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Ruben Bromiker Department of Neonatology Shaare Zedek Medical Center

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Presentation on theme: "Ruben Bromiker Department of Neonatology Shaare Zedek Medical Center"— Presentation transcript:

1 Ruben Bromiker Department of Neonatology Shaare Zedek Medical Center
Neonatal Jaundice Ruben Bromiker Department of Neonatology Shaare Zedek Medical Center

2 Physiologic Jaundice Healthy infants
up to 12mg% in 3rd day; in premature, 5th day. No hemolysis or bleedings No underlying metabolic disease 5

3 Mechanism Production: Volemia, RBC span (90 days)
Ineffective erythropoyesis Turnover of non Hb heme proteins 6

4 Mechanism Enterohepatic recirculation: Glucuronidase
Bilirubin monoglucuronide Intestinal bacteria Intestinal motility and stooling 7

5 Mechanism Bilirubin Uptake : ligandin Conjugation : UDPG-T activity
Hepatic excretion of bilirubin 8

6 Neonatal Hyperbilirubinemia
Visible jaundice: Adults: >2mg% Newborns: >6mg Up to 50% of all newborns may develop jaundice

7 Source of Bilirubin Metabolism of heme 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. 2

8 Metabolism Heme Biliverdin + CO + Fe Indirect (unconjugated) bilirubin
Heme Oxygenase + O2 Heme Biliverdin + CO + Fe Biliverdin reductase Indirect (unconjugated) bilirubin Binds to albumin in plasma 3

9 Conjugation Indirect bilirubin Liver Gut
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 4

10 Jaundice: Physical examination
Blanch skin with a finger  Jaundice Significant when appears at palms or below knees. Transcutaneous bilirubinometer Bruising, cephalohematoma, others. Organomegaly 13

11 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.

12 Jaundice: Laboratory Total serum bilirubin
Blood type, Rh, Coombs infant and mother Smear (morphology and reticulocytes) Hematocrit 14

13 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 15

14 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 9

15 Non Physiologic Jaundice: Anamnesis
Familial: G6PD, spherocytosis, metabolic, enzymes. Siblings: Immune, breast milk. Pregnancy: Infections, drugs, diabetes. Delivery: Trauma, cord clumping, asphyxia. 10

16 Bilirubin toxicity: Disrupted BB barrier Hyperosmolarity Anoxia
Cerebral Penetration: As free indirect bilirubin or bound when disrupted BBB Disrupted BB barrier Hyperosmolarity Anoxia Hypercarbia Prematurity 16

17 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

18 Bilirubin toxicity: Kernicterus
Neuronal injury + yellow staining of brain  incidence in hemolytic disease (especially RH) Localization Basal ganglia Cranial nerve and cerebral nuclei Hippocampus Anterior horn of spinal cord 18

19 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 19

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

21 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. 21

22 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 11

23 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 12

24 Treatment Options for Jaundiced Breast-fed Infants

25 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

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: hm also adequate. Irradiation generates photochemical reaction in the extravascular space of the skin A higher illuminated area increases effectiveness 22

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 23

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) 23

33 Treatment: Phototherapy mechanism
Main Pathway Bilirubin Lumirubin 24

34 Phototherapy: Technique
Fluorescents ,spots or biliblankets More than 5mw/cm2 at hm Naked , covering eyes Increase fluids 10-20% Check bilirubin every 12-24hs Stop: 13±1mg% in term, 10±1mg% in preterm Check 12-24hs later for rebound

35 Phototherapy: Side effects
Increased water loss Diarrhea Retinal damage Bronze baby, tanning Mutations in DNA?  shield scrotum Disturb of mother-infant interaction.

36 Exchange transfusion: Technique
Irradiated PC < 7 days + FFP. Warmed Double of blood volume. Open incubator, monitors Route UV: push-pull, over > 1hr Artery-vein: Isovolumetric

37 Exchange transfusion: Complications
Hypocalcemia-hypomagnesemia (CPD) Hypoglycemia (monitor Dx after exchange) Acid base disturbances Hyperkalemia Cardiovascular: Embolizations, arrhythmia, perforation, arrest.

38 Exchange transfusion: Complications
Bleeding Thrombocytopenia, loss of factors. Infections Hemolysis GVHD Other Fever, hypothermia, NEC?

39 Neonatal Jaundice: Other treatments
Phenobarbital:  conjugation Oral agar:  enterohepatic circulation Metalloporphyrins: inhibit bilirubin production. Competitors of heme oxygenase IVIGg: inhibits hemolysis. Binds to FC receptor of reticuloendothelial cells

40 Management of Hyperbilirubinemia in the Healthy Term Newborn*

41 Diagnostic approach to neonatal jaundice
Measure Bilirubin Non physiologic Blood type, Rh, Coombs Hematocrit, Smear, Reticulocytes Increased direct bili Increased indirect bili Coombs + Sepsis TORCH Biliary Atresia Cholestasis Inspissated Bi Hepatitis CF Tyrosinosis Galactosemia Coombs - ­Hematocrit ABO Rh minor group Polycytemia N or ¯Hematocrit RC shape Normal Bleedings Enterohepatic Metabolic Drugs Other Abnormal Specific and non specific Abnormalities

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