Obstructive jaundice

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Contents

Introduction

This chapter will discuss the clinical, diagnostic and therapeutic approach to a patient presenting with obstructive jaundice, as demonstrated by Diagnostic and therapeutic approach to a patient with jaundice. CBD, common bile duct; ERCP, endoscopic retrograde cholangiopancreatography; PTC, percutaneous transhepatic cholangiography; CT, computed tomography.

Diagnostic and therapeutic approach to a patient with jaundice. CBD, common bile duct; ERCP, endoscopic retrograde cholangiopancreatography; PTC, percutaneous transhepatic cholangiography; CT, computed tomography.

History and examination

The first step is a detailed history. If pain is present, and that pain is consistent and of a biliary origin, then a history of repeated episodes, associated nausea, radiation to the back and symptoms of fever should be elicited. Pain may also be due to malignancy and is then more constant and is usually associated with weight loss. The patient should be asked if they have noted pale stools or dark urine. Generalised itch in more chronic obstruction is also a symptom that may not be volunteered spontaneously. A history of intermittent fever suggests the potentially serious consequences of unrelieved cholangitis.

A history of prior surgery should be obtained both in relation to anaesthetic agents such as halothane and to surgery for biliary disease, which may result in early or late complications of bile duct surgery. A history of previous endoscopic retrograde cholangiopancreatography (ERCP) and sphincterotomy should be elicited, because sphincter stenosis due to the diathermy damage may occur months to years after the procedure.

The history should determine whether the patient is at risk for hepatitis, either from sexual contact or intravenous drug use, and whether any family members have been affected by hepatitis recently or in the past. A full drug history should also be obtained because of the risk of hepatotoxic drug reactions, which are of various types and include antibiotics such as flucloxacillin, sulphas, erythromycin, nitrofurantoin and other agents such as oestrogens and paracetamol. Excess vitamin A intake, an occasional feature of health food fanatics, may lead to hypercarotenaemia, which gives the skin a jaundiced appearance with normal sclera and liver function tests (LFT).

On examination, once the bilirubin is more than double the normal level, icterus should be evident in the sclera. On examining the abdomen, a palpable mass, either a pancreas, which is fixed and that the palpating hand may get above, or a gall-bladder, which the palpating hand will not get above and that moves down on respiration, may be elicited. If malignancy is suspected, other masses in the abdomen (particularly the liver) and the left prescalene (Virchow) node should be looked for. Evidence of skin scratching as a response to pruritus should be noted.

Investigations

Liver function tests

A ward test of the urine in obstructive jaundice will demonstrate the presence of bilirubin and the absence of urobilinogen. The plasma bilirubin will be elevated and will be principally in the conjugated form. Small changes only should occur in the alanine aminotransferase (ALT) and the aspartate aminotransferase (AST), which are indicative of hepatocyte injury. Alkaline phosphatase will be more markedly elevated with levels more than double those of the transaminases. The alkaline phosphatase is normally higher in children and will also be elevated in bony disease, the latter being differentiated either by alkaline phosphatase isoenzymes or by the gamma glutamyl transpeptidase (γ-GT). If the bilirubin is elevated but the alkaline phosphatase, γ-GT and transaminases are normal, one of the congenital hyperbilirubinaemias should be considered. Examples are Gilbert's syndrome, a conjugated hyperbilirubinaemia due to a deficiency in glucuronyl transferase activity, or Dubin Johnson syndrome, also a conjugated hyperbilirubinaemia, but due to a defect in the transport of bilirubin. Neither requires treatment. The abnormalities in bilirubin become more evident during infective or traumatic episodes.

Coagulation studies should be performed. If abnormal, and particularly if surgical, intervention is likely, vitamin K should be given.

If LFT suggests that the process is hepatitic, viral serology and autoimmune antibodies should be investigated. Liver biopsy may be required for confirmation, but only after obstructive causes have been ruled out first by ultrasound, to prevent the potential problem of bile fistula if a major duct is punctured by the biopsy needle.

Ultrasound and computed tomography scans

Ultrasound is the key technique in distinguishing medical from surgical jaundice, and should be performed on all cases of jaundice if LFT are not absolutely confirmatory of a hepatitic picture.

If the LFT are obstructive, but ultrasound shows non-dilated ducts, then there are four possibilities. First, the ultrasound may have been performed so early that the ducts have not yet dilated, in which case the scan should be repeated after 24–48 hours. Second, in the presence of defective liver function, a sudden bilirubin load from haemolysis or absorption of a large haematoma may produce jaundice. Third, the patient has cirrhosis, preventing dilation of the ducts (the extrahepatic ducts, however, will still dilate if the obstruction is outside the liver). Fourth, primary sclerosing cholangitis produces multiple strictures with segmental duct dilation occurring late. The diagnosis is usually indicated on ERCP, but liver biopsy may be required to confirm the diagnosis and the extent of hepatic damage secondary to the obstruction.

If the ultrasound shows a mass, usually in conjunction with dilated ducts, then the next step is a computed tomography (CT) scan to determine whether the lesion will be surgically resectable. This is then followed by ERCP to determine the nature of the obstruction.

Endoscopic retrograde cholangiopancreatography

This may demonstrate that a duct stone is the cause of the jaundice. If the patient is unfit for surgery, has cholangitis as a result of the stone or has already had a cholecystectomy, then the ideal treatment is ERCP/sphincterotomy and stone extraction. If the patient has an intact gall bladder containing stones, the history is typical of stone disease and he or she is fit (the majority), then it is best to treat by a laparoscopic cholecystectomy with intraoperative cholangiography, followed by laparoscopic duct exploration if a stone is still present in the duct. If the latter is unsuccessful, the duct can be explored by open operation immediately or by performing a post-operative ERCP and sphincterotomy to remove the stone.

If ERCP demonstrates a benign stricture, it should be dilated to improve the patient's clinical condition and then a decision can be made as to whether repeated dilations should be performed, or whether surgical bypass should be undertaken.

If ERCP demonstrates a malignant stricture and CT shows the lesion is not resectable or the patient is not fit for surgery, a stent is inserted, as definitive palliative treatment. Because stents obstruct and have to be replaced in 3–4 months, if the patient is fit enough, likely to live long enough, surgical bypass provides better palliation. Curative resection is uncommon. If ERCP fails to define the ductal system adequately, so surgery cannot be appropriately planned, then a percutaneous transhepatic cholangiogram may need to be performed. Such failure may be due to technical difficulties in accessing the papilla (prior gastrectomy, duodenal diverticulum) or because the stricture is so tight that contrast cannot be made to pass into the upper duct system.
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