Causes of Jaundice: Signs and Symptoms
Causes of Jaundice: Signs and Symptoms
Causes of Jaundice: Signs and Symptoms
Pale-colored stools
Dark-colored urine
Skin itching
Nausea and vomiting
Rectal bleeding
Diarrhea
Fever and chills
Weakness
Weight loss
Loss of appetite
Confusion
Abdominal pain
Headache
Swelling of the legs
Swelling and distension of the abdomen due to the accumulation of fluid (ascites)
Causes of jaundice
Old red blood cells travel to your liver, where they’re broken down. Bilirubin is the
yellow pigment formed by the breakdown of these old cells. Jaundice occurs when
your liver doesn’t metabolize bilirubin the way it’s supposed to.
Your liver might be damaged and unable to perform this process. Sometimes the
bilirubin simply can’t make it to your digestive tract, where it normally would be
removed through your stool. In other cases, there may be too much bilirubin trying to
enter the liver at once or too many red blood cells dying at one time.
alcohol misuse
liver cancer
thalassemia
cirrhosis (scarring of the liver, usually due to alcohol)
gallstones (cholesterol stones made of hardened fat material or pigment
stones made of bilirubin)
hepatitis A
hepatitis B
hepatitis C
hepatitis D
hepatitis E
pancreatic cancer
G6PD deficiency
biliary (bile duct) obstruction
sickle cell anemia
acute pancreatitis
ABO incompatibility reaction
drug-induced immune hemolytic anemia
yellow fever
Weil’s disease
other blood disorders such as hemolytic anemia (the rupture or destruction of
red blood cells that leads to a decreased number of red blood cells in your
circulation, which results in fatigue and weakness)
an adverse reaction to or overdose of a medication, such as an
acetaminophen (Tylenol)
Risk factors
Major risk factors for jaundice, particularly severe jaundice that can cause
complications, include:
Blood type. If the mother's blood type is different from her baby's, the
baby may have received antibodies through the placenta that cause
abnormally rapid breakdown of red blood cells.
Complications
High levels of bilirubin that cause severe jaundice can result in serious
complications if not treated.
Bilirubin is toxic to cells of the brain. If a baby has severe jaundice, there's a
risk of bilirubin passing into the brain, a condition called acute bilirubin
encephalopathy. Prompt treatment may prevent significant lasting damage.
Listlessness
Difficulty waking
High-pitched crying
Fever
Kernicterus
Hearing loss
The goals of testing are to determine the cause of jaundice and to evaluate the severity of the
underlying condition. Initial testing, usually a physical exam conducted by a healthcare
practitioner, is generally focused on the liver. Specific additional tests, such as viral hepatitis
testing and/or testing to evaluate increased red blood cell destruction, may be ordered along
with or following the initial tests based on the clinical findings and the healthcare practitioner's
suspicions of the cause of the jaundice.
Laboratory tests
Some tests are used to detect liver damage and evaluate liver function and may include:
Some tests may be used to detect infections that affect the liver, such as:
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis E
Cytomegalovirus (CMV)
Epstein-Barr virus (EBV)
Tests used to detect decreased red blood cell survival may include:
Non-laboratory tests
Imaging tests and liver biopsies may be used to help evaluate the status and structure of the
liver, gallbladder, and bile ducts. Testing may include:
Abdominal ultrasound
CT (computed tomography) scan
MRI (magnetic resonance imaging) scan, often including MRCP (magnetic resonance
cholangiopancreatogram, to visualize the pancreas and bile ducts)
Endoscopic retrograde cholangiopancreatography (ERCP, a direct imaging of the
pancreas and bile ducts)
Liver biopsy
Normal /
Total bilirubin Increased
increased
Normal /
Unconjugated bilirubin Increased Normal
increased
Normal / Decreased /
Urobilinogen Decreased
increased negative
Normal
Alanine transferase and
Increased
aspartate transferase levels
Large spleen
Pathophysiology[edit]
Jaundice itself is not a disease, but rather a medical sign of one of many possible underlying pathological
processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin in
blood.
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 tetrapyrrole pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is
"unconjugated," "free" or "indirect" bilirubin. Approximately 4 milligrams of bilirubin per kilogram of blood is
produced each day.[33] The majority of this bilirubin comes from the breakdown of heme from expired red blood
cells in the process just described. Approximately twenty percent comes from other heme sources, however,
including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as
muscle myoglobin and cytochromes.[33]
Liver events[edit]
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-glucuronyl transferase.
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal
bacteria convert some bilirubin into urobilinogen. From there, 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 feces and urine, respectively
reatment
Mild infant jaundice often disappears on its own within two or three weeks.
For moderate or severe jaundice, your baby may need to stay longer in the
newborn nursery or be readmitted to the hospital.
Treatments to lower the level of bilirubin in your baby's blood may include:
Treatment varies based on the medical condition responsible for causing jaundice,
and the associated symptoms and complications. Treatments may include the
following:
supportive care,
IV fluids in cases of dehydration,
medications for nausea/vomiting and pain,
antibiotics,
antiviral medications,
blood transfusions,
steroids,
chemotherapy/radiation therapy, and
phototherapy (newborns).