysfunction to acute bilirubin encephalopathy (ABE) and kernicterus.
    
    • ABE
      describes the acute manifestations of bilirubin toxicity seen in the 1st wk after birth.
      
    • Kernicterus:
      Chronic form of BIND, with significant mortality or permanent sequelae including choreoathetoid type of cerebral palsy, gaze abnormalities, hearing loss, and dental dysplasia.
      
  • Rate of progression of BIND depends on rate of increase of bilirubin levels, duration of hyperbilirubinemia, albumin-binding reserves, unbound bilirubin level, host susceptibility, and comorbidities.
    
  • Death is due to respiratory failure and progressive coma or intractable seizures.
    
• Risk factors for severe hyperbilirubinemia:
  
  • Jaundice observed in 1st 24 hr
    
  • Predischarge total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) (see “Diagnosis”) in high-risk or high–intermediate-risk zone
    
  • Lower gestational age, 35–38 wk
    
  • Exclusive breastfeeding, especially if inadequate with excessive weight loss
    
  • Isoimmune or other hemolytic disease
    
  • Sibling with neonatal jaundice
    
  • Cephalohematoma or excessive bruising
    
  • Ethnicity: East Asian
    
• Severe hyperbilirubinemia is associated with perinatal factors: Low birth weight, macrosomia from maternal diabetes, infection, polycythemia
  
• Hyperbilirubinemia neurotoxicity risk factors:
  
  • Isoimmune hemolytic disease
    
  • G6PD deficiency
    
  • Asphyxia
    
  • Sepsis
    
  • Acidosis
    
  • Albumin <3 mg/dL
    
• Postphototherapy (post-PT) bilirubin rebound to bilirubin levels of concern may occur:
  
  • At high risk are newborns <37 wk gestation, patients with hemolytic disease, patients treated for <72 hr.
    

• Unconjugated hyperbilirubinemia:
  
  • Physiologic jaundice
    
  • Jaundice in breastfed infants:
    
    • Breastfeeding failure jaundice
      : Exaggeration of physiologic jaundice due to inadequate ingestion/production of sufficient volume of breast milk in the 1st wk of life
      
    • Breast milk jaundice
      : Begins days 3–5, peaks within 2 wk but lasts up to 8 wk; caused by increased β-glucuronidase in breast milk
      
    • May be exacerbated by dehydration
      
  • Specific hemolytic conditions:
    
    • Blood group isoimmunization due to ABO, Rh, and minor blood group incompatibility; ABO is most common: Rh disease is unusual (RhoGAM prevents).
      
    • Red cell enzyme deficiencies: G6PD deficiency
      
    • Red cell membrane defects: Hereditary spherocytosis and elliptocytosis
      
  • Sepsis: Bacterial, viral, or protozoal
    
  • Birth trauma:
    
    • Increased heme load from resolving cephalohematoma or ecchymosis
      
  • Polycythemia:
    
    • Caused by maternal–fetal transfusion
      
    • Fetal–fetal transfusion
      
    • Infants of diabetic mothers
      
  • Congenital hypothyroidism
    
  • Defective hepatic conjugation:
    
    • Gilbert syndrome (familial partial defect in glucuronyl transferase activity) is benign.
      
    • Crigler–Najjar syndrome (congenital absence of glucuronyl transferase), lifelong unconjugated hyperbilirubinemia
      
  • Intestinal obstruction such as ileus, functional or anatomic, increases enterohepatic circulation
    
• Conjugated hyperbilirubinemia:
  
  • Failure of hepatic excretion of conjugated bilirubin
    
  • Causes include neonatal hepatitis, congenital biliary atresia, extrahepatic biliary obstruction, shock liver from neonatal asphyxia, neonatal hemosiderosis
    

DIAGNOSIS

• Sleepiness, poor intake, and inadequate urine output may be present.
  
• Early phase of ABE:
  
  • Feeding difficulties with poor suck; decreased urine output
    
  • Fussiness, irritability, hypotonia
    
  • Lethargy with altered awake–sleep pattern
    
• Intermediate phase of ABE:
  
  • High-pitched cry, irritability
    
  • Increased tone with backward arching of neck (retrocollis) and trunk (opisthotonos) alternating with hypotonia
    
  • Fever
    
• Signs of advanced ABE:
  
  • Pronounced retrocollis–opisthotonos
    
  • Semicoma, seizures
    
  • Bicycling movements
    

• Yellowish discoloration of skin, sclera, and body fluids due to bilirubin deposition. Indicates elevated serum bilirubin level.
  
• Evidence of dehydration: Mottled, prolonged capillary refill
  
• Increasing levels of bilirubin affect skin color progressing in cephalocaudal direction:
  
  • Blanch skin with digital pressure to reveal underlying skin color
    
  • Face: Bilirubin levels >6–8 mg/dL
    
  • Feet: Bilirubin levels >12–15 mg/dL
    
  • Visual diagnosis of jaundice is unreliable, especially in darkly pigmented infants.
    
• Neurologic dysfunction is identified by abnormal tone—hypotonia, hypertonia, or variability; setting sun sign—sclera visible below upper eyelid.
  
• Clues to contributing conditions
  

• Clinical diagnosis considering risk factors
  
• TSB mandatory in any infant with suspected or obvious jaundice
  
• Initial TSB should be fractionated into indirect (unconjugated) and direct (conjugated) bilirubin
  

• Interpret TSB according to infant’s age in hours, not days, to determine risk and need for treatment. Chart progression
  
• Identify TSB level or TcB
  
• TcB correlates well with TSB if available.
  
• Further evaluation is recommended for these newborns with jaundice:
  
  • Occurs in the 1st 24 hr of life
    
  • Persists beyond the 1st wk of life
    
  • TSB levels reach level to initiate
    intensive
    PT
    
  • Conjugated bilirubin is >10% or >2 mg/dL.
    
  • Any signs of ABE
    
• Serum albumin, electrolytes, BUN, Cr, calcium
  
• CBC with differential and RBC morphology
  
• Reticulocyte count
  
• Maternal and infant blood type
  
• Direct Coombs test on cord blood:
  
  • Hospital routines vary: Some will test newborns from all type O mothers.
    
  • If not available, direct Coombs test on infant’s blood
    
• Sepsis evaluation in ill-appearing infant
  
• Further inpatient workup is directed at suspected cause:
  
  • Red cell enzyme assay: G6PD
    
  • Liver function tests
    
  • Urine-reducing substances
    
  • Metabolic or endocrine studies