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The Neonate- Full neonatal exam- SGA/LGA- Preterm- Jaundice- Infections- Cold stress cycleJaundice Readings and Quiz Fully comprehend how neonatal jaundice relates to bilirubin metabolism Define and contrast physiological (breast milk) jaundice and pathological jaundice Outline the diagnosis, manage...

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The Neonate -

Full neonatal exam SGA/LGA Preterm Jaundice Infections Cold stress cycle

Jaundice Readings and Quiz 1. 2.

Fully comprehend how neonatal jaundice relates to bilirubin metabolism Define and contrast physiological (breast milk) jaundice and pathological jaundice 3. Outline the diagnosis, management, and treatment of neonatal jaundice that is within the scope of the midwife 4. Identify when medical referral is needed for complications of jaundice 5. Awareness of neonatal risk factors and maternal history associated with pathological jaundice (e.g. Rh disease, ABO incompatibility and G6PD [glucose-6phosphate deydrogenase enzyme]) Physiological • one of the most common physiological problems in the newborn 60% of term infants (80% preterm) part of the normal physiology of the neonate • Due to normal neonatal adaptation to extra-uterine life Pathological • Arises from factors that alter the neonates usual physiological processes • Common pathologies: ABO incompatibility, Rhesus factor incompatibility • Uncommon pathologies: Biliary atresia, Glucose-6-phosphate dehyrogenase (G6PD) deficiency Breastfeeding • early onset: feeding related (‘breastfeeding failure’ or ‘breastfeeding’ jaundice) • late onset: constituents in breastmilk cause an increase in UCB in the body (‘breastmilk jaundice’ • Video 1: Jaundice: Means yellowing - Can be also called Icterus Yellow pigment in the skin, sclera and mucous membranes. Yellow pigment caused by bilirubin – which is found in bile Contributes to yellow in urine and brown in faeces The bilirubin is broken down by the spleen by reticuloendothelial system: macrophage system 1

Bilirubin metabolism When broken down the RBC is split into globin (-> amnio acids) and heme (->iron and protoporphyrin which goes into unconjugated bilirubin which is lipid soluble NOT water soluble) Unconjugated bilirubin is taken to the liver where it is conjugated by UGT (uridine glucosyl transferase) where it becomes water soluble. Drains into the bile duct. The common bile duct drains into the small intestine. The bilirubin is converted into urobilinogen which is transferred into stercobilin which makes the brown colour of faeces/ Some of the urobilinogen is reabsorbed into the blood and taken to the liver or kidneys as urobilin which makes the yellow colour of urine. If the liver cells are immature or damaged serum bilirubin levels increase which causes jaundice. Takes >2.5mg/dl to give yellow appearance. High levels of unconjugated bilirubin in the blood: ineffective haematopoiesis (poor formation of RBC) or extravascular haemolytic anaemia (broken down too early) – both overwhelm RBC breakdown causing levels to increase. Conjugated: lots of bile, some is reabsorbed into the blood, makes urine very yellow and the liver as bilirubin is stored in the interstitial space. Newborns have a low level of UGT to convert bilirubin. It can cause brain damage if left untreated. Treatment: phototherapy as this changes the shape of the unconjugated bilirubin making it more water soluble. Video 2 Jaundice of the skin and conjunctiva Can be early signs of a greater issue… is it benign or pathological? Jaundice is caused by elevated levels of unconjugated levels of bilirubin in the blood. As conjugated bilirubin is excreted through newborn stool. Hyperbilirubinemia/jaundice - High number of RBC - Shorter RBC lifespan - Slower liver conjugation - Increased reabsorption of conjugated bilirubin Lipid soluble bilirubin can cross the blood brain barrier and cause brain damage causing kernicterus: hearing loss, brain damage and death. Pathological jaundice: Immediately begin a work up for possible sepsis and blood group incompatibility. Other causes of jaundice could be things that decrease liver function: Hypoxic liver injury or G6PD deficiency Treatment is phototherapy or transfusion of blood.

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Learning Activity Quiz on jaundice – 1.

Bilirubin is a product of red blood cell / haemoglobin breakdown.

2. a.

Haemolysis is increased in neonates more than adults. True or False? Why? List 2 reasons Immature liver cells and enzymes fHb has a lower life expectancy thus higher turnover (increased haemolysis) Breakdown due to transition from a low 02 environment to high 02 Higher GI reabsorption Low input in BF babies Have more RBC than adults

3.

Bilirubin is conjugated in the Hepatocytes, which are cells of the Liver.

4.

Water soluble bilirubin is called conjugated bilirubin or urobilinogen

or stercobilin a. Does it cause Kernicterus? Yes or No b. Why? Kernicterus is a rare and preventable brain damage that occurs to newborns that have jaundice. It occurs when serum bilirubin levels are too high. Unconjugated bilirubin is deposited in the brain by diffusing across the blood brain barrier as it is fat soluble and can’t be excreted readily by the body. If left untreated can be fatal. 5. Jaundice is not clinically apparent until the serum bilirubin (SBR) level is approx. 80/85 μmol/L. 6. How does Early feeding for the neonate aid bilirubin excretion? Yes as it increases gut movements which aids in excretion – helps the bile duct empty bile as food moves through the GI tract. Conjugated Bilirubin is excreted in the gut by way of biliary excretion (CG is stored in bile ducts after it’s production in the liver). Bile is only secreted to aid in food digestion (enzymes can breakdown fats for uptake by the body) so without food activating peristalsis, bile won’t be secreted and bilirubin won’t convert to it’s final exreted forms (stercobilonigoen and urobilin) 7. Bilirubin must bind with albumin in the blood steam to travel to the liver to be conjugated. True or False? “Bilirubin binds to albumin and is transported to the liver, where it is conjugated” 8. The sclera becomes yellow first. True or False? High concentrations of elastin which bilirubin likes to bind to. 9. Stercobilinogen is produced in the small intestine and responsible for the brown colour in feces. a. What colour would baby’s stool be that has high levels of stercobilinogen? brown/meconium coloured 3

10. Would delayed cord clamping increase bilirubin levels in the neonate? Yes or No Why? Because there are greater levels of RBC in the blood stream. Higher erthythrocytes/RBCs; potential for increased haemolysis as more blood from cord during DCC

Section 2 Multiple choice Bilirubin Metabolism 1. Jaundice is caused by: a. Excess of uric acid in the blood b. Excess of haemoglobin in the blood c. Excess of bilirubin in the blood d. Excess of potassium in the blood

2. a. b. c. d.

Bilirubin is a waste product released during the breakdown of: Mast cells Erythrocytes White cells Platelets

3.

Pre-hepatic jaundice is caused by anything which causes an increased rate of haemolysis (breakdown of________): a. Blood plasma b. Haem c. Haematology d. Platelet

4.

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of________ in the biliary system. a. Human gastrointestinal tract b. Secretin c. Digestion d. Bile

5.

It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the ________, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. a. Stool b. Toilet c. Blood d. Faeces

6. a. b. c. 4

Breastmilk can increase the incidence of jaundice because: Decreased volume of colostrum reduces gut motility Difficulty to latch, poor suck, delayed lactation Factors in breastmilk that increase unconjugated bilirubin

d.

A breastmilk fat binds to bilirubin so it cannot be metabolised

Jaundice metabolism Jaundice is a medical condition with yellowing of the skin or whites of the eyes and is is due to excessive production OR decreased elimination of bilirubin • HYPERBILIRUBINAEMIA refers to an excessive blood level of accumulated bilirubin • By age 96 hours/4 days old, serum bilirubin levels are 137-154 µmol/L Bilirubin is clinically noticeable at ~ 85 µmol/L PRODUCTION Bilirubin production occurs in the spleen – RBC are broken into unconjugated bilirubin. TRANSPORTATION binds to albumin and taken to the liver hepatocytes Cannot travel without it as it is fat soluble and doesn’t dissociate in the blood. CONJUGATION The liver cells use the enzyme to change albumin-UCB into water soluble form called conjugated bilirubin which is excreted into the duodenum and small intestine. CB is better for the neonate as it can be excreted readily and does not cross the blood brain barrier. EXCRETION In faeces as stercobilinogen and urine as uroblinogen. NEONATAL PHYSIOLOGY AND JAUNDICE: Neonates are more at risk of increased bilirubin because: 1. They are born with more RBCs than needed for life ex utero and Foetal RBC lifespan is shorter 80 -100 days than adults (120d) 2. Increased entero-hepatic reabsorption of conjugated-bilirubin due to initial lower levels of gut bacteria (until microbes colonise) 3. The immature neonatal liver (enzymes) are unable to metabolise the unconjugated bilirubin for excretion so UCBs build up in fatty deposits (e.g. sclera & skin) Note: Meconium contains up to 175g bilirubin that can be reabsorbed back into the bloodstream (entero-hepatic portal system)

Increased Production: RBC Haemolysis

Decreased Excretion: Low gut microbial activity

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Decreased Metabolism: mmature Liver enzymes

THREE TYPES OF JAUNDICE Physiological • one of the most common physiological problems in the newborn 60% of term infants (80% preterm) part of the normal physiology of the neonate • Due to normal neonatal adaptation to extra-uterine life Pathological • Arises from factors that alter the neonates usual physiological processes • Common pathologies: ABO incompatibility, Rhesus factor incompatibility • Uncommon pathologies: Biliary atresia, Glucose-6-phosphate dehyrogenase (G6PD) deficiency Breastfeeding • early onset: feeding related (‘breastfeeding failure’ or ‘breastfeeding’ jaundice) • late onset: constituents in breastmilk cause an increase in UCB in the body (‘breastmilk jaundice’) MIDWIFERY MANAGEMENT History and assessment to establish if jaundice is pathological or physiological Clinical history of mother/family• Maternal vs Baby Blood group and Rhesus Factor • Baby- age/gestation? Preterm leading to very immature neonatal adaptation • Family genetic factors? RBC issues, Enzyme deficiencies, Hx of jaundiced babies History of labour, Type of birth • Instrumental leading to bruising/cephalhaematoma/birth trauma? Maternal Fever? Behaviour overall • Feeding pattern, disinclination to feed, sleepy/lethargy etc • Is this a well baby? TERM BABY 1. Take history and clinically assess to establish if jaundice is pathological or physiological 2. If physiological – advise: • Frequent feeds – 3 hourly day & night • Show mother ways to wake baby up • Assess output, fecal and urine colour 3. Follow up next day and continue to monitor baby’s jaundice levels (Kramer’s Rule), alertness, feeding patterns and output • If in doubt, take or arrange for SBR, urgent analysis and follow up ‘phone with result’ There is no evidence that supports this practice. Risks outweigh any perceived advantage: high UV levels – sunburn and Melanoma development (Ghazi et al., 2012) 6

• • • •

Neonatal jaundice in first 24 h Jaundiced neonate whose mother has rhesus antibodies Preterm baby whose SBR > 200 μmol/L Neonate who has clinical signs of obstructive jaundice (pale stools, dark urine) • Prolonged hyperbilirubinemia >7-10 days in term and 2 weeks in prem infant – could be pathological Unconjugated patholgies: Breastmilk jaundice, Infection, Hypothyroidism, Pyloric stenosis Conjugated pathologies: Biliary Atresia, Enzyme defects KRAMERS RULE – ONLY FOR TERM BABIES: Kramer’s tool (grading jaundice by its progression from the head downwards) helps visually identify the degree of jaundice. Under Kramer’s rule, clinical jaundice is first obvious in the face and progresses downwards to the toes as it increases in intensity When looking for jaundice (visual inspection): Check the NAKED BABY in bright & preferably natural light Examine the SCLERA, GUMS & BLANCHED SKIN or GUMS with gloved finger (useful across all skin tones)

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Zone

Average serum bilirubin

1

100 µmol/l jaundice terminating at the neck

2

150 µmol/L jaundice terminating at the umbilicus/upper arms

3

200 µmol/L jaundice from umbilicus to knees

4

250 µmol/L jaundice to lower arms/below knees to the point wrists/ankles

5

>250 µmol/L jaundice from top to toe

Double check Maternal Blood group: • Pre-warns if likely to have ABO or RH incompatibility while red blood cell antibody screening in pregnancy alerts to any sensitisation Perform heel prick for Neonatal Serum bilirubin (SBR): • bilirubin total good estimate of indirect bilirubin ONGOING MANAGEMENT Hydration Effective, frequent (3-hourly) and early breastfeeding • Increases bowel motility Phototherapy? Blue light on bare skin in a warm room • enhances bilirubin excretion • ABO or Rhesus Pathologies: • Exchange Transfusion (Blood Transfusion) • Replacing neonatal blood with fresh Rhesus-negative blood (generally only needed for babies with haemolytic disease) WHEN TO REFER TO PEADIATRICIAN Reason

Recommenda

Jaundice in first 24 hours

Transfer

Bilirubin > 250 micromol/L in first 48 hours

Consultation

Bilirubin > 300 micromol/L at any time

Consultation

Late jaundice: visible or >150 micromol/l from 2 weeks in term infant and 3 weeks in preterm infant

Consultation

Significant jaundice in previous infant

Consultation

TO REMEMBER • Ensuring early frequent feeds (3 hourly) is the best means of minimising the chance of physiological jaundice • Jaundice appearing before 24 hours of age= abnormal. • What constitutes normal levels of bilirubin depends on the age/gestation of infant, speed of increase, and condition of infant. • Infants with transitory hyperbilirubineamia (without kernicterus) do not appear to have any long-term problems.

Narrative: the risks of diagnostic testing (amniocentesis) for down syndrome sometimes outweighs the benefits of finding out. 1/1000 risk for miscarriage. With high risk results refer to Maternal Fetal Medicine. Don’t say that everything will be alright – may not be Establish a clear understanding that the screening is not always accurate. 8

Termination is offered but should be educated on the normal lives down syndrome babies can have. Important that normal processes are adhered to in abnormal circumstances such as when the neonate is diagnosed with fetal/neonatal conditions/diseases. Guthrie test is very sensitive and can pick up carriers of the disease – needs official diagnosis.

Neonatal energy triangle: Metabolism, thermoregulation and respiratory adaptation – the three biggest challenges faced by the preterm infant Fetus prepares for transition primarily in the third trimester by storing glycogen and producing catecholamines and depositing brown fat – this makes a preterm infant less prepared for life. Thermal and glycaemic stability together with effortless respiration are critical physiological functions. Body temperature, oxygen levels and glucose are variables that are important to neonatal health. All three are essential for the regulation of enzymes and cellular function. Neonatal hypoxia, hypothermia and hypoglycaemia are signs of a failure to transition – and can affect neonatal survival. AT birth glucose levels are 70% of the mothers serum levels. Intermittent feeding ensures glucose homeostasis. After clamping the cord the neonates glucose levels drop, reaching their lowest at 1-2 hours after. Glycogenolysis is replaced by gluconeogenesis so that the brain is not fuel deficient. The neonate also decreases insulin production, and increases glucagon, epinephrine, growth hormone, and cortisol secretion. Lipolysis also occurs creating ketone bodies which can be used as a fuel source, competing with glucose allowing neonates to mobilise their glucose stores. IN SUMMARY postnatal metabolic adaptation is characterised by vigorous ketogenesis. Impaired metabolic adaptation Hypoglycaemia is the result of inadequate hepatic glucose production that cannot meet the demand or excessive insulin production. Delayed feeders or preterm infants are at risk. Early insitituion of feeding IV dextrose is paramount to the preterm baby. Concurrent conditions such as hypoxia and hypothermia may occur as the baby doesn’t have the fuel to initiate such actions like breathing and keeping warm. These will also cause issues for babies in maintaining blood glucose levels. AT RISK babies - Mothers with diabetes - Mothers with drug treatment - Intrapartum glucose administration for mothers Neonatal factors - Preterm - IGUR - Perinatal hypoxia - Hypothermia - Infection 9

- Polycythaemia - Syndromes Babies with these risk factors should undergo glucose testing. Signs associated with hypoglycaemia: - Change in level of consciousness: lethargy, drowsiness, coma - Changes in behaviour: irritable, jitteriness, poor feeding, hypotonia - Changes in vital signs As glucose is important for the brain, abnormal levels that prevail for a long time have the potential to induce long term neurological injury. There is debate over the levels at which are appropriate as these depend on BW, feeding method, gestation, PN age. One policy states: levels should be above 2.5mmol/l in a preterm infant 3.5mmol/l for those with anticipated levels eg SGA Questions: Most glycogen stores take place at? After birth there is a decrease in the blood level of..? Glucose What is a sign of hypoglycaemia? Hypothermia What infants are at risk of hypoglycaemia? Born to diabetic mothers and SGA The level of hypoglycaemia that results in serious sequelae is well researched? False THERMOREGULATORY AND RESPIRATORY ADAPTATION Fetal mechanisms for the cold stress response are not active in utero as the mother constitutes as a heat reservoir for the baby – babies temp usually being 0.5 degrees higher than its mother’s core temp. When the infant is born into a wet and cold environment – temperatures drop rapidly between 0.2-1º/min. In a term infant the response is to increase involuntary muscle activity, vasoconstriction and non-shivering thermogenesis (shivering is not apart of the human newborn thermal response). Term infants are able to increase their metabolic rate for a few hours – and thus effectively be thermoregulated, however after that energy stores deplete and hypothermia can be induced. Hypothermia in newborns are associated with adverse outcomes, preterm infants are at increased risk, why?..

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Large surface area to body mass ratio Low stores of subcutaneous fat Decreased brown fat Greater water content Immature skin Poorly developed metabolism mechanism Delayed development of skin blood flow (vasoconstriction is poor)

Premature newborns are unable to maintain adequate temperatures without an external heat source. In a premature newborn if the normal mechanisms in response to cold stress pursued to the extreme, this may lead to peripheral and pulmonary vasoconstriction which decreases oxygenation. This is because metabolic activity creates a high demand for oxygen – decreasing its availability elsewhere. Hypoxia with an accumulation of lactic acidosis resulting from anaerobic respiration can switch off the production of surfactant. Neutral thermal environment: ambient temperature where a newborn can maintain normal body temperature with minimal metabolic rate and oxygen consumption. Newborns can have a normal core temperature and still be c...