Neonatal hyperbilirubinemia.Bilirubinaemia of Newbornpptx

SreevidhyaJS 96 views 53 slides May 27, 2024
Slide 1
Slide 1 of 53
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53

About This Presentation

Neonatal Hyperbilirubinaemia


Slide Content

Neonatal Hyperbilirubinemia By Dr Sreevidhya JS,BHMS,MD(Paediatrics) Asso prof/HOD Dept of OBG MNR Homoeopathic Medical College Sangareddy,Telangana State

A Case of Hyperbilirubinaemia This is a jaundiced, 4 day old, 3.1 kg, appropriate for gestational age (AGA) Asian female infant born at term to a 25 year old A+ primiparous woman with gestational diabetes. The pregnancy was otherwise uneventful. Labor was augmented with Pitocin.

The baby was discharged home on day of life 2 at which time her weight was down 4% from birth weight and she had mild facial jaundice. In the hospital, she was breast fed every 3 hours and had 2 wet diapers and one meconium stool over a 24 hour period. On day 3, her parents gave her water on two occasions as she appeared hungry despite regular and frequent breast feeding attempts. 

In addition, they noted an increase in the degree of jaundice, but failed to address it after being reassured by family members that jaundice is common. They also had an appointment to see their pediatrician the following day.

In the office, on day 4, mother reports that she is breastfeeding the baby every three hours and that there have been 2 wet diapers per day. The urine is described as dark yellow in color and the stools appear dark green.

Exam: P 102, RR 55, BP 63/45. Weight 2.7 kg (25%ile), length 50 cm (75%ile), head circumference 34 cm (75%ile). 

The infant is jaundiced and irritable. The anterior fontanel is slightly sunken, the oral mucosa is tacky, and there is jaundice to the lower extremities. No cephalohematoma or bruising is present. The sclera of both eyes are icteric. Muscle tone and activity are normal. The remainder of the physical exam is normal.

The total bilirubin is 20 mg% . She is admitted to the hospital for phototherapy, and lactation consultation. By the following day, the bilirubin has decreased to 12 mg% and she is discharged home on breast milk feedings. baby is scheduled for follow-up with both the pediatrician and the lactation consultant.

What is the Neonatal Jaundice? Neonatal Jaundice(also called Newborn jaundice) is a condition marked by high levels of bilirubin in the blood . The increased bilirubin cause the infant's skin and whites of the eyes (sclera) to look yellow.

Neonatal Jaundice Visible form of bilirubinemia Adult sclera >2mg / dl Newborn skin >5 mg / dl Occurs in 60% of term and 80% of preterm neonates

Bilirubin Metabolism Heamoglobin  Haeme +Globin ↓ Heme Oxygenase Biliverdin + Carbon Monoxide Biliverdin I Reductase ↓ + Iron Bilirubin

Rt Hepatic Duct+ Lt Hepatic Duct→Common hepatic duct Gall Blader → Cystic duct Common hepatic duct + Cystic duct→ Common bile duct Common bile duct + Pancreatic duct→Hepatopancreatic duct

Conjugated bilirubin Hepatopancreatic duct→Descending part of duodenum→(Bacterial flora) Conjugated bilirubin→Urobilinogen (50%)→ Vein→Portal vein→Inferior vena cava→Rt Atrium→Rt Ventricle→Pulmonary Artery→Lt Atrium→Lt Ventricle→Aorta→Kidney→Excreated out(Urobilinogen)

Remaining 50%→Stercobilinogen + Feces → Yellow colored Feces

Congugated bilirubin is not reabsorbed from bowel unless it is deconjugated by intestinal enzyme beta glucuronidase which is present in intestinal mucosa – Enterohepatic circulation

Causes of Unconjugated hyperbilirubinemia Starts from spleen to liver Hemolytic anaemia Rh incompactability Heriditory sperocytosis Glucose 6 phosphate dehydrogenase deficiency Cephalohematoma Maternal diabetis Chronic fetal hypoxia

5.Gilbert syndrome 6.Crigler Naja Syndrome 7.Congenital hypothyroidism

Conjugated Hyperbilirubinemia Obstructive causes- Hepatic or Intrahepatic, Congenital hepatic fibrosis CaroIi’s disease Progressive familial intrahepatic cholestasis Alagille syndrome OATP1B1-DEFECT-Rotor syndrome Defect in multidrug resistant protein-DUBIN JOHNSON SYNDROME

Extrahepatic Extrahepatic biliary atresia –Kasai procedure –Diagnose by HIDA SCAN Choledochal cyst Obstruction - stones Primary biliary sclerosis Primary sclerosing collangitis

Non Obstructive Bacterial Infection Viral infections Parasitic Infection Metabolic Problems

Other causes 1.Physiological Jaundice 2.Breast milk Jaundice 3.Breast feeding Jaundice

Special characteristic in neonates 1.More billirubin produced Much more Hemolysis The life-length of hemolysis(90 days)

Special characteristic in neonates Less albumin in neonates Decreased ligandin

Special characteristic in neonates Decreased Clearence ↓UGT1A1 Activity

Special characteristic in neonates High workload of the hepato-enteric circulation Increased enterohepatic circulation Decreased bacteria and decreased gut motility Poor evacuation of bilirubin laden meconium

Increased rbc’s Shortened rbc lifespan Immature hepatic uptake & conjugation Increased enterohepatic Circulation

Grading of extent of jaundice by Kramer

Clinical assessment of jaundice Area of body Face Upper trunk Lower trunk & thighs Arms and lower legs Palms & soles Bilirubin levels mg/dl 4- 6 6 - 8 8-1 2 1 2 -1 4 > 15

Physiological jaundice Characteristics Appears after 24 hours Maximum intensity by 3rd day in term & 5 th day in preterm Serum level less than 15 mg / dl Clinically not detectable after 14 days Disappears without any treatment Note: Baby should, however, be watched for worsening jaundice

Why does physiological jaundice develop? Increased bilirubin load Defective uptake from plasma Defective conjugation Decreased excretion Increased entero-hepatic circulation

Term Preterm 1 2 3 4 5 6 10 11 1 2 1 3 14 Age in Days 15 10 5 Bilirubin level mg/dl Course of physiological jaundice

Pathological jaundice Appears within 24 hours of age Increase of bilirubin > 5 mg / dl / day Serum bilirubin > 15 mg / dl Jaundice persisting after 14 days Stool clay / white colored and urine staining clothes yellow Direct bilirubin> 2 mg / dl

Causes of jaundice Appearing within 24 hours of age Hemolytic disease of NB : Rh, ABO Infections: TORCH, malaria, bacterial G6PD deficiency Appearing between 24-72 hours of life Physiological Sepsis P o l y c y th e m ia Concealed hemorrhage Intraventricular hemorrhage Increased entero-hepatic circulation

Causes of jaundice After 72 hours of age Sepsis Cephalhaematoma Neonatal hepatitis Extra-hepatic biliary atresia Breast milk jaundice Metabolic disorders

R i s k f a c t o r s f o r j a u n d i c e JAUNDICE J - jaundice within first 24 hrs of life A - a sibling who was jaundiced as neonate U - unrecognized hemolysis N – non-optimal sucking/nursing D - deficiency of G6PD I - infection C – cephalhematoma /bruising E - East Asian/North Indian

Common causes in India Physiological Blood group incompatibility G 6 PD deficiency Bruising and cephalhaematoma Intrauterine and postnatal infections Breast milk jaundice

Approach to jaundiced baby Ascertain birth weight, gestation and postnatal age Assess clinical condition (well or ill) Decide whether jaundice is physiological or pathological Look for evidence of kernicterus* in deeply jaundiced NB *Lethargy and poor feeding, poor or absent Moro's, opisthotonus or convulsions

W o r k u p Maternal & perinatal history Physical examination Laboratory tests (must in all)* Total & direct bilirubin* Blood group and Rh for mother and baby* Hematocrit, retic count and peripheral smear* Sepsis screen Liver and thyroid function TORCH titers, liver scan when conjugated hyperbilirubinemia

Management Rationale: reduce level of serum bilirubin and prevent bilirubin toxicity Prevention of hyperbilirubinemia: early feeds, adequate hydration Reduction of bilirubin levels: phototherapy, exchange transfusion, drugs

Mechanism of bilirubin reduction by phototherapy -Structural isomerization by light Bilirubin → lumirubin(more soluble structure)→ Excreted into bile,urine without conjugation -Photoisomerization Z isomers of bilirubin are converted into E isomers Bilirubin( less toxic form), clearence is slow.

Principle of phototherapy Teaching Aids: NNF NJ - 44 Native bilirubin Photo isomers of bilirubin I n s ol u b l e Soluble 4 5 - 4 6 n m of light

Administrating Phototherapy Ambient room temperature-25 to 28 degree C to prevent hypothermia or hyperthermia Remove all clothes of the baby except the diaper. Cover the baby’s eyes with an eye patch Place the baby under the lights in a cot If weight is more than 2 kg in an incubator or radiant warmer,if baby is small Distance between baby and light 30-45 cm

Babies under phototherapy

Phototherapy Frequent extra breast feeding every 2 hourly Turn baby after each feed Temperature record 2 to 4 hourly Weight record- daily Monitor urine frequency Monitor bilirubin level

Side effects of phototherapy Increased insensible water loss Loose stools Skin rash Bronze baby syndrome Hyperthermia Upsets maternal baby interaction May result in hypocalcemia

Choice of blood for exchange blood transfusion Double volume exchange transfusion should be performed when infant shows signs of bilirubin encephalopathy irrespective of TSB Levels Infants with Rh isoimmunization include Cord bilirubin is 5 mg/dL Cord haemoglobin is 10g/dl or less Baby at birth showing signs of hydrops or cardiac decompensation in presence of low pcv -exchange transfusion with Packed red blood cells

Prolonged indirect jaundice Causes Crigler Najjar syndrome Breast milk jaundice Hypothyroidism Pyloric stenosis Ongoing hemolysis, malaria

Conjugated hyperbilirubinemia Suspect High colored urine White or clay colored stool Caution  Always refer to hospital for investigations so that biliary atresia or metabolic disorders can be diagnosed and managed early

Kernicterus Kernicterus is damage to the brain centers of infants caused by increased levels of unconjugated-indirect bilirubin which is free (not bound to albumin).

Thank you
Tags