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Last updated: October 25, 2022 Revisions: 26

• 1.1.1 Types of Jaundice
• 1.2 Bilirubinuria
• 2.1.1 Liver Screen
• 2.2 Imaging
• 3 Management
• 4 Key Points

Introduction

Jaundice refers to the yellow discolouration of the sclera and skin (Fig. 1) that is due to hyperbilirubinaemia , occurring at bilirubin levels roughly greater than 50 µmol/L.  

Figure 1 – Yellowing of the sclera

Pathophysiology

Jaundice results from high levels of bilirubin in the blood. Bilirubin is the normal breakdown product from the catabolism of haem , and thus is formed from the destruction of red blood cells.

Under normal circumstances, bilirubin undergoes conjugation within the liver , making it water-soluble. It is then excreted via the bile into the GI tract, the majority of which is egested in the faeces as urobilinogen and stercobilin (the metabolic breakdown product of urobilingoen). Around 10% of urobilinogen is reabsorbed into the bloodstream and excreted through the kidneys. Jaundice occurs when this pathway is disrupted .

Figure 2 – Bilirubin is produced as a byproduct of haem metabolism

Types of Jaundice

There are three main types of jaundice: pre-hepatic, hepatocellular, and post-hepatic.

Pre-Hepatic

In pre-hepatic jaundice, there is excessive red cell breakdown  which overwhelms the liver’s ability to conjugate bilirubin. This causes an unconjugated hyperbilirubinaemia.

Any bilirubin that manages to become conjugated will be excreted normally, yet it is the unconjugated bilirubin that remains in the blood stream to cause the jaundice.

Hepatocellular

In hepatocellular (or intrahepatic) jaundice, there is dysfunction of the hepatic cells . The liver loses the ability to conjugate bilirubin, but in cases where it also may become cirrhotic, it compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction.

This leads to both unconjugated and conjugated bilirubin in the blood, termed a ‘mixed picture’.

Post-Hepatic

Post-hepatic jaundice refers to obstruction of biliary drainage . The bilirubin that is not excreted will have been conjugated by the liver, hence the result is a conjugated hyperbilirubinaemia.

Table 1 – Potential Causes for Jaundice, divided into pre-hepatic, hepatocellular, and post-hepatic

Bilirubinuria

A good estimation of which type of jaundice is present (prior to any further investigation) can be made from observing the colour of the urine.

Conjugated bilirubin can be excreted via the urine (as it is water soluble), whereas unconjugated cannot. Consequently, dark (‘coca-cola’) urine manifests in conjugated or mixed hyperbilirubinaemias, whereas normal urine is seen in unconjugated disease.

Moreover, those with an obstructive picture will likely note pale stools, due to the reduced levels of stercobilin entering the GI tract, which normally colours the stool.

Investigations

In many cases, the likely underlying cause can be elicited from the history , with the investigations simply confirming suspicions. Hence, whilst a complete list of investigations is given below, these should be tailored to the clinical features of the patient.

Laboratory Tests

Any patient presenting with jaundice should have the following bloods taken:

• Liver function tests (LFTs), as summarised in Table 2
• Coagulation studies (PT can be used as a marker of liver synthesis function)
• FBC (anaemia, raised MCV, and thrombocytopenia all seen in liver disease) and U&Es
• Specialist blood tests , as summarised below as part of a liver screen

Table 2 – LFT serum markers. *as an estimate, if the AST:ALT ratio >2, this is likely alcoholic liver disease, whilst if AST:ALT is around 1, then likely viral hepatitis as the cause

Liver Screen

A liver screen can be performed for patients whereby there is no initial cause for liver dysfunction , tailored to whether acute or chronic liver failure

Table 3 – Acute and Chronic Liver Screens *Autoantibodies include anti-mitochondrial antibody (AMA), anti-smooth-muscle antibody (Anti-SMA), and anti-nuclear antibody (ANA), used to identify a variety of autoimmune liver conditions, such as primary sclerosing cholangitis (PSC)

The imaging used will depend on the presumed aetiology. An  u ltrasound abdomen is usually first line, identifying any obstructive pathology present or gross liver pathology (albeit often user dependent).

Magnetic Resonance Cholangiopancreatography (MRCP) is used to visual the biliary tree, typically performed if the jaundice is obstructive , but US abdomen was inconclusive or limited, or as further work-up for surgical intervention.

A liver biopsy can be performed when the diagnosis has not been made despite the above investigations.

The definitive treatment of jaundice will be dependent on the underlying cause . Obstructive causes may require removal of a gallstone through Endoscopic Retrograde CholangioPancreatography (ERCP) or stenting of the common bile duct.

Symptomatic treatment is often needed for the itching caused by hyperbilirubinaemia. An obstructive cause may warrant cholestyramine (acting to increase biliary drainage), whilst other causes may respond to simple anti-histamines.

Identify and manage any complications where possible. Monitor for  coagulopathy , treating promptly (either vitamin K or fresh frozen plasma (FFP) is needed) if any evidence of bleeding or rapid coagulopathy, and treat hypoglycaemia orally if possible (otherwise 5% dextrose is needed).

Where patients become confused from decompensating chronic liver disease (‘hepatic encephalopathy’), laxatives (lactulose or senna) +/- neomycin or rifaximin may be used, in attempt to reduce the number of ammonia-producing bacteria in the bowel.

Figure 3 – Images from a laparoscopic cholecystectomy

• Jaundice refers to the yellow discolouration of the sclera and skin that is due to hyperbilirubinaemia
• Causes can be broken down into pre-hepatic, hepatocellular, and post-hepatic
• Most cases will warrant initial blood tests and ultrasound imaging, however this should be tailored to the clinical presentation
• Definitive treatment of jaundice will be dependent on the underlying cause
• Ensure to monitor for complications, such as coagulopathy, encephalopathy, or infective sequelae

This leads to both unconjugated and conjugated bilirubin in the blood, termed a ‘mixed picture'.

[start-clinical]

[end-clinical]

Table 3 - Acute and Chronic Liver Screens *Autoantibodies include anti-mitochondrial antibody (AMA), anti-smooth-muscle antibody (Anti-SMA), and anti-nuclear antibody (ANA), used to identify a variety of autoimmune liver conditions, such as primary sclerosing cholangitis (PSC)

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Original Author(s): Dr Phil Jordan and Dr Umberto Piaggio Last updated: 16th February 2021 Revisions: 19

• 1 Introduction
• 2.1 Physiological jaundice
• 2.2 Pathological jaundice
• 3 Risk factors and history
• 4 Clinical Presentation
• 5.1 Bilirubin
• 5.2 Further investigations
• 5.3 As needed
• 6.1 Phototherapy
• 6.2 Fluid intake
• 6.3 Exchange Transfusion
• 6.4 IV Immunglobulin
• 7 Complications
• 8 Prognosis
• 9 References

Introduction

Jaundice is t he yellow colouring of skin and sclera caused by the accumulation of bilirubin in the skin and mucous membranes.

Neonatal jaundice  occurs in 60% of term infants and 80% of preterm infants [1] and is caused by hyperbilirubinaemia that is unconjugated (divided into physiological or pathological) or conjugated (always pathological).  High levels of unconjugated bilirubin have acute harmful effects as well as long term damage if left untreated, such as kernicterus .

10% of breast fed babies are jaundiced at 1 month.

Types of Jaundice

Physiological jaundice.

Jaundice in a healthy baby, born at term, is normal and may result from:

• Increased red blood cell breakdown: in utero the fetus has a high concentration of Hb (to maximise oxygen exchange and delivery to the fetus) that breaks down releasing bilirubin as high Hb is no longer needed
• Immature liver not able to process high bilirubin concentrations

Starts at day 2-3, peaks day 5 and usually resolved by day 10.   The baby remains well and does not require any intervention beyond routine neonatal care.

Physiological jaundice can progress to pathological jaundice if the baby is premature or there is increased red cell breakdown e.g. Extensive bruising or cephalohaematoma following instrumental delivery.

Pathological jaundice

Jaundice which requires treatment or further investigation.

• Onset less than 24 hours
• ?previous siblings treated for jaundice/family history/maternal rhesus status
• Maternal blood group (type O most likely to produce enough IgG antibodies to cause haemolysis)
• Requires investigation and treatment
• Onset after 24 hours
• likely dehydrated ?breast fed baby establishing feeding
• increased haemolysis due to bruising/cephalohaematoma
• Unwell neonate: jaundice as a sign of congenital or post-natal infection
• Metabolic: Hypothyroid/pituitarism, galactosaemia
• Breast milk jaundice: well baby, resolves between 1.5-4 months
• GI: biliary atresia, choledhocal cyst

Risk factors and history

Risk factors for pathological hyperbilirubinaemia: to be asked in history

• Prematurity, low birth weight, small for dates
• Previous sibling required phototherapy
• Exclusively breast fed
• Jaundice <24 hours
• Infant of diabetic mother

Clinical Presentation

• Colour: All babies should be checked for jaundice with the naked eye in bright, natural light (if possible). Examine the sclera, gums and blanche the skin. Do not rely on your visual inspection to estimate bilirubin levels, only to determine the presence or absence of jaundice.
• Drowsy: difficult to rouse, not waking for feeds, very short feeds
• Neurologically: altered muscle tone, seizures-needs immediate attention
• Other: signs of infection , poor urine output, abdominal mass/organomegaly, stool remains black/not changing colour

Investigations

• Transcutaneous bilirubinometer (TCB) can be used in >35/40 gestation and >24 hours old for first measurement. TCB can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment
• Serum bilirubin to be measured if <35/40 gestation, <24 hours old or TCB >250 µmol/L
• Infants that are not jaundice to the naked eye do not need routine bilirubin checking.  
• Total and Conjugated Bilirubin is important if suspected; liver or biliary disorder, metabolic disorder, congenital infection or prolonged jaundice. Do not subtract conjugated from total to make management decisions for hyperbilirubinaemia.

Further investigations

• Serum bilirubin for all subsequent levels
• Blood group (Mother and Baby) and DCT
• FBC for haemoglobin and haematocrit
• U&Es if excessive weight loss/dehydrated
• Infection screen if unwell or <24 hours including Microbiological cultures if infection suspected: blood, urine, CSF. Consider TORCH screen.
• Glucose-6-phosphate dehydrogenase especially if Mediterranean or African origin
• LFTs if suspected hepatobiliary disorder

Phototherapy

Figure 1 – NICE treatment threshold graph [3]

• Above: If level is on or above the phototherapy line for their gestation and age (in days) phototherapy should be initiated and bilirubin monitored
• >50µmol/L below, clinically well with no risk factors for neonatal jaundice do not routinely repeat level
• <50µmol/L below, clinically well repeat level within 18 hours (risk factors present) to 24 hours (no risk factors present)
• Repeat bilirubin 4-6 hours post initiation to ensure not still rising, 6-12 hourly once level is stable or reducing.
• NB. Maximum skin coverage, eye protection for babies, breaks for breastfeeding/nappy changes/cuddles to be coordinated to maximise phototherapy
• Stop phototherapy once level >50µmol/L below treatment line on the threshold graphs
• Check for rebound of hyperbilirubinaemia 12-18 hours after stopping phototherapy

Fluid intake

Do not give additional fluids with phototherapy unless indicated and if possible expressed maternal milk is preferred. If phototherapy intensified or feeding poorly consider NGT feeding or IV fluids.

Give consideration to underlying cause i.e. infection, biliary obstruction

Exchange Transfusion

This is the simultaneous exchange of the baby’s blood (hyperbilirubinaemic) with donated blood or plasma (normal levels of bilirubin) to prevent further bilirubin increase and decrease circulating levels of bilirubin.

Performed via umbilical artery or vein and is indicated when there are clinical features and signs of acute bilirubin encephalopathy or the level/rate of rise (>8.5µmol/L/hour) of bilirubin indicates necessity based on threshold graphs. This will require admission to an intensive care bed.

IV Immunglobulin

IVIG can be used as adjunct to intensified phototherapy in rhesus haemolytic disease or ABO haemolytic disease.

Complications

Kernicterus , billirubin-induced brain dysfunction, can result from neonatal jaundice. Bilirubin is neurotoxic and at high levels can accumulate in the CNS gray matter causing irreversible neurological damage . Depending on level of exposure, effects can range from clinically undetectable damage to severe brain damage.

Depends on underlying cause but if correctly and promptly treated prognosis is excellent.

Always refer to local trust guidelines.

1st Author: Dr Phil Jordan

Senior Reviewer: Dr Umberto Piaggio

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Neonatal Jaundice

Sep 23, 2014

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Neonatal Jaundice. Neonatal Ward Dr. Ziyu Hua. Classification of neonatal jaundice. Physiological jaundice. Pathological jaundice. Etiology of physiological jaundice. In the first few days after birth, haemoglobulin concentration falls rapidly.

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Presentation Transcript

Neonatal Jaundice Neonatal Ward Dr. Ziyu Hua

Classification of neonatal jaundice Physiological jaundice Pathological jaundice

Etiology of physiological jaundice In the first few days after birth, haemoglobulin concentration falls rapidly. Red cell life span of newborn infants is 70 days which is much shorter than that of adults(120 days). Hepatic bilirubin metabolism is less efficiency.

Jaundice is important as A sign of another disorder, e.g. infection, hemolysis Kernicterus: a severe complication of neonatal jaundice, indirect bilirubin (UB) deposited in the brain (basal ganglia).

Warning There are no bilirubin levels which are known to be safe or which will definitely cause kernicterus. Infants who experience severe hypoxia, hypothermia or any serious illness may be susceptible to damage from hyperbilirubinemia.

Severity of jaundice The jaundice starts on the head and face, spreads down the trunk and limbs. How to measure: Observation by eye: blanching the skin Transcutaneous jaundice meter Blood sample: minibilirubin meter

Gestation Preterm infants may be damaged by a lower bilirubin level than term infants. Age from birth is important, higher tolerance with increasing age.

Rate of change Rate of rise tends to be linear until reaching plateau. Rapid rise with increasing harm. Serial measurement of serum bilirubin, suitable intervention when necessary.

Etiology of pathological jaundice Age of onset is a useful guide to likely cause of jaundice. Within 24 hrs During 24 hrs to 2 wks After 2 wks

Jaundice within 24 hrs of age Hemolytic disorders: UB, rise rapidly, high level Rhesus hemolytic disease: jaundice, anemia, hydrops, hepatosplenomegaly; antenatal identify, fetal therapy. ABO incompatibility: less severe, more common, slight or without anemia, peak in the first 12—72hrs. G6PD deficiency: epidemiology; some drugs, infection, hypoxia.

Jaundice within 24 hrs of age Hemolytic disorders Spherocytosis: less common, family history; spherocytes found on the blood film. Congenital infection: conjugated bilirubin, other abnormal clinical signs.

Jaundice at 24 hrs to 2 wks of age Physiological jaundice Infection: unconjugated hyperbilirubinemia; abnormal metabolism of bilirubin; pneumonia, sepsis, hepatitis, urinary tract infection. Other causes: bruising, polycythaemia (venous hematocrit >65%); Crigler-Najjar syndrome (inherited deficiency of enzyme glucuronyl transferase)

Jaundice at 24 hrs to 2 wks of age Breast milk jaundice: prolonged, unconjugated hyperbilirubinemia; unknown cause; declined bilirubin with interruption of breast-feeding; may be harmless. It is unnecessary to stop breast-feeding when breast milk jaundice is diagnosed.

Jaundice at >2 wks of age(persistent) Unconjugated hyperbilirubinemia: Infection, particularly of urinary tract. Congenital hypothyroidism: neonatal biochemical screening; clinical manifestations (constipation, dry skin, coarse facies, hypotonia) Breast milk jaundice: most common, 15% affected; disappears by 3-4 wks of age.

Jaundice at >2 wks of age(persistent) Conjugated hyperbilirubinemia: Neonatal hepatitis syndrome(TORCH), biliary atresia; Dark urine and unpigmented pale stools; Biliary atresia should be diagnosed as soon as possible.

Management No study could prove that supplement with water or dextrose solution would reduce jaundice. Effective treatments: Phototherapy, intense phototherapy Exchange transfusion

Phototherapy Overhead light, blanket, and both of them Blue light: wavelength 450nm, visible Photodegradation: UB is converted into a water-soluble pigment, harmless, excreted in urine Side effects: Uncomfortable eyes, retinal damage in animal, dehydration, rash, diarrhoea, abnormal temperature Phototherapy should not be used indiscriminately.

Exchange transfusion(ET) Indications: Bilirubin rises to the dangerous level; Continues to rise above the recommended level in spite of intensive phototherapy. Transfusion via: cord vessels, peripheral vessels Blood volume: twice infant’s blood volume It should be consider seriously whether to use ET.

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