Jaundice is a medical condition which shows yellowing of skin, mucous membranes, and eye whites. 

The normal serum level of bilirubin is less than 1 milligram per deciliter (mg/dL). 

As serum bilirubin level increases then skin discoloration shifts from yellow to green due to prolonged biliverdin buildup. 

Bilirubin has two components:  

Unconjugated  

Conjugated 

Yellow color skin with white eyes suggests carotenoderma from excessive carotene-rich foods. 

Male infants have higher risk of neonatal jaundice, unrelated to bilirubin production rates compared to female infants. 

Infrequent in adults, prevalence linked to liver diseases, hemolytic disorders, and obstructions. 

East Asians and American Indians have a higher incidence, while Africans have a lower incidence.  

Endogenous and exogenous competitors reduce albumin binding affinity for bilirubin. It is a small fraction of unconjugated bilirubin remains unbound. 

Bilirubin is produced in reticuloendothelial system as product of heme catabolism, formed through oxidation-reduction reactions. 

Liver struggles with bilirubin breakdown due to hemolysis. Liver diseases further hinder bilirubin processing and removal. 

Causes of jaundice as: 

Blood diseases 

Genetic syndromes 

Liver diseases 

Blockage of bile ducts 

Good prognosis with treatment, but complications can arise if not promptly treated for conditions like hemolytic disease of the newborn or G6PD deficiency.  

Kernicterus poses a continued risk, with increased incidence possibly stemming from misunderstanding jaundice in healthy full-term babies as harmless. 

Neonatal jaundice usually harmless, but kernicterus can be fatal in underdeveloped countries. 

Jaundice occurs in newborns and adults. 

Skin Examination 

Head and Neck Examination 

Abdominal Examination 

Acute Presentation as: 

Rapid onset of symptoms 

Often accompanied by systemic signs of illness 

Subacute Presentation as: 

Symptoms develop over weeks to months 

Gradual worsening of jaundice and associated symptoms 

Phototherapy, IVIG, and exchange transfusion are commonly used for neonatal jaundice treatment. 

Photo isomers of bilirubin are excreted in bile and urine. Lumirubin has a shorter serum half-life than E isomers. 

If the excessive bilirubin is increased due to red blood cell breakdown, the treatment involves discontinuation of medications that cause hemolysis and manage autoimmune disorders. 

Supportive measures include intravenous fluids to maintain hydration to ensure adequate nutrition and manage symptoms. 

Critical Care/Intensive Care

Phototherapy is recommended for newborns with jaundice, while adults can benefit from natural light exposure for well-being. 

Physician should arrange frequent feeding sessions to promotes increased bowel movements for eliminating bilirubin from the body. 

Hydration may be beneficial in promoting bilirubin excretion through urine and stools. 

Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort. 

Critical Care/Intensive Care

Cholestyramine: 

It binds to bile acids in the intestine to form a complex excreted in feces, which reduce reabsorption and interrupt enterohepatic circulation. 

Critical Care/Intensive Care

Surgery is not needed for normal jaundice in infants but is needed for atresia-caused jaundice. 

The initial diagnosis phase involves evaluation of the patient medical history and physical examination to confirm diagnosis. 

Pharmacologic therapy is very effective in the treatment phase as it includes the use of bile acid sequestrant and phototherapy. 

The regular follow-up visits with the physician are schedule to check the improvement of patients along with treatment response.