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اليرقان المرضي عند الوليد Pathologic jaundice


اليرقان المرضي عند الوليد Pathologic jaundice

المعلومة

Pathologic jaundice is diagnosed when there is clinical jaundice in the first 24 hours of life or serum bilirubin level increasing at a rate of >5 mg/dL/day.
A peak serum bilirubin level higher than that mentioned above in a term infant and >15 mg/dL in a preterm infant should always be considered pathologic until proven otherwise.

يُشخَّص اليرقان المرضي عندما يوجد يرقان سريري خلال الـ 24 ساعة الأولى من الحياة أو عندما يرتفع مستوى بيلروبين المصل بمعدل أكبر من 5 مغ/دل/اليوم .

إن ارتفاع مستوى بيلروبين المصل بمعدل أكبر من المذكور أعلاه عند الوليد بتمام الحمل أو أكبر من 15 مغ/دل/اليوم عند الخديج ؛ يجب اعتباره يرقان مرضي حتى يثبت العكس .

المرجع

Thomas P,Wayne H,Robert R.(2005).Pediatrics just the facts.The McGraw-Hill Companies.
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NEONATAL JAUNDICE

• The yellow discoloration of the skin caused by accumulation of bilirubin is called jaundice or icterus. Nearly all newborns develop transient hyperbilirubinemia (serum bilirubin >2 mg/dL) and nearly 65% are clinically jaundiced (serum bilirubin >5 mg/dL).
• Bilirubin is derived primarily from the breakdown of heme in the reticuloendothelial system. Unconjugated bilirubin is released into the circulation and is rapidly
bound reversibly to albumin and transported to the liver. Bilirubin enters the liver cell by a process of carrier-mediated diffusion by binding to ligandin (Y protein) and Z protein. Nonpolar and water-insoluble unconjugated bilirubin is conjugated inside liver cells by bilirubin uridine 5′-diphosphate (UDP)-glucuronyl transferase enzyme. Water-soluble conjugated bilirubin is then actively excreted into the bile canaliculi by the liver cells. Conjugated bilirubin cannot be reabsorbed from the intestine and most of it is converted to urobilinoids which are excreted in stool and urine. A small amount of conjugated bilirubin is converted back to unconjugated form by enteric mucosal enzyme, b-glucuronidase, and reabsorbed by way of enterohepatic circulation.
• Unconjugated hyperbilirubinemia, also known as indirect hyperbilirubinemia, can be either physiologic or pathologic. In absence of neurologic injury, unconjugated
hyperbilirubinemia is not associated with any specific symptoms except those related to the underlying etiology.
• Jaundice is typically apparent first in the face and then
follows a cephalocaudal progression as the degree of jaundice increases. Palms and soles are the last to be jaundiced and suggest severe jaundice and an infant at risk for bilirubin encephalopathy. In absence of neurologic
injury, unconjugated hyperbilirubinemia is not associated with any specific symptoms except symptoms related to underlying etiology.
Physiologic jaundice in term infants is characterized
by a progressive rise in serum bilirubin to a mean peak
of 5–6 mg/dL by the third day of life in both White and Black infants and to a peak of 10–14 mg/dL by the fifth day in oriental infants. This peak is followed by a gradual decline to baseline by the fifth day of life in White and Black infants and by the seventh to the tenth day in oriental infants. Physiologic jaundice in a preterm infant appears earlier, can reach a higher peak, and declines more gradually.
The underlying mechanisms for physiologic jaundice in newborn are related to (a) increased bilirubin production
because of larger RBC mass and shorter life span; (b) hepatic immaturity resulting in defective uptake, diminished conjugating capacity, and impaired excretion; and (c) increased enterohepatic circulation in newborn.
Pathologic jaundice is diagnosed when there is clinical
jaundice in the first 24 hours of life or serum bilirubin level increasing at a rate of >5 mg/dL/day. A peak serum bilirubin level higher than that mentioned above in a term infant and >15 mg/dL in a preterm infant should always be considered pathologic until proven otherwise.
1. Most disorders causing unconjugated hyperbilirubinemia
do so via one or more of the same mechanisms that produce physiologic jaundice described above.
2. The most common pathologic cause of increased bilirubin production in the newborn is isoimmune hemolytic disease, because of blood group incompatibility between mother and fetus. Other causes of hemolysis as mentioned under causes of hemolytic anemia can also result in pathologic jaundice.
3. Sepsis, polycythemia, and extravasated blood can lead to increased bilirubin production.
4. Defects in hepatic uptake of bilirubin such as Gilbert
syndrome and defects in hepatic conjugation such as Type I and Type II glucuronyl transferase deficiency are uncommon causes of pathologic jaundice. Other rare causes of glucuronyl transferase inhibition are Lucey-Discroll syndrome and pyloric stenosis.
Breast milk jaundice: Nearly 30–60% of all breast-fed infants develop exaggerated unconjugated hyperbilirubinemia
toward the end of the first week of life when physiologic jaundice would normally be decreasing.
1. Breast-fed infants are three times more likely to
develop serum bilirubin levels of >12 mg/dL and six times more likely to develop levels of >15 mg/dL than formula-fed infants. Jaundice can persist beyond 2–3 weeks in about 25% of all breast-fed infants and can rarely persist for up to 3 months. It can recur in 70% of future pregnancies.
2. The great majority of infants with breast milk jaundice
have serum bilirubin concentrations around 10 mg/dL. Less than 1% have level >20 mg/dL but rarely levels as high as 30 mg/dL have been reported.
3. The etiology of breast milk jaundice is not ellestablished.
Increased enterohepatic circulation appears to be the most important mechanism.
Increased concentration of fatty acids and presence of a progesterone metabolite, pregnane-3a-20b diol in breast milk have been suggested to play a role by inhibiting hepatic glucuronyl transferase.
4. Interruption of nursing and use of formula feeding for 1–3 days causes a prompt decline in bilirubin but is only recommended for infants with serum bilirubin on centrations that put them at risk for kernicterus.
• The initial evaluation of a jaundiced infant should
include determination of total and direct serum bilirubin
in addition to a detailed family, maternal, and infant’s history. Evaluation of an infant with pathologic jaundice should include blood group and Rh type determination for mother and infant, direct Coomb’s test, hemoglobin or hematocrit, peripheral blood smear and reticulocyte count.
Treatment options for an infant with unconjugated
hyperbilirubinemia include phototherapy, exchange transfusion, and rarely pharmacologic therapy.
1. Phototherapy is the most common treatment in use
for neonatal jaundice. Phototherapy converts bilirubin by isomerization and photooxidation into more water-soluble photoproducts that can bypass the liver’s conjugating system and be excreted without further metabolism. Factors that determine the efficacy of phototherapy include spectrum of light, irradiance of light source, distance of infant from light source, and surface area of infant
exposed to light. Side effects of phototherapy are minimal and include concerns about light toxicity to the retina, increased insensible fluid loss, bronze baby syndrome, and risk of overheating.
2. Exchange transfusion is indicated for immediate treatment of severely jaundiced infants at risk of developing kernicterus. A double volume blood exchange transfusion replaces nearly 85% of the circulating red blood cells and lowers serum bilirubin by 50%. The overall mortality is reported to be about 0.3% and significant morbidity occurs in 1–5% of the patients. In addition, exchange transfusion carries the usual risks of any blood product transfusion.
3. Pharmacologic treatment is not used commonly. Tinand zinc metalloporphyrins have been shown to inhibit enzymes necessary for heme breakdown and can reduce bilirubin production; however, further clinical trials on efficacy and safety are required. Intravenous immunoglobin (IVIG) administration soon after birth can also reduce hemolysis and bilirubin production in patients with isoimmune hemolytic jaundice. Phenobarbital can increase bilirubin elimination by induction of microsomal enzymes in liver.
Because it takes 3–7 days to be effective, it is not helpful in the management of majority of infants with unconjugated hyperbilirubinemia.

Thomas P,Wayne H,Robert R.(2005).Pediatrics just the facts.The McGraw-Hill Companies

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dr.msh
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كأنّه أعطيت لنا على أساس أنه اليرقان الذي يحدث بين الومين 3-10 من تاريخ الولادة Shocked

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KMG
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كلام صحيح أخي خالد فيما يتعلق باليرقان الفيزيولوجي :
عند الوليد بتمام الحمل : يبدأ البيلروبين بالارتفاع منذ اليوم 3 , يصل للذروة باليوم 5 , يعود للسواء باليوم 10 :


• Physiologic jaundice in term infants is characterized
by a progressive rise in serum bilirubin to a mean peak
of 5–6 mg/dL by the third day of life in both White and Black infants and to a peak of 10–14 mg/dL by the fifth day in oriental infants. This peak is followed by a gradual decline to baseline by the fifth day of life in White and Black infants and by the seventh to the tenth day in oriental infants. Physiologic jaundice in a preterm infant appears earlier, can reach a higher peak, and declines more gradually. "

أما المعلومة هنا فتتحدث عن اليرقان المرضي ...

" يُشخَّص اليرقان المرضي عندما يوجد يرقان سريري خلال الـ 24 ساعة الأولى من الحياة أو عندما يرتفع مستوى بيلروبين المصل بمعدل أكبر من 5 مغ/دل/اليوم .

إن ارتفاع مستوى بيلروبين المصل بمعدل أكبر من المذكور أعلاه عند الوليد بتمام الحمل أو أكبر من 15 مغ/دل/اليوم عند الخديج ؛ يجب اعتباره يرقان مرضي حتى يثبت العكس . "

dr.msh's picture
dr.msh
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آسف، اختلطت عليّ كلمة Pathologic مع كلمة Physiologic Embarrased

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KMG
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