Neonatal jaundice

• Nearly every newborn is a little jaundiced, because red cell breakdown is brisk, the liver's conjugating enzyme is immature, and gut bacteria are not yet established enough to keep bilirubin from being reabsorbed.
• "Physiological" jaundice starts after the first day, rises slowly, is unconjugated, and fades by about two weeks in term babies and three weeks in preterm babies. "Pathological" jaundice arrives in the first 24 hours, rises fast, may be conjugated, or outlasts the usual time course, and always demands a cause.
• The danger is unconjugated bilirubin crossing an immature blood-brain barrier and depositing in the basal ganglia, producing acute bilirubin encephalopathy and, if unchecked, permanent kernicterus.
• Management rests on three pillars: measure the bilirubin and its form, check for haemolysis (ABO or rhesus incompatibility, G6PD deficiency, bruising), and apply phototherapy, intravenous immunoglobulin or exchange transfusion at the hour-specific thresholds for gestational age.
• Conjugated (direct) jaundice in any newborn is never physiological. Pale stools and dark urine are the warning signs, and urgent referral for cholestasis, including biliary atresia, is mandatory.

By the end of this page you should be able to:

1. Tell physiological from pathological jaundice by timing, bilirubin species and rate of rise, and list the main causes in each group.
2. Explain why newborns are prone to unconjugated hyperbilirubinaemia, from fetal red cell lifespan to UGT1A1 immaturity and enterohepatic circulation.
3. Describe haemolytic jaundice from ABO and rhesus incompatibility and from G6PD deficiency, and interpret the Coombs (direct antiglobulin) test.
4. Recognise breastfeeding and breast milk jaundice as two different things, and manage each without stopping breastfeeding.
5. Explain how kernicterus and acute bilirubin encephalopathy arise and show themselves, and state the bilirubin levels that raise the risk.
6. Read an hour-specific bilirubin threshold table and decide when phototherapy, intensified phototherapy, intravenous immunoglobulin and exchange transfusion are indicated.
7. Investigate prolonged jaundice and conjugated jaundice, and name the cholestatic causes, including biliary atresia.
8. Adapt jaundice care to low-resource settings.

Unconjugated bilirubin is lipid soluble and travels in plasma bound to albumin. It can cross cell membranes and, when the blood-brain barrier is immature, enter brain tissue. Conjugated bilirubin is water soluble, cannot cross the blood-brain barrier in the same way, and appears in the urine. That single distinction organises the whole topic.

Jaundice is almost universal in the first week of life: roughly 60 to 80 percent of the 134 million babies born each year develop some degree of jaundice, and about 18 percent (around 24 million) are diagnosed with clinically significant hyperbilirubinaemia. ^[4] Up to 35 percent of first-month hospital readmissions are for jaundice. ^{[4] [1]}

Among term infants about 50 percent and among preterm infants about 80 percent are affected. ^[3] In high-income settings, kernicterus has been driven down to roughly 1 case per 100,000 live births, whereas in low-income regions, particularly sub-Saharan Africa and South Asia, estimates run from 25 to 38 cases per 100,000 live births; the incidence of severe neonatal jaundice in sub-Saharan Africa and Southeast Asia exceeds 600 per 10,000 live births against only 3 to 4 per 10,000 in Europe and the Americas. ^[3] The vast majority of infants with severe disease reside in sub-Saharan Africa and South Asia. ^[4]

A useful bedside rule is that jaundice visible in the first 24 hours is haemolysis or another pathology until proven otherwise, and any term baby still jaundiced after day 14 (or preterm after day 21) needs the prolonged-jaundice assessment below.

Bilirubin is a breakdown product of haem, mostly from senescent red blood cells. Haem becomes biliverdin, and biliverdin reductase converts it to unconjugated bilirubin, which binds albumin in plasma and travels to the hepatocyte. There UGT1A1 (uridine diphosphate-glucuronosyltransferase 1A1) attaches glucuronic acid to make conjugated, water-soluble bilirubin, which the canalicular transporter MRP2 excretes into bile. The bowel bacteria then convert it to stercobilin in the stool and to urobilinogen, some of which is reabsorbed (enterohepatic circulation).

Three neonatal facts overload this system:

1. Fetal red cells live only 70 to 90 days, against 120 days in adults, so the bilirubin load per kilogram is higher from birth. ^[3]
2. Hepatic UGT1A1 activity is low at birth and rises over the first weeks, so conjugation lags behind production.
3. Intestinal beta-glucuronidase activity is high in the newborn, deconjugating bilirubin in the gut and sending it back into the circulation instead of out into the stool; this is worsened by delayed passage of meconium and by poor early feeding.

Unconjugated bilirubin is lipophilic and, in excess, crosses the immature blood-brain barrier and binds to the basal ganglia, brainstem and cerebellar nuclei. Albumin binds most of it in plasma, but once the binding sites are saturated, or when competing substances (certain drugs, free fatty acids in sick, hypoalbuminaemic infants) displace it, the free fraction rises. This is the link between high unconjugated bilirubin and brain injury. Conjugated bilirubin does not cause kernicterus in the same way, which is why direct hyperbilirubinaemia points to a cholestatic cause rather than a neurotoxic risk in the short term.

ABO incompatibility. A mother of blood group O has naturally occurring anti-A and anti-B IgG antibodies that cross the placenta and destroy the red cells of a group A or group B fetus. Jaundice appears early (often within the first day), is often deep, and is accompanied by anaemia and reticulocytosis. The direct antiglobulin test (DAT, the Coombs test) on the baby's red cells is positive. Disease is usually milder than rhesus disease but is far more common. Management includes phototherapy, intravenous immunoglobulin when the bilirubin is rising despite it, and, rarely, exchange transfusion.

Rhesus (Rh) incompatibility. An RhD-negative mother carrying an RhD-positive fetus becomes sensitised and makes anti-D antibodies that haemolyse fetal and neonatal red cells. This tends to be more severe than ABO disease: early and deep jaundice, pronounced anaemia, hepatosplenomegaly, and a positive DAT. Anti-D immunoglobulin given to RhD-negative women in pregnancy and after delivery has made this condition uncommon in well-served settings, which is why rhesus haemolytic disease is often seen where antenatal screening and prophylaxis are missed.

G6PD deficiency. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked red cell enzyme defect. It is the most common red cell enzymopathy worldwide and is concentrated where malaria is or was endemic. It produces a haemolytic, unconjugated jaundice, sometimes triggered by oxidative stress (infection, certain drugs, naphthalene in mothballs, fava beans in later life), but neonatal jaundice can occur without any trigger, and it is a leading preventable cause of severe neonatal jaundice in sub-Saharan Africa and South Asia. ^[3][4] Because the haemolysis can be episodic and the G6PD level can be falsely normal during an acute haemolytic crisis, the assay is best sent after the baby recovers, and testing policy follows ethnic origin and local prevalence as the NICE guideline advises. ^[1]

Other production causes. Cephalhaematoma, subgaleal haemorrhage and bruising from delivery increase haem breakdown. Sepsis can haemolyse red cells and also depress conjugation, so a sick, jaundiced neonate needs cultures and prompt treatment.

It helps to think of all unconjugated jaundice as "too much input or not enough conjugation". The relevant defects range from the benign to the catastrophic:

• Physiological immaturity. Low UGT1A1 activity at birth.
• Prematurity. More immature UGT1A1, lower albumin, and delayed meconium.
• Gilbert syndrome. A common, benign reduction in UGT1A1 activity of roughly 30 percent. Unconjugated bilirubin usually sits between 17.1 and 102.6 micromol/L and stays mostly under 85.5 micromol/L; it is commoner in men and declares itself in adolescence, not the newborn (covered in more detail in the topic on isolated hyperbilirubinaemia). ^[2]
• Crigler-Najjar syndrome. Type 1 has no enzyme activity and total bilirubin of 342 micromol/L or more from birth, does not respond to phenobarbital, carries a high risk of encephalopathy, and needs phototherapy and plasma exchange in the first week of life with liver transplantation as the cure. Type 2 has under 10 percent activity and bilirubin of 102.6 to 342.0 micromol/L; phenobarbital lowers it by 25 to 30 percent, and childhood treatment is considered once it exceeds 200 micromol/L. ^[2]
• Hypothyroidism and galactosaemia. Metabolic conditions that depress conjugation. Routine metabolic screening (including screening for congenital hypothyroidism) is part of the prolonged-jaundice assessment precisely to catch these. ^[1]
• Drugs and sepsis. Some drugs inhibit UGT1A1, and sepsis can do both: produce and reduce conjugation.

This text refers to the inherited disorders of bilirubin only briefly, because they are covered in detail in the MedGrasp topic on isolated hyperbilirubinaemia.

These are two different entities, and confusing them causes needless worry and unnecessary bottle feeding.

• Breastfeeding jaundice is an early, unconjugated jaundice caused by inadequate milk intake: the baby is dehydrated and sleepy, passage of meconium is delayed, and enterohepatic circulation rises. Breastfeeding more often, with proper positioning and skilled support, prevents and reverses it. Temporary supplementation with expressed breast milk may be needed if the baby is very sleepy, but stopping breastfeeding is not the treatment.
• Breast milk jaundice appears from about days 2 to 3, rises slowly and may persist for 3 to 12 weeks, despite good feeding and adequate weight gain. Constituents of breast milk are thought to slow conjugation. It is benign and does not require stopping breastfeeding; reassure the parents and follow the bilirubin. ^[2]

Both are driven by the same physiology: low early intake and increased enterohepatic recirculation. The two differ in timing, severity and clinical course, which is how you tell them apart at the bedside.

A conjugated (direct) fraction making up more than a small part of the total is abnormal at any age in the newborn. It is the liver's conjugating machinery working while the export pathway or the biliary tree is blocked. These babies are not treated by nomograms; they need diagnosis.

• Biliary atresia. Fibro-obliteration of the extrahepatic bile ducts, presenting with progressive conjugated jaundice after the first two weeks, pale (acholic) stools, dark urine that stains the nappy, a firm enlarged liver and, later, splenomegaly. It is an emergency in the truest sense: the Kasai portoenterostomy is time-critical, and delay worsens outcome. Any baby with prolonged jaundice and a conjugated bilirubin above 25 micromol/L should be referred urgently to a centre with paediatric hepatology and surgery. ^[1]
• Neonatal hepatitis. Inflammation of the liver in the newborn from infection (congenital infections such as cytomegalovirus and Toxoplasma, and other viral or bacterial infections), metabolic disease, genetic cholestasis, or the aftermath of perinatal insults. It can look like biliary atresia clinically; imaging and, eventually, biopsy or cholangiography separate them.
• Choledochal cyst. A cystic dilatation of the bile duct, sometimes presenting as conjugated jaundice, sometimes as a mass or pain, diagnosed by ultrasound and solved surgically.
• Neonatal cholestasis more generally. Sepsis, total parenteral nutrition, prematurity and haemolysis can all produce a conjugated rise, particularly in sick, small babies on intensive care.
• Parenteral nutrition-associated cholestasis. The liver needs enteral stimulation; prolonged exclusive parenteral nutrition in preterm or surgical babies switches on cholestasis. Prevention and treatment centre on introducing and advancing enteral feeds, cycling the parenteral nutrition, and using liver-protective lipid formulations where available.
• Alagille syndrome, progressive familial intrahepatic cholestasis and metabolic diseases. Rare genetic causes of cholestasis that may present in the neonatal period; they sit behind biliary atresia and neonatal hepatitis in frequency but belong in the differential.

Because NICE advises against subtracting the conjugated bilirubin from the total when applying treatment thresholds, ^[1] and because conjugated jaundice is worked up and treated on its own merits rather than by the unconjugated nomograms, the correct first step in any baby who looks cholestatic is referral, not phototherapy.

This is the complication that makes neonatal jaundice a public health issue.

Acute bilirubin encephalopathy is the early, reversible stage of bilirubin-induced neurotoxicity. The early signs are lethargy, poor feeding, diminished or abnormal muscle tone (hypotonia that can become hypertonia), a high-pitched cry and irritability. ^[2][4] Left untreated, it progresses to rigidity, opisthotonus, fever, seizures and apnoea; severe cases can end in death. ^[2] The onset is insidious and, with rare exceptions, only unconjugated hyperbilirubinaemia at clinically important levels does this.

Kernicterus is the chronic, irreversible end state, defined as permanent bilirubin-induced brain damage, with athetoid cerebral palsy, sensorineural hearing loss (often out of proportion to the movement disorder), gaze palsy and, in some survivors, cognitive impairment and dental enamel dysplasia. ^[2][4]

The risk of kernicterus rises with three independent factors in the NICE guideline: a serum bilirubin above 340 micromol/L in a baby of 37 weeks or more gestation; a rapidly rising level of more than 8.5 micromol/L per hour; and any clinical feature of acute bilirubin encephalopathy. ^[1] Severe jaundice is defined by most guidelines as 342 micromol/L (20 mg/dL) or more, and hazardous as 513 micromol/L (30 mg/dL) or more. ^[4]

Take a history that covers the risk factors directly:

• gestational age, birth weight and mode of delivery
• maternal ABO and Rh(D) status, antenatal screening and anti-D, plus family history of jaundice or haemolytic disease
• feeding method and frequency, stool and urine output, and weight loss
• when the jaundice first appeared, how fast it is deepening, and whether it extends to the trunk or legs
• drugs, infection, birth trauma, cephalhaematoma or bruising
• ethnic origin (G6PD is commoner in particular populations) and any family history of red cell disorders

On examination:

• inspect in bright, preferably natural, light: look at the sclerae and gums and blanch the skin on the nose with gentle pressure; be aware that yellowing can be much harder to see in darker skin. ^[1]
• grade by colour and extent, but never rely on visual inspection alone to estimate the bilirubin. ^[1]
• check for anaemia (pallor), hepatosplenomegaly (haemolysis or cholestasis), bruising, cephalhaematoma, sepsis and signs of acute bilirubin encephalopathy.
• check for pale or chalky stools and dark urine staining the nappy in any baby with prolonged or deep jaundice.

Bilirubin measurement. Measure serum bilirubin in the first 24 hours of life or in any baby under 35 weeks gestation. In babies of 35 weeks or more who are more than 24 hours old, use a transcutaneous bilirubinometer first; if it gives a value above 250 micromol/L, confirm with a serum value, and use serum for all subsequent measurements once the level is at or above the treatment threshold. ^[1] Visual inspection alone is never enough to estimate the level. ^[1]

Cord blood bilirubin, end-tidal carbon monoxide and the cord direct antiglobulin test (Coombs) must not be used to predict significant hyperbilirubinaemia. ^[1]

Underlying cause screen (significant hyperbilirubinaemia). ^[1]

• serum bilirubin (baseline, to judge response to treatment)
• blood packed cell volume (haematocrit)
• blood group of mother and baby
• direct antiglobulin test (Coombs): positive in rhesus and ABO haemolytic disease, negative in Gilbert syndrome and Crigler-Najjar disease, and positive in autoimmune haemolysis
• full blood count and blood film, where clinically indicated
• glucose-6-phosphate dehydrogenase levels, taking ethnic origin into account
• microbiological cultures of blood, urine and (if infection is suspected) cerebrospinal fluid.

Why each test is done. The Coombs test looks for maternal antibody bound to the baby's red cells and is the diagnostic signature of immune haemolysis. The packed cell volume tells you how bad the anaemia is; the reticulocyte percentage (high in haemolysis, under 1.5 percent in Gilbert syndrome) and blood film tell you whether the bone marrow is being driven to replace lost cells; haptoglobin falls and lactate dehydrogenase rises in haemolysis; the Coombs test is negative in inherited enzyme and conjugation disorders. ^[2]

Prolonged jaundice assessment (term 14 days; preterm 21 days). ^[1]

• look for pale, chalky stools or dark urine that stains the nappy
• measure the conjugated bilirubin (report as total, direct and unconjugated)
• full blood count
• mother's and baby's blood group and direct antiglobulin test
• consider a urine culture if there is clinical suspicion of infection
• confirm that routine metabolic screening, including screening for congenital hypothyroidism, has been done.

A conjugated (direct) bilirubin above 25 micromol/L may indicate serious liver disease and needs expert advice. ^[1]

The table below is the consensus, hour-by-hour guide for babies of 38 weeks gestation or more, from the NICE guideline. ^[1] It is only an illustration of the principle (age in hours on one axis, threshold on the other); thresholds differ between countries' guidelines, and assay variability means local laboratories should be consulted, especially where the measured bilirubin sits near a cut-off. ^[1]

Practical points that come with the thresholds: ^[1]

• The bilirubin is interpreted by postnatal age in hours, not by days or by "mild, moderate, severe".
• Do not subtract the conjugated bilirubin from the total when making decisions about management, and do not use an albumin-to-bilirubin ratio.
• For babies less than 38 weeks, or for preterm or sick babies, other charts and a lower threshold are used, and the national guideline or neonatal unit protocol takes over.
• Do not start phototherapy unless the level exceeds the phototherapy threshold for that age.
• If a well baby of 38 weeks or more has a level below but within 50 micromol/L of the phototherapy threshold, repeat the measurement within 18 hours (risk factors present) or 24 hours (no risk factors); if it is more than 50 micromol/L below, do not routinely repeat it.
• Once phototherapy is running, repeat the serum bilirubin in 4 to 6 hours, then every 6 to 12 hours while it is stable or falling; stop phototherapy once the level is at least 50 micromol/L below the phototherapy threshold; recheck for rebound 12 to 18 hours after stopping. ^[1]
• Intensify phototherapy (extra irradiance from another light source or a higher output) if the serum bilirubin is rising by more than 8.5 micromol/L per hour, is within 50 micromol/L of the exchange transfusion threshold after 72 hours, or is not falling within 6 hours of starting phototherapy. When it then falls to 50 micromol/L below the exchange threshold, the intensity can be reduced. ^[1]
• High-risk babies (bilirubin above 340 micromol/L, rapidly rising over 8.5 micromol/L per hour, or any clinical feature of acute bilirubin encephalopathy) need the response that follows, including exchange transfusion.

Other major guidelines (the American Academy of Pediatrics 2022 revision is the most widely cited, and Canadian, Japanese and WHO guidance also exist) publish their own hour-specific, gestation-specific nomograms, and they do not agree on every number. ^[4] Use the chart your service adopts, apply it consistently, and say so in your notes rather than mixing two thresholds in one baby.

Phototherapy is the first-line treatment for hyperbilirubinaemia of any severity, even when an exchange transfusion is imminent. ^[4] It works by converting unconjugated bilirubin into water-soluble photoisomers that can be excreted without conjugation. Modern devices use blue-green light with a wavelength around 460 to 490 nm. Standard phototherapy delivers 8 to 10 microwatts per square centimetre per nanometre to one body surface, and intensive phototherapy delivers 30 microwatts per square centimetre per nanometre or more. ^[4] The effect depends on irradiance, spectrum, the area of skin exposed and the duration of exposure. ^[4]

Good phototherapy practice: ^[1]

• place the baby on the back (or prone as needed) with maximal skin exposed, nothing between the light and the skin except a nappy on boys
• give eye protection and routine eye care while under the lights
• keep a thermoneutral environment, monitor temperature and hydration, and weigh daily
• encourage short breaks of up to 30 minutes for breastfeeding, nappy change and cuddles; during intensified phototherapy do not interrupt the light but continue enteral or intravenous feeds. ^[1]

Do not use sunlight as treatment. ^[1] It is uncontrolled, causes sunburn, dehydration and hyperthermia, and is unreliable. In low-resource settings where electric phototherapy cannot be assured, filtered sunlight in a purpose-built, ventilated, light-filtering enclosure has been studied as a non-inferior alternative for daytime treatment, and is better than exposing the baby to direct sun or to no treatment at all. ^[4]

Intravenous immunoglobulin. In rhesus or ABO haemolytic disease, give IVIG at 500 mg/kg over 4 hours as an adjunct to continuous intensified phototherapy when the serum bilirubin keeps rising by more than 8.5 micromol/L per hour. ^[1] This can reduce the need for exchange transfusion, though results are variable and the evidence is strongest in rhesus disease.

Exchange transfusion. A double-volume exchange is the rescue treatment for a level that reaches the exchange threshold on the chart above, or for any clinical feature or sign of acute bilirubin encephalopathy. ^[1] Do not stop intensified phototherapy during the exchange; do not use a single-volume exchange, albumin priming or routine intravenous calcium. ^[1] After the exchange, continue intensified phototherapy, measure the serum bilirubin within 2 hours, and manage further by the thresholds. ^[1] The NICE guideline requires that parents be told the exchange needs an intensive care bed and what it involves and what the side effects are. ^[1]

Feeding. Encourage mothers with a jaundiced baby to breastfeed frequently and to wake the baby for feeds. ^[1] Give lactation support. Do not give extra water, which dilutes electrolytes and worsens enterohepatic recirculation; if additional feeds are needed, maternal expressed milk is the first choice. ^[1] Feeding is itself the treatment in breastfeeding jaundice and helps re-establish the bowel transit that clears bilirubin in every baby.

The management of conjugated jaundice is diagnosis first: assess liver function, image the biliary tree by ultrasound (and, where available, hepatobiliary scintigraphy or intraoperative cholangiography), look for infection and metabolic disease, and refer early to paediatric hepatology and, for biliary atresia, to paediatric surgery. Vitamin K is given to correct the coagulopathy of cholestasis, nutrition is supported (medium-chain triglyceride feeds and fat-soluble vitamins), and the bile flow is optimised where a drug or sepsis is the cause. Kasai portoenterostomy is time-critical, which is why any conjugated jaundice beyond the first two weeks triggers an urgent pathway.

• Acute bilirubin encephalopathy and kernicterus, as above, the main preventable neurological harm.
• Dehydration and poor feeding, which in turn worsen hyperbilirubinaemia by slowing meconium and bilirubin clearance.
• Anaemia and hydrops in severe rhesus disease.
• Sepsis, which may mimic or accompany haemolysis and is a common precipitant.
• Phototherapy side effects: loose stools, temperature instability, skin changes, reduced vitamin B6 and folate in prolonged courses, and the rare possibility of long-term effects, which is why phototherapy is not used when the level is below threshold.
• Exchange transfusion complications: hypocalcaemia if calcium is not handled correctly, arrhythmia, thrombosis, the need for repeat treatment if rebound is not caught.

Physiological jaundice is self-limiting and benign, and even most treated hyperbilirubinaemia leaves no sequelae. The prognosis worsens with delay: once neuronal injury from bilirubin has occurred it is permanent, although mild cases may show only subtle cognitive, motor or hearing deficits years later. ^[3] With prompt phototherapy and, where needed, exchange transfusion, the outcome for haemolytic disease in centres with good blood-banking is excellent. Biliary atresia has a different prognosis, determined by the timing of Kasai surgery and the need for liver transplantation; in well-served systems a substantial proportion of affected children reach adulthood with their native liver.

• Antenatal screening and anti-D immunoglobulin for Rh-negative women, to prevent rhesus sensitisation, plus blood grouping.
• Avoidance of triggers for G6PD deficiency: certain drugs (sulfonamides, nitrofurantoin, chloramphenicol, primaquine and others), mothball (naphthalene) exposure and, later in life, fava beans; universal newborn G6PD screening in high-prevalence regions reduces severe jaundice admissions.
• Vitamin K and good delivery practice reduce bruising and haemorrhage, both causes of jaundice.
• Universal bilirubin screening before discharge with transcutaneous or serum measurement in the first 24 to 48 hours, and earlier if the baby leaves hospital sooner, identifies at-risk infants before bilirubin reaches neurotoxic levels; this is one of the most evidence-supported interventions for preventing severe hyperbilirubinaemia. ^[3][4]
• Parent education: parents are taught how jaundice looks and told to return urgently if the baby becomes yellow in the first 24 hours, if feeding fails, or if stools turn pale or urine dark.
• Feeding support: early, frequent, effective breastfeeding prevents breastfeeding jaundice and the dehydration that both deepens jaundice and hides it until it is advanced.

• Preterm babies. Lower UGT1A1 and albumin, slower meconium, longer jaundice and lower thresholds; phototherapy is needed earlier and for longer.
• Breastfed babies. See the two entities above; do not stop breastfeeding for jaundice. Supplement only when the baby is too sleepy to feed, using expressed breast milk first. ^[1]
• Babies with darker skin. Visual screening is less sensitive; transcutaneous or serum bilirubin should be used rather than relying on the eye. ^[1]
• Babies born outside hospital in low-income settings. A large minority of babies in sub-Saharan Africa and South Asia are born with limited or no access to routine bilirubin screening and to phototherapy; this underlies the difference in kernicterus rates. ^[4]

• Screen early and often. Train midwives and community health workers to assess the sclerae, gums and blanched skin during any postnatal contact, and to send high-risk babies (visible jaundice in the first 24 hours, a previous sibling who needed phototherapy, preterm, exclusive breastfeeding without good intake) for measurement, even if a laboratory is far away. ^[1][3]
• Use what works. Transcutaneous bilirubinometers are relatively cheap, non-invasive and battery-friendly and are recommended by WHO screening advice; point-of-care serum assays can confirm hazardous levels. ^[4]
• Support breastfeeding and feeding in every contact; it prevents and treats the commonest form.
• Keep phototherapy running. Invest in simple, well-maintained LED or fluorescent devices, their protective goggles and spares, and in keeping them in use. ^[1]
• Filtered sunlight phototherapy, in a purpose-built, ventilated, light-filtering enclosure with temperature and body-temperature monitoring, has been shown to be non-inferior to conventional phototherapy for daytime treatment and is better than direct sun or no treatment at all where electric phototherapy cannot be assured; it needs more research and pilot work at a given site. ^[4]
• Plan referrals before the emergency: agree where a baby can go for exchange transfusion, keep compatible blood available, and refer promptly once the threshold is approached or any sign of encephalopathy appears.
• Refer cholestasis early. Pale stools and dark urine in the second or third week are easy to miss, and late Kasai surgery changes a child's life.

• Neonatal jaundice is a sign, not a disease. It is split by whether the bilirubin is unconjugated (physiological, haemolytic or metabolic) or conjugated (cholestatic), and that distinction drives the whole work-up.
• Physiological jaundice starts after day 1, is unconjugated, peaks in the first week and resolves by day 14 in term babies and day 21 in preterm babies. ^[2]
• Pathological jaundice starts in the first 24 hours, rises fast, is conjugated, or lasts beyond the usual time course.
• Unconjugated bilirubin can cross the blood-brain barrier and injure the basal ganglia, producing acute bilirubin encephalopathy and, if unchecked, irreversible kernicterus.
• Haemolytic causes (ABO, rhesus, G6PD) produce early, deep jaundice with a positive Coombs test in immune haemolysis; anaemia and reticulocytosis confirm the process.
• Breastfeeding jaundice (poor intake, early) and breast milk jaundice (late-presenting, good feeder, benign) are different; neither requires stopping breastfeeding.
• Conjugated (direct) jaundice is never physiological. Pale stools, dark urine or jaundice beyond two weeks mean urgent referral for biliary atresia and other cholestasis.
• Measure serum bilirubin in the first 24 hours or in babies under 35 weeks; otherwise start with transcutaneous measurement. Always confirm a level above 250 micromol/L by serum testing.
• The risk of kernicterus rises with bilirubin above 340 micromol/L (in babies of 37 weeks or more), a rise above 8.5 micromol/L per hour, or any clinical sign of acute bilirubin encephalopathy.
• Phototherapy is first-line treatment; it is intensified for a rising or unresponsive level and is stopped once the level is at least 50 micromol/L below threshold, with rebound testing at 12 to 18 hours.
• IVIG (500 mg/kg over 4 hours) is given with intensified phototherapy for rhesus and ABO disease when the bilirubin continues to rise by more than 8.5 micromol/L per hour.
• Double-volume exchange transfusion is used for an exchange threshold or for the clinical signs of acute bilirubin encephalopathy, with phototherapy continued throughout.
• Visual screening alone is unreliable, especially in dark skin; use objective bilirubin measurement and withhold phototherapy when the level is below threshold.
• Do not use sunlight as treatment; in low-resource settings filtered sunlight phototherapy is a studied bridge where electric phototherapy is unavailable.

Isolated hyperbilirubinaemia and inherited disorders of bilirubin (Gilbert, Crigler-Najjar, Dubin-Johnson and Rotor syndromes); haemolytic anaemias generally; G6PD deficiency; blood group and rhesus incompatibility in the newborn; biliary atresia and neonatal cholestasis; conjugated hyperbilirubinaemia and liver disease in infants; intravenous immunoglobulin and exchange transfusion in neonatal practice; breastfeeding support in the postnatal period.