- a yellowish pigmentation of the skin, the conjunctiva membranes over the sclerae, and other mucous membranes.
- caused by hyperbilirubinemia.
- Normal conc. Of bilirubin is 0.2 – 1.2 mg/dL.
- 1.5 mg/dL (>26µmol/L), three times the usual value of approximately 0.5 mg/dL, for the coloration to be easily visible.
- Jaundice comes from the French word jaune, meaning yellow.
How dose JAUNDICE happen
- Bilirubin is normally produced as by product of hemoglobin metabolism.
- 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. 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.
- the heme is then turned into unconjugated bilirubin in the macrophages of the spleen.
- this unconjugated bilirubin is not water soluble then it bound to albumin and sent to liver.
- in the liver it is conjugated with glucuronic acid making it soluble in water. Much of it goes into the bile, and thus out into the small intestine.
Types of jaundice :
- Prehepatic (haemolytic) jaundice.
- Hepatocellular jaundice.
- Post hepatic jaundice ( obstructive jaundice ).
Prehepatic (haemolytic) jaundice.
- Excessive destruction of red cells.
- Unconjugated hyperbilirubinaemia.
- most important to surgeons is hereditary spherocytosis, in which splenectomy may be necessary.
- Failure to remove bilirubin from blood stream.
- Medical rather than surgical conditions.
- Surgical intervention may aggravate hepatocellular injury.
Post-Hepatic (Obstructive) Jaundice
- blockage of any duct (intrahepatic or extrahepatic) that carries bile from the liver to the gallbladder or to the small intestine, which prevent excretion of conjugated Bilirubin
- jaundice due to biliary obstruction; This can occur at various levels within the biliary system.
- may result from Obstruction within the lumen, Pathology in the wall or External compression ( EC ).
Etiology of obstructive jaundice
The most Common are :
- Common bile duct stones, LO (most common).
- Carcinoma of the head of pancreas, EC (2ed most common).
- Malignant porta hepatis lymph nodes, EC Metastatic tumors (usually from the gastrointestinal tract or the breast).
Biliary obstruction can be intra or extrahepatic.
- Hepatitis; is inflammation of the liver with diffuse or patchy necrosis. Causes of hepatitis include viruses, drugs, and alcohol.
- Cirrhosis; results from chronic inflammation of the liver e.g. Alcoholic hepatitis or chronic hepatitis B. or PBC is a chronic, autoimmune progressive, granulomatous destruction of the intrahepatic ducts, more common in females.
- Drugs; such as anabolic steroids ,chlorpromazine and ceftriaxone directly cause cholestasis.
Extra hepatic causes are subdivided into intraductal and extraductal.
1- Intraductal causes include neoplasms, stone disease, biliary stricture, parasites, primary sclerosing cholangitis, AIDS-related cholangiopathy, and biliary tuberculosis.
2- Extraductal obstruction caused by external compression of the biliary ducts may be secondary to neoplasms, pancreatitis, or cystic duct stones with subsequent gallbladder distension.
Gallstones may pass through the CBD and cause obstruction, larger stones can become lodged in the CBD and cause complete obstruction.
– Mirizzi syndrome is the presence of a stone impacted in the cystic duct or the gallbladder neck, causing inflammation and external compression of the common hepatic duct and thus biliary obstruction.
- Periampullary carcinomas, gallbladder carcinomas & cholangiocarcinomas.
- Metastatic tumors and the secondary adenopathies in the porta hepatis.
Approach to jaundice
– Jaundice, pale stools, dark urine and pruritus.
– pain : (intermittent and severe, dull ache, backache, no pain )
– episodes of indigestion or dyspepsia.
– loss of appetite and weight.
– general malaise and breathlessness.
– Abdominal pain may be misleading; some patients with CBD stones have painless jaundice, whereas others with hepatitis have pain in the RUQ .
– Age ,sex , occupation.
– drugs, alcohol intake.
– Hx of injections , infusions.
– Hx of recent travel , blood transfusion ,contact with other jaundice patient.
– History of anemia, previous malignancy.
– known GS disease, previous biliary surgery, hepatitis.
On physical examination signs of jaundice (skin, sclera , mucos membranes).
– A high fever and chills suggest a coexisting cholangitis.
– Enlarged liver or shrunken liver.
– Needle tracks (over the limbs).
Features of cirrhosis & liver failure:
– Changes in Mental state for example loss of concentration.
– spider naevi.
– Ascites and collateral circulation, caput medusae.
– Palmar erythema, bruising & oedema.
– Dupuytrens, testicular atrophy, Gynaecomastia.
– Finger clubbing & leuconychia.
Courvoisier sign(palpable GB):
- when the gallbladder is palpable and the patient is jaundice, the bile duct is unlikely to be obstructed by a stone because previous attacks of inflammation will have caused the gallbladder to become thick-walled, fibrotic and non-distensible.
- it may be associated with pancreatic malignancy.
- Scratch marks over the limbs suggest prolonged cholestasis or high-grade biliary obstruction.
Early signs of liver failure
- Body hair loss
- Spider naevi “ more than 9 indicates a state of a progressive disease
- Palmer erythema “Thenar and hypothenar”
- Dupuytrens contracture
Late signs of liver failure
- Ill looking, wasted patients.
- Testicular atrophy.
- Liver flap.
- Encephalopathy with cogwheel limb rigidity.
- Intellectual change.
- Convulsions & coma.
- Serum Bilirubin: Conjugated Bilirubin >35 mmol/l
- ALP : raised
- gamma-glutamyl transpeptidase (GGT): raised
- ALT & AST : No significant increase
- Blood Glucose : Raised if pancreas is involved
- Serum Protein : Normal
- Urine : -ve urobilinogen, +ve Bilirubin
- Feces : pale
- Prolonged PT
Jaundice Lab Studies:
- Serum bilirubin: Regardless the cause conjugated serum bilirubin values are usually elevated.
- Extrahepatic obstruction: This is typically associated with considerable direct and
- indirect bilirubin elevation.
- Initially, an increase in the conjugated bilirubin level occurs without affecting the unconjugated bilirubin level because obstruction of the CBD prevents excretion of already conjugated bilirubin into the duodenum.
- Conjugated bilirubin that does reach the intestine is deconjugated by intestinal bacteria.
- Unconjugated bilirubin easily crosses the intestinal epithelial barrier into the blood. It accumulates in the blood because the uptake mechanism and the hepatic cells are overburdened by bilirubin that has already been conjugated but cannot be excreted.
- Therefore, indirect bilirubin levels rise even in persons with obstructive jaundice.
- Intrahepatic obstruction: Both conjugated and unconjugated bilirubin fractions may increase in varying proportions.
- The unconjugated fraction may be increased because of the inability of the damaged cells to conjugate.
Alkaline phosphatase (ALP): ALP is markedly elevated in persons with biliary obstruction. However, high levels of this enzyme are not specific to cholestasis.
- ALP levels are elevated in nearly 100% of patients, they exceed 5 times the upper limit.
- Intrahepatic obstruction:
- ALP levels are usually less than 3 times the upper limit of the normal reference range.
These levels are elevated in patients with diseases of the liver, biliary tract, and pancreas when the biliary tract is obstructed. Levels parallel the levels of ALP and 5-prime-nucleotidase in conditions associated with cholestasis. The extreme sensitivity of GGT, as opposed to ALP, limits its usefulness; however, the level helps distinguish hepatobiliary disease as the cause of an isolated rise in ALP.
Serum transaminases: Levels of these are only moderately elevated, may be markedly increased in cholangitis.
Extrahepatic obstruction: Usually,AST & ALT levels are not elevated unless secondary acute parenchymal damage is present. A 3-fold or more increase in ALT strongly suggests pancreatitis.
Intrahepatic obstruction: ALT elevations are due to intrahepatic disease. ALT and AST levels are usually elevated to the same degree in patients with viral hepatitis and those with drug-induced liver damage.
Prothrombin time (PT):
- This may be prolonged because of malabsorption of vitamin K. Little or no improvement occurs in patients with parenchymal liver disease.
- include serologic assays for acute viral hepatitis, Hepatitis A, B, & C.
- The presence of antimitochondrial antibodies, usually in high titers, is indicative of PBC.
- Urine bilirubin normally is absent.
- When it is present, dark-colored urine seen in patients with obstructive jaundice or jaundice due to hepatocellular injury.
Jaundice Imaging Studies:
- Plain XR
- CT scan
Plain XR are of limited value, few calculi are radiopaque.
- Is the least expensive, safest, most sensitive for visualizing the biliary system. Current accuracy is close to 95%.
- It is used for the initial evaluation of extrahepatic obstruction is suggested by the presence of dilated bile ducts.
- Visualization of the pancreas, kidney, and blood vessels is also possible.
- Bowel gas may obscure visualization of the CBD.
- The cystic duct is also poorly imaged.
- It is less useful as diagnostic in obese
CT scan is usually considered more accurate.
- In addition, it helps visualize liver structures.
- The addition of intravenous contrast helps define vascular structures and the biliary tract.
- Spiral CT scan gives a better resolution & reduce the presence of air artifacts.
- spiral CT cholangiography is used to visualize radiolucent stones, ducts & tumors.
- Resolution is low as s. bilirubin levels increase & patient is asked to hold his breath.
Magntic Resonance Cholangiopancreatography provides a sensitive noninvasive method of detecting biliary and pancreatic duct stones, strictures, or dilatations or cancer.
Absolute contraindications include
- the presence of a cardiac pacemaker,
- cerebral aneurysm clips,
- ocular or cochlear implants, & foreign bodies.
- Relative contraindications include the presence of cardiac prosthetic valves, neurostimulators, metal prostheses, and penile implants.
Endoscopic Retrogade Cholangiopancreatography
is a procedure to visualize both the biliary and pancreatic duct systems. Endoscopically, the ampulla of Vater is identified and cannulated. A contrast agent is injected into these ducts, and x-ray images are taken to evaluate their caliber, length, and course.
- It is especially useful for lesions distal to the bifurcation of the hepatic ducts,
ERCP has a therapeutic application
- obstructions can be relieved by the removal of stones, sphincterotomy.
- the placement of stents and drains.
- Complications of this technique include pancreatitis, perforation, biliary peritonitis, sepsis, hemorrhage, and adverse effects from the dye.
Percutaneous Tanshepatic Cholangiography is performed by a radiologist using fluoro-scopic guidance.
- Useful for lesions proximal to the CHD.
- The technique requires considerable experience.
- Complications include peritonitis with possible intraperitoneal hemorrhage, sepsis, cholangitis, subphrenic abscess, and lung collapse.
- The accuracy of PTC in elucidating the cause and site of obstructive jaundice is 90-100% for causes within the biliary tract.
Endoscopic ultrasound (EUS) combines endoscopy and US to provide remarkably detailed images of the pancreas and biliary tree.
- It uses higher-frequency ultrasonic waves compared to US (3.5 MHz vs 20 MHz) and allows diagnostic tissue sampling(FNA).
- EUS has been reported to have up to a 98% diagnostic accuracy in patients with obstructive jaundice.
- The sensitivity of EUS for the identification of focal mass lesions <3 cm in diameter has been superior to that of CT & MRCP.
- EUS is more portable than ERCP or MRCP.
- EUS can be followed immediately by therapeutic ERCP.
- The positive of EUS-FNA for cytology in patients with malignant obstruction has been reported to be as high as 96%.
- Treatment of the underlying cause is the objective of the medical treatment of biliary obstruction.
- Bile acid–binding resins, cholestyramine (4 g) or colestipol (5 g), dissolved in water or juice 3 times a day may be useful in the symptomatic treatment of pruritus associated with biliary obstruction.
- Deficiencies of vitamins A, D, E, and K may happened, include an individualized regimen for replacement of these vitamins as needed in the patient’s treatment.
- Antihistamines may be used for the symptomatic treatment of pruritus
- Treatment with parentally administered naloxone and, more recently, nalmefene, has improved pruritus in some patients.
Complications in jaundiced pts.
1. Bleeding (¯ clotting factors)
2. Infections – reduced resistance to bacterial infection.
3. Renal failure. Absorption of endotoxins from the .gut (hepatorenal syndrome)
Specific measures are needed:
1. Vit. K 10 mg IM or 1mg IV .
2. Systemic antibiotics.
3. Adequate hydration.
4. Mannitol “osmotic diuretics” 200 ml .
5. Urethral catheter “good urinary output”.
Jaundice surgical intervention
- surgical intervention depends on the cause of biliary obstruction.
- Laparoscopic cholecystectomy remains the treatment of choice for symptomatic gallstones. If failed open cholecystectomy.
- Resectability of neoplastic causes of biliary obstruction varies with respect to the location and extent of the disease.
- Liver transplantation may be considered in appropriate patients.
Jaundice Nursing Care Plan
– Documentation of patient age as it helps in the diagnosis of the patient and the underlining cause.
– Applying phototherapy treatment , to facilitate alternative ways of bilirubin excretion.
– In case of Infantile jaundice, the nurse have to completely undress the enfant
– Closing the enfants gonads and eyes, to protect eyes from intensive light and temperature.
– Scheduling of patient turning program. Normally 2 hours program.
– Trying to obtain bilirubin level within normal ranges.
– Fluids administration, to prevent dehydration.
Nursing evaluation: the enfant bilirubin level should go to normal levels within 7 days of treatment.