Jaundice is caused by accumulation of unconjugated (before conjugation process takes place in liver) bilirubin due to immature development of the baby's liver. This condition is deemed as a normal transitional condition in the 1st week of life and is called as Physiological jaundice.
However, if the serum bilirubin level rises too excessively, it may be because for due concern. Unconjugated bilirubin can penetrate the blood-brain barrier and is neurotoxic (toxic to the brain-neuro). It can cause death in newborns. Infants who survive would have lifelong neurologic sequelae. Increased levels of unconjugated-indirect bilirubin which is free (not bound to albumin) may cause kernicterus damage to brain centers of those infants.
Such conditions frequently warrants diagnostic evaluation to ensure that neonatal jaundice does not turn fatal.
Be alert if the child presents with following symptoms, including jaundice, pale skin/pallor (RBCs destroyed), severe tiredness (due to low oxygen carrying capacity as a result of low RBC after being destroyed) and dark urine.
These are the signs of glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Ernest Beutler, M.D. (a leading expert in this field) has to say about neonatal icterus (jaundice), "Icterus neonatorum with no evidence of immunologic incompatibility occurs in some the infants with G6PD deficiency. The jaundice may be quite severe and, if untreated, may result in kernicterus. Hence G6PD deficiency is a preventable cause of mental retardation, and this aspect of the disorder has considerable public health significance."
G6PD deficiency is due to a problem with an enzyme called G6PD found in the red blood cells of the blood. It is more prevalent in males but females could be a carrier and remain asymptomatic- no symptoms at all.
This deficiency can cause hemolytic anemia-breaking up of the RBC , usually after exposure to certain medications, foods, or even infections.Most people with G6PD deficiency don't show any symptoms, while others develop symptoms of anemia only after RBCs have been destroyed, a condition called hemolysis. In these cases, the symptoms disappear once cause, or the trigger, is removed.
A normal life is certainly possible, if child is aware that the condition is lifelong and must be cautious of certain medicines and chemical exposure. Keeping the list of medicine, chemical and food to be avoided is always a wise thing to do. Always present the list to the medical doctor whenever seeking treatment.
Some children with G6PD must not consume asprin. Check with a specialist or paediatrician first.
In conclusion, patients must be informed this is not a life threatening disease and one can live a normal life provided if he is not exposed to the triggering factors.
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