Jaundice is the yellow discolouration of skin and sclerae caused by accumulation of bilirubin in tissues. Bilirubin is a breakdown product of haem from red blood cell destruction.
Unconjugated bilirubin crosses the blood-brain barrier and is directly neurotoxic. Conjugated bilirubin does NOT cause kernicterus.
| Feature | Physiological | Pathological |
|---|---|---|
| Onset | Day 2–4 | First 24 hours |
| Duration (term) | Resolves by day 10–14 | Persists >14 days |
| Duration (preterm) | Resolves by day 21 | Persists >21 days |
| Rate of rise | Slow (<85 μmol/L/day) | Rapid (>85 μmol/L/day) |
| Conjugated component | None (<20 μmol/L) | Present (>20 μmol/L) |
| SBR level | Below treatment threshold | May exceed threshold |
| Stool/urine colour | Normal | Pale stools, dark urine (if conjugated) |
Pale stools + dark urine in a jaundiced neonate = biliary atresia until proven otherwise. Urgent split bilirubin + surgical referral.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is X-linked recessive. Prevalence is very high in the GCC — up to 10–25% of males in some Arab and African populations. Females are mostly carriers but can be affected if homozygous.
G6PD protects RBCs from oxidative stress. Deficiency leads to oxidative haemolysis when triggered — often severe and sudden in neonates.
All GCC neonates should be screened for G6PD deficiency (mandatory in UAE, Qatar, Saudi Arabia). G6PD-deficient neonates have lower phototherapy/exchange thresholds.
Jaundice progresses in a cephalocaudal direction. Kramer's rule correlates clinical zone with approximate SBR — but is unreliable and should NOT be used as sole assessment. Use transcutaneous bilirubinometer or SBR.
Visual assessment is unreliable in dark-skinned neonates. Always confirm with TcB or SBR. Kramer zones are for orientation only.
Phototherapy converts unconjugated bilirubin in skin and superficial capillaries into water-soluble isomers (photoisomers and lumirubin) via photoisomerisation and photooxidation. These isomers are excreted in bile and urine without requiring hepatic conjugation.
Blue-green light: 425–490 nm (blue light most effective). Special blue fluorescent tubes or LED devices are most efficient. Standard white light is less effective.
Standard: ≥6 μW/cm²/nm
Intensive: ≥30 μW/cm²/nm — measured at skin surface
Determined by SBR plotted on the NICE Bhutani nomogram thresholds adjusted for gestational age and postnatal age in hours. Lower thresholds apply for:
Single overhead lamp. Baby supine. Exposes front surface only. Effective for mild-moderate jaundice. Ensure lamp is at correct distance per manufacturer specification (usually 35–50 cm).
Overhead lamp plus fibre-optic biliblanket beneath the baby. Exposes both anterior and posterior surfaces simultaneously. Doubles effective skin surface area — used for moderate-high bilirubin levels or near exchange threshold.
Multiple devices, high-irradiance blue LED or special blue fluorescent tubes. Device distance reduced to <10 cm from skin surface. Used when SBR is near or above exchange threshold. Irradiance ≥30 μW/cm²/nm required. Monitor temperature closely — hyperthermia risk.
Bronze baby syndrome occurs when phototherapy is given to neonates with conjugated (direct) hyperbilirubinaemia. The skin develops a grey-green/bronze discolouration due to accumulation of phototherapy byproducts.
Phototherapy can be stopped when SBR has fallen to at least 50 μmol/L below the treatment threshold and is falling.
Consult blood bank early — irradiated CMV-negative blood may require 2–4 hours to prepare.
| Parameter | Timing | Concern |
|---|---|---|
| Glucose | Before, during, after | Hypoglycaemia — citrated blood depletes calcium |
| Calcium (iCa) | Every 50–100 mL exchanged | Hypocalcaemia (citrate binds Ca²⁺) |
| Potassium | Before, after | Hyperkalaemia from old blood / haemolysis |
| SBR | Immediately post-exchange, then 2h | Rebound rise expected — check at 2h |
| FBC + coagulation | Post-exchange | Thrombocytopenia common |
| Complication | Mechanism | Prevention / Management | Severity |
|---|---|---|---|
| Hypocalcaemia | Citrate in donor blood chelates calcium | Monitor iCa q50mL; IV calcium gluconate 10% if symptomatic (jitteriness, apnoea, prolonged QT) | Common |
| Hypoglycaemia | Glucose-poor donor blood; rebound insulin surge post-exchange | Monitor glucose before, during, after; IV dextrose as required | Common |
| Hypothermia | Cold blood infused; exposed neonate | Warm blood to 37°C; maintain incubator/warmer; monitor temperature q15min | Common |
| Thrombocytopenia | Dilutional; platelet-poor stored blood | Post-exchange FBC; platelet transfusion if <50 × 10⁹/L and symptomatic | Common |
| NEC | Gut ischaemia during exchange; UVC compromise | Hold enteral feeds 4–6h pre/post exchange; monitor for abdominal distension, bilious aspirates | Serious |
| Air embolism | Air entering UVC during push-pull | Purge all lines; closed system; nurse monitors for sudden deterioration | Rare — fatal |
| Graft vs Host Disease | Donor lymphocytes — in immunocompromised neonate | Always use irradiated blood | Preventable |
| Bilirubin rebound | Extravascular bilirubin re-equilibrates | Check SBR at 2h post-exchange; continue intensive phototherapy | Expected |
Kernicterus is a PREVENTABLE cause of brain damage. Recognition of early ABE and immediate escalation are essential nursing responsibilities. Every at-risk neonate requires neurological assessment every 4 hours.
| Phase | Clinical Features | Reversibility | Action |
|---|---|---|---|
| Phase 1 (Early) |
|
Potentially reversible | Intensify phototherapy immediately; escalate to senior; consider exchange transfusion urgently |
| Phase 2 (Intermediate) |
|
Partially reversible | EMERGENCY — exchange transfusion NOW; senior and neonatologist at bedside |
| Phase 3 (Advanced) |
|
Largely irreversible | Exchange transfusion still indicated to prevent further damage; ITU involvement; family communication |
Kernicterus is the chronic, permanent neurological damage resulting from severe unconjugated hyperbilirubinaemia. Bilirubin stains the basal ganglia, cerebellum, and brainstem nuclei.
Subtle, long-term neurodevelopmental effects (auditory processing difficulties, cognitive delay, behavioural problems) may occur even without classic ABE — BIND spectrum. All treated neonates need neurodevelopmental follow-up.
These factors lower the bilirubin threshold at which neurotoxicity occurs — lower treatment thresholds should be used:
G6PD deficiency is the leading cause of kernicterus in the GCC. All at-risk neonates must be screened and threshold adjusted accordingly.
Neurological assessment q4h in all at-risk neonates (near-threshold SBR, haemolysis, G6PD, preterm). Document tone, activity, cry character, feeding behaviour.
Note for GCC families: Jaundice can be difficult to see on darker-skinned babies. Check the whites of the eyes (sclerae) — yellowing is easier to detect there.
Effective breastfeeding is the best prevention for significant neonatal jaundice. Adequate milk intake promotes gut motility and bilirubin excretion (enterohepatic circulation is reduced).
Parents must be taught to inspect nappy contents. Pale/chalky stools combined with dark urine in a jaundiced baby is an emergency — this pattern indicates conjugated (obstructive) jaundice, most importantly biliary atresia.
Biliary atresia pathway: Kasai portoenterostomy must be performed within 60 days of life for best outcome. Delayed diagnosis leads to liver cirrhosis and death without transplant.
G6PD deficiency is a common inherited condition in GCC families. Boys are more commonly affected. The condition means the baby's red blood cells are more fragile and can break down quickly when exposed to certain triggers.
This rapid blood cell breakdown releases bilirubin, causing severe jaundice that can be dangerous to the brain.
High-yield for DHA, DOH (Abu Dhabi), SCFHS (Saudi Arabia), QCHP (Qatar) nursing licensing examinations. Review these key concepts, tables, and triggers — neonatal jaundice is a consistently tested topic across all GCC boards.
| Feature | Physiological | Pathological |
|---|---|---|
| Onset | Day 2–4 | Within 24 hours |
| Term resolution | By day 14 | Persists >14 days |
| Preterm resolution | By day 21 | Persists >21 days |
| Rate of rise | <85 μmol/L/day | >85 μmol/L/day |
| Conjugated component | Absent (<20 μmol/L) | Present (>20 μmol/L) |
| Cause | Physiological RBC turnover | HDN, G6PD, sepsis, biliary atresia |
| Stool/urine | Normal | Pale stools + dark urine (conjugated) |
| Area | Key Point |
|---|---|
| Eye shields | Apply before light on; check q4h; remove for feeding |
| Clothing | Nappy only — maximise skin exposure |
| Position | Supine; reposition q2h |
| Temperature | Monitor q2–4h; hypo and hyperthermia risk |
| Fluids | Increase feeds 10–20%; insensible losses increased |
| SBR monitoring | Intensive: q6–12h; standard: q12–24h |
| TcB after phototherapy | NOT reliable — use SBR only |
| Wavelength | Blue-green 425–490 nm most effective |
| Intensive irradiance | ≥30 μW/cm²/nm at skin surface |
| Interruptions | Only for feeding and skin-to-skin |
| Complication | Cause | Key Sign | Prevention |
|---|---|---|---|
| Hypocalcaemia | Citrate in donor blood | Jitteriness, apnoea, prolonged QT | Monitor iCa q50mL; IV calcium gluconate if symptomatic |
| Hypoglycaemia | Glucose-poor blood; rebound insulin | Jitteriness, seizure, apnoea | Monitor glucose before/during/after |
| Hypothermia | Cold blood infused | Temperature drop, apnoea | Warm blood to 37°C; maintain warming |
| Thrombocytopenia | Dilution; platelet-poor stored blood | Bleeding, petechiae | Post-exchange FBC; platelet transfusion if indicated |
| NEC | Gut ischaemia; UVC compromise | Distension, bloody stools, bilious aspirates | Hold feeds 4–6h pre/post exchange |
| Air embolism | Air in UVC lines | Sudden collapse, cardiac arrest | Purge all lines; closed system; vigilant nurse |
| GvHD | Donor lymphocytes | Rash, diarrhoea, pancytopenia (weeks later) | Always use irradiated blood |
| Bilirubin rebound | Extravascular bilirubin re-equilibrates | SBR rises at 2h post-exchange | Check SBR at 2h; continue intensive phototherapy |
Inheritance: X-linked recessive — males affected; females are carriers (but can be affected if homozygous). Screen all GCC male neonates. Common in Arabs, Africans, South Asians.
Yellow discolouration of the face/sclerae. Jaundice progresses cephalocaudally — face first, then trunk, arms, legs, and finally palms/soles (Zone 5 = severe).
To protect the retina from damage by blue-spectrum phototherapy light. Shields must be applied before the light is switched on, checked every 4 hours for position and damage, and removed during feeding and skin-to-skin contact.
Phototherapy bleaches bilirubin in superficial skin layers. The TcB device measures skin bilirubin — after phototherapy, superficial levels are falsely lowered while serum levels may remain high. Always use serum bilirubin (SBR) once phototherapy has commenced.
1. Athetoid/dyskinetic cerebral palsy
2. Sensorineural hearing loss
3. Upward gaze palsy
4. Dental enamel dysplasia (green teeth)
These result from bilirubin deposition in the basal ganglia, cochlear nuclei, oculomotor nuclei, and subthalamic nuclei.
Mother blood group O, baby blood group A or B. Group O mothers have anti-A and anti-B IgG antibodies which cross the placenta and haemolyse fetal/neonatal RBCs. Unlike Rh HDN, ABO HDN can occur in the first pregnancy.
Acute bilirubin encephalopathy Phase 2 (intermediate phase). Opisthotonus is severe backward arching of the whole body — a sign of basal ganglia involvement by bilirubin. This is a neonatal emergency. Intensify phototherapy immediately and prepare for urgent exchange transfusion.