We should consider ascending cholangitis in any patient with fever and features of obstructive jaundice till prove otherwise.
The diagnosis of ascending cholangitis is a clinical diagnosis. Patients usually have the classic Charcot triad of abdominal pain, fever, and jaundice.
Now we will discuss each component of this Liver Functions Tests separately.
Bilirubin = 101 umol/L.
Bilirubin results are expressed as direct, indirect or total bilirubin. Total bilirubin is a combination of direct and indirect bilirubin. Her we have total bilirubin level of 101.
The cause of hyperbilirubiaemia can be prehepatic, intrahepatic, and posthepatic.
- Prehepatic causes of hyperbilirubinaemia include hemolysis and hematoma resorption, this usually leads to elevated levels of unconjugated (indirect) bilirubin.
- Intrahepatic disorders can lead to unconjugated or conjugated hyperbilirubinemia. The conjugated (direct) bilirubin level is often elevated by alcohol, infectious hepatitis, drug reactions, and autoimmune disorders.
- Posthepatic disorders cause conjugated hyperbilirubinemia. Gallstone formation is the most common and benign posthepatic process that causes jaundice; however, the differential diagnosis also includes serious conditions such as biliary tract infection, pancreatitis, and malignancies.
ALP = 348 U/L
ALP is an enzyme found throughout the body, but it is mostly found in the liver, bones, kidneys, and GIT.
Bile duct obstruction results in increased synthesis of ALP by bile duct epithelial cells and release of ALP into the serum. Alkaline phosphatase may be increased even if only a few small bile ducts are obstructed, and serum bilirubin is normal.
Alkaline phosphatases are a group of isoenzymes, located on the outer layer of the cell membrane; they catalyze the hydrolysis of organic phosphate esters present in the extracellular space. The mechanism of the increase in alkaline phosphatase in hepatobiliary disorders is due to increased enzyme synthesis and not to reduced hepatobiliary excretion of the enzyme.
Because alkaline phosphatase is newly synthesized in response to biliary obstruction, its serum level may be normal in the early phase of acute biliary obstruction even when the serum aminotransferases are already at their peak.
GGT = 483 U/L
Obtaining gamma glutamyl transpeptidase (GGT) levels is used to identify the source of elevated ALP as both are elevated in hepatobiliary disease. Accordingly, we can tell that the elevated ALP in this case is due to liver disorder rather than bones disorder.
ALT = 161 U/L
ALT, which stands for alanine transaminase, is an enzyme found mostly intracellularly in the hepatocytes. When liver cells are damaged, they release ALT into the bloodstream. High levels of ALT may indicate liver damage from hepatitis, infection, cirrhosis, liver cancer, or other liver diseases. Also medication can affect the results.
Traditionally, ALP is elevated in cholestatic conditions while ALT is elevated in hapatitic condition. For this patient both levels are elevated. So, we have a mixed picture.
ALB = 40 g/L
This is to check the synthetic functions of the liver as albumin is synthesized in the liver. The normal liver usually produces around 10 grams of albumin per day.
The most common cause of low albumin level is chronic liver failure caused by cirrhosis. Serum albumin concentration is usually normal in chronic liver disease until cirrhosis or significant liver damage has developed.
Total Protein = 72 g/L
Total protein help us to identify the Albumin/Globulin ratio.
Total protein = Albumin + Globulin
Normal Albumin/Globulin ratio is between 1.1 and 2.5.
Low or reverse A/G ratio may reflect:
- Overproduction of globulin such as multiple myeloma or autoimmune diseases
- Underproduction of albumin as in liver cirrhosis
- Loss of albumin from the circulation as with nephrotic syndrome
High A/G ratio may reflect:
- Underproduction of immunoglobulin this can be seen in some genetic deficiencies and in some leukemias.
In this patient the ratio was 40/(72-40) = 1.25, that is within normal range.
This patient has sepsis secondary to ascending cholangitis. CT scan showed few intra-hepatic abscesses.
The treatment should start as early as the diagnosis was suspected.
- Resuscitate the patient with IV fluids. Target MAP of 65-90 mmHg with urine output more than 0.5 ml/Kg/hr.
- Early antibiotics (Gentamycin + Amoxicillin or Ceftriaxone or Tazocin).
- Opiates for pain control.
- Antiemetics for nausea and vomiting.
Because of high biliary intraductal pressure, biliary secretion of antibiotics is impaired. So, biliary drainage is the next step. It can be best done by therapeutic ERCP.
Depending on the etiology of biliary obstruction the possible procedures are:
- endoscopic retrograde cholangiopancreatography ERCP
- sphincterotomy +/- biliary stone removal
- PTC (percutaneous transhepatic cholangiography)
- Ultrasound-guided drainage
- lithotripsy if stone >2cm
- open surgical decompression
Then the surgical tram should consider the definitive treatment of the cause, for example cholecystectomy, biliary stent,,, etc.