Jaundice - baby, swollen, symptoms, Definition, Description, Demographics, Causes and symptoms
PHYSIOLOGIC JAUNDICE (non-pathologic unconjugated hyperbilirubinemia). 1 . more difficult to define and jaundice should be followed closely. Definition. Jaundice is the yellow color of skin and mucous membranes due to accumulation of bile pigments in blood and their deposition in body tissues. Jaundice is the yellowing of the skin and/or eyes and is a classic symptom of viral hepatitis. Learn what causes the symptom and how it is.
This is called hyperbilirubinemia. This is called jaundice. Depending on the cause of the hyperbilirubinemia, jaundice may appear at birth or at any time afterward. During pregnancy, the placenta excretes bilirubin.
When the baby is born, the baby's liver must take over this function. There are several causes of hyperbilirubinemia and jaundice, including the following: Physiologic jaundice occurs as a "normal" response to the baby's limited ability to excrete bilirubin in the first days of life.
About 2 percent of breastfed babies develop jaundice after the first week. It peaks about two weeks of age and can persist up to three to 12 weeks. Breast milk jaundice is thought to be caused by a substance in the breast milk that increases the reabsorption of bilirubin through the intestinal tract. It is caused by failure to initiate breastfeeding, resulting in dehydration, decreased urine production and accumulation of bilirubin. Late preterm infants, those who are born between 34 weeks and 36 weeks, are more susceptible to this problem because they do not have the coordination and strength to maintain a successful breastfeeding.
However, it is also very common in full-term newborns and usually gets better once breastfeeding is established. Jaundice may occur with the breakdown of red blood cells due to hemolytic disease of the newborn Rh diseaseor from having too many red blood cells that break down naturally and release bilirubin. Jaundice related to inadequate liver function.
Jaundice may be related to inadequate liver function due to infection or other factors. Who is affected by hyperbilirubinemia? About 60 percent of term newborns and 80 percent of premature babies develop jaundice. Infants of diabetic mothers and of mothers with Rh disease are more likely to develop hyperbilirubinemia and jaundice.
Why is hyperbilirubinemia a concern? Although low levels of bilirubin are not usually a concern, large amounts can circulate to tissues in the brain and may cause seizures and brain damage. This is a condition called kernicterus. What are the symptoms of hyperbilirubinemia? The following are the most common symptoms of hyperbilirubinemia.
However, each baby may experience symptoms differently. How is hyperbilirubinemia diagnosed? The timing of the appearance of jaundice helps with the diagnosis.
Abdominal pain frequently accompanies jaundice, and its character may point to a specific diagnosis. Although hepatocellular jaundice is usually painless, a dull ache or "heavy sensation" in the right upper quadrant may attend acute hepatitis of any cause. Pain associated with alcoholic hepatitis, especially when accompanied by fever, jaundice, and leukocytosis, may be sufficiently severe to simulate an acute surgical abdomen Mendenhall, f Right upper quadrant abdominal pain occurring episodically over months to years, and especially when radiating to the right scapular area, right shoulder, or around the upper abdomen and back in a girdle distribution, suggests gallstones.
Persistent epigastric or right upper quadrant pain possibly radiating to the back suggests carcinoma of the head of the pancreas. Fever frequently accompanies jaundice caused by acute hepatitis, although it usually lasts no more than a few days. Fever associated with chills usually points to biliary obstruction, especially due to stones or stricture and, less frequently, to malignancy.
Generalized pruritus usually points to biliary tract obstruction as the cause of jaundice. Recent onset localizes the level to the large ducts i. A long-standing history of pruritus extending over months to years in a middle-aged woman suggests primary biliary cirrhosis as the culprit. However, pruritus may occasionally occur with viral hepatitis too. Arthritis or urticaria appearing within a month of onset of jaundice and disappearing shortly before the onset points to hepatitis B virus infection Alpert et al.
Arthritis may also accompany or precede autoimmune hepatitis Golding et al.
- HOMOLOGOUS SERUM JAUNDICE AND ITS RELATION TO METHODS OF PLASMA STORAGE
- Hyperbilirubinemia and Jaundice
True arthritis may also accompany hemochromatosis, although this disease rarely causes jaundice Bassett et al. Bone pain simulating joint pain may accompany any long-standing cholestatic condition due to vitamin D depletion and calcium deficiency. The jaundiced patient requires thorough documentation of all recent drug and toxin exposures.
After asking for a list of the patient's drugs, the physician should specifically ask about pain relievers, tranquilizers, and birth control pills or other estrogens that the patient may forget to mention. Chemicals, especially organic compounds used occupationally or at home, may be hepatotoxins.
Alcohol intake should be documented, preferably by estimating the number of grams or ounces of alcohol imbibed per day rather than the number of drinks consumed. Alcohol abusers are often reluctant to tell the truth about their habit, and the physician may need to talk to the patient's spouse, other family members, or friends to obtain a complete picture. Potential contact with hepatitis viruses and other infectious agents should also be determined. This involves asking about contacts with other icteric or potentially hepatitic patients, recent transfusions, needle or narcotic use, and ingestion of raw shellfish.
Recent foreign travel to areas of poor sanitation carries a risk of exposure to hepatitis A virus or Entamoeba histolytica. The homosexual male is at high risk for development of hepatitis A or B infection Keeffe, Occupational exposure to barnyard animals, slaughterhouses, or stagnant water may implicate leptospirosis.
A patient who is immunologically compromised is a potential target for cytomegalovirus or herpes virus infection, while work in an institution i. A young icteric individual with a sore throat and rash may have infectious mononucleosis. A patient with bacterial sepsis due to a wide variety of bacteria may have jaundice without cholangitis or biliary obstruction Gottlieb et al, Surgical history, whether recent or remote may be implicated in the cause of jaundice Lamont and Isselbacher, Within the first three postoperative weeks, jaundice may be due to a variety of problems that include: Biliary tract surgery in the remote past may have produced a biliary stricture, although these are usually clinically evident within 2 years of operation.
When investigating a case of jaundice potentially related to surgery, it is important to examine the operative record for transfusion, anesthesia, x-rays, drugs, and potential hypotension or hypoxia, as well as the surgeon's dictated note of intraoperative events and his visual and palpation impression of the patient's liver, biliary tree, and pancreas.
Other systemic conditions may have complications related to the liver. For example, patients with inflammatory bowel disease are predisposed to primary sclerosing cholangitis, cholangiocarcinoma, chronic hepatitis, cirrhosis, and hepatic amyloid. If a significant section of terminal ileum has been involved by or resected for Crohn's disease, the patient may also have gallstones Allan, ; Warren and Kern, Cystic fibrosis, hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency and other hereditary metabolic diseases with prominent hepatic effects i.
Systemic lupus erythematosus sometimes directly affects the liver Runyon, LaBrecque, and Anuras, Acutely or subacutely decreased hepatic oxygenation of any cause may simulate the hepatic manifestations of viral hepatitis. A family history of jaundice, liver disease, or anemia especially when requiring splenectomy should be sought. A positive family history of liver disease may implicate the genetically transmitted nonhemolytic hyperbilirubinemias i.
Physical Examination In most instances, physical examination of the jaundiced patient confirms a diagnosis suspected by history or provides diagnostic proof in its own right. A general examination of the patient furnishes numerous diagnostic clues.
At any given level of jaundice, the patient with hepatocellular disease appears more acutely ill than the individual with obstruction. Indeed, unless his course is complicated by cholangitis, the obstructed patient generally does not appear acutely ill at all. The patient's age renders some diagnoses more likely than others. Carcinoma of the pancreas is an increasingly prominent cause of jaundice over 40 years of age.
The incidence of hepatitis A virus is greatest in youth, but hepatitis B and non-A, non-B virus infections may occur at any age. Gallstones may uncommonly occur in adolescence but become increasingly common in middle age.
A green cast to the jaundice indicates prolonged obstruction, while an orange-yellow color is more compatible with a hepatocellular mechanism. Disorientation, obtundation, or a simple slowing of mental processes such as speech or recall incriminate disturbed hepatocellular function rather than obstruction as a cause of jaundice. Examination of the skin may reveal bruising resulting from disturbed blood coagulation mechanisms. Spider telangiectases are small cutaneous arteriovenous anastomoses that blanch when pressure is exerted on the central point of the vascular complex.
They are most liable to appear on the upper body including trunk, arms, hands, neck, and face. Although they may occasionally occur singly in normal people and more commonly during pregnancy, their presence generally indicates chronic hepatocellular disease. Scratch marks confirm a patient's history of pruritus.
Decreased axillary and pubic hair and a change from a male to female escutcheon over the genitals suggests cirrhosis. Dupuytren's contracture may also accompany chronic liver disease. Xanthelasma and tuberous xanthomas are fatty deposits appearing on eyelids and over the buttock and extensor surfaces of the extremities respectively and are commonly seen in long-standing biliary obstruction with hyperlipidemia, especially primary biliary cirrhosis.
Auscultation over the liver including the lower right anterior chest should be performed prior to manual manipulation of the area. Hepatic friction rubs are usually due to malignancy or inflammatory disease involving Glisson's capsule Simpson, Abnormal auscultatory sounds may be better appreciated with the patient standing rather than recumbent. Palpation of the liver is the single most crucial step in evaluation of the jaundiced patient.
An appreciation of its size, surface characteristics, and tenderness are central to understanding the cause of the patient's illness. Liver size should always be expressed in terms of centimeters of total span.
This involves determining the position of the lower hepatic border by palpation, percussion, or ballotment and that of the upper border by percussion and measuring the distance between the two marks.
Liver span is dependent on the height and lean body mass of the patient and especially on the percussion technique of the examiner Castell et al.
However, a "normal" liver span does not guarantee that the organ is functionally or histologically normal. Observer variation regarding liver size can usually be resolved with an objective measurement such as a liver scan. Very large livers are likely to be congested or fatty or to be involved with cirrhosis, neoplasm, or amyloid.
A rapidly shrinking liver combined with deepening jaundice and clinical deterioration indicates acute liver failure, usually secondary to a virus or toxin. A hard or nodular liver is probably fibrotic or infiltrated with tumor. Although the normal liver is slightly tender to palpation, unusual hepatic tenderness is often the result of acute hepatitis of any cause, abscess, or rapid hepatic enlargement secondary to vascular congestion or fatty infiltration. Splenomegaly is frequently found in the jaundiced patient, although its specific etiology is variable.
Splenomegaly without hepatomegaly may result from primary hemolytic disease especially hereditary spherocytosis or from portal vein occlusion of any cause. Enlarged spleens commonly result from portal hypertension caused by liver disease or hepatic venous obstruction. In these instances, hypersplenism with hemolysis may contribute to the patient's jaundice.
Splenomegaly due to portal hypertension is often associated with ascites and, in later stages, a prominent abdominal venous pattern. An enlarged spleen may also occur in viral hepatitis as a nonspecific reticuloendothelial response to infection.
Finally, concurrent hepatomegaly and splenomegaly may not be related as cause and effect, but both may be due to involvement by another process, most commonly tumor particularly hematologic or storage disease. Ascites in the jaundiced patient is an ominous sign, usually signifying severly decompensated cirrhosis with portal hypertension or malignancy studding the peritoneum or invading the liver. Occasionally, ascites may be due to massive or subacute hepatic necrosis or hepatic vein obstruction, but is a rare feature of isolated portal vein occlusion.
Bilateral lower extremity edema often accompanies ascites, although the latter frequently occurs without evidence of other fluid accumulation. If bilaterally equal leg edema arises in a jaundiced patient who does not have ascites or cardiovascular-renal disease, carcinoma of the pancreas with inferior vena cava obstruction must be considered. An abdominal venous pattern extending over the anterior abdominal wall in a patient with ascites usually means that the patient has portal hypertension.
Occasionally it can indicate an obstruction of the inferior vena cava with collateral flow Missal et al. If the venous pattern is secondary to portal hypertension, blood in the vessels will flow away from the umbilicus.
If the patient has caval obstruction, blood in the dilated veins will flow superiorly at all levels. An everted umbilicus in a patient with massive ascites indicates chronic abdominal distention and usually means cirrhosis.
Dark urine resembling tea, which develops a green foam on shaking, is caused by bile pigment. Its presence excludes hemolysis or a hepatic uptake or conjugating defect of bilirubin metabolism acting alone as a cause of jaundice. The stool of patients whose jaundice is due to hemolysis is brown.
Patients with mild to moderate hepatocellular jaundice also have brown stools, although as their hepatic excretory ability increasingly fails, their stool may turn a clay color. Patients with obstructive jaundice often have clay-colored stools. A jaundiced patient with a positive reaction for blood in a clay-colored stool suggests carcinoma of the pancreas or ampulla of Vater.
Laboratory Tests Laboratory tests usually serve to confirm the pathophysiology of jaundice. Sometimes they may demonstrate a specific etiology as well Chopra and Griffin, The complete blood count may provide evidence for hemolysis by demonstrating anemia in a patient without blood loss or a blood smear with spherocytes or other oddly shaped erythrocytes.
Hemolysis may be proven via a reticulocyte count, Coomb's test, or other specific tests of erythrocyte enzymes. Leukocytosis and neutrophilia are unusual in viral hepatitis, although common in cholangitis and alcoholic hepatitis. Eosinophilia plus jaundice is suspicious for toxic hepatitis on a basis of hypersensitivity.
A jaundiced patient without urinary bilirubin has either hemolysis or a hepatic defect in bilirubin uptake or conjugation.
Jaundice | Icterus | MedlinePlus
Marked persistent proteinuria in a jaundiced patient is suspicious for amyloid. Liver function tests are nonspecific indicators of liver disease. None of them alone provides a sensitive evaluation of liver function. Many of the enzymes tested have potential sources other than the liver. Their interpretation is possible only in the light of a thorough history and meticulous physical examination.
Even then, their value is often realized only alter serial determinations have been obtained. Normal serum bilirubin concentration is usually no greater than 1. Serum alkaline phosphatase derives from liver, bone, placenta, intestinal mucosa, and certain tumors.
In most instancies, only sources from liver and bone are clinically important. Alkaline phosphatase is often elevated to at least three times the upper limit of normal in patients with jaundice due to intra- or extrahepatic obstruction but is usually less than this figure in hepatocellular jaundice.
However, patients with acute alcoholic liver disease may have alkaline phosphatase elevations higher than five times the upper limit of normal without an obstructive component. The enzyme is also frequently elevated in diffuse hepatic infiltration i. An alkaline phosphatase elevated out of proportion to serum bilirubin may mean hepatic infiltrative disease or partial biliary obstruction associated with choledochohthiasis. In jaundiced women with a long history of hyperphosphalasia and pruritus, a diagnosis of primary biliary cirrhosis is likely Tornay, Although the test is not specific for primary biliary cirrhosis, it is almost always negative in extrahepatic obstruction, the most important differential diagnostic problem of this disease.
Transaminase elevations are common in both hepatocellular and obstructive jaundice, although higher values are generally achieved in the former case. Unexpectedly elevated transaminases due to obstruction are caused by transient mechanisms such as floating gallstones or to sphincter of Oddi spasm.
In these instances, the transaminases fall rapidly toward normal over 48 hours. Transaminase elevations associated with hepatocellular jaundice gradually decline over weeks. In viral hepatitis both enzymes are often elevated to or higher than ten times the upper limit of normal, and the two are more nearly equal or the SGPT is frequently higher. In general, transaminase elevations greater than are usually due to viral or toxic hepatitis, decrease in hepatic oxygen supply i.
Prothrombin precursor is a protein manufactured by the liver whose full expression of activity in coagulation relies on a vitamin K-dependent carboxylase Corrigan et al. The concentrations of circulating prothrombin precursor and fully functional prothrombin may be measured independently.
RELATION OF THE SPLEEN TO JAUNDICE
Moderately severe hepatocellular disease results in reduction of both proteins, while extrahepatic obstruction, due to impairment of vitamin K absorption, will cause a fall of functional prothrombin alone.
Prognostically, a rise of the precursor concentration indicates return of hepatic synthetic capacity even though the patient's prothrombin time remains abnormal. In practice, the prothrombin time may be prolonged more than 3 seconds over control in both hepatocellular and obstructive jaundice.
Parenteral administration of vitamin K 10 mg will correct the prothrombin time of the obstructed patient to normal within 24 hours, while that of the hepatocellular icteric patient will improve only partially or not at all.
A prothrombin time at least 10 seconds over control in a jaundiced patient and the inability to correct it with vitamin K is a poor prognostic sign. Albumin is synthesized in the liver. Because the protein has a relatively long half-life approximately 2 weeksits serum concentration will usually not fall significantly until liver disease has been present for at least 1 to 2 weeks.
However, elevated total serum globulins, especially when exhibiting a broad gamma electrophoretic distribution and when unexplained by other chronic inflammatory conditions, are a generally reliable indicator of chronic hepatocellular disease.
A serum protein electrophoretic pattern missing an alpha-1 peak suggests alpha-1 antitrypsin deficiency and should be followed by a specific assay for alpha-1 antitrypsin.
Serologic assays for hepatitis A and B viruses should be performed in cases of acutely developing jaundice.
Hepatitis A virus does not produce chronic liver disease, so only hepatitis B virus serology will be meaningful in patients with chronic hepatocellular disease Lemon, ; Friedman and Dienstag, Antibody titers against delta agent, Epstein-Barr virus, herpesvirus and cytomegalovirus, and urine culture for cytomegalovirus can also be obtained in selected cases.
In special cases, serological tests for leptospirosis, syphilis, and Entamoeba histolytica are also available. Imaging Evaluation Although a thorough history and physical examination still provide the best clinical diagnostic assessment of the jaundiced patient, new imaging procedures designed to identify biliary obstruction or other potential surgical causes of jaundice i.
In the past 10 to 15 years, the development of high-resolution ultrasound and computerized tomography CT and advanced techniques and equipment for performing percutaneous transhepatic cholangiography PTCendoscopic retrograde cholangiopancreatography ERCPand hepatobiliary scintigraphy HBS have revolutionized the investigation of jaundice.
Imaging investigation should start with a chest x-ray and plain film of the abdomen. The former may furnish clues such as cardiac enlargement with pulmonary venous engorgement, mass lesion in the chest, bony erosion of the ribs and spine, pleural effusions, or an elevated right diaphragm. Abdominal sonography is a valuable screening test in the jaundiced patient Ferruci, ; Meire, The demonstration of biliary ductal dilation, gallstones, hepatic mass lesion, or an enlarged or abnormally shaped pancreas directs further investigation or therapy.
Sonography is noninvasive, readily available in most hospitals, does not involve radiation exposure, and is cheaper than CT or other procedures in which the bile ducts are directly opacified. It may also allow guided biopsy or drainage of lesions in the liver or pancreas. Sonography is frequently more successful at identifying ductal dilation rather than its level or cause, but may also miss early cases of obstruction in which the biliary tree has not had sufficient opportunity to dilate.
Finally, the procedure may be difficult to perform in the postoperative patient with surgical wounds, dressings, and drains that prevent close apposition of the sonographic probe to the abdominal wall. Nevertheless, in most patients sonography should be the initial imaging procedure directed at the biliary tree. Computerized tomography has the advantage of surveying the entire abdomen as well as the hepatobiliary-pancreatic axis Lee and Evens, ; Kreel, In addition to reliably detecting ductal dilation, CT is superior to sonography in determining the level and cause of obstruction.
The pancreas is displayed more reliably and accurately by CT than by sonography. The obese patient and patients with prior biliary-enteric bypass procedures in whom the bile ducts may not be well seen sonographically might best be first examined by CT. Like sonography, CT allows accurate guided biopsy or drainage of otherwise inaccessible lesions. It is expensive, however, involves radiation exposure, and is not available at some health care facilities.
Optimal interpretation of CT for the jaundiced patient often involves administration of intravenous or oral contrast to opacity the bile ducts and bowel repectively ; some patients may not tolerate these agents due to drug allergy or to abdominal pain or ileus.
Residual intestinal barium may also prevent x-ray transmission and create artifact. Although CT usually defines an abnormally shaped pancreas with high accuracy, it may not always distinguish the cause of the misshapen gland i. ERCP may then be necessary to complete the evaluation. CT is particularly useful in patients with equivocal sonographic data or a strong suspicion of pancreatic disease or biliary obstruction despite negative sonography.
Until recently, hepatobiliary scintigraphy had little to contribute to the differential diagnosis of jaundice except in the instance of neonatal hepatitis versus biliary atresia or the occasional need for objective assessment of liver size. However, the development of new radionuclide agents with improved hepatic extraction and biliary excretion, improved imaging techniques, and the application of computer assistance to interpretation of dynamic scans have transformed HBS into an accurate modality for the diagnosis of large bile duct obstruction and may also prove useful in demonstrating intrahepatic cholestasis Lieberman and Krishnamurthy, When evaluating the patency of the extrahepatic bile ducts by HBS, the scintigraphic image of the liver provides an added advantage to uncover unsuspected abscess or neoplasm.
HBS does not have the resolution needed to diagnose specifically gallstones or tumor in the biliary system. Consequently, HBS, when used for uncovering extrahepatic obstruction, provides functional data i.
However, because biliary obstruction may exist for several weeks before the proximal ducts dilate sufficiently to be visualized by ultrasound or CT, HBS may provide a more rapid assessment of biliary patency then is obtainable by other noninvasive means Kaplun et al. Percutaneous transhepatic cholangiography involves passage of a thin needle into the liver under fluoroscopic guidance and injection of contrast into the biliary tree Lintott, The procedure is easily available, its cost is generally less than that of ERCP, and a local anesthetic injection over the right flank is the only sedative or anesthetic medication required.
A dilated, obstructed duct may be decompressed percutaneously by passage of a guide wire and cannula through the right flank incision. If the ducts are not visualized or if a nonobstructed biliary tree is found, one can immediately perform a needle liver biopsy through the anesthetized incision in the patient's right side.
The patient should have a normal clotting mechanism and intravenous antibiotics should be administered before the procedure to guard against cholangitis and septicemia should an obstruction be revealed.