OBSTRUCTIVE JAUNDICEPATHOPHYSIOLOGY AND WORKUP

DR.KIRAN KUMAR.G

APOLLO BGS HOSPITALS

DEFINITION

Failure of normal amount of bile to reach intestine

due to mechanical obstruction of the extra hepatic biliary tree or within the porta hepatis

JAUNDICE Jaundice (derived from French word ‘jaune’ for yellow) or icterus (Latin

word for Jaundice)

Yellowing of sclera at 3 mg%

Bilirubin has got high affinity for elastin and sclera has high elastin

content

Yellowing of skin and mucous membrane at 6 mg%

D/D beta carotenemia,Quinacrine therapy malingering with picric acid

They doesn’t stain mucous membrane and sclera

Bilirubin level rise upto three weeks than stabilise

BILIRUBIN METABOLISM

PHYSIOLOGICAL FACTS

Total bile flow-600ml/day(500-1000ml/day)

Hepatocyte component is -450ml/day

Can be bile salt dependent due to biliary glutathione and ductular

bicarbonate secretion

Cholangiocyte component-150ml/day

It depends on secretin stimulation

Total serum bilirubin is 0.3-1.2 mg/dl

With conjugated bilirubin<15 %

1mg/dl of bilirubin=17 mmol/l

PHYSIOLOGY OF OBSTRUCTION

Normal secretory pressure of bile is 15-25 cm of water

At 35 cm of water there is suppression of bile flow

High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile

Dilatation of bile duct and intra hepatic biliary radicals(IHBR)

IHBR dilatation may be absent if there is secondary hepatic fibrosis or

cirrhosis

PATHOPHYSIOLOGY

Increase in biliary pressure leads to

Disruption of tight junctions between hepatocytes and bile duct cells with

increased permeability

Reflux of bile contents in liver sinusoids

Neutrophil infiltration,increased fibrinogenesis and deposition of reticulin

fiberes in portal triad

Reticulin fibers gets converted in to type 1 collagen

Laying down of collagen fibers leads to hepatic fibrosis obstruction of

sinusoids and secondary biliary cirrhosis and portal hypertension

Fibrosis can also lead to atrophy of obstructed liver

EFFECTS OF OBSTRUCTIVE JAUNDICE ON VARIOUS

SYSTEMS

CHANGES IN LIVER BLOOD FLOW

Acute obstruction

increase in hepatic arterial blood flow

No change in portal venous blood flow

Chronic obstruction

Decrease in total liver blood flow , dilatation of sinusoids and elevation of

portal pressure

CARDIOVASCULAR EFFECTS

Decreased cardiac contractability

Reduced left ventricular pressure

Impaired response to beta agonist drugs

Decreased peripheral vascular resistance

Bradycardia due to direct effect of bile salts on SA node.

Net result

Hypotensive patient

Exaggerated hypotensive response to bleeding

More prone to postoperative shock

RENAL FAILURE

10 % incidence with 70 % mortality

Factors responsible are

Decresed cardic function

Increased levels of ANP resulting in hypovolemia

Decreased effect of bile salts on kidney mediated by increased

prostaglandin E2

Endotoxemia

Resulting in

Renal vasoconstriction

Shunting of blood from cortex

Activation of complement system peritubular and glomerular fibrin

deposition leading to tubular and cortical necrosis

IMMUNE SYSTEM

Defects in cellular immunity

Impaired T cell proliferation

Decreased neutophil chemotaxis

Defective bacterial phagocytosis

Depressed function of RE system ie Kupffer cells

WOUND HEALING

Delayed wound healing

High incidence of wound dehiscence

Decresed activity of enzyme Propyl hydroxylase in the skin

This helps in incorporation of proline in collagen

Defective synthesis of collagen

COAGULATION FACTOR DEFECTS

Prolongation of Prothrombin time

Loss of calcium

Endotoxin induced damage to factor XI ,XII ,platelets

Low grade DIC with increased fibrin degradation products

Thrombocytopenia from hyperspleenism

Decreased absroption of fat solube vitamins A,D,E,K

ITCHING

Retained bile salts

Levels does not correlete well

Itching disappears in terminal liver failure but bile salt

level still increased

Other theory

Due to endogenous opiate peptides

Inducing opiod receptor mediated scratching

activity of central origin

BIOCHEMICAL EFFECTS

Bilirubin

Rise by 25-43 micromol/litre/day

Mechanism of hyperbilirubinemia

Biliary venous & biliary regurgitation of conjugated bilirubin due to

disruption of tight intracellular junction

Trans hepatocytic regurgitation due to reversal of the secretory polarity

of hepatocytes

Rupture of dilated canaliculi in to sinusoids due to necrosis of

hepatocytes

ALKALINE PHOSPHATSE

Most sensitive indicator

Factor responsible are

Biliary component regurgitation

Increase in hepatic synthesis

Why Bilirubin levels plateau

Increased excretion of bile pigments by kidney by products other than

bilirubin not giving DIAZO reaction

With increasing levels of conjugated bilirubin

A portion get covalently bounded to serum albumin

This protein bound bilirubin-Delta bilirubin,is not measurable by routine

technique

HISTORY AND CLINICAL EXAMINATION

The sensitivities of history, physical examination, and blood tests alone

range from 70% to 95%,whereas the specificities are approximately

75%.

The overall accuracy of clinical assessment of hepatic and posthepatic

causes of jaundice ranges from 87% to 97%.

6.Lindberg G, BjÃjrkman A, Helmers C: A description of diagnostic strategies in jaundice. Scand J Gastroenterol 18:257, 19837. Lumeng L, Snodgrass PJ, Swonder JW: Final report of a blinded prospective study comparing current non-invasive approaches in the differential diagnosis of medical and surgical jaundice. Gastroenterology 78:1312, 19808. Martin W, Apostolakos PC, Roazen H: Clinical versus actuarial prediction in the differential diagnosis of jaundice. Am J Med Sci 240:571, 19609. Matzen P, Malchow-Möller A, Hilden J, et al: Differential diagnosis of jaundice: a pocket diagnostic chart. Liver 4:360, 198410. O'Connor K, Snodgrass PJ, Swonder JE, et al: A blinded prospective study comparing four current non-invasive approaches in the differential diagnosis of medical versus surgical jaundice. Gastroenterology 84:1498, 1983

HISTORY

Previous dyspepsia, fat intolerance

Jaundice- onset, course, itching

Pain

Pyrexia

Weight loss

Dark urine and clay coloured stools

Travel to endemic area

Contact with jaundice patient

History of upper abdominal operation

Drug intake ie ATT

History of injection in preceding six months

CLINICAL EXAMINATION

Age

Anaemia - hemolysis, cancer , cirrhosis

Gross weight loss-malignancy

Hunched up position-chronic pancreatitis or ca pancreas

Fetor, flapping tremors,personality changes-impending hepatic coma

Skin changes-Bruising,purpuric spots,spider naevi,palmar

erythema,white nails,loss of secondary sexual characters

ABDOMINAL EXAMINATION

Dilated peri umbalical veins- cirrhosis & portal collateral

circulation

Ascitis-Cirrhosis or malignant disease

Nodular liver

Courvoisier’s Law-palpable non tender gall bladder in

jaundice patient-malignant biliary obstruction

Exceptions

Double impaction of stones

Impaction of pancreatic calculus at ampulla of vater

Mirizzi syndrome

BIOCHEMICAL INVESTIGATIONS

Routine investigations-Hb,TLC,DLC, Blood sugar, RFT ,Serum electrolytes

Urinary bilirubin,Urobilinogen

Serum Bilirubin-Total and Direct

SGOT,SGPT,ALP.GGTP and 5- Nucleotidase

PT and Serum Albumin

ALKALINE PHOSPHATSE(ALP)

ALP levels are elevated in nearly 100 % of patients with extra hepatic

obstruction except in some cases of intermittent obstruction.

Values usually greater than 3 times the upper limit of reference range,

and in most typical cases, they exceed 5 times the upper limit.

An elevation less than 3 times the upper limit is evidence against

complete extra hepatic obstruction.

AST and ALT

Serum enzymes that provide evidence of hepato cellular damage.ALT found

primarily in the liver, where as AST also found in heart ,kidney, skeletal

muscle and brain

AST is less specific for liver function. The levels of AST and ALT should be

done simultaneously since ALT can confirm the hepatic origin of the less

specific but more sensitive AST.

In extra hepatic obstruction usually AST levels are not elevated(< 10 times

the upper reference limit)

GAMMA –GLUTAMYL TRANSPEPTIDASE(GGTP)

Correlates with ALP level

Most sensitive indicator of biliary tract disease

Better indicator of obstruction in children – levels are independent of age

Helpful in the diagnosis of acute biliary tract obstruction in contrast to ALP

because ALP requires synthesis of fresh ALP and hence lags behind the

onset of obstruction

5- NUCLEOTIDASE

The principal value is to confirm the hepatic origin of an elevated

ALP

This is particularly helpful in children, pregnant women and patients

who may have bone disease resulting in rise of ALP

It is more useful than ALP/GGTP in detecting hepatic metastasis

OTHER LAB INVESTIGATIONS

Prothrobin time

Serum albumin

Stool for occult blood

Presence of occult blood in the stools of a patient with jaundice must raise the

suspicion of malignancy.

Obstructive jaundice Medical jaundice

Serum Bilirubun conjugated unconjugated

++++

++++

Urobilinogen ↓ ↑

Urinary Bilirubin + 0

Urinary Bile salts + 0

Serum ALP ↑ No change

Serum GGTP ↑ No change

Serum 5-nucleotidase

↑ No change

Transaminases Mildly raised Markedly raised

ETIOLOGY

TYPES OF BILIARY OBSTRUCTION

Complete obstruction

Intermittent obstruction

Chronic incomplete obstruction

Segmental obstruction

INTERMITTENT OBSTRUCTION

Symptoms and typical biochemical changes

Clinically jaundice may or may not be present

Causes

CBD stones

Periampullary tumours

Duodenal diverticulum

Choledochal cyst

Biliary parasites

hemobilia

CHRONIC INCOMPLETE OBSTRUCTION

With or without classical symptoms or biochemical changes

Pathological changes in bile ducts or liver

Causes

Strictures of CBD

Stenosis of biliary-enteric anastamosis

Chronic pancreatitis

Cystic fibrosis

Sphincter of oddi stenosis

SEGMENTAL OBSTRUCTION

one or more segment of intrahepatic biliary tract obstructed

Causes

Traumatic

Intrahepatic stones

Sclerosing cholangitis

Cholangiocarcinoma

BILIARY OBSTRUCTION

INTRINSIC Ductal calculi

Primary - Develop de novo in bile ducts

Secondary - Migrate from gall bladder Acute Cholangitis Biliary Strictures

Idiopathic

Iatrogenic Sclerosing Cholangitis Parasites Haemobilia Benign Biliary Tumours Cholangiocarcinoma Carcinoma of ampulla of vater and Periampullary tumours Intraductal secondary tumour seeding

BILIARY OBSTRUCTION

EXTRINSIC

Mirizzi syndrome

Pancreatitis- acute and chronic

Pancreatic pseudocyst

Carcinoma of gall bladder

Carcinoma of pancreas

Cystic tumours of pancreas

Metastatic carcinoma

Hepatocellular carcinoma

BILIARY OBSTRUCTION

CONGENITAL AND GENETIC DISORDERS

Biliary atresia

Choledocal cyst

Caroli’s disease

Progressive familial intra hepatic cholestasis

Primary biliary cirrhosis

Alpha 1 antitrypsin defeciency

Tyrosinemia

Neonatal hepatitis

Wilson disease

Others - dyskinesia of sphincter of odi

IMAGING GOALS

To confirm the presence of an extrahepatic obstruction

To determine the level of the obstruction, to identify the specific cause of the

obstruction

To provide complementary information relating to the underlying diagnosis

(eg., Staging information in cases of malignancy).

Ultrasonography

Ultrasound of the abdomen is an extremely useful and accurate method for identifying gallstones and pathologic changes in the gallbladder consistent with acute cholecystitis. Abdominal ultrasound, if performed by an experienced operator, should be part of the routine evaluation of patients suspected of having gallstone disease, given the high specificity (>98%) and sensitivity (>95%) of this test for the diagnosis of cholelithiasis[1] ( Table 54-1 ). In addition to identifying gallstones, ultrasound can also detail signs of cholecystitis such as thickening of the gallbladder wall, pericholecystic fluid, and impacted stone in the neck of the gallbladder. It is often the initial screening test for patients with suspected extrahepatic biliary obstruction ( Fig. 54-7 ). Dilation of the extrahepatic (>10 mm) or intrahepatic (>4 mm) bile ducts suggests biliary obstruction. Intraoperative ultrasound is now used frequently to further evaluate intrahepatic lesions, assess resectability, and determine involvement of vascular structures

.

MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP)

• Noninvasive test to visualize the hepato biliary tree

• No contrast

• Fluid found in the biliary tree is hyper intense on T2-weighted images. Surrounding

structures do not enhance and can be suppressed during image analysis.

• Sensitive in detecting biliary and pancreatic duct stones, strictures, or dilatations

within the biliary system.

• MRCP combined with conventional MR imaging of the abdomen can provide

information about surrounding structures (eg, pseudocysts, masses).

• ERCP and MRCP similarly effective in detecting malignant hilar and perihilar

obstruction

• MRCP is better able to determine the extent and type of tumor as compared to

ERCP

Absolute contraindications cardiac pacemaker cerebral aneurysm clips ocular or cochlear implants

Fluid stasis in the adjacent duodenum or ascitic fluid may produce image artifacts on MRCP, making it difficult to clearly visualize the biliary tree.

ENDOSCOPIC ULTRASOUND (EUS)

Combines Endoscopy and US

Higher-frequency ultrasonic waves compared to traditional US (3.5 mhz vs 20 mhz) and allows diagnostic tissue sampling via EUS-guided fine-needle aspiration (EUS-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 in pancreas has been reported to be superior to that of CT scanning, both traditional and spiral, particularly for tumors smaller than 3 cm in diameter.

Compared to MRCP for the diagnosis of biliary stricture, EUS has been reported to be more specific (100% vs 76%) and to have a much greater positive predictive value (100% vs 25%), although the two have equal sensitivity (67%).

The positive yield of eus-fna for cytology in patients with malignant obstruction has been reported to be as high as 96%.

Investigations

Metastasis poor Surgical risks

No metastasisGood Surgical

Risks

Non operative procedures

Operative Procedures

Non resectable

tumoursResectable

tumours

Biliary –enteric Bypass

Surgically placed stents

Percutanesly placed Stents

Endoscopically placed stents

Palliative resection

Curative resection

Malignant Obstructive jaundice

WORKUP AND MANAGEMENT OF POSTHEPATIC JAUNDICE 

three possible clinical scenarios:DUCTAL OBSTRUCTION

SUSPECTED CHOLANGITIS

SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT

CHOLANGITIS

SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS

SUSPECTED CHOLANGITIS

A clinical picture compatible with acute suppurative cholangitis (charcot's triad or raynaud's pentad) the most likely diagnosis is choledocholithiasis.

Appropriate resuscitation, correction of any coagulopathies if present, and administration of antibiotics

ERCP is indicated for diagnosis and treatment

If ERCP is unavailable or is not feasible (e.g., Because of previous roux-en-y reconstruction), transhepatic drainage or surgery may be necessary

Mainstay of treatment of severe cholangitis is not just the administration of appropriate antibiotics but rather the establishment of adequate biliary drainage.

SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS

Choledocholithiasis is the most common cause of biliary obstruction.

Strongly suspected if the jaundice is episodic or painful or if usg has shown presence of gallstones or bile duct stones.

Patients with suspected cbd stones should be referred for lap cholecystectomy with either preoperative ERCP, intra operative cholangiography

Preoperative ERCP in this setting of jaundice is prefered Diagnostic yield is high Therapeutic-clearing the CBD of stones in 95% of cases.

Many authors, however favor fully laparoscopic approach, in which CBD stone is detected in the OR by means of intraoperative cholangiography and laparoscopic biliary clearance is performed when choledocholithiasis is confirmed.

The optimal approach in a particular setting should be dictated by local expertise. 

SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS

No gallstones are seen Clinical presentation is less acute (e.g., constant abdominal or back pain) Associated constitutional symptoms (e.g., weight loss, fatigue, and long-standing

anorexia) Possible causes of may be classified into three categories depending on the location

of the obstructing lesion the upper third of the biliary tree the middle third the lower (distal) third

 

Upper-third obstruction Polycystic liver disease  Caroli diseas HCC Oriental cholangiohepatitis Hemobilia(e.g.,afterbiliaryma

nipulation) Iatrogenic bile duct injury Cholangiocarcinoma

(Klatskin'stumor)  Sclerosing cholangitis Papillomas of the bile duct

Mid-third obstruction Cholangiocarcinoma Sclerosing cholangitis Papillomas of the bile duct Gallbladder cancer Choledochal cyst Intrabiliary parasites Mirizzi syndrome Extrinsic nodal compression

(e.g., lymphoma) Iatrogenic bile duct injury Cystic fibrosis Benign idiopathic bile duct

stricture

Lower-third obstruction Cholangiocarcinoma Sclerosing cholangitis Papillomas of the bile duct Pancreatic tumors Ampullary tumors Chronic pancreatitis Sphincter of Oddi dysfunction Papillary stenosis Duodenal diverticula Penetrating duodenal ulcer Retroduodenal adenopathy

(e.g., lymphoma, carcinoid

ETIOLOGY

DIAGNOSIS AND ASSESSMENT OF RESECTABILITY

Involvement of the SUPERIOR MESENTERIC VEIN, THE PORTAL VEIN, THE SUPERIOR MESENTERIC ARTERY, and the PORTA HEPATIS and on whether there is evidence of significant LOCAL ADENOPATHY or EXTRAPANCREATIC

EXTENSION OF TUMOR indicates UNRESECTABILITY

The majority of lesions will be clearly unresectable, either because of tumor extension or because of the presence of hepatic or peritoneal metastases

NON OPERATIVE MANAGEMENT

DRAINAGE PROCEDURES 

   

In the majority of patients with malignant obstructions, treatment is palliative rather than curative.

Cholangiography and decompression of obstructed biliary system

In the absence of preexisting or concomitant hepatocellular dysfunction, drainage of one half of the liver is generally sufficient for resolution of jaundice

Routine preoperative drainage of an obstructed biliary system does not benefit patients who will soon undergo resection.90,91

There is evidence suggesting that in patients with either pancreatic 92,93 or hepatic malignancies, routine preoperative direct cholangiography with decompression is associated with a higher incidence of postoperative complications when tumor resection is ultimately carried out.

90. Pitt HA, Gomes AS, Lois JF: Does preoperative percutaneous biliary drainage reduce operative risk or increase hospital cost? Ann Surg 201:545, 198591. McPherson GA, Benjamin IS, Hodgson HJ, et al: Preoperative percutaneous transhepatic biliary drainage: results of a controlled trial. Br J Surg 71:371, 198492. Povoski SP, Karpeh MS Jr, Conlon KC, et al: Preoperative biliary drainage: impact on intraoperative bile cultures and infectious morbidity and mortality after pancreaticoduodenectomy. J Gastrointest Surg 3:496, 199993. Sohn TA, Yeo CJ, Cameron JL, et al: Do preoperative biliary stents increase postpancreaticoduodenectomy complications? J Gastrointest Surg 4:258, 2000

OPERATIVE MANAGEMENT AT SPECIFIC SITES BYPASS AND RESECTION

UPPER-THIRD OBSTRUCTION

PALLIATION.

Because the left hepatic duct has a long extrahepatic segment and is more accessible, the preferred bypass -is a left hepaticojejunostomy

Laparoscopic bypass techniques that make use of segment 3 have been developed, but their performance has yet to be formally assessed

RESECTION FOR CURE

The hilar plate is taken down to lengthen the hepatic duct segment available for subsequent anastomosis.

A formal hepatectomy or segmentectomy is required to ensure an adequate proximal margin of resection

If the resection is carried out proximal to the hepatic duct bifurcation, several cholangiojejunostomies have to be done to anastomose individual hepatic biliary branches.

The results of aggressive hilar tumor resections that included as much liver tissue as was necessary to obtain a negative margin appear to justify this approach.

In cases of left hepatic involvement, resection of the caudate lobe is indicated as well.

MIDDLE-THIRD OBSTRUCTION

Palliation.

Surgical bypass of middle-third lesions is technically simpler

Hepaticojejunostomy is done distal to the hepatic duct bifurcation,

Exposure of the hilar plate or the intrahepatic ducts is unnecessary.

Resection for cure.

Tumors in this part usually quite amenable to resection along with the lymphatic chains in the porta hepatis.

Mirizzi syndrome -extrinsic obstruction of the CBD, either by causing inflammation of the gallbladder wall or via direct impingement.

Treatment of this syndrome - Hepaticojejunostomy

Lower-third obstruction

Palliation

The preferred bypass technique for lower-third lesions is a Roux-en-Y choledochojejunostomy.

Cholecystojejunostomy carries a higher risk of complications and subsequent development of jaundice

Resection for cure.

Resection of a lower-third lesion usually involves a pancreaticoduodenectomy though transduodenal ampullary resection may be an acceptable alternative for a small adenoma of the ampulla

For optimal results, pancreaticoduodenectomy is best performed in specialized centers.

postoperative adjuvant therapy may improve the prognosis after resection of a pancreatic adenocarcinoma

PALLIATION IN PATIENTS WITH ADVANCED MALIGNANT DISEASE

When a patient has advanced malignant disease, drainage of the biliary system for palliation is not routinely indicated, because the risk of complications related to the procedure may outweigh the potential benefit

The best treatment for a patient with asymptomatic obstructive jaundice and liver metastases may be supportive care alone.

  Biliary decompression is indicated if cholangitis or severe pruritus interferes with

quality of life.

Stent placed with ercp to be the palliative modality of choice for advanced disease,

Upper-third lesions may be managed most easily through the initial placement of an internal/external catheter at the time of ptc.

 

Metal expandable stents remain patent longer than large conventional plastic stents

RCTs suggest that surgical biliary bypass should be reserved for patients who are expected to survive for 6 months or longer because bypass is associated with more prolonged palliation at the cost of greater initial morbidity.

  The role of prophylactic gastric drainage at the time of operative biliary drainage

remains controversial,101,102

RCTs demonstrated a reduced incidence of subsequent clinical gastric outlet obstruction when this measure was employed.

When a pancreatic malignancy is present, intraoperative celiac ganglion injection should be performed for either prophylactic or therapeutic pain

POSTOPERATIVE JAUNDICE

The development of jaundice in the postoperative setting is approximately 1% of all surgical patients after operation.120

When jaundice occurs after a hepatobiliary procedure, Attributable to specific biliary causes, Retained cbd stones, Postoperative biliary leakage (through reabsorption of bile leaking into the peritoneum) injury to the cbd Development of biliary strictures

JAUNDICE WITHIN 48 HOURS OF THE OPERATION

Breakdown of rbc –due to multiple blood transfusions , The resorption of a large hematoma, Transfusion reaction. Known underlying hemolytic anemia and may be precipitated specific drugs (e.G.,

Sulfa drugs in a patient who has G6PD deficiency). Gilbert syndrome may first manifest itself early in the postoperative period. Intraoperative hypotension or hypoxemia or the early development of heart failure

can lead to hyperbilirubinemia within 5 to 10 days after operation. The hyperbilirubinemia may be associated with other end-organ damage (e.G.,

Acute tubular necrosis). Impairment of renal function causes a decrease in bilirubin excretion and can be

responsible for a mild hyperbilirubinemia.

Jaundice developing 7 to 10 days after operation In association with a medication-induced hepatitis attributable to an anesthetic agent.

Incidence of 1/10,000 after an initial exposure.

Administration of antibiotics or other medications used in the perioperative setting

Jaundice associated with intrahepatic cholestasis is often a manifestation of a sepsis, particularly in patients with mods

Jaundice may occur in as many as 30% of patients receiving total parenteral nutrition (tpn).

It may be due to steatosis, particularly with formulas containing large amounts of carbohydrates.

Decreased export of bilirubin from the hepatocytes may lead to cholestasis

Acalculous cholecystitis or even ductal obstruction may develop as a result of sludge in the gallbladder and the cbd.

Unsuspected hepatic or post-hepatic causes (e.G., Occult cirrhosis, choledocholithiasis, or cholecystitis)

A rare cause of postoperative jaundice is the development of thyrotoxicosis.

A diagnosis of exclusion- is so-called benign postoperative cholestasis, a primarily cholestatic, self-limited process with no clearly demonstrable cause that typically arises within 2 to 10 days after operation.

Mechanism-combination of an increased pigment load, impaired liver function, and decreased renal bilirubin excretion caused by varying degrees of tubular necrosis.

The predominantly conjugated hyperbilirubinemia may reach 40 mg/dl and remain elevated for as long as 3 weeks.

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