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Neonatal jaundice is well understood from a French word which means yellow . It is a common and frequent clinical condition and a major serious problem during the neonatal period. It is characterized by manifestation of a yellow pigmentation on the skin of the newborn progressing down wards to other tissues of the infant’s body. Premature infants are said to be at a high risk of developing neonatal jaundice as compared to full term newborns. The yellow pigmentation on the skin is caused by excess secretion of bilirubin in the infants skin.
Bilirubin is said to be a yellowish – red pigment present in the skin.
Normally and in general circumstances there exists small amounts of bilirubin in everyone’s blood. When excess secretion of bilirubin occurs, it is dumped in the bloodstreams and finally deposited in the tissues for temporary storage. Bilirubin is also formed in blood streams especially when red blood cells are broken down. Infants have high levels of red blood cells in their blood volumes which tend to increase the bilirubin load in their bodies.
This bilirubin is then carried to the liver where it is processed and finally excreted from the body (Axe, 2007, pp. 13).
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In his research study, Colon (2006) has argued that neonatal jaundice may occur in infants as a result of both physiologic and pathological processes in the newborns (pp. 6). Generally, infants have got too much red blood cells in their bodies, it is a natural process therefore, for the infant’s body to break down excess red blood cells leading to formation of large amounts of bilirubin.
It is as a result of this breakdown that causes excess secretion of bilirubin in the body which makes the skin to turn yellow in color.
On the other hand infants’ liver is immature and in most cases it is unable to process bilirubin as quickly as it would have done at an older age. This inability of the liver to process bilirubin leads to delay in the elimination of excess bilirubin resulting to accumulation which leads to skin discoloration.
To a greater extend, the disease is related to pathological processes present during the neonatal period which include different types of hemolytic disorders, increased enterohepatic circulation, bilirubin conjugation, and decreased hepatic uptake of bilirubin. One of the most important steps in treatment of neonatal hyperbilirubinemia is to prevent induced bilirubin neurological dysfunction which involves kernicterus in its acute and chronic forms which are very serious conditions.
There are different methods of treatment with each having specific indications of phototherapy and exchange transfusion medication (Tian, Zucker, Wei, 2005, pp. 5). According to Iozzio (2005), during Normal metabolism of lipophilic, bilirubin results predominantly from catabolism of red cells which circulate in blood mainly as convalent conjugates with albumin. After their absorption by the liver, they are converted into two different isomeric monoglucuronides and diglucuronide (pp. 11). The water soluble glucuronides are then excreted to the bile juice with the assistance of canalicular multidrug resistance that is usually associated with the transportation of proteins. In the absence of the glucuronidation factor bilirubim cannot be excreted in the bile or urine.
In infant’s hepatic activity is deficient and the lifespan of red blood cells is shorter than in adults resulting to accumulation and increased formation of bilirubin which eventually results to jaundice (Stables, Rankin, 2005, pp. 19). Phototherapy turns bilirubin to a yellow photoisomer and a colorless oxidation substance that that is less lipophilic than bilirubin and do not require hepatic conjugation for excretion . The photoisomer is therefore excreted in bile while the oxidized substances are predominantly excreted in urine.
The significance of performing this kind of therapy is to reduce the concentration of circulating bilirubin or keep it from increasing. Phototherapy achieves this goal by use of light energy which shapes the structure of bilirubin converting it into molecules which can be secreted even when normal conjugation is deficient (Chivrier, Eskenazi, 2007, pp. 57). The absorption of the light by dermal and subcutaneous bilirubin induces a certain percentage of the pigment to undergo a chain of photochemical reactions that occur at different times.
Such reactions produce yellow stereoisomers of bilirubin and colorless derivatives of lower molecur weight. These products are less lipophilic as compared to bilirubin and they can be excreted in the bile or urine without the need for conjugation. Relatively, the contributions of various reactions to the overall elimination of bilirubin are unknown although studies suggest that photoisomerization is more important than photodegration. Therefore, bilirubin elimination relays heavily on the rates of formation as well as on the rates of clearance of the photoproducts (Ryan, 2006, pp. 23).
The process of photoisomerization occurs more rapidly during phototherapy and isomers appear in the blood long before the level of plasma bilirubin begins to decline. Absorption of light by normal bilirubin produces transient excited state of bilirubin molecules. These fleeting intermediates react with oxygen to evolve colorless substances of lower molecular weight which are rearranged to become structural isomers. It is important to understand that jaundice is not a disease but a disorder that occurs due to underlying pathological processes that emerge at some point along the normal physiological pathway of metabolism bilirubin.
In his argument, Winter (2004) has stated that neonatal jaundice can be classified into three classes depending on which part of the physiological mechanism is affected by the pathology. For instance, at the pre –hepatic stage, jaundice occurs as result of anything that causes an increase in the rate of hemolysis of red blood cells (pp. 43). In tropical continents, diseases such as malaria can cause jaundice . Specific genetic diseases such as sickle anemia glucose dehydrogenise deficiency can lead to increased red blood lysis which later translates to hemolytic jaundice.
That is when red blood cells complete their life span of approximately 120 days, they get damaged and their membranes become fragile and prone to rapture. The hemoglobin secreted to the blood is phagocytosed by macrophages and it is splitted into heme and globin portions. The globin being protein in nature becomes degraded into amino acids and they perform no other role in the body. Two reactions at this point occur on the heme molecule. The very first reaction is the oxidation of the heme molecule to form biliverdin.
The next reaction involves the reduction of the biliverdin molecule into the yellow color tetrapyrol pigment bilirubin which is cytosolic enzyme biliverdin reductase. At the hepatic event stage, hepatic jaundice is caused by factors such as acute hepatitis, whereby cell neurosis reduce the liver‘s ability to metabolize and excrete bilirubin leading to its accumulation in the blood system. The unconjucated bilirubin is then transferred to the liver through the blood streams.
However, due to the fact that this bilirubin is insoluble in water, it is transported again via the blood streams to the serum albumin. Once at the liver it is conjugated with glucuronic so that it becomes water soluble. This process is catalyzed by a certain enzyme found in the system known as UDP- glucuronide transferase (Ginsberg, Slikker, 2004, pp. 22). According to Balsanek (2004), bilirubin takes light more strongly in the blue region of the spectrum near 460mn, a certain region in which penetration of tissue by light increases remarkably with the wavelength (pp16).
The rate at which bilirubin photopructs are formed is highly dependent on the intensity and wavelengths of light used. Only wavelengths that can penetrate tissues are absorbed by bilirubin and have phototherapeutic effects. Studies spell out clearly that the blue light is the most effective for phototherapy but due to the transmittance of skin increasing concurrently with the increase in wavelength the best wave lengths to use are preferably between the ranges of 460 – 490nm.
Full term and almost near term babies should be treated in bassinets and not incubators to allow light sources to be brought closer to within 10 – 15 cm of the infant therefore increasing the radiance and efficacy. For high intensive phototherapy, an auxiliary light source should be placed below the infant or bassinet. On the other hand if the infant is placed in an incubator the light rays should be kept in perpendicular to the surface of the incubator in order to reduce loss of efficacy due reflectance.
Lastly, at the post hepatic events stage, the conjugated bilirubin is excreted to the liver into the biliary and cystic ducts as a component of bile. Intestinal bacteria work on it and convert it into stercobilinogen which is later oxidized to stercobilin and passed out inform of faeces. It is then reabsorbed back to the system by intestinal cells and later transported through blood streams to the kidneys and excreted out inform of urine as an oxidized product of urobilin. Therefore, the two factors that are stercobilin and urobilin are the products that are most responsible for the coloration of faeces and urine.
Neonatal jaundice is normally a harmless condition that is registered among infants around the second day after birth extending to day 8 of normal birth around day 14 of premature births. Serum bilirubin declines to a certain level that does not require intervention. Jaundice is presumably an end product of metabolic and physiological adjustments after birth. Extreme cases can lead to a brain damaging condition known as kernicterus. Neonatal jaundice is also a risk factor to hearing loss in childhood.
Understanding Neonatal Jaundice and Its Treatment. (2016, Dec 05). Retrieved from https://studymoose.com/neonatal-jaundice-essay
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