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Physiologic Jaundice

Physiologic Jaundice. Healthy infant Term AGA. 60hs Jaundiced Pressure on leg  yellow Phys ex: Otherwise normal Lab:up 12mg%. Mechanism. Production: Volemia, RBC span (90 days) Ineffective erythropoyesis Turnover of non Hb heme proteins. Mechanism.

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Physiologic Jaundice

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  1. Physiologic Jaundice • Healthy infant Term AGA. 60hs • Jaundiced • Pressure on leg  yellow • Phys ex: Otherwise normal • Lab:up 12mg%

  2. Mechanism • Production: • Volemia, • RBC span (90 days) • Ineffective erythropoyesis • Turnover of non Hb heme proteins

  3. Mechanism • Enterohepatic recirculation: • Glucuronidase • Bilirubin monoglucuronide • Intestinal bacteria • Intestinal motility and stooling

  4. Mechanism • Bilirubin Uptake : ligandin • Conjugation : UDPG-T activity • Hepatic excretion of bilirubin

  5. Source of Bilirubin • Metabolism of heme. 6-10 mg/kg/day. (adults 3-4mg/kg/day) • 1gr Hemoglobine produces 34mg of bilirubin • 75%: from old RBCs released from RES • 25%: from ineffective erythropoyesis, myoglobine, cytochromes, catalase, peroxidase.

  6. Metabolism Heme Oxygenase + O2 Heme Biliverdin + CO + Fe Biliverdin reductase Indirect (unconjugated) bilirubin Binds to albumin in plasma

  7. Indirect bilirubin Conjugation • Liver Uptake (binds to ligandin) Endoplasmic reticullum • Bilirubin Mono and diconjugated bilirubin UDPG-T Liver Excretion Gut • Elimination • Enterohepatic recirculation • Urobilinoids • Stool • Beta glucuronidase • Bacteria

  8. Jaundice: Physical examination • Blanch skin with a finger  Jaundice • Significant when appears at palms or below knees. • Transcutaneous bilirubinometer • Bruising, cephalohematoma, others. • Organomegaly

  9. Dermal Zones of Jaundice After leaving RES bilirubin binds to albumin, initially with low affinity, thus bilirubin precipitates in the proximal parts of the body before it does it distally. So jaundice appears first proximally, and later distally.

  10. Jaundice: Laboratory • Total serum bilirubin • Blood type, Rh, Coombs infant and mother • Smear (morphology and reticulocytes) • Hematocrit

  11. Jaundice: Laboratory • Antibody identification • Direct bilirubin: • When more than 2 weeks old or signs of cholestasis • If prolonged: • LFT, TORCH, sepsis work-up, metabolic, thyroid • G6PD

  12. Non Physiologic Jaundice • Onset at < 24 hs • Bilirubin  over levels for phototherapy • Bilirubin rise > 0.5 mg%/hr • Signs of underlying illness • Vomiting, lethargy, poor feeding,  weight • Age > 8 days in term or 15 days in premature

  13. Non Physiologic Jaundice: Anamnesis • Familial: • G6PD, spherocytosis, metabolic, enzymes. • Siblings: • Immune, breast milk. • Pregnancy: • Infections, drugs, diabetes. • Delivery: • Trauma, cord clumping, asphyxia.

  14. Bilirubin toxicity • Healthy full-term infants: • Abnormality in ABR • Hypotony: reverses with  bilirubin levels • Very rarely kernicterus • Low birth weight infants: • Damage most probably due to accompanying factors than to high bilirubin.

  15. Bilirubin toxicity: Cerebral Penetration: As free indirect bilirubin or bound when disrupted BBB • Disrupted BB barrier • Hyperosmolarity • Anoxia • Hypercarbia • Prematurity

  16. Bilirubin toxicity: Factors Unbound indirect bilirubin •  Albumin concentration • 1gr albumin binds 8.5mg bilirubin • Displacement from albumin site • FFA • Drugs: Sulfonamides • Correction of acidosis

  17. Bilirubin toxicity: Acute encephalopathy • I) Hypotonia, lethargy, high pitched cry, poor suck • II) Hypertonia of extensor muscles • opistotonus, rigidity, oculogyric crises, retrocollis • III) Return of hypotonia after 1 week

  18. OPISTOTONUS

  19. Bilirubin toxicity: Kernicterus Neuronal injury + yellow staining of brain  incidence in hemolytic disease (especially RH) • Basal ganglia • Cranial nerve and cerebral nuclei • Hippocampus • Anterior horn of spinal cord Localization

  20. Bilirubin toxicity: Chronic complications • Athetosis • Sensorial deafness • Limited upward gaze • Intellectual deficits • Dental dysplasia

  21. Breast Feeding Jaundice • Bilirubin  after 4 days of age. Healthy infants • Resolves after holding breast milk for 1-2 days • Presentation • Early: 2-4 days of age • Late: after 4 days of age

  22. Breast Feeding Jaundice: Mechanism • Interference with hepatic conjugation • Beta glucuronidase in milk • Reduced bacterial colonization of gut • Caloric intake intestinal motility recirculation • FFA suggested to reduce bilirubin metabolism

  23. Treatment Options for Jaundiced Breast-fed Infants

  24. Isoimmune hemolytic disease of the newborn • Rh , or minor types (Kell, Duffy, E, C,c) • 15% of people are Rh- • Coombs + • Maternal sensitization d/t previous pregnancy, transfusion, amniocentesis, abortion

  25. Erythroblastosis Fetalis –Hemolytic Disease of Newborn (HDN)

  26. IHDN: Pregnancy Management • Coombs titers >1/16 or previous history of severe disease  Amniocentesis for optical density • High levels, and clinical signs of hydrops Intrauterine transfusion • Intraperitoneal, intravascular or intracardiac • Repeated transfusions  switched fetal blood type

  27. IHDN: Newborn Management • Check immediately after birth • Hematocrit • Bilirubin • Blood type • 50% will only need phototherapy • 24% will be anemic and cord bilirubin >4mg% exchange transfusion

  28. IHDN: Prevention Anti D (Rh) immune globulin indications • At 28 weeks • within 72 hours since birth. • Procedures or suspected transplacental hemorrhage.

  29. ABO hemolytic disease of the newborn • 15% of pregnancies mother O infant A or B • 20% will develop significant jaundice • 10% will need phototherapy. • Presentation: • Early jaundice (<24hs of life) • Many times Combs -, but there are antibodies • Blood smear: spherocytes

  30. Treatment: Phototherapy • Bilirubin best absorbs light at 450 hm. • The best is to provide it with blue light. • White range: 380-700 hm also adequate. • Irradiation generates photochemical reaction in the extravascular space of the skin • A higher illuminated area increases effectiveness

  31. Treatment: Phototherapy Mechanism • Photoisomerization: • Natural Isomer 4Z,15Z  4Z,15E hydrosoluble  blood  biliar secretion (unconjugated) • Slow excretion and fast reisomerization  reabsorbed. • Photooxydation: Small polar products. Slow

  32. Treatment: Phototherapy mechanism • Structural isomerization: • Ciclization to lumirubin (irreversible)  bile and urine • Fast excretion not reabsorption. • Related to dose of phototherapy (intensity of light)

  33. Phototherapy: Technique • Fluorescents ,spots, LED or biliblankets • More than 5mw/cm2 at 425-475hm • Naked , covering eyes • Increase fluids 10-20% • Check bilirubin every 4-8 hs • Stop: 13±1mg% in term • Check 6-12 hs later for rebound

  34. IVIG No IVIG With IVIG Macrophage Fc Receptor RBC

  35. In Conclusion • Bilirubin is potentially toxic to the central nervous system • Bilirubin is normally cleared from the body by hepatic conjugation with glucuronic acid and elimination in bile • Pathologic conditions can increase bilirubin production or reduce elimination • The goal of therapy is to lower the concentrationof circulating bilirubin or keep it from increasing

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