Biliary Mud: What is it? Causes, Symptoms, Diagnosis, Treatment and Prevention

It is a deposit of small stones or crystals formed by cholesterol, calcium bilirubin, and other calcium salts.

Bile muds or muds are also known as microlithiasis, pseudolithiasis, or bile sand.

When the gallbladder does not become empty, the particles present in the bile, such as cholesterol or calcium salts, can form a muddy precipitate.

As a result of staying in the gallbladder for so long and become what we commonly know as the gallbladder mud.

The relationship between gallstones and gallbladder symptoms is not well known.

Researchers debate the importance of biliary sludge; some think it is not essential, while others believe that having bile sludge increases the risk of forming gallstones.

The disagreement stems from the fact that most biliary slime people do not develop any symptoms; they usually disappear independently. Only a small number of people who have bile sludge develop gallstones.

 

Mud in the gallbladder is usually an incidental finding.

In asymptomatic cases, the gallbladder sediment may exist for decades.

Incidental findings of gallstones occur during the evaluation of the patient due to abdominal pain or some gastrointestinal disorder.

Although most patients are asymptomatic, a more detailed investigation suggests a pathogenicity potential similar to cholelithiasis.

Causes

The prevalence and other vital statistics are unknown.

Since it is often an asymptomatic condition and is mainly found incidentally.

Some studies suggest possible causes such as:

  • Excessive weight loss in a short period can lead to sludge formation in the bile.
  • Excess alcohol makes the liver work harder. The liver with a more significant load produces more bile liquid.
  • Fluctuations in hormones during pregnancy can lead to sludge formation in the gallbladder.
  • Fasting conditions in the long term.
  • Consumption of fatty foods.
  • Liver cirrhosis .
  • Inability to feed by mouth for some reason (parental nutrition).
  • Operations of the digestive tract.
  • Organ transplant.
  • Sickle cell anemia.
  • AIDS.
  • Use of medications such as Ceftriaxone, octreotide, and cyclosporine.

symptom

Biliary colic occurs when the gallbladder contraction causes gallstones or sediments to clog the cystic duct and separate the gallbladder wall.

The most common presentation of symptoms is characterized by a relief of pain that coincides with the relaxation of the gallbladder, which occurs between 30 and 90 minutes.

These episodes are typically sporadic. The patient will describe a dull and intense pain in the upper right quadrant or epigastrium.

This pain often radiates to Collin’s sign in the right scapula.

The onset is usually postprandial with the ingestion of fatty food.

The pain lasts 1 to 5 hours and is initially intense but resolves gradually as the gallbladder relaxes.

Possible associated symptoms include nausea, jaundice, fever, vomiting, and diaphoresis.

In cases where biliary colic is accompanied by cholelithiasis, there is likely intolerance to fats, indigestion, dyspepsia, bloating, and belching.

Medical conditions that can cause pain in the gallbladder are:

Biliary colic is the intermittent obstruction of a bile duct or bile duct (sometimes called uncomplicated biliary disease), acute cholecystitis, and inflammation of the gallbladder tissue.

It is essential to remember that these nonspecific symptoms can occur in people, whether gallstones are present or absent.

That is why a differential diagnosis is essential.

Differential diagnosis

After the symptoms, the physical examination is the second principal component of the clinical presentation.

Because biliary colic and acute cholecystitis have similar symptoms, the physical examination is beneficial in distinguishing the actual condition.

In uncomplicated biliary colic, the abdominal examination is benign; the patient is afebrile.

The clinical picture is complicated by fever, tachycardia, hypotension, and jaundice in conditions such as cholecystitis, cholangitis, or pancreatitis.

Therefore, if some of these symptoms occur, the suspicion must be high for one of these complications.

Bowel sounds may be absent or hypoactive.

Acute cholecystitis is associated with Murphy’s sign. The ascending cholangitis is characterized by findings known as Charcot’s triad, which is characterized by pain in the upper right quadrant, jaundice, and fever.

In choledocholithiasis or obstruction of the bile duct, jaundice is usually present due to the accumulation of bilirubin.

Severe cases may present with ecchymosis, flank edema (Gray Turner’s sign), and periumbilical region (Cullin’s sign).

Acute pancreatitis is due to the sediments lodged in the ampulla of Vater, which transiently obstructs the pancreatic duct.

This condition is characterized by acute and severe pain radiating to the back in the epigastric and abdominal areas.

Symptoms include nausea and emesis.

These episodes may be recurrent.

When evaluating biliary colic, it is pertinent to recover the clinical picture thoroughly with a consideration of the risk factors and a detailed physical examination in search of suggestive clues to the diagnosis.

It is necessary to perform laboratory tests, appropriate images, and clinical correlation.

This constellation of findings taken together, which helps to determine the diagnosis and differentiate them, can be summarized as follows:

    • Laboratory studies include a complete blood count with differential, liver function panel, amylase, and lipaseGenerally, these tests are repeated frequently to monitor patients closely and observe trends.
  • The images include vertical abdominal and supine radiographs to rule out intestinal obstruction, visceral perforation, kidney stones, or chronic calcified pancreatitis.
  • Ultrasound is the recommended procedure for gallbladder or biliary conditions. Many conditions arise incidentally in the ultrasound, observing inflammation of the gallbladder.
  • Computed tomography is less sensitive than ultrasound for gallbladder sludge, but it is better than ultrasound to detect gallstones in the bile duct. This is very useful for the evaluation of abdominal pain.
  • Magnetic resonance cholangiopancreatography is a noninvasive test to visualize gallstones in the biliary tract, including the bile duct. It is done in those cases that are highly suspicious of choledocholithiasis.
  • The scintigraphy detects the obstruction of the cystic duct, but it is not helpful for other obstructive pathologies.
  • Endoscopic retrograde cholangiopancreatography is used to obtain images of the bile ducts.

The typical findings in laboratory tests and images for various pathologies that are commonly found are associated with pathologies such as:

  • Mud without complications
  • Typical findings in laboratory tests.
  • It is unnecessary to perform them unless there is suspicion of acute cholecystitis.
  • Asymptomatic biliary sludge is usually an incidental finding when other pathologies develop.
  • It is found on ultrasound and computed tomography.

Acute cholecystitis:

Typical laboratory findings include elevated white blood cells and values ​​to detect liver inflammation.

Ultrasound provides information such as the thickening of the gallbladder wall.

It also detects the fluid surrounding the gallbladder and distension of the gallbladder.

A key finding is Murphy’s sonographic sign.

Cholangitis:

The suspicion of this complication is high in increased leukocytes, bilirubin, aspartate aminotransferase blood tests, and the alanine aminotransferase test, despite treatment with antibiotics.

In addition, blood culture is positive in 30 to 60% of patients.

Coledocolitiasis:

Typical laboratory findings include increased aspartate aminotransferase blood tests and the alanine aminotransferase test, followed by an increase in bilirubin level, which is associated with a higher predictive value.

If the pancreatic duct is also blocked, the lipase and amylase increase.

Magnetic resonance or magnetic resonance cholangiopancreatography shows gallstones in the bile duct.

Treatment

Biliary sludge often does not require pharmacological treatment; home treatments and controlled nutrition reduce or eliminate these conditions.

A planned diet, low in fat, low cholesterol, and low in sodium can reduce the chances of developing bile mud.

However, the doctor may recommend a treatment to help dissolve the sediment and avoid possible future complications, such as the appearance of stones.

In patients with symptomatic biliary sludge with biliary pain, cholecystitis, cholangitis, or pancreatitis, cholecystectomy, surgery to remove the gallbladder.

When treating gallbladder sludge, the goal should be to treat its risks.

Endoscopic spirometry is another option for surgical candidates affected with cholangitis and pancreatitis.

Ursodeoxycholic acid is beneficial in preventing recurrent acute mucous membrane formation and pancreatitis.

Risk factor’s

The prognosis of the gallbladder mud is not entirely known.

However, deduced from the fact that these patients have risk factors and pathogenicity similar to those with stones in the gallbladder, it is believed that they also have a similar prognosis.

In addition, the symptomatic pimples of the gallbladder can cause biliary complications, in which a cholecystectomy can be justified.

About gallstones, only 10% of asymptomatic cholelithiasis become symptomatic in the first five years. This number doubles in 20 years.

About 15-19% of patients with gallstones have choledocholithiasis.

The prognosis in these patients correlates with the general clinical picture and the complications that may arise.

The origin and evolution of gallbladder clay and gallbladder stones are similar, almost in the same way they share the risk factors.

The sludge can resolve spontaneously or can precipitate the formation of gallstones. Complications include biliary colic, cholecystitis, cholangitis, and acute pancreatitis.

In patients with biliary colic, 1 to 3% of patients develop complications.

Bile sludge consists of bile and particulate material.

The established risk factors for cholesterol gallstones are female sex, fertile women, advanced age, European or Native American background, and the Western diet.

Women with multiple pregnancies are at increased risk, probably due to hormonal changes in pregnancy, such as high progesterone.

Specifically, this hormone decreases the contractility of the gallbladder.

Certain medications also present a risk. These include estrogen, such as oral contraceptives, which can cause an increase in biliary cholesterol release.

In addition, fibril anti-lipid drugs and somatostatin-like medications may predispose to gallstone formation, although by different mechanisms.

Obese populations are at greater risk.

By further assessing the etiology, people with metabolic syndrome may be predisposed to developing cholesterol gallstones compared to those with a body weight appropriate for their age and height.

The main characteristics of this syndrome are obesity, insulin resistance, diabetes mellitus type II, hypertension, and hyperlipidemia.

It is believed that this is secondary to the release of hepatic cholesterol.

A positive family history of gallstones also correlates with the development of cholelithiasis.

Other factors include pre-existing diseases such as Crohn’s disease or those who have suffered burns, significant trauma, or total parenteral nutrition.

Other etiologies include spinal cord injuries, prolonged fasting, an extreme diet with fat restriction, and rapid weight loss.

People who undergo gastric bypass are also at greater risk.

Prevention

In order to prevent biliary sludge, specific modifiable lifestyle measures must be taken, and the prevention of symptoms implies changes in the diet.

Some recommendations include eating breakfast in small portions as soon as the patient wakes up in the mornings.

In addition, it is advisable to eat multiple small meals at regular intervals.

Eating less but much more frequent meals can aggravate the symptoms.

Reducing calories, fatty foods, and high cholesterol are also important.