Jaundice: Wikis

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Jaundice
Jaundice08.jpg

A person with jaundice from hepatic failure.
ICD-10 R17.
ICD-9 782.4
DiseasesDB 7038
MedlinePlus 003243
MeSH D007565

Jaundice, also known as icterus (attributive adjective: icteric), is a yellowish discoloration of the skin, the conjunctival membranes over the sclerae (whites of the eyes), and other mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL[1] ( >35 nmol/l), three times the usual value of approximately 0.5 mg/dL[1], for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.

One of the first tissues to change color as bilirubin levels rise in jaundice is the conjunctiva of the eye, a condition sometimes referred to as scleral icterus. However, the sclera themselves are not "icteric" (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly conjunctival icterus.[2] See photographic illustration on the right.

Contents

Signs and symptoms

This is a 4-year old boy diagnosed with Glucose-6-phosphate dehydrogenase deficiency showing Jaundice in the sclera.
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Eyes

It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. Alexander Pope, in "An Essay on Criticism" (1711), wrote: “All seems infected that the infected spy, As all looks yellow to the jaundiced eye.”[3] Similarly in the mid-19th century the English poet Lord Alfred Tennyson wrote in the poem “Locksley Hall”: “So I triumphe'd ere my passion sweeping thro' me left me dry, left me with the palsied heart, and left me with a jaundiced eye.”

Differential diagnosis

Types of jaundice

When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

Category Definition
Pre-hepatic The pathology is occurring prior to the liver.
Hepatic The pathology is located within the liver.
Post-Hepatic The pathology is located after the conjugation of bilirubin in the liver.

Pre-hepatic

Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers. Rat fever (leptospirosis) can also cause jaundice.

Laboratory findings include:

  • Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
  • Serum: increased unconjugated bilirubin.
  • Kernicterus is not associated with increased bilirubin

Hepatic

Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann-Pick disease, type C. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Laboratory findings include:

  • Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a condition not associated with increased bilirubin.

Post-hepatic

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".

Not one test can differentiate between various classifications of jaundice. A combination of liver function tests is essential to arrive at a diagnosis.

Table of diagnostic tests[4]
Function test Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal / Increased Increased
Conjugated bilirubin Increased Normal Increased
Unconjugated bilirubin Normal / Increased Normal
Urobilinogen Normal / Increased Decreased / Negative
Urine Color Normal Dark
Stool Color Normal Pale
Alkaline phosphatase levels Normal Increased
Alanine transferase and Aspartate transferase levels Increased
Conjugated Bilirubin in Urine Not Present Present

Neonatal jaundice

Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur, leading to significant lifelong disability; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. A Bili light is often the tool used for early treatment, which often consists of exposing the baby to intensive phototherapy. Bilirubin count is lowered through bowel movements and urination so regular and proper feedings are especially important.[5]

Pathophysiology

In order to understand how jaundice results, the pathological processes that cause jaundice to take their effect must be understood. Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin.

When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As each red blood cell traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this. Cellular contents, including hemoglobin, are subsequently released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice. Two reactions then take place with the heme molecule. The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon monoxide. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is "unconjugated," "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day.[6] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 percent comes from other heme sources, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.[6]

Hepatic events

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

Diagnostic approach

Most patients presenting with jaundice will have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel will include blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include GGT and prothrombin time (PT).

Some bone and heart disorders can lead to an increase in ALP and the aminotransferases, so the first step in differentiating these from liver problems is to compare the levels of GGT, which will only be elevated in liver-specific conditions. The second step is distinguishing from biliary (cholestatic) or liver (hepatic) causes of jaundice and altered lab results. The former typically indicates a surgical response, while the latter typically leans toward a medical response. ALP and GGT levels will typically rise with one pattern while AST and ALT rise in a separate pattern. If the ALP (10–45) and GGT (18–85) levels rise proportionately about as high as the AST (12–38) and ALT (10–45) levels, this indicates a cholestatic problem. On the other hand, if the AST and ALT rise is significantly higher than the ALP and GGT rise, this indicates an hepatic problem. Finally, distinguishing between hepatic causes of jaundice, comparing levels of AST and ALT can prove useful. AST levels will typically be higher than ALT. This remains the case in most hepatic disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage may see fairly normal ALT levels, with AST 10x higher than ALT. On the other hand, if ALT is higher than AST, this is indicative of hepatitis. Levels of ALT and AST are not well correlated to the extent of liver damage, although rapid drops in these levels from very high levels can indicate severe necrosis. Low levels of albumin tend to indicate a chronic condition, while it is normal in hepatitis and cholestasis.

Lab results for liver panels are frequently compared by the magnitude of their differences, not the pure number, as well as by their ratios. The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (10), some other form of liver damage (above 1), or hepatitis (less than 1). Bilirubin levels greater than 10x normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15x tends to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5x normal tend to indicate obstruction, while levels greater than 10x normal can indicate drug (toxic) induced cholestatic hepatitis or Cytomegalovirus. Both of these conditions can also have ALT and AST greater than 20× normal. GGT levels greater than 10x normal typically indicate cholestasis. Levels 5–10× tend to indicate viral hepatitis. Levels less than 5× normal tend to indicate drug toxicity. Acute hepatitis will typically have ALT and AST levels rising 20–30× normal (above 1000), and may remain significantly elevated for several weeks. Acetaminophen toxicity can result in ALT and AST levels greater than 50x normal.

References

  1. ^ a b Guyton, Arthur, and John Hall, John. Textbook of Medical Physiology, Saunders, September 2005, ISBN 978-0-7216-0240-0
  2. ^ Findarticles.com, accessed Nov. 22, 2008
  3. ^ From The Dictionary of Cliches by James Rogers (Ballantine Books, New York, 1985).
  4. ^ Goljan, Edward F., Rapid Review Pathology 2nd edition. Pg. 368–369. 2007.
  5. ^ O'Keefe, Lori (2001-05-05). "Increased vigilance needed to prevent kernicterus in newborns". American Academy of Pediatrics 18 (5): 231. http://aapnews.aappublications.org/cgi/content/full/18/5/231. Retrieved 2007-06-27. 
  6. ^ a b Pashankar, D; Schreiber, RA (July 2001). "Jaundice in older children and adolescents". Pediatrics in Review 22 (7): 219–226. doi:10.1542/pir.22-7-219. PMID 11435623. 

External links

Infants


1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

Medical warning!
This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead.

JAUNDICE (Fr. jaunisse, from jaune, yellow), or Icterus (from its resemblance to the colour of the golden oriole, of which Pliny relates that if a jaundiced person looks upon it he recovers but the bird dies), a term in medicine applied to a yellow coloration of the skin and other parts of the body, depending in most instances on some derangement affecting the liver. This yellow colour is due to the presence in the blood of bile or of some of the elements of that secretion. Jaundice, however, must be regarded more as a symptom of some morbid condition previously existing than as a disease per se. Cases with jaundice may be divided into three groups.

1. Obstructive Jaundice. - Any obstruction of the passage of bile from the liver into the intestinal canal is sooner or later followed by the appearance of jaundice, which in such circumstances is due to the absorption of bile into the blood. The obstruction is due to one of the following causes: (I) Obstruction by foreign bodies within the bile duct, e.g. gallstones or parasites; (2) inflammation of the duodenum or the lining membrane of the duct; (3) stricture or obliteration of the duct; (4) a tumour growing from the duct; (5) pressure on the duct from without, from the liver or other organ, or tumours arising from them. Obstructions from these causes may be partial or complete, and the degree of jaundice will vary accordingly, but it is to be noted that extensive organic disease of the liver may exist without the evidence of obstructive jaundice.

The effect upon the liver of impediments to the outflow of bile such as those above indicated is in the first place an increase in its size, the whole biliary passages and the liver cells being distended with retained bile. This enlargement, however, speedily subsides when the obstruction is removed, but should it persist the liver ultimately shrinks and undergoes atrophy in its whole texture. The bile thus retained is absorbed into the system, and shows itself by the yellow staining seen to a greater or less extent in all the tissues and many of the fluids of the body. The kidneys, which in such circumstances act in some measure vicariously to the liver and excrete a portion of the retained bile, are apt to become affected in their structure by the long continuance of jaundice.

The symptoms of obstructive jaundice necessarily vary according to the nature of the exciting cause, but there generally exists evidence of some morbid condition before the yellow coloration appears. Thus, if the obstruction be due to an impacted gallstone in the common or hepatic duct, there will probably be the symptoms of intense suffering characterizing hepatic colic (see Colic). In the cases most frequently seen - those, namely, arising from simple catarrh of the bile ducts due to gastro-duodenal irritation spreading through the common duct - the first sign to attract attention is the yellow appearance of the white of the eye, which is speedily followed by a similar colour on the skin over the body generally. The yellow tinge is most distinct where the skin is thin, as on the forehead, breast, elbows, &c. It may be also well seen in the roof of the mouth, but in the lips and gums the colour is not observed till the blood is first pressed from them. The tint varies, being in the milder cases faint, in the more severe a deep saffron yellow, while in extreme degrees of obstruction it may be of dark brown or greenish hue. The colour can scarcely, if at all, be observed in artificial light.

The urine exhibits well marked and characteristic changes in jaundice which exist even before any evidence can be detected on the skin or elsewhere. It is always of dark brown colour resembling porter, but after standing in the air it acquires a greenish tint. Its froth is greenish-yellow, and it stains with this colour any white substance. It contains not only the bile colouring matter but also the bile acids. The former is detected by the play of colours yielded on the addition of nitric acid, the latter by the purple colour, produced by placing a piece of lump sugar in the urine tested, and adding thereto a few drops of strong sulphuric acid.

The contents of the bowels also undergo changes, being characterized chiefly by their pale clay colour, which is in proportion to the amount of hepatic obstruction, and, to their consequent want of admixture with bile. For the same reason they contain a large amount of unabsorbed fatty matter, and have an extremely offensive odour.

Constitutional symptoms always attend jaundice with obstruction. The patient becomes languid, drowsy and irritable, and has generally a slow pulse. The appetite is usually but not always diminished, a bitter taste in the mouth is complained of, while flatulent eructations arise from the stomach. Intolerable itching of the skin is a common accompaniment of jaundice, and cutaneous eruptions or boils are occasionally seen. Yellow vision appears to be present in some very rare cases. Should the jaundice depend on advancing organic disease of the liver, such as cancer, the tinge becomes gradually deeper, and the emaciation and debility more marked towards the fatal termination, which in such cases is seldom long postponed. Apart from this, however, jaundice from obstruction may exist for many years, as in those instances where the walls of the bile ducts are thickened from chronic catarrh, but where they are only partially occluded. In the common cases of acute catarrhal jaundice recovery usually takes place in two or three weeks.

The treatment of this form of jaundice bears reference to the cause giving rise to the obstruction. In the ordinary cases of simple catarrhal jaundice, or that following the passing of gallstones, a light nutritious diet (milk, soups, &c., avoiding saccharine and farinaceous substances and alcoholic stimulants), along with counter-irritation applied over the right side and the use of laxatives and cholagogues, will be found to be advantageous. Diaphoretics and diuretics to promote the action of the skin and kidneys are useful in jaundice. In the more chronic forms, besides the remedies above named, the waters of Carlsbad are of special efficacy. In cases other than acute catarrhal, operative interference is often called for, to remove the gallstones, tumour, &c., causing the obstruction.

2. Toxaemic Jaundice is observed to occur as a symptom in certain fevers, e.g. yellow fever, ague, and in pyaemia also as the effect of certain poisons, such as phosphorus, and the venom of snake-bites. Jaundice of this kind is almost always slight,, and neither the urine nor the discharges from the bowels exhibit changes in appearance to such a degree as in the obstructive variety. Grave constitutional symptoms are often present, but they are less to be ascribed to the jaundice than to the disease with which it is associated.

3. Hereditary Jaundice

Under this group there are the jaundice of new-born infants, which varies enormously in severity; the cases in which a slight form of jaundice obtains in several members of the same family, without other symptoms, and which may persist for years; and lastly the group of cases with hypertrophic cirrhosis.

The name malignant jaundice is sometimes applied to that very fatal form of disease otherwise termed acute yellow atrophy of the liver (see Atrophy).


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Simple English

Jaundice (also called icterus) is when the skin and the whites of the eyes become a yellow color.[1] People with jaundice have a problem with their liver, which stops it from removing dead red blood cells properly. These blood cells contain a chemical called bilirubin.[1] Bilirubin causes the yellow coloring of the skin. Jaundice is common in newly born babies. It usually starts the second day after birth. [2]

Jaundice can also be caused by other diseases, like malaria, hepatitis, or gallstones.

Jaundice is the most common of all liver problems. The yellow colour of the skin and mucous membranes happens because of an increase in the bile pigment, bilirubin, in the blood.[2]

The bile, made by the liver, is a vital digestive fluid needed for proper nutrition. It also stops decaying changes in food. If the bile is stopped from entering the intestines there is an increase in gases and other products. Normally, the production of bile and its flow is constant.

Contents

Types of Jaundice

There are three types of jaundice:

  • haemolytic jaundice - caused by destruction of red blood cells. This causes increased bilirubin formation and anaemia
  • obstructive jaundice - caused by a blockage in the pathway where bilirubin is made in the liver cells and where bile goes into the duodenum
  • hepatocellular jaundice - caused by damage to liver cells. The damage could be from a viral infection or toxic drugs.

Yellow discoloration of the skin and the whites of the eyes happens in all types of jaundice.

Symptoms

The symptoms of jaundice are:[3]

  • extreme weakness
  • headache
  • fever
  • loss of appetite
  • tiredness
  • severe constipation
  • nausea
  • yellow coloration of the eyes, tongue, skin and urine.
  • dull pain in the liver region.
  • Obstructive jaundice may also cause intense itching.

Causes

Jaundice is a sign of that the liver is not working. It may be caused by a blockage of the bile ducts which release bile salts and pigment into the intestines. The bile then gets mixed with blood and this gives a yellow colour to the skin[3]. The blockage of the bile ducts could be caused by:

  • gallstones
  • inflammation (swelling) of the liver, called hepatitis. This is caused by a virus. The virus can spread and may lead to epidemics caused by:
    • overcrowding
    • dirty surroundings
    • insanitary conditions
    • contamination of food and water.

Other causes of jaundice are pernicious anaemia and diseases affecting the liver such as typhoid, malaria, yellow fever and tuberculosis.

Dietary Treatment

The simple form of jaundice can be cured quickly by diet and exercises. Recovery will be slow in serious cases which have been caused by a blockage or pressure in the bile ducts. The patient should rest until the acute symptoms of the disease subside.

The patient should be put on a juice diet for a week. The juice of oranges, lemons, grapes, pears, carrots, beets and sugarcane can be used. A hot water enema should be given every day during this period to make sure the bowel empties completely. This stops decomposed, poisonous material going into the blood stream. The juice diet may be continued till the acute symptoms subside.

After the juice diet, the patient may start an all-fruit diet for further three to five days. The patient should have three meals a day of fresh, juicy fruits such as apples, pears, grapes, oranges, and pineapples, but no bananas.

Afterward a simple diet may be started on the following lines :

Getting up : A glass of warm water with juice of half a lemon.

Breakfast : One fresh juicy fruit such as apple, pear, mango, papaya, or some grapes, or berries. One cup wheat dalia or one slice of whole meal bread with a little butter.

Mid-morning : Orange or pear juice.

Lunch : Raw vegetable salad, two small chapatis of whole wheat flour, a steamed leafy vegetable such as spinach, methi saag or carrot and a glass of buttermilk.

Mid-afternoon : Coconut water or apple juice.

Dinner : One cup strained vegetable soup, two chapatis of whole meal, baked potato, and one other leafy vegetable like methi, spinach, etc.

Before bed : A glass of hot skimmed milk with honey if desired.

All fats like ghee, butter, cream and oils must not be eaten for at least two weeks. After that a little butter and olive oil may be used in the diet. A light carbohydrate diet, without fats, best obtained from vegetables and fruits should be eaten.

The patient should take plenty of fresh vegetables and fruit juices. Dandelion leaves, radishes with leaves, endive should be added to the daily raw vegetable salad. Raw apples and pears are especially helpful. Barley water, drunk several times during the day, is considered good for jaundice. One cup of barley should be boiled in six pints of water and simmered for three hours.

Digestive upsets must be avoided. No food that will ferment or decay in the lower intestines, like pulses and legumes, should be included in the diet. Drinking a lot of water with lemon juice will protect the damaged liver cells.

A person with jaundice can get better quite easily with the above diet and build up his sick liver until it works normally once again. A repeat of liver trouble can be stopped with:

  • reasonable care in the diet and life style,
  • regular, moderate exercise
  • frequent exposure to sunshine and fresh air
  • enough rest.

Research has shown that the liver has an excellent ability to fix itself provided all essential nutrients are eaten. Diets high in complete proteins, Vitamin C, and Vitamin B, particularly Choline which helps digest fats, and Vitamin E can help the liver recover. It is essential to keep the diet for a long time to prevent a repeat of the trouble.

References

  1. 1.0 1.1 Marks, Jay. "Jaundice signs, symptoms and treatment" (in English). MedicineNet. http://www.medicinenet.com/jaundice/article.htm. Retrieved 2010-05-04. 
  2. 2.0 2.1 "Jaundice in Healthy Newborns" (in English). The Nemours Foundation. http://kidshealth.org/parent/pregnancy_newborn/common/jaundice.html. Retrieved 2010-05-15. 
  3. 3.0 3.1 "Jaundice signs and symptoms" (in English). MedicineNet. http://www.jaundicesymptoms.net. Retrieved 2010-09-09. 

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