Cholelithiasis and Homoeopathy

Dr Beenadas

Gallblader
The gallbladder is a 4-inch sac with a muscular wall that is located under the liver. Here, most of the bile fluid (about 2 – 5 cups a day) is removed, leaving a few tablespoons of concentrated bile.

The gallbladder serves as a reservoir until bile is needed in the small intestine to digest fats. This need is triggered by a hormone called cholecystokinin, which is released when food enters the small intestine.

Cholecystokinin signals the gallbladder to contract and deliver bile into the intestine. The force of the contraction propels the bile down the common bile duct and into the small intestine, where it emulsifies (breaks down) fatty molecules.

This part of the digestive process enables the emulsified fat along with important fat-absorbable nutrients (such as vitamins A, D, E, and K) to pass through the intestinal lining and enter the blood stream.

Gallstones are concretions that form in the biliary tract, usually in the gallbladder.. Migration of gallstones may lead to occlusion of the biliary and pancreatic ducts, causing biliary colic and acute complications, such as acute cholecystitis, ascending cholangitis,  acute pancreatitis,  fibrosis and loss of function of the gallbladder.Magnetic resonance cholangiopancreatography (MRCP) showing 5 gallstones in the common bile duct (arrows). In this image, bile in the duct appears white; stones appear as dark-filling defects. Similar images can be obtained by taking plain radiographs after injection of radiocontrast material in the common bile duct, either endoscopically (endoscopic retrograde cholangiography) or percutaneously under fluoroscopic guidance (percutaneous transhepatic cholangiography), but these approaches are more invasive.

Pathophysiology
When bile is concentrated in the gallbladder, certain substances become supersaturated, which then precipitate from solution as microscopic crystals. The crystals are trapped in gallbladder mucus, producing gallbladder sludge. Over time, the crystals grow, aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and stones produces the complications of gallstone disease.

The 2 main substances involved in gallstone formation are cholesterol and calcium bilirubinate.

Cholesterol gallstones (80%)
Liver cells secrete cholesterol into bile along with phospholipid (lecithin), termed unilamellar vesicles. Liver cells also secrete bile salts. Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. This happens mainly in the gallbladder, where bile is concentrated by reabsorption of electrolytes and water.

If bile contains a relatively high proportion of cholesterol to begin with, then as bile is concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol carrying capacity of the micelles and residual vesicles is exceeded. At this point, bile is supersaturated with cholesterol, and cholesterol monohydrate crystals may form. Thus, the main factors that determine whether cholesterol gallstones will form are: (1) the amount of cholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentration and extent of stasis of bile in the gallbladder.

Calcium, bilirubin, and pigment gallstones – 10-20%

Bilirubin, is secreted into bile by liver cells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water soluble and stable, but a small proportion consists of unconjugated bilirubin. Unconjugated bilirubin, like fatty acids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calcium enters bile passively along with other electrolytes.

In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may be present in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize from solution and eventually form stones. Oxidations cause the bilirubin precipitates to take black color, and stones formed in this manner are termed black pigment stones.

The bacteria hydrolyze conjugated bilirubin, and the resulting increase in unconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals. Bacterial hydrolysis of lecithin leads to the release of fatty acids, which complex with calcium and precipitate from solution. The resulting concretions have a claylike consistency and are termed brown pigment stones,, which form in the bile ducts. Brown pigment stones are possibly related to liver flukes.

Mixed gallstones
Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosal inflammation. Lytic enzymes from bacteria and leukocytes hydrolyze bilirubin conjugates and fatty acids. As a result, cholesterol stones may accumulate a substantial proportion of calcium bilirubinate and other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calcium resembling an eggshell that may be visible on plain x-ray films.

Frequency
Gallstones are uncommon in children. Beginning at puberty, the concentration of cholesterol in bile increases. The incidence in women falls with menopause.

Race : White individuals, have a relatively high prevalence of gallstones. Gallstone disease is less common in Asians and Africans.

Sex :  Women are more likely to develop cholesterol gallstones than men, especially during their reproductive years, when the incidence of gallstones in women is 2 to 3 times that in men. The difference appears to be attributable mainly to estrogen, which increases biliary cholesterol secretion.Pigment gallstones affect men and women equally. 

Age :Gallstones continue to form throughout adult life, and the prevalence is greatest at advanced age.

History : Gallstone disease may be thought of as having the following 4 stages: (1) the lithogenic state, in which conditions favor gallstone formation; (2) asymptomatic gallstones; (3) symptomatic gallstones, characterized by episodes of biliary colic; and (4) complicated cholelithiasis –  Symptoms occurring within the gallbladder or when lodge in the common bile duct.

• Asymptomatic gallstones
  • Gallstones may be present in the gallbladder for decades without causing symptoms or complications and discovered incidentally. In most cases, do not require any treatment.
  • Gallstones often coexist with other gastrointestinal conditions –  chronic abdominal pain, heartburn, postprandial distress, bloating, flatulence, constipation, or diarrhea
• Biliary colic
  • Biliary colic occurs when gallstones  impact in the cystic duct during a gallbladder contraction, increasing gallbladder wall tension. In most cases, the pain resolves over 30 to 90 minutes as the gallbladder relaxes and the obstruction is relieved.
  • Episodes of biliary colic are sporadic and unpredictable. The patient localizes the pain to the epigastrium or right upper quadrant and may describe radiation to the right scapular tip. It may be accompanied by nausea and vomiting.
• Complications of gallbladder stones
  • Acute cholecystitis causes the gallbladder to become distended and progressively inflamed. In severe cases, gallbladder empyema, occurs.
  • Chronic cholecystitis – due to repeated attacks of acute cholecystitis and localized ischemia. The chronically fibrotic gallbladder may become shrunken and adherent to adjacent viscera.
  • Gallbladder cancers commonly invade the adjacent liver and common bile duct, producing jaundice.
  • Occasionally, a large stone may erode through the wall of the gallbladder into an adjacent viscus, producing a cholecystoenteric fistula and may obstruct the small intestine, a phenomenon termed gallstone ileus.
• Complications of stones in the common bile duct
  • Patients who have passed one stone tend to pass more stones over the subsequent months.
  • May impact distally in the ampulla of Vater and  produce biliary colic indistinguishable from that caused by cystic duct stones. Because impaction of common bile duct stones occludes the flow of bile from the liver to the intestine, pressure rises in the intrahepatic bile ducts, leading to increased liver enzymes and jaundice.
  • Bacterial overgrowth in stagnant bile above an obstructing common duct stone produces ascending cholangitis- Charcot triad – fever, jaundice, and right upper quadrant pain.
  • A stone impacted in the ampulla of Vater may transiently obstruct the pancreatic duct, leading to in situ activation of pancreatic proteases and triggering an attack of acute pancreatitis.
  • Stone impaction in the distal common bile duct is often relieved spontaneously within hours to days by passage of the stone into the intestine.
  • Porcelain Gallbladders. Gallbladders are referred to as porcelain when their walls have become so calcified that they look like porcelain on an x-ray. Porcelain gallbladders have been associated with a very high risk of cancer,

Physical

• In acute cholecystitis, tenderness to palpation over the gallbladder,  can be elicited by having the patient inhale while the examiner maintains steady pressure below the right costal margin -Murphy sign. Localized rebound tenderness, guarding, or rigidity may occur with pericholecystic inflammation.
• Patients with acute cholecystitis, ascending cholangitis, or acute pancreatitis, in addition to abdominal pain, may exhibit fever and may be tachycardic and hypotensive. In severe cases, bowel sounds are often absent or hypoactive.
• Choledocholithiasis with obstruction of the common bile duct produces cutaneous and scleral icterus that evolves over hours to days as bilirubin accumulates.
• The Charcot triad of severe right upper quadrant tenderness with jaundice and fever is characteristic of ascending cholangitis.
• Acute gallstone pancreatitis is  characterized by epigastric tenderness. In severe cases, retroperitoneal hemorrhage may produce ecchymoses of the flanks and periumbilical ecchymoses -Cullen sign and Grey-Turner sign.

Causes
Cholesterol gallstones, black pigment gallstones, and brown pigment gallstones have different pathogenesis and different risk factors.

• Cholesterol gallstonesare associated with female gender, European or Native American ancestry, and increasing age. Other risk factors include the following:
  • Obesity: The metabolic syndrome of truncal obesity, insulin resistance, type II diabetes mellitus, hypertension, and hyperlipidemia is associated with increased hepatic cholesterol secretion.
  • Pregnancy: Cholesterol gallstones are more common in women who have experienced multiple pregnancies. A major contributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reduces gallbladder contractility, leading to prolonged retention and greater concentration of bile in the gallbladder.
  • Gallbladder stasis: Other causes of gallbladder stasis associated with increased risk of gallstones include high spinal cord injuries, prolonged fasting with total parenteral nutrition, and rapid weight loss associated with severe caloric and fat restriction (eg, diet, gastric bypass surgery).
  • Drugs: Estrogens administered for contraception or for treatment of prostate cancer increase the risk of cholesterol gallstones. Drugs that increase hepatic elimination of cholesterol via biliary secretion  increase the risk of cholesterol gallstones.
  • Heredity: About 25% of the predisposition to cholesterol gallstones appears to be. A rare syndrome of low phospholipid-associated cholelithiasis occurs in individuals with a hereditary deficiency of the biliary transport protein required for lecithin secretion.

• Black pigment gallstonesoccur disproportionately in individuals with high heme turnover.
  • Disorders of hemolysis associated with pigment gallstones include sickle cell anemia, hereditary spherocytosis, and beta-thalassemia.
  • In cirrhosis, portal hypertension leads to splenomegaly. This, in turn, causes red cell sequestration, leading to a modest increase in hemoglobin turnover. About half of all cirrhotic patients have pigment gallstones.
• Prerequisites for formation of brown pigment gallstones include colonization of bile with bacteria and intraductal stasis. This condition causes recurrent cholangitis and predisposes to biliary cirrhosis and cholangiocarcinoma. The etiology is unknown, but liver flukes have been implicated.

Risk Factors:

• Studies recently found that a mutation in the gene ABCG8 significantly increase a person’s risk of gallstones. This gene controls a cholesterol pump that transports cholesterol from the liver to the bile duct.
• People with diabetes are at higher risk for gallstones, and have a higher-than-average risk for gallbladder disease without stones.
• Being overweight is a significant risk factor for gallstones.

Prevention :Diet may play a role in gallstones.

Fats. Although fats (particularly saturated fats found in meats, butter, and other animal products) have been associated with gallstone attacks,   Fiber. High intake of fiber has been associated with a lower risk for gallstones.  Nuts. Studies suggest that people may be able to reduce their risk of gallstones by eating more nuts (peanuts and tree nuts, such as walnuts and almonds).

Fruits and Vegetables. had the lowest risk of developing symptomatic gallstones that required removal of the gallbladder.

Lecithin. Lecithin is a key component of bile. It contains choline and inositol, two compounds that are important for the breakdown of fat and cholesterol. Low levels of lecithin may precipitate the formation of cholesterol gallstones. Dietary lecithin is available in health food stores and is found in eggs, soybeans, liver, wheat germ, and peanuts. There is no evidence, however, that lecithin supplements or foods containing it can prevent gallstones in humans.

Sugar. High-intake of sugar has been associated with an increased risk for gallstones.

Alcohol. A few studies have reported a lower risk for gallstones with alcohol consumption.  Preventing Gallstones during Weight Loss   Maintaining a normal weight and avoiding rapid weight loss are the keys to reducing the risk of gallstones.

Diagnosis
Blood tests showing high levels of pancreatic enzymes (amylase and lipase) usually indicate a diagnosis of pancreatitis. Elevated levels of the liver enzyme alanine aminotransferase (ALT) are very specific in identifying gallstone pancreatitis.

Imaging techniques are useful in confirming a diagnosis – Ultrasound, computed tomography (CT) scan, along with laboratory tests, can determine the severity of the condition.

Laboratory Tests

• Bilirubin and the enzyme alkaline phosphatase are usually elevated in acute cholecystitis, and especially choledocholithiasis (common bile duct stones
• Levels of liver enzymes known as aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are elevated when common bile duct stones are present. A threefold or more increase in ALT strongly suggests pancreatitis.

A high white blood cell count is a common finding in many (but not all) patients with cholecystitis.

A number of techniques –  endoscopic retrograde cholangiopancreatography (ERCP), endoscopic ultrasound (EUS) and magnetic resonance cholangiography (MRC) –  effective for detecting common bile duct stones. Only ERCP, however, allows removal of the stones.

Imaging Techniques
Ultrasound. Ultrasound is a simple, rapid, and noninvasive and diagnostic method to detect gallstones, acute cholecystitis. Air in the gallbladder wall may indicate gangrene. X-Rays. Standard x-rays of the abdomen may detect calcified gallstones.

Some remedies of gall-stone colic

• Chelidonium majus
• China officinalis
• Aconitum napellus
• Nux vomica -KENT says : “The proper medicine relaxes the circular fibres in the canal, and lets the stone pass. The remedy that ameliorates, or some of its cognates, will overcome the tendency to form stones.
• Berberis vulgaris”An excellent remedy for renal calculi; also for gall-stones associated with renal disease”. Sticking pains under border of false ribs on right side, shoot from hepatic region down through abdomen”. FARRINGTON.
• Dioscorea villosa -Hard, dull pain, gall bladder, at 7 p.m. -Better hard pressure.
• Magnesium phosphoricum
• Podophyllum peltatum -“sweat profuse, dropped off the prover’s fingers”.
• Lithium carbonicum
• Kalium bichromicum
• Carduus marianus -Liver engorged. Gall-stones.
• Iris versicolor -Also set down for gall-stone colic.
• Baptisia tinctoria
• Leptandra virginica
• Chionanthus virginica
• Lycopodium clavatum clavatum
• Natrium sulphuricum
• Apis mellifica
• Cocculus indicus
• Ipecacuanha
• Hydrastis canadensis
• Bryonia alba  KENT says : “It has inflammation of the liver, and many other liver symptoms.
• Kalium carbonicum
• Chamomilla
• Veratrum album
• Calcarea carbonica
• Mercurius solubilis
• Nitri spiritus dulcis -HERING says : “incarcerated gall-stones (with yolk of egg beaten up and applied inwardly and outwardly)….
• Aether-FARRINGTON : “In the passage of gall-stones, when remedies fail to relieve, I find that ether, externally and internally, is very good, acting better than chloroform”.
• Chloroformium-“Cholestric gall-stones and biliary colic”.
• CLARKE says : “Choloform will dissolve gall-stones, and cases have been treated by injection of chloroform into gall bladder”.

Dr Beenadas
Department of MM
Govt. Homeopathic Medical College. Calicut