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11 D old , bottle-feeding infant parents c/o his poor appetite for 24 hrs ,, BP 82/52,PR 150,temp. 36.2 ,, O/E mild dehydrated ,mild jaundice ,,,, which of the following is mot important diagnostic study : <ul><li>Bilirubin level </li></ul><ul><li>Lumber puncturee </li></ul><ul><li>Periphral smear </li></ul><ul><li>Reticulocyte count </li></ul><ul><li>TSH </li></ul><ul><li>No need Inx as this is milk-feeding juindice,just advised the mother to breast feed child and FU after 24 hrs </li></ul>
Jaundice is the visible manifestation of chemical bilirubinemia In neonates, evaluation of sclera is difficult because of physiological photophobia Almost 60% Term and 80% Preterm will have TSB >85umlo/l (>5 mg/ dl) in the first week of life and become clinically juindiced * *Nelson Textbook of Pediatrics. 17th ed A recent EBM review suggests that a relationship b/w height of TSB & likelihood of developing kernicterus does exist , 50% of infants with kernicterus had TSB > 511 umol/l (>29.9 mg/dL)^ ^N Engl J Med 2006;354:1889-1900 Identify those at risk of developing neurological dysfunction
Heamoglobin Heme Globin Biliverdin Unconj. Bili. Conj.bili. bile Entrohep. Circulation (UDP)-glucuronyl transferase <ul><li>Entrohepatic circulation result : </li></ul><ul><li>Deconjugated to unconj. Bili. </li></ul><ul><li>Reduced to stercobilinogen </li></ul>unconj. Bili urine stool
b/w 24-72 hrs of life Appearing > 72 hrs Hemolytic disease of newborn: Rh, ABO and minor group incompatibility Infections: intrauterine viral, bacterial; malaria G-6PD deficiency Physiological Sepsis neonatorum Polycythemia Concealed hemorrhages: cephalhematoma, SAH, IVH. Increased enterohepatic circulation Sepsis neonatorum' Neonatal hepatitis Extra hepatic biliary atresia Breast milk jaundice Metabolic disorders Time of apperance cause remains uncertain in 1/3 of cases multifactorial in origin <24 hrs of life
Physiological jaundice · First appears b/w 24-72 hrs of age · Maximum level seen on 4-5th D in term and 7th D in preterm neonates · Does not exceed 15 mg/ dl ( 257 umol/l) · Clinically disappear at 14 Ds. · No Rx required but baby should observed closely for signs of worsening Pathological jaundice · Clinical jaundice detected < 24 hrs of age · Rise in TSB by > 5 mg/ dl/ day ( >86 umol/l/day) · TSB > 15 mg/ dl ( > 257 umol/l) · Clinical jaundice persisting > 14 Ds · Clay/white colored stool and/or dark urine staining the clothes yellow · allways search for the cause Physiological/pathological
Breast milk jaundice Prolonged physiological jaundice appear in 2 nd wk of life Common in solely breast fed baby The bili. rarly high enough to require treatment If TSB> 15 mg/dl at 3 wks, cessation of breast milk 48 hrs will decrease TSB & breast milk can be resumed w/out risk of recurrence of jaundice Due to the presence of maternal glucuronidase in breast milk Breast feeding jaundice Appear first few days of life Occurs in formula-fed infants who feed poorly or in those not being fed at all Result of persistent intestinal glucuronidase activity during early breastfeeding when there is limited milk intake Milk associated juindice
Conjugated hyperbilirubinemia Rare in the newborn period and is defined as a conj. bilirubin level of > 2mg/dl (>34umol/l) or (>20 % of TSB) Never discharge baby with conjugated hyperbili. w/out attempting to find the cause (never physiological) Conjugated bili. is not toxic but its presence usually indicative of a serious underlying disorder
Complication BIND : Acute Bilirubin Induce Neurological Defect caused by toxic effects of unconjugated bilirubin on CNS Kernicterus : Is the chronic , permanent clinical sequelae of bilirubin toxicity
Risk factors for neurotoxicity Hypoproteinemia Acidosis Hypothermia Hypoglycemia Drugs(sulfonamides or salicylates) Asphyxia Prematurity Hyperosmolarity Infection facilitate move. of bili. from vascular to tissues alter the permeability of the blood-brain barrier Nelson Textbook of Pediatrics 17 th edi.
AAP recommends predischarge measurement of the TSB / TcB & assessment of clinical risk factors.
Timing of FU determined by : length of stay in the nursery, presence or absence of risk factors for hyperbilirubinemia and risk of other neonatal problems Earlier ,close & more frequent follow-up should be provided for those who have risk factors for hyperbilirubinemia
Approach to a jaundiced baby Mother blood group Prenatal / natal / postnatal history Birth wt Gestation age Juindice started Color of stool and urine Familial causes of jaundice Infant feeding and elimination Infant’s behavior Symptoms of encephalopathy Medications (directly o r via breast milk) History
Skin findings ( bruising /petechia … etc hmrg) Wt compared to birth wt & hydratin Dysmorphic features CVS examination for sign of anemia / murmur Abd. hepatosplenomegaly or masses Neurological examination Exam. Hypothyroidism 2 nd wk of life, motteled skin, coars face,larg tongue,hourse cry Hypoglycemia, hyponatremia, small genitalia Hypopituitarism Infants of diabetic mothers polycythemia /immaturity glucuronyl transferase enzyme system
Clinical Assessment of jaundice Clinical jaundice first appears in face then progress downward as it increases in intensity Assessment should be done in natural light, press baby's skin( preferably over a bony part) till it blanches. The underlying skin is noted for yellow color. Umol/l Range of bilirubin (mg/100 ml) Area of body 51.4 - 137 3-8 face 85.6 – 205.6 5-12 Upper trunk 137 - 274 8-16 Lower trunk and thigh 188 - 308 11-18 Arm and lower limb > 257 > 15 Palms and soles
Clinical estimation of bilirubin has to be confirmed by laboratory methods. TSB results should be interpreted in relation to the infant’s age in hours Various methods for measuring bilirubin in the lab are used Remember :
Portable handheld devices that allow transcutaneous measurement of bilirubin (TCB) Studies have documented that the results from TCB are equivalent to TSB in term and preterm infants * *Bhutani V, Pediatrics 2000;106:e17 Available studies suggest that the use of TCB could reduce the frequency of outpatient blood sampling for TSB ^ ^December 2007/ Pediatric EM Reports
There is no evidence upon which to base the decision as to when followup should occur Availability of the neonate’s primary care physician Distance the family must travel to receive care Reliability of the parents How close the TSB level is to the treatment threshold Presesnse of clinical symptoms suggestive neurotoxicity Follow up guideline Factors impacting this decision include : Pead. EM book ,Jill barin,2008
Guidline for phototherapy--- Rosen American Academy of Pediatrics. Subcommittee on Hyperbili.Clinical practice guideline
Guidline for exchange Tx --- Rosen American Academy of Pediatrics. Subcommittee on Hyperbili.Clinical practice guideline
<ul><li>SnMP is a structural analog of heme </li></ul><ul><li>It blocks the site on heme oxygenase where conversion of heme to bilirubin occurs. </li></ul><ul><li>Still under investigation </li></ul><ul><li>Administered parenterally in a small dose (6 micromoles/kg) </li></ul><ul><li>Some preterm infants still needed phototherapy but none needed exchange transfusion </li></ul><ul><li>Virtually 100% efficacy </li></ul><ul><li>Can also be used repeatedly for patients with Crigler-Najar (effects last several days). </li></ul><ul><li>Stanate ® -currently being patented </li></ul>
11 D old , bottle-feeding infant parents c/o his poor appetite for 24 hrs ,, BP 82/52,PR 150,temp. 36.2 ,, O/E mild dehydrated ,mild jaundice ,,,, which of the following is mot important diagnostic study : <ul><li>Bilirubin level </li></ul>B. Lumber puncture C. Periphral smear D. Reticulocyte count E. TSH F. No need Inx as this is milk-feeding juindice,just advised the mother to breast feed child and FU after 24 hrs
Neonatal jaundice is common, but hyperbilirubenemia Induced neurotoxicity is critical Estimates TSB based on clinical examination are not reliable Jaundiced infants exhibiting signs & symptoms suggestive of a concurrent serious illness require more extensive diagnostic testing and empirical Rx For infants at higher risk, decisions will need to be made on an individual basis Conj. Hyperbilirubinemia is never physiological