Presented at Belfast City Hospital Physician's Meeting.
Topic - A case of Focal Segmental Glomerulosclerosis with all the complications of nephrotic syndrome and transplant recurrence of FSGS.
Presented at Belfast City Hospital Physician's Meeting.
Topic - A case of Focal Segmental Glomerulosclerosis with all the complications of nephrotic syndrome and transplant recurrence of FSGS.
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
Neonatal jaundice occurs in 60% of term and 80% of preterm babies. Despite Neonatal jaundice is one of the commonest neonatal conditions, there are no national practice guidelines for its management in our country. Lack of uniform guidelines and standard practice parameters for diagnosis and management of neonatal jaundice often leads many babies to develop unnoticed hyperbilirubinemia causing kernicterus and long term poor neurological sequelae. This review after briefly discussing the epidemiology and pathophysiology of neonatal jaundice provides evidence-based pragmatic guidelines for the diagnosis and management of neonatal jaundice in resource-limited countries like Afghanistan
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
NEONATAL JAUNDICE- ALL YOU NEED TO KNOW
1. NEONATAL JAUNDICE
A PRESENTATION BY MARY NYAMBURA MUONGOYA
DEFINITION
Neonatal jaundice referstothe yellowishdiscolorationof the white partof the eyes (sclera) andskinina
newbornbabydue to bilirubindepositioninthese tissuessecondary tohighserumbilirubinlevels
(hyperbilirubinemia) thatoccurswhenthe rate of productionexceedsthe rate of elimination.
EPIDEMIOLOGY
Jaundice isa commonneonatal problem.
65% of newbornsdevelopclinical jaundice withabilirubinlevel above 5mg/dLduring the firstweekof
life.
However,significantjaundice occursin6 % of term babies
BILIRUBIN METABOLISM
There are six basicstepsinthe metabolismof bilirubinthese are;
1) Production
Bilirubinisthe endproductof heme( ironprotopophyrin)catabolism.
There are three mainsourcesof heme;
o The firstis the breakdown of effete(senescent) RBCS by cellsof the
reticuloendothelial system.
o The secondis throughineffective erythropoiesis (destruction of developing
erythroidcellsinmarrow.
o The third isa non-erythropoieticcomponent,resultingfromturnoverof
nonhemoglobinsourcesof hemee.g.cytochromes,catalase,peroxidase and
myoglobin.
In the newborninfant,the normal destructionof the circulatingredbloodcellsinthe
RES accounts forapproximately 75% of the dailyproductionof bilirubin.The other25%
of the dailyproductionof bilirubinisderivedfromsourcesother thansenescentred
bloodcells(listedabove)
The conversionof the heme moietytobilirubinrequiresthe sequentialactionof two
enzymes;
o Heme oxygenase-toformbiliverdin,carbonmonoxide andiron
o Biliverdinreductase- thisisareducednicotinamide adeninedinucleotide
phosphate (NADPH) dependentenzymethatcatalyzesconversionof biliverdin
to bilirubin.
Each 1 g of hemoglobinbreakdownresultsinthe productionof 34 mg of bilirubin(1mg/dL=
17.2umol/L of bilirubin).
2. 2) Transport
Bilirubinistransportedinplasmaboundtoalbumin.Humanalbuminhasasingle,tight,high
affinity (orprimary) bindingsite forbilirubinandone ormore weaker,lower affinitybinding
sites.
The capacity of serumalbumintobindbilirubinisknownasthe bindingcapacityandthe
strengthof the bilirubin- albuminbondisreferredtoasthe bindingaffinity.
The amount of free bilirubinisverylow atphysiological pH.
The bindingcapacity,bindingaffinityandamountof free bilirubincanbe estimatedbyIvitro
measurementsandprovidea measure,albeitonlyapproximate,of the amountof bilirubinthat
may be available tocause neuronal injury.
3) Hepaticuptake
Hepatocyteshave aselective andhighlyefficientsystemforremovingunconjugatedbilirubin
fromplasma.Thismechanismrequiresseveral differentorganicaniontransport proteins.
Variantsof one of these,organicaniontransporter2(OATP2),maybe importantindetermining
the riskof severe hyperbilirubinemiainAsianinfants.
In the hepatocyte, the transportedbilirubinisboundtoligandin,acytosolicprotein,that
facilitatestransfertothe endoplasmicreticulum,the site of bilirubinconjugation.
4) Conjugation
Carriedoutby the microsomal enzyme uridine diphosphate glucoronyl transferasewhichis
encodedbythe UGT1A1 gene to formbilirubinmonoglucoronideanddiglucoronide.
5) Excretion
The conjugatedbilirubinisexcretedintothe bile.itisthentransportedtothe small intestine where
In the presence of normal gutflora,the conjugatedbilirubinismetabolizedfurthertostercobilins
and excretedinthe stool.
6) Enterohepaticcirculation
Intestinal betaglucuronidasehydrolyzesthe conjugatedbilirubinthusreleasingfreebilirubin
whichisthenreabsorbedandtransportedbythe portal circulationtothe liver.
POSSIBLE CLINICAL OUTCOMES OF HYERBILIRUBINEMIA
Jaundice
Acute bilirubinencephalopathy
Chronicbilirubinencephalopathy/kernicterus
RISK FACTORS FOR NNJ (MNEMONIC-JAUNDICE)
Jaundice withinthe first24hours
A siblingwhowasjaundicedasaneonate
Unrecognizedhemolysis
3. Nonoptimal sucking/nursing
Deficiencyof G6PD
Infections
Cephalohematoma/bruising
East Asian/NorthIndian
SYMPTOMS (visible form of bilirubinemia is ≥ 5mg/dl)
Scleral yellowing
Skinyellowing
Mucous membrane yellowing
Nail yellowing
Excesssleepiness
Poorfeeding
Physical examcluestosome etiologies:
o Sepsis:lethargy,temperature instability,poorfeeding,vomiting,apneaortachypnea
o Hemolytic disease: pallor,hepatosplenomegaly
o Extravascularhemolysis: birthtraumaassociatedwithcephalohematomaorbruising
o Polycythemia:ruddycomplexion
o Cholestaticjaundice:persistentjaundicefor3 weeks,darkurine orlight-coloredstools
WHERE TO LOOK FOR SKIN JAUNDICE
Forehead
Tip of the nose
Chest
Knees
Palmsand soles
CLINICAL ASSESSMENT / EVALUATION
VISUALINSPECTION
Examine babyinbrightnatural lightor white fluorescentlight.
Baby shouldbe naked.
Examine blanched skinandgums.
N/B: NORMAL BILIRUBIN LEVELS ARE 1- 1.5mg/dl
Kramer’s rule is usedto determinethe extentof jaundice.
Level 1-headandneck - 5mg/dl
Level 2- upper trunk above the umbilicus - 5-10mg/dl
Level 3- lowertrunkand thighs-10-12mg/dl
5. Measurementof serumbilirubin
o Transcutaneousbilirubinometer
o Serumbilirubinlevels
ETIOLOGY
Causesof neonatal jaundice canbe broadlydividedintotwo;
Causesof unconjugated( indirect) hyperbilirubinemia
Causesof conjugated( direct) hyperbilirubinemia
CAUSES OFUNCONJUGATED (INDIRECT/WATERINSOLLUBLE)HYPERBILIRUBINEMIA
PHYSIOLOGICCAUSES
o IncreasedRBCmass (polycythemia)
o Shorterlife spanof fetal RBCS(80-90 days ina term infant)
o Relativelylowactivityof the enzyme glucoronyl transferase- terminfantshave 1%
of adultactivity,preterminfantshave 0.1%. before birththisenzymeisactively
downregulatedsince bilirubinneedstoremainunconjugatedIordertocross the
palcentato avoidaccumulationinthe fetus.
o Immature hepaticuptake
o Relativelylowconversionof bilirubintourobilinogenbygutflora.
PATHOLOGIC CAUSES
o HEMOLYTIC CAUSES
o CAUSES INTRINSICTOTHE RBCS
Membrane defects- spherocytosis,elliptocytosis,pyknocytosis,and
stomatocytosis
Enzyme defects- G6PDdeficiency,pyruvatekinasedeficiency,hexokinase
deficiency
Globinsynthesisdefects- α thalassemia,sickle celldisease
o CAUSES EXTRINSICTO THE RBCS
Alloimmunity- ABOorrhesusincompatibility,anti-kell,anti-duffy
Systemicconditions- sepsis,sequesteredblood(e.g. cephalohematoma,
bruising,intracranial hemorrhage)
o NON HEMOLYTIC CAUSES
Breastmilkjaundice
a) Breastmilkhas an enzyme calledlipoproteinlipase thatproduceshigh
concentrationsof nonesterifiedfree fattyacidsthatinhibithepatic
glucoronyl transferase ladingtodecreasedbilirubinconjugationand
thushyperbilirubinemia.
6. b) Breastmilkcontainsa metabolite of progesterone called3-α-20beta
pregnanediolthatinhibitsactionof uridine diphosphoglucuronicacid
glucoronyl transferase leadingtodecreasedbilirubinconjugation.
c) At birth,the gut issterile andnormal gutflora take time to establish.In
the absence of gut flora,bilirubinisdeconjugatedbybrushborderbeta
glucuronidase andisreabsorbed.
Breastfeedingjaundice
Pyloricstenosis
Polycythemia
a) Due to maternal-fetaltransfusion
b) Fetal-fetaltransfusion
c) Infantsof diabeticmothers
Sepsis
a) bacterial
b) viral
c) protozoa
Hypothyroidism-causesdecreasedbilirubinuptake intothe hepatocyte.
Extravascularhemorrhage (whichresultsinreabsorptionof hemolyzed
blood)
a) Cephalohematoma
b) CNShemorrhage
c) Extensive bruising
CriglerNajjarsyndrome (autosomal recessive diseasescausedbyvarious
mutationsinthe UGT1 gene.CriglerNajjarsyndrome type1refersto
congenital absence of UDP glucuronyl transferasecauseslifelong
unconjugatedhyperbilirubinemia.CriglerNajjartype 2is causedby a
reductioninUDP glucoronyl transferaseandhasa milderphenotype)
Gilbert’ssyndrome (familialpartial defectinglucuronyl transferaseactivity
due to mutationsinthe promotorregioninthe UGT1gene)
Lucy-Driscoll syndrome(severe unconjugatedhyperbilirubinemiathoughtto
be due to inhibitionof infant'sglucuronyltransferasebyunidentified
maternal serumfactors)
N/B: THE CAUSES OF UNCONJUGATED HYPERBILIRUBINEMIA CAN ALSO BE GROUPED
INTO TWO MAIN CATEGORIES: OVERPRODUCTION OF BILIRUBIN AND DECREASED
CONJUGATION OF BILIRUBIN. OVERPRODUCTION COULD BE DUE TO HEMOLYTIC OR NON
7. HEMOLYTIC CAUSES WHILE DECREASED CONJUGATION COULD BE DUE TO THE
SYNDROMES ABOVE OR HYSIOLOGIC JAUNDICE.
DEFINITION OF PATHOLOGIC JAUNDICE
Clinical jaundiceinthe first24 hours of life
Clinical jaundicelasting>14 daysof life
Increase of bilirubin>5 mg / dl / day
Total bilirubin>331.5 ᶙmol/L
Directbilirubin>34ᶙmol/L( > 2 mg / dl)
Stool clay/ white coloredandurine stainingclothesyellow
DEFINITION OF PHYSIOLOGIC JAUNDICE
Appearsafter24 hours
Clinicallynotdetectableafter14 days
Maximumintensityby4th-5thdayinterm & 7th dayin preterm
Serumlevel lessthan15 mg/ dl
Disappearswithoutanytreatment
jaundice occurswhenbilirubinnormally increasesfrom1.5mg/dL incord bloodto a meanof
6.5 mg/dLon day 3, followedbyagradual decline tonormal adultlevelsof 1.5 mg/dLby day 10
or 12 of life
MECHANISMS OF PHYSIOLOGIC JAUNDICE
Increasedproductionof bilirubin ( approx 2-3Xona perkilogrambodyweightbasis,thanadults)
o Increasedineffectiveerythropoiesis
o IncreasedRBCmass/erythrocyte volume
o Short RBC life span(80-90)
Decreasedhepaticuptake- low concentrationof the bindingproteinligandininthe hepatocytes
hence decreaseduptake from intothe hepatocyteendoplasmicreticulum.
Decreasedhepaticconjugation- decreased activityof glucoronyl transferase
Increasedenterohepaticcirculation-conjugatedbilirubinisexcretedthroughthe bileintothe
intestine,where it sisdecconjugatedbyamucosal enzyme,βglucuronidase andreabsorbedinto
the enterohepaticcirculationbefeore itcanbe excretedwiththe stool. Newbornshave a
paucityof gut floraand relative caloricdeprivationinthe firstdaysof life,bothof which
promote physiologichyperbilirubinemiathroughincreasedenterohepaticcirculation.
Diminishedbindingtoalbuminandbilirubinbindingprotein
Physiologicjaundice canbe aggravatedby;
8. Immaturity
Cephalohematoma
Birthasphyxia
Hypothermia
Infection
breastfeeding
CAUSES OFCONJUGATED(DIRECT/WATERSOLUBLE)HYPERBILIRUBINEMIA
HEPATIC CAUSES
o INFECTIONS
o Neonatal idiopathichepatitis
o HepatitisA
o HepatitisB
o TORCH
o Bacterial infectionse.g.E.Coli andurinarytract infections
o METABOLIC
o α1 antitrypsin deficiency
o galactosemia
o tyrosinemia
o Fructosemia
o DubinJohnson syndrome- anautosomal recessive diseasecausedbya
mutationinABCC2 onchromosome 10q24 that resultsinalterationsin
bilirubinexcretionviaMRP2.In normal circumstances,bilirubin
diglucoronideispredominantlyexcretedintothe canaliculusbyacarrier
proteinlocalizedtothe MRP2 on the canalicularmembrane.
o Hypopituitarism
o Cysticfibrosis
o Glycogenstorage disorders
o Cerebrohepatorenaldisease ( Zellweger)
o Rotor syndrome- anautosomal recessive diseasecausedbymutationsin
SLCO1B1 andSLCO1B3 on chromosome 12 that resultinthe absence of
OATP1B1 and OATP1B3 on the basolateral surface of hepatocytes.
o DRUGS
o TPN
o Neonatal hemosiderosis
o shockliverfromneonatal asphyxia
POST HEPATIC CAUSES/ EXTRAHEPATIC CAUSES
9. Biliaryatresia- aprogressive diseasecharacterizedbyinflammationandfibrosisof the
extrahepaticbiliarytractresultinginpartial orcomplete obliterationof the extrahepaticbile
ducts.
Choledochal cyst- acysticdilatationof the biliarytract,maybe exclusivelyextrahepaticor
include dilatationsof the intrahepaticbiliarytract.
Alagille syndrome
Bile plugsyndrome
COMPLICATIONS
ACUTE BILIRUBIN ENCEPHALOPATHY
Acute bilirubinencephalopathyis characterizedby;
o Lethargy
o Highpitchedcrying
o Poorfeeding/refusaltofeed
o Irritability
o Jitteriness
o Apnea
o Seizures
o Opisthotonus andretrocolis
o Sunsettingof eyes
o sluggishmoro reflex
KERNICTERUS- causedbybilirubintoxicitytothe basal gangliaandbrainstemnuclei
o Choreoathetoidcerebral palsy
o Upward gaze palsy
o Sensorineural hearingloss
o Dental dysplasia
o Intellectual retardationandlearningdisabilities
MANAGEMENT
PRIMARYPREVENTION
Ensuringadequate feeding
Breastfedinfantsshouldhave 8to 12 feedingdper24 hours.
Formula-fed,full terminfantsshouldconsume 150 kcal per kg perday.
10. DEFINITIVE MANAGEMENT
Treat basedon
TSB
Gestational age and
Cause of jaundice (non-Shemolyticvs.hemolytic)
There are five maintreatmentmodalitiesusedin the managementof jaundice;
PHOTOTHERAPY
AIM: Loweringthe total serumbilirubinconcentration.
LIGHTS: In practice,lightisusedinthe white,blue,turquoise andgreenwavelengths.
Bilirubinabsorbslightprimarilyaround450- 460 nm.
The bestlightis narrow spectrumblue lightsinthe range of 425- 475 nmbut white lampsin
the range of 380-700 nmcouldbe used.
Althoughgreenlighttheoreticallypenetratesskinbetter,ithasnotbeenshown
unequivocallytobe more efficientinclinical use thanblue orwhite light.Besides,green
lightmakesbabieslooksickandisunpleasanttoworkin.
MECHANISMS:
Backgroundknowledge :Thereare fourstructural isomersof bilirubinnamelythe ZZ,ZE,EE
ANDEZ isomerswiththe ZZisomerbeingthe stable more insoluble form.
o Photo-isomerization/configurationalisomerization- thisisaveryrapidand
reversiblereactionthatinvolvesconversionof insoluble toxicformZ isomertonon-
toxicpolarE isomerwhichdiffusesintobloodandisexcretedinbile.
o Structural isomerization- thisisanirreversiblereactionthatinvolves consistingof
intramolecularcyclizationresultingin conversionof bilirubintolumirubinwhichis
rapidlyexcretedinbileandurine. Thisprocessisenhancedbyincreasingthe
intensityof light.Lumirubinisthe primarypigmentfoundinbileduring
phototherapy.
o Photo-oxidation- slow andminorreactioninvolvingphotooxidationof bilirubinto
watersoluble polymersformingacolorlessbyproduct.Thisreactioniscatalyzedby
riboflavin.
INDICATIONS:
o Total serumbilirubin>18mg % in terminfantsand>15 mg % in preterminfants.
o Adjuvanttoexchange transfusion.
o Prophylacticphototherapyfor;ELBW,extremelypreterminfants,babieswithDCT
positivity,baby’swhosemotherisICTpositive
PROCEDURE:
o Selectblue lightsinthe range of 425-475 nm
o Setthe distance fromthe skintobe 45 cm (IPTdistance is15-20 cm)
o Shieldeyes andgenitalia
11. o Change positiononce every2-4hours
o TSB levelscheckedevery10-12hours
o Frequenttemperaturemonitoringanddailyweightcheck
SIDE EFFECTS:
IMMEDIATE LATE
LOOSE STOOLS RISKOF SKIN MALIGNANCY
DEHYDRATION-insensiblewaterlossmay
occur
DAMAGE TO INTRACELLULAR DNA
HYPO/HYPERTHERMIA RETINALDAMAGE
RASHES TESTICULAR DAMAGE
BRONZEBABY SYNDROME
HYPOCALCEMIA
12. EXCHANGE TRANSFUSION
INDICATIONS:
Alloimmune hemolyticdisease of the newborn
o Remove circulatingbilirubintoreduce levelsandpreventkernicterus
o Replace antibody-coatedredcellswithantigen-negativeredcells
o To remove antibodiesassociatedwithredbloodcell hemolysis.
Severe hyperbilirubinaemia secondary to alloimmune haemolyticdiseaseof
the newborn isthe mostcommon reason forexchangetransfusion in the
neonatalintensivecare unit.
Treatment/correctionof Severe anaemia(where there isnormal orincreased
circulatingbloodvolume)
Polycythemia(toreduce haematocrit,usuallyaccomplishedwithpartial exchange
transfusionusingnormal salinereplacement)
Significantunconjugatedhyperbilirubinaemiawithriskof kernicterusdue toany
cause whenintensivephototherapyisunsuccessful
Antibodiesinmaternal autoimmune disease
Severe disturbancesof bodychemistry
PARENTAL CONSENT:
Informedwrittenconsentmustbe obtained.
Consentisdocumentedonaconsentform(AgreementtoTreatmentCR0111).
Consentforbloodisdocumentedonthe reverse side of form CR0111.
In special circumstances (e.g. baby transferred, a shocked anaemic baby with a
parent not available) verbal consent by a parent is acceptable provided it is
documented in baby's clinical record and written consent obtained as soon as
possible
AIM:
Decreasingthe serumbilirubinlevels(thisreducesthe riskof braindamage
(kernicterus))
Decreasingthe sensitizedorabnormal redbloodcells
Remove the offendingantibodysothatongoinghemolysiswill be decreased.
13. EXCHANGE VOLUME:
BloodVolume =70-90 ml/kgfortermand 85-110 ml/kgforpreterminfants
One bloodvolume removes65% of baby's redcells.
Two bloodvolumesremove 88%
ALIQUOTS:
WEIGHT OF NEONATE ALIQUOT VOLUME
<1000 grams 5ml
1000-2000 grams 10ml
>2000 grams 15ml
TECHNIQUE:
Exchange transfusionsare performedusingeither one catheterortwo catheterpush-pull
method. Thisset-upisa jointresponsibilitybetweenmedical andnursingstaff,butthe
specialistdoingthe exchange hasoverall responsibilityforthe procedure.
1. Two Catheter Push-pull Technique
Bloodisremovedfromthe arterywhile infusingfreshbloodthroughaveinatthe same rate.
In Out
Umbilical vein Peripheral artery
or Umbilical vein Umbilical artery
or Peripheral vein Peripheral artery2
or Peripheral vein Umbilical artery
2. One Catheter Push-pull Technique
Thiscan be done throughan umbilical venouscatheter.Exceptionally,anumbilical artery
cathetercan be used.
14. Ideally,the tipof the UVCshouldbe inthe IVC/rightatrium(atorjust above the diaphragm) but
can be usedif itis inthe portal sinus.For 'high'UVC placement,positionshouldbe checkedby
an X-ray.Thisis notalwaysnecessaryfora low position.A low positionedcatheterisusually
removedaftereachexchange.
Withdrawbloodover2 minutes,infuseslightlyfaster.
MONITORING AND DOCUMENTATION:
1. Recordbaseline observationspriortocommencingexchangetransfusion.
- Axilla/rectal temperature
- Heart rate
- Respiratoryrate
- Bloodpressure
- Oxygensaturationandcolour
2. Continuouslymonitorandrecordat 15 minute intervalsonthe recordof Exchange
Transfusionsheet(CR5730),the followingobservations:
- Skintemperature
- Heart rate
- Respiratoryrate
- Oxygensaturation
- BloodPressure (non-invasive)
3. Recordaxilla/rectal temperaturerecorded15minutes aftereach donor pack is
commenced,and then every30 minutesduring the transfusion.
4. Observe foranychangesinneurological status - drowsiness,irritability.
5. Recordbloodin/bloodoutonthe Recordof Exchange Transfusionsheet(CR5730).Keepa
runningtotal.
6. Recordbloodresultsonthe Exchange TransfusionResultsSheet(CR5729)
7. Maintaincontinuouselectronicmonitoringof vital signsforatleasttwohourspost
transfusion(orlongerif baby'sconditionisnot stable).
The entire procedure shouldtake 1-2hoursand shouldbe performedusingaseptic
technique
15. COMPLICATIONS
Be aware of thispossibility,observe the babycarefully andhave resuscitation
equipmentready
During Exchange
Air embolus Ensure the linesare correctlysetup.
Watch the linescontinuouslyforair.
Turn the line off instantlyif airisseen.
Neverhave a3 way tap opentoair and the baby
Be verycareful if there are large swingsinintrathoracicpressure.
Volume imbalance The nurse is responsible forrecordingthe volume balance throughoutthe
exchange.
Arrhythmias Can occur from a varietyof causes.
Setthe monitortohave an audible QRScomplex.
Acidosis Bloodfor exchange transfusionispreservedinCPD(citrate,phosphate,
dextrose) andcanbe quite acidotic.
Checkthe baby's bloodpHbefore,during (usually half way),andafterthe
exchange
Checkmore frequentlyforasick,unstable orsmall baby.
16. Respiratory distress MonitorrespirationandSpO2 constantly.
Hyperkalemia CPD bloodcan have highpotassium[K+] levels.
Check[K+] at the start of each bag.
Monitorthe QRS complex.(forarrhythmia,wideningQRS)
MonitorK+ witheachbloodgas.
Anemia/Polycythemia Checkthe PCV of eachbloodbag.
Agitate the bagevery 15 minutes.
FluctuatingBP and
cerebral blood flow
Monitorrate of bloodinandout carefully.
After Exchange
Infection Prophylacticantibioticsare notindicated.
Observe closelyforsignsof infection.
Hypocalcaemia Monitorcalcium[Ca++] and give replacementCa++in IV fluidsasper
clinical guidelines
Hypoglycaemia Unlikelyduringthe exchange asCPDbloodhas19mmol/L [glucose].
Howeverreboundhypoglycaemiamayoccurafterwards.
Commence a10% glucose infusionpostexchange,orif the exchange is
interrupted.
Hypernatraemia CPD bloodhasa high[Na+].Monitor [Na+] witheachgas.
Thrombocytopenia Verycommon,andmore severe aftermore exchanges(due toincreased
plateletconsumption).
Recoversina few days.
Monitorplatelets seriallyforaweekpostexchange.
17. Polycythaemiaor
anaemia
From poorlymixedorpackedblood.
Coagulopathy or
neutropenia
More likelythe multiple transfusions.
Necrotisingenterocolitis Umbilical catheterrelated(especiallywithalow UVC) and maybe due to
BP and bloodvolume fluctuations.
Take care withfeedingpostexchange
Blood transmitted
infections
For a detailedlistrefertoBloodProducts - RBC guideline
Graft versusHost
disease
There have beenseveral case reports.
It seemstobe more likelywithmore preterminfants,intrauterine
transfusions,multiple exchanges,andrelateddonors.
Irradiate the donorblood.
Drug therapy
IVIG
Metallopophyrintin/zinc
REASONS OF REFERRAL
Onsetof jaundice within24hours
Rapidlyrisingbilirubingreaterthan6mg/dl/day(103umol/L/day)
Clinical jaundicebelowumbilicus(12-15mg/dl /205-257umol/L)
Clinical jaundicetill the solesof the feet
G6PD deficiency
s/sx of sepsis