Jaundice in newborns

Jaundice with a yellowing of the skin and eyes caused by hyperbilirubinemia (elevated serum bilirubin concentration) is caused. The serum bilirubin levels that trigger a jaundice, vary depending on the skin color and the body, jaundice, but will generally be visible on the sclera in an amount of 2-3 mg / dl (34-51 micromol / L) and the face a value of about 4-5 mg / dl (68-86 .mu.mol / l). With increasing bilirubin levels jaundice in the direction of the head seems to advance to toe, while to the umbilicus at a value of about 15 mg / dL (258 mol / l) and to the feet at about 20 mg / dl (340 progresses .mu.mol / l). Slightly more than half of all newborns in the first week of life have a visible jaundice. Consequences of hyperbilirubinemia Hyperbilirubinemia is harmless or dangerous depending on the cause and degree of severity. Some causes of jaundice are potentially dangerous regardless of the bilirubin levels. But hyperbilirubinemia any etiology is a concern when high enough. The threshold for concern varies depending on the age health apnea of ??prematurity In newborns, the state is of concern when it> 18 mg / dl (> 308 .mu.mol / l) comes to a value; Risk of hyperbilirubinemia in newborns ? 35 weeks of gestation. However, having children, the premature birth, small for gestational age, and / or sick (z. B. sepsis, hypothermia, or hypoxia) have a much greater risk. In such infants, although the risk increases with increasing hyperbilirubinemia, there is no hyperbilirubinemia levels that are considered safe; the treatment based on age and clinical factors. There is now operational limits to initiate phototherapy based on the gestational age. NeurotoxizitätIst the most important consequence of neonatal hyperbilirubinemia. Acute encephalopathy can follow a variety of neurological impairment, including cerebral palsy and sensorimotor deficits; the perception is usually spared. Kernicterus is the most severe form of neurotoxicity. Although now rare, kernicterus still occurs, but can be prevented in most cases. Kernicterus is an injury to the brain caused by deposits unconjugated bilirubin in the basal ganglia and brainstem nuclei veruracht either acute or chronic hyperbilirubinemia. Normally, bilirubin is bound to serum albumin and remains in the intravascular space. However, bilirubin can cross the blood-brain barrier and cause under certain conditions kernicterus, if the serum bilirubin concentration is significantly increased if the serum albumin concentration is remarkably low (for example, in premature infants.) If bilirubin is mixed with albumin by competitive binding include competitive bonds drugs (such. as sulfisoxazole, ceftriaxone, aspirin) and free fatty acids as well as hydrogen ions (eg. as in fasting, septic or acidotic infants). Risk of hyperbilirubinemia in newborns ? 35 SSW The risk is based on the total serum bilirubin levels. (Adapted from Bhutani VK, Johnson L Sivieri Em. Predictive ability of a predischarge hour-specific serum bilirubin for Subsequent significant hyperbilirubinemia in healthy term and near-term newborns Pediatrics 103 (1): 6-14, 1999.) The majority pathophysiology bilirubin is produced by the breakdown of hemoglobin in conjugated bilirubin (and other substances). Unconjugated bilirubin bound to albumin in the blood for transport to the liver, where it is taken up by hepatocytes and conjugated by the enzyme UDP-glucuronosyltransferase with glucuronic acid to make it water-soluble. The conjugated bilirubin is excreted in the bile into the duodenum. In adults conjugated bilirubin is reduced by intestinal bacteria to Urobilin and excreted. However, newborns have less bacteria in their digestive tract, so fewer bilirubin is reduced to Urobilin and excreted. They also have the enzyme ?-glucuronidase cleaves the bilirubin. The now unconjugated bilirubin may be absorbed into the circulation and recycled. This process is called enterohepatic circulation of bilirubin called (see also bilirubin Metabolism). Mechanisms of hyperbilirubinemia hyperbilirubinemia may by one or caused more of the following processes: Decreased Increased production hepatic uptake Decreased conjugation Prevented excretion Prevented bile flow (cholestasis) Increased enterohepatic circulation etiology classification There are several ways to classify the causes of hyperbilirubinemia and discuss. Since temporary jaundice is common in healthy newborns (in contrast to adults in whom jaundice always means a disorder), hyperbilirubinemia can be classified as physiological or pathological. It can also be classified according to whether the hyperbilirubinemia unconjugated, conjugated or both. It can also be classified according to the underlying mechanism (see Table: Causes of neonatal hyperbilirubinemia) .Ursachen Most cases involve conjugated hyperbilirubinemia. Among the most common causes of neonatal jaundice physiological hyperbilirubinemia are breastfeeding breast milk Pathologic hyperbilirubinemia due to hemolytic disease liver dysfunction (eg., Caused by parenteral nutrition, leading to cholestasis, neonatal sepsis, neonatal hepatitis) can be a conjugated or mixed hyperbilirubinemia to lead. Physiological hyperbilirubinemia occurs in almost all newborns. This is due to the fact that it comes with the shorter life of the red blood cells to increased Bilirubinproduktion, the clearance is reduced by insufficient conjugation of UDP-glucuronosyltransferase and the low bacterial colonization of the intestine with an increased hydrolysis of conjugated bilirubin to an increase in enterohepatic circuit leads. the bilirubin level in the 3rd or 4th day of life while rise (in Asian children at the age of 7) to 18 mg / dl and then drop off again. Jaundice caused by breast-feeding develops in one-sixth of breastfed infants during the first week of life. Breastfeeding increases the entero-hepatic circulation of bilirubin in some infants who have a reduced milk recording with simultaneous dehydration or low caloric intake. The increased enterohepatic circulation can also result from reduced intestinal bacteria that convert bilirubin to unabsorbed metabolites. Breast milk jaundice is different from jaundice caused by breastfeeding. It develops after the first 5-7 days of life, and has peaked at about 2 weeks. It is believed that the jaundice caused by an increased concentration of ?-glucuronidase in breast milk, resulting in an increase in the deconjugation and reabsorption of bilirubin. Pathological hyperbilirubinemia is diagnosed in neonates appears when Jaundice in the first 24 hours after the first week or> 2 weeks continues. Serum total bilirubin to> 5 mg / dl / day increases the serum total bilirubin is> 18 mg / dl The infant symptoms or signs of severe disease has some of the most common pathological causes are immune and non-immune hemolytic anemia G6PD deficiency hematoma absorption sepsis hypothyroidism causes of neonatal hyperbilirubinemia mechanism causes Increased enterohepatic circulation breast milk (breast milk jaundice) breastfeeding problems (jaundice through breastfeeding) drug-induced paralytic Darmv Closure (magnesium sulphate or morphine) fasting or other cause for Hypoperistalsis Hirschsprung’s disease Intestinal atresia or stenosis, including pancreatic annularly meconium ileus or Mekoniumpfropf syndrome pyloric stenosis * swallowed blood overproduction distribution of extravascular blood (eg. B. bruising, petechiae; pulmonary, cerebral or occult bleeding) polycythemia due maternofetaler or fetofetaler transfusion or by delayed cord clamping overproduction due to hemolytic anemia Certain medications and drugs in neonates with G6PD deficiency (eg. as paracetamol, alcohol, anti-malarials, aspirin, bupivacaine, corticosteroids, diazepam, nitrofurantoin, oxytocin, penicillin, phenothiazine, sulfonamides) Maternofetale blood group incompatibility (z. B. Rh, AB0) erythrocyte enzyme deficiency (z. B. of G6PD or pyruvate kinase) spherocytosis thalassemias (?, ?-?) hypofunction due to bile duct obstruction ?1 antitrypsin deficiency * biliary atresia * * Choledochal cystic fibrosis * (Thickened bile) Dubin-Johnson syndrome and Rotor syndrome * Parenteral Nutrition tumor or Band * (extrinsic obstruction) sub-function due to metabolic-endocrine conditions Crigler-Najjar syndrome (familial nonhemolytic jaundice types 1 and 2) drugs and hormones Gilbert’s syndrome hypermethioninemia hypopituitarism and anencephaly hypothyroidism Lucey-Driscoll syndrome Maternal diabetes prematurity Tyrosinosis Mixed overproduction and underactive asphyxia intrauterine infections Maternal diabetes respiratory distress syndrome sepsis Fetal erythroblastosis syphilis TORCH infections Jaundice can also occur after the neonatal period. TORCH = toxoplasmosis, other pathogens, rubella, cytomegalovirus and herpes simplex. Adapted from Poland RL, Ostrea EM Jr: Neonatal. In Care of the high-risk neonate, ed. 3, ed. Klaus and MH AA Fanaroff. Philadelphia, WB Saunders Company, 1986. Clarification History The history of the current disease should be documented age of onset and duration of jaundice. Important associated symptoms include lethargy and poor nutrition (suggesting possible kernicterus), which can progress to stupor, hypotension, or seizures and eventually hypertension. A documentation of the feedings can give indications of possible problems breastfeeding or malnutrition. Therefore, it should also belong to the history of what was fed to the child, how much and how frequently, how often urinates the child or bowel movements had (which may indicate possible problems with breastfeeding or malnutrition) how well the child takes the breast or the bottle whether the mother feels that her milk is injected and whether swallows child during feedings and appears after nursing sick. A review of body systems should investigate as respiratory distress syndrome, fever, irritability or lethargy (sepsis) for symptoms and causes; Hypotension and Still problems (hypothyroidism, metabolic disorder); and repeated episodes of vomiting (intestinal obstruction). The history should pay attention to maternal infections (toxoplasmosis, other pathogens, rubella, cytomegalovirus and herpes simplex [TORCH] infections), as well as diseases that cause early hyperbilirubinemia as maternal diabetes, maternal Rh factor and maternofetale blood group incompatibility. Also a possible history of a delayed or difficult birth (hematoma or forceps injury) should be included. Family history should query whether hereditary diseases in the family are known to cause jaundice including G6PD deficiency, thalassemia and spherocytosis and whether siblings had jaundice. A documentation of previous medication should especially note medicines that can cause jaundice such. As ceftriaxone, sulfonamides, Malariamittel.Körperliche study the clinical impression and the vital signs are checked. The skin is examined for the extent of jaundice out. A gentle pressure on the skin can help to recognize the jaundice. Also bruising and petechiae (signs of anemia) are documented. The physical examination should focus on signs of certain underlying diseases. The overall appearance is on Plethora studied (maternofetale transfusion); Macrosomia (maternal diabetes); Lethargy or extreme irritability (sepsis or infection); as well as on dysmorphic signs in the face as macroglossia (hypothyroidism), flat nasal bridge or bilateral epicanthus (Down syndrome). In the study of head and neck all the bruising and swelling of the scalp with a view to Cephalhematoma special attention. The lung is listening to rattling, wheezing and decreased breath sounds (pneumonia). The abdomen is on expansion, mass (hepatosplenomegaly) or pain (bowel obstruction) was investigated. The neurological examination should for signs of hypotension or weakness (metabolic disorder, hypothyroidism, sepsis) achten.Warnhinweise The following findings are of particular importance: jaundice in the first day of life serum total bilirubin> 18 mg / dl rate of increase of total bilirubin in serum > 0.2 mg / dl / h (> 3.4 mol / l / h) and> 5 mg / dl / day conjugated bilirubin> 1 mg / dl (> 17 micromol / l) when serum total bilirubin <5 mg / dL or> 20% of total bilirubin in serum (indication of neonatal cholestasis) jaundice that occurs after the first 2 weeks of life, lethargy, irritability, shortness of breath assessing the findings the assessment should initially focus on the distinction between pathological physiological jaundice. History, physical examination and temporal occurrence can also provide information, but usually the serum total bilirubin and conjugated bilirubin levels will beurteilt.Zeitaspekt Jaundice occurs in the first 24-48 hours, or continues to> 2 weeks, is likely pathological. Jaundice that occurs only after 2 or 3 days is more likely related to physioligischer jaundice, jaundice caused by breast feeding or breast milk jaundice. One exception is the sub function of bilirubin by metabolic factors (eg. As Crigler-Najjar syndrome, hypothyroidism, medications), which often becomes apparent only after 2 to 3 days. In this case, the höchse value of bilirubin in the first week it should be noted at a concentration of <5 mg / dL / day, which may persist for an extended period. Since most newborns in the United States h are discharged from the hospital or from the children's ward within 48, many cases of hyperbilirubinemia can only be detected after discharge. Physical findings in neonatal jaundice findings at the time of jaundice cause General examination fever, tachycardia, dyspnea within the first 24 h Accumulates at> 5 mg / dl / day (> 86 mol / l / day) pneumonia, TORCH infection, sepsis lethargy, Can occur hypotension during first 24-48 h> 2 weeks last hypothyroidism, metabolic disorder Macrosomia 24-48 h Accumulates at> 5 mg / dl Maternal diabetes petechiae within the first 24 h Accumulates at> 5 mg / dl Hemolytic states (eg. B. maternofetale blood group incompatibility, erythrocyte enzyme deficiency, hereditary spherocytosis, thalassemia, sepsis) plethora within the first 24 h Accumulates at> 5 mg / dl Maternofetale or fetofetale transfusion, delayed cord clamping Head and neck Bilateral oblique palpebral fissures, flat nose, macroglossia, flat occiput first 2-3 days down syndrome (possibly duodenal atresia, Hirschsprung’s disease, bowel obstruction, further distance 1 to 2 cloves) Cephalohematoma 24-48 h if necessary Accumulation at> 5 mg / dl birth trauma macroglossia 24-48 h Can> 2 weeks last hypothyroidism abdominal examination abdominal distention, decreased bowel sounds may delayed onset (2-3 days or later) bowel obstruction (eg. As cystic fibrosis, Hirschsprung’s disease, intestinal atresia or stenosis, pyloric stenosis, biliary atresia) TORCH = toxoplasmosis, other Krankheitser simplex lively, rubella, cytomegalovirus and herpes. Tests The diagnosis results from the skin color of the child and is confirmed by the measurement of Serumbilirubinspiegels. Invasive techniques for transcutaneous measurement of bilirubin in infants are increasingly being used in connection with a measurement of bilirubin in serum. The risk of hyperbilirubinemia is based on age-specific bilirubin. A bilirubin of> 10 mg / dl (> 170 .mu.mol / l) in premature infants and> 18 mg / dl (> 308 .mu.mol / l) at newborns makes further clarification is required, incl. Hct, blood smear, reticulocyte count, direct Coombs test, direct and total bilirubin, blood group and Rh factor from both the child and the mother. Other studies such. As blood, urine and Liquorkulturen to rule out sepsis and the study of erythrocyte enzymes to exclude rarer causes of hemolysis are indicated depending on the history and physical examination. These tests can be carried dl (> 428 mol / l)> 25 mg / for all newborns with an initial bilirubin. Treatment Treatment of hyperbilirubinemia depends on the underlying disease. Additionally, treatment for hyperbilirubinemia may even be necessary. Clinical Calculator: hyperbilirubinemia in newborns Review The physiological jaundice usually has no clinical relevance and disappear after a week. By the frequent feeding commercial baby foods, the incidence and severity of hyperbilirubinemia can be reduced because the peristalsis in the gastrointestinal tract excited and the frequency of bowel movements is increased, which in turn reduces the enterohepatic circulation of bilirubin. It seems to play no matter what food is selected. Jaundice through breastfeeding can be reduced by increasing the frequency of feeding. When the bilirubin is further increased to> 18 mg / dl with a mature born infant with jaundice due to breast-feeding, a temporary change from breast milk to finished infant formula may be necessary; Also phototherapy may be displayed at higher values. The interruption of breastfeeding is only required for one to two days, the mother should be encouraged to regularly pump out so that they once bilirubin decreases with her infant, can continue breastfeeding immediately. In addition, it should be assured that by the jaundice there is no damage and they can resume breastfeeding without risk. It is not advisable to substitute with water or dextrose, as this can interfere with milk production in the mother. A targeted treatment of hyperbilirubinemia include phototherapy (phototherapy) exchange transfusion phototherapy Phototherapy is the treatment of choice, usually using fluorescent white light. (The most effective for intensive phototherapy is blue light having a wavelength of 425-475 nm.) In the phototherapy light is used, which leads to the formation of photoisomers of bilirubin, which are more water soluble and rapidly excreted without glucuronidation by the liver and the kidneys can be. It provides an immediate treatment of hyperbilirubinemia and kernicterus prevention. For newborns ? 35 SSW were born is the phototherapy an option if the value of the unconjugated bilirubin is> 12 mg / dl (> 205.2 mol / l ), and h is at values ??of> 15 mg / dl at the age of 25-48, 18 mg / dl at the age of 49-72 h and at 20 mg / dl at the age of> 72 h indicated (risk of hyperbilirubinemia in newborns ? 35 weeks). Phototherapy is not indicated for conjugated hyperbilirubinemia. For newborn babies, who were born <35 SSW, the thresholds of bilirubin levels for treatment are lower because preemies have a greater risk of neurotoxicity. The earlier the premature babies, the lower the threshold (see table: Recommended limits * for the start of phototherapy or exchange transfusion in infants <35 weeks). Recommended limits * for the start of phototherapy or exchange transfusion in babies <35 SSW gestational age (weeks) phototherapy (total serum bilirubin, mg / dl) exchange transfusion (total serum bilirubin, mg / dl) <28 5-6 11-14 28 to <30 6-8 12-14 30 to <32 8-10 13-16 32 to <34 10 to 12 15 to 18 34 to <35 12-14 17-19 * Consensus-based recommendations, adapted from MJ Maisel, Watchko JF, Bhutani VK, Stevenson DK: An approach to the management of hyperbilirubinemia in the preterm infant less than 35 weeks of gestation. Journal of Perinatology 32: 660-664, 2012. Since the visible jaundice may disappear under the phototherapy, although the serum bilirubin remains elevated, the skin color can not be used as a measure of the severity of hyperbilirubinemia. Attention should be paid to the fact that the blood is protected for the determination of bilirubin from bright light as it quickly to a photo-oxidation of bilirubin in the sample tube kann.Austauschtransfusion This treatment can remove bilirubin rapidly from the circulation, and is indicated for severe hyperbilirubinemia, the most often occurs in the context of an immunologically mediated hemolysis. By an umbilical vein catheter small amounts of blood are withdrawn to remove partially hemolyzed and antibody-bearing erythrocytes and circulating lgs The blood is replaced with uncoated donor red blood cells, which do not have the erythrocyte membrane antigen, binds to circulating antibody. That is, the blood type is used O when the newborn is sensitized to AB antigens and Rh-negative blood is used when the newborn is sensitized to Rh antigens. Since red blood cells from adult donors own more ABO antigen sites than fetal cells, a type-specific transfusion will intensify hemolysis. Since only unconjugated bilirubin can cause kernicterus, the indication for exchange transfusion should not be made due to the total, but the conjugated bilirubin. At-term infants are specific indications for exchange transfusion bilirubin levels of ? 20 mg / dl at the age of 24-48 hours, or ? 25 mg / dl at the age of> 48 hours further when the phototherapy not to a decrease in the serum concentration of 1- leads or 2 mg / dl (17-34-mol / l) within 4-6 hours after its beginning but, irrespective of the bilirubin when clinical signs of kernicterus occur. If the bilirubin is> 25 mg / dl in the initial investigation, exchange transfusion in the event should be prepared that the phototherapy alone in bilirubin levels is not enough to cut. There are limits to infants who were born at <35 SSW proposed (see table recommended thresholds * for starting phototherapy or exchange transfusion in newborns 35 weeks). Previously used some doctors criteria, which were based solely on the patient's weight, but these criteria were replaced by the above described specific guidelines. In most cases, 160 ml / kg of concentrated red blood cells are replaced (twice the total blood volume of the child) over 2-4 hours. Alternatively, it is possible to have two consecutive blood exchange transfusion of 80 ml / kg over 1-2 h to carry out. For an exchange of blood 20 ml of blood is removed and then immediately replaced by 20 ml of transfused blood. This process is repeated until the entire desired amount is replaced. In critically ill or premature infants portions are of 5-10 ml used to avoid sudden large changes in blood volume. The aim is to reduce the bilirubin about 50%, knowing that it can come to 60% of the value before transfusion within 1-2 hours at a rebound of hyperbilirubinemia. When risk factors for the development of kernicterus present (z. B. fasting, sepsis, acidosis), it is common to strive for about 1-2 mg / dl lower target value. Bei persistierenden hohen Bilirubinwerten kann es erforderlich sein, die Austauschtransfusion zu wiederholen. Allerdings gibt es Risiken und Komplikationen bei diesem Verfahren, und der Erfolg der Phototherapie hat die Häufigkeit der Austauschtransfusionen reduziert. Fazit Neugeborenen-Gelbsucht wird durch erhöhte Bilirubin-Produktion verursacht, verringerter Bilirubin-Clearance oder durch einen erhöhten enterohepatischen Kreislauf. Ein gewisser Grad an Gelbsucht ist bei Neugeborenen norma. Das Risiko variiert je nach dem Alter, dem Bilirubinwert, der Frühgeburtlichkeit und der Gesundheit des Neugeborenen. Die Behandlung hängt von Ursache und Ausmaß der Bilirubin-Erhebung ab; je früher der Säugling, geboren wurde, desto geringer der Schwellenwert für die Behandlung. Zur gezielten Behandlung gehört die Phototherapie und die Austauschtransfusion.

Health Life Media Team

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