Disorders of Gall Bladder and Homoeopathic management

Dr Appu Gopalakrishnan

General Considerations
The right and left hepatic ducts join to form the common hepatic duct. It joins the cystic duct to form the common bile duct which ranges in length from 2-9 cm. It passes behind the duodenum through the head of the pancreas to join the pancreatic duct and opens into the second part of the duodenum at the ampulla of Vater. The gallbladder, situated below and in close contact with the liver, is pear-shaped, and has a capacity of 50 mL. Its fundus lies beneath the tip of the right ninth costal cartilage. In 10% of people the gallbladder has a mesentery (floating gallbladder) and it is freely movable. The liver secretes 600 to 700 mL of bile in 24 hours at a pressure of 15-25 cm of water. The gallbladder concentrates the bile ten-fold by absorption of water and electrolytes. Bile secretion is inhibited when the pressure in the common bile duct exceeds 30 cm water. Vagus, which is the motor nerve, probably maintains the tone of the gallbladder. Gallbladder contracts in response to cholecystokinin (CCK) secreted by the duodenal mucosa. Cholecystokinin also causes relaxation of the sphincter. Drugs like morphine and pethidine cause spasm of the sphincter of Oddi and glyceryl trinitrate relaxes it.

Symptomatology of Biliary Tract Disease
The most obvious sign is jaundice which may be constant and progressive or fluctuating. This may or may not be associated with pain. Acute inflammatory lesions cause severe pain in the right hypochondrium, referred to the right shoulder. Obstruction to the cystic duct or common bile duct causes colicky pain with periodic waxing and waning. Unlike as in renal colic, mild constant pain persists between spasms. Persistence of continuous pain for more than five hours should suggest complications such as infection or perforation of the gallbladder. The fundus of an enlarged gallbladder can be palpated at the lateral border of the right rectus abdominis as a globular firm mass. Sometimes an elongated or floating gallbladder may reach as low as the right iliac fossa. Obstruction of the common bile duct due to external pressure as in carcinoma of the head of the pancreas causes enlargement of the gallbladder (Courvoisier’s law).

Since the gallbladder may enlarge only intermittently, repeated examinations may be necessary to detect it. Gall stones lead to chronic infection and thickening of the gallbladder, and this restricts enlargement. Tenderness over the gallbladder is elicited over the right hypochondrium. Murphy’s sign is sudden catching pain felt on inspiration when the palpating finger exerts gentle pressure below the liver edge at the right border of the right rectus abdominis. The Boas’s sign is tenderness, sometimes elicited over the region of the right scapula. Gallbladder pain may occasionally radiate to the chest and this may be mistaken for angina pain. Gallbladder disease and ischemic heart disease coexist in many instances.

Investigation of the Gallbladder and Bile Ducts

Radiographs: Plain radiograph taken in the anteroposterior and right lateral positions may reveal radiopaque

calculi. Only 10% of biliary calculi are radiopaque. Opacities due to renal calculi, calcified lymph nodes and fecoliths have to be differentiated from gall stones. An enlarged gallbladder may throw a soft tissue shadow. Gas in the biliary tree and pancreatic calculi are also seen at times.

Ultrasonography: It is the most useful noninvasive method to detect dilated biliary passages, gallbladder and calculi. This is the investigations of first choice.

CT scan: It demonstrates dilated biliary passages, intra and extrahepatic lesions and the gallbladder. The neighboring organs can also be well-visualized.

Contrast radiography: With the advent of noninvasive procedures such as ultrasound, CT scan and MRI which are much more effective in bringing out the abnormalities, the cumbersome and less precise investigations such as oral cholecystogram, intravenous cholangiography and blind percutaneous transhepatic cholangiography are seldom performed at present. Still in particular situations, USS guided or CT guided needling procedures and biopsies are done.

Endoscopic retrograde cholangiopancreatography (ERCP): This is an elegant method for visualizing the

biliary and pancreatic duct systems. It utilizes endoscopy and radiography simultaneously. The ampulla of Vater is cannulated through a side-viewing duodenoscope and the contrast is injected. The pancreatic duct, bile duct, and their tributaries are visualized in over 80% of cases. The ERCP also facilitates the collection of specimens for biopsy, cytology, and analysis of the juices. Therapeutically, ERCP has been employed to remove stones from the ducts and relieve strictures and even malignant obstructions. Endoscopic ultrasound scan (EUS) is a very sensitive imaging modality for terminal CBD lesions.

Operative cholangiography: The bile duct can be opacified during surgery by injecting contrast medium and its progress is followed.

Choledochoscopy: Visualization of the intra- and extrahepatic biliary system intraoperatively is possible by the choledochoscope which is introduced into the common bile duct. Stones and lesions missed by other investigations can be detected.

Barium meal: A properly conducted barium meal examination may give valuable clues in hepatobiliary disease. Distortion of the stomach and duodenum, abnormalities of the duodenum produced by ampullary carcinoma or pancreatic tumours, presence of fistulae, and regurgitation of the barium through the incompetent biliary sphincter are all useful diagnostic findings. This is seldom done at present since direct visualization is possible by endoscopy.

Radionuclide imaging: Scintiscans using 131I rose-bengal or 99mTc-pyridoxylidene iminodiacetic acid derivative (HIDA) when given intravenously is taken up by the liver and excreted in bile. The biliary tree can be visualized.

Duodenal biliary drainage: Bile can be collected for examination through a duodenal tube after injecting cholecystokinin.

CHOLECYSTITIS : This may be acute or chronic.

ACUTE CHOLECYSTITIS
Obstruction to the gallbladder neck or cystic duct by gall stones, mucus plugs, neoplasms or other foreign bodies leads to stasis and infection. Initially the lesion is sterile but soon infection by E. coli and Streptococcus fecalis supervenes. Anaerobes such as fusobacteria and Bacteroides are also common. Inflammation may be mild or fulminant. The gallbladder may become filled with pus (empyema of the gallbladder) and the organ may burst after perforation, leading to severe biliary peritonitis and shock. Invasion by gas-forming organisms leads to the presence of gas in the wall of the gallbladder (emphysematous gallbladder) or in its cavity.

CLINICAL FEATURES
The disease is more common in middle-aged women. Sudden severe pain in the epigastrium and right hypochondrium referred to right shoulder, fever, vomiting and restlessness should suggest acute cholecystitis. Deep jaundice is rare unless the biliary tree is diffusely involved or the common bile duct is blocked. Heavy fatty meals at night, violent exercise, travel or even abdominal palpation in some cases may precipitate the attack. Pain may be colicky or continuous. The abdomen may be rigid. In some cases the gallbladder may be enlarged and palpable but local tenderness and rigidity preclude proper palpation.

Murphy’s sign and Boas’s sign may be positive. General features of infection like fever, rigor, and neutrophil leukocytosis accompany these attacks. The condition subsides with treatment but recurs after varying intervals. Perforation of the gallbladder, ascending cholangitis, and shock occur in severe cases.

Differential diagnosis of acute cholecystitis includes hepatitis, cholangitis, gastric perforation, pancreatitis, appendicitis, acute intermittent porphyria and peritonitis. Pain may radiate to the chest, which could be mistaken for angina pectoris.

Diagnosis
The condition should be suspected clinically. Polymorphonuclear leukocytosis with a shift to the left is usually seen. The ultrasound scan may demonstrate stones in more than 90% of cases. Radionuclide scan (HIDA) is typical. It may demonstrate the bile ducts without visualizing the gallbladder.

Treatment
Conservative treatment consists of bed rest, analgesics and intravenous fluids to give symptomatic relief. Antibiotics like penicillin, cephalosporins and cotrimoxazole reach the bile in adequate amounts and these have to be employed judiciously. Metronidazole is to be given if anaerobic infection is suspected. In more than 90% of cases the condition subsides with conservative treatment within 3- 4 days.

Surgical Management
Elective cholecystectomy can be done within three months after the acute phase subsides. The surgical mortality is about 0.5 to 1%. With the advent of laparoscopic cholecystectomy the operation has become more simple and less traumatizing.

Acute gangrenous cholecystitis is seen in the elderly and immunosuppressed individuals. The gallbladder may rupture at the fundus giving rise to local peritonitis, adhesions with other viscera or formation of internal biliary fistula. Acute gangrenous cholecystitis should be suspected in any individual if the pain and toxemia increase despite treatment, and shock supervenes. The mortality is 15-20%. Initial treatment consists of massive antibiotic therapy and supportive measures. Emergency cholecystectomy or cholecystostomy and drainage of abscesses are indicated if the condition deteriorates in spite of adequate conservative measures.

CHRONIC CHOLECYSTITIS
This is the most common medical lesion affecting the gallbladder, and it is invariably due to cholelithiasis. The gallbladder is thickened and fibrotic and the mucosa may be destroyed by scarring.

CLINICAL FEATURES
Vague upper abdominal pain, colic, gaseous distension after fatty meal or recurrent episodes of acute cholecystitis should suggest the possibility of chronic cholecystitis. Peptic ulcer, hiatus hernia, and chronic pancreatitis have to be excluded by investigations. Murphy’s sign may be positive and in the absence of hepatic disease it is very suggestive of cholecystitis. Calculi may be seen in plain radiographs of the abdomen. Oral cholecystogram, cholangiogram, ultrasonography and ERCP help to localize the lesion.

Course and Prognosis

The condition persists for several years with exacerbations and remissions. There is increased risk of malignancy.

Treatment
Medical treatment consists of dietary adjustment, reduction of weight, antispasmodics, antacids, and antibiotics. Early cases may subside completely. Drugs which dissolve cholesterol gall stones are worth a trial. Chenodeoxycholic acid in a dose of 13-15 mg per kg body weight given orally at bed time is effective in dissolving these stones in a period of 6-24 months. Recurrence may occur on stopping therapy. Side effects include mild diarrhea and elevation of serum cholesterol. Ursodeoxycholic acid is a better drug in this class and in a dose of 10 mg/kg given twice daily, it acts faster. Troublesome diarrhea does not occur. Rowachol is a mixture of essential fatty acids capable of dissolving gall stones. Medical treatment is generally not preferred on along term basis. Shock wave lithotripsy disintegrates the stones. This helps in quicker resolution. Surgical removal of the gallbladder is indicated if medical treatment fails. With the availability of laparoscopic cholecystectomy in many centers in India at reasonable cost, this has become more popular as the definitive long-term treatment.

Typhoid cholecystitis: The biliary tract may be colonized by Salmonella typhi. More commonly chronic

cholecystitis may occur in typhoid carriers. Typhoid bacilli form a nidus around which calculi may

form. The gallbladder becomes chronically infected with Salmonella and this perpetuates the fecal carrier state. Cholecystectomy helps in clearing the focus of infection and the carrier state.

Carcinoma of the Gallbladder
It is a rare condition in South India, but is more common in the Gangetic belt of India. It is seen more in people above the age of 50 years. Around 90% cases are adenocarcinomas. It presents with progressive biliary obstruction. Chronic calculous cholecystitis predisposes to malignancy.

Cholangiocarcinoma
This is a rare slow-growing adenocarcinoma arising from any part of the biliary tree from the bile canaliculi to the sphincter of Oddi. Progressive jaundice occurs depending on the site of obstruction.

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.

ImagingTechniques
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.

HOMOEOPATHIC MANAGEMENT

Repertorial approach

1.SHROYEN’S SYNTHESIS

ABDOMEN – INFLAMMATION – Gallbladder

bell. berb. but-ac. calc. card-m. chel. chin. coli. coloc. curc. eberth. fel guat. Hed. lyc. mag-m. mag-s. malar. mand. morg. morg-g. Nat-s. nux-v. parathyr. prot. ptel. tarax.

ABDOMEN – INFLAMMATION – Gallbladder – acute : bell. crot-h. parathyr. pyrog.

ABDOMEN – INFLAMMATION – Gallbladder – chronic : beryl. coli. eberth. hydroq. parathyr. quinhydr.

ABDOMEN – INFLAMMATION – Gallbladder – suppurated : eberth.

ABDOMEN – INFLAMMATION – Gallbladder – septic lach.

ABDOMEN – GALLSTONES

bell. berb. calc. calc-f. card-m. chel. chin. chion. chlf. chol. cupr. dios. eberth. euon. euon-a. euonin. fab. fel fuma-ac. jug-c. lach. lith-c. lob. mand. mang. morg-g. morg-p. nat-sal. nit-s-d. nux-v. podo. ptel. tarax. thlas. vichy-g.

ABDOMEN – PAIN – Liver – colic; gallstone
ars. bamb-a. Bapt. BELL. BERB. Bry. cal-bil. Calc. CARD-M. Cham. Chel. CHIN. Chion. Chlf. Chlol. Coloc. cupr. dig. Dios. Fab. hep. Ip. Iris kali-ar. Kali-bi. Kali-c. Lach. laur. Lept. Lith-c. LYC. mag-bcit. Mag-m. Mag-s. mand. mang. merc. Merc-d. NAT-S. Nux-v. ozone podo. puls. rhus-t. Sep. sil. staph. sulph. tab. ter. trios. VERAT.

2.MURPHY

Diseases – CHOLECYSTITIS, gallbladder : card-m. chel. chion. Chol. Lach. lept. morg-g. myric. Phos. podo. pyrog.

Diseases – CHOLECYSTITIS, gallbladder – septic : bry. bufo Lach. Phos. Pyrog.

THERAPEUTICS

• 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.
• Podophyllum peltatum -“sweat profuse, dropped off the prover’s fingers”.
• Carduus marianus -Liver engorged. Gall-stones.
• Iris versicolor -Also set down for gall-stone colic.
• Nitri spiritus dulcis -HERING says : “incarcerated gall-stones (with yolk of egg beaten up and applied inwardly and outwardly)….
• Ether-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”.
• Carlsbad waters: Almost specific, RUDDOCK says, for gall-stone colic. 

Belladonna: Extreme sensitiveness: especially to jarring. Face red: hot. Hyperaesthesia: extreme irritability of whole economy or nerve centres. Extreme irritability.

Chelidonium: Pains from region of liver, shooting towards back and shoulder. Pain in region of liver, extending quickly down across navel into intestines. Biliary calculi: chill: intense pain in gall-bladder region; vomiting; clay-coloured stools. Cutting pains and stitches: constriction like a cord. Pain in the inner angle of right shoulder blade, running into chest. Yellow tongue with intended edges. Liver region tense and tender.

China: FARRINGTON says: ‘Bell. Is useful in cholelithiasis, but the remedy to cure the condition permanently is Cinchona. Unless some symptom or symptoms call specifically for another drug, put your patient on a course of Cinchona.

Pain in the hepatic region, worse from touch. Shooting in region of liver, tenderness and pain on touching the part. Liver region sensitive to least pressure. Obstruction in gallbladder with colic; periodic reccurence; yellow skin and conjunctivae; constipation with dark greenish scybala. Biliary calculi. Intensely sensitive to touch, to motin, to cold air. Periodicity: pains come on regularly at a given time each day; or every night at 12 o’ clock. Drenching night sweats.

Nux-vom: Gall-stone colic with sudden severe pains on right side; spasms of abdominal muscles with stitching pains in  liver. Jaundice, aversion to food, fainting turns; gall-stones. Constipation nearly always. Liver swollen, indurated, sensitive, with pressure and stinging. Cannot bear tight clothing. Oversensitive, irritable, touchy. Ineffectual urging to stool, irregular peristalsis. Chiily, if he uncovers or moves.

Berberis: “An excellent remedy for renal calculi; also for gall-stones associated with renal disease. Pain shooting. The patient cannot make the slightest motion, sits bent over to painful side with relief. Symptom peculiar to Berberis is a bubbling feeling as if water coming up through the skin. Stitching pains under border of false ribs in right side, shoot from hepatic region down through abdomen.” FARRINGTON.

Radiating pains from a particular point puts Berb almost alone for radiating pains. Has cured renal colic many times, bcoz of its well-known ability to shoot out in every direction. It cures gall-stone colic when little twinges go in every direction from that locality. The liver is full of suffering. Sudden stabbing like a knife pucturing the liver. Dreadful suffering.

Berberis, when indicated, will let the little gall-sone loos, and it will pass through, and the patient will take a long breath…… Anything that is spasmodic can be relieved instantly.” KENT.

Dioscorea:  Hard, dull pain, gall-bladder, at 7 p.m. Neuralgia and spasmodic affections of liver and gall-ducts. Cutting, squeezing, twisting pain. Colic begins at umbilicus and radiates to all parts of body, even extremities. A constant pain, aggravated at regular intervals by paroxysms of intense suffering. Unbearably sharp, cutting, twisting, griping or grinding pains; dart about and radiates to distant parts. Worse doubling up. Better stretching out, or bending back. Better hard pressure.

Podophyllum:  Pod indicated in biliary colic. Stools constipated and clay-coloured. Tongue yellow or white, takes imprint of teeth. Pain liver, inclined to rub part with hand. Colic at daylight every morning. Better bending forward: external warmth.

Lithium carb:  Gall-stones. Violent pain in hepatic region between ilium and ribs. Soreness and pain in bladder: sharp, sticking. Red nose is characteristi

Cardus marianus:  Liver engorged. Gall-stones. Tongue, white centre with red intended edges. Crawling sensation , like the passage of a small body like a pea through a narrow canal on posterior side of liver extending to pit of stomach.

Iris:  Gall-stone colic. Cutting pain, region of liver: < motion. Tongue dry, coated dry, coated on each side: red streak in centre. Great burning distress in epigastrium.

Leptandra: Burnings, liver: near gall bladder. Dull aching, liver < near gall bladder. Yellow coated tongue. Jaundice. Better lying on stomach or side.

Chionanthes: A great liver and gall-stone-colic medicine. Better lying on abdomen. Heat with aversion to cover. Very bitter eructations. Hot, bitter, sour, sets teeth on edge. Hypertrophy of liver: obstruction: jaundice. Soreness. Nausea and retching with desire for stool. Sensation of double action in stomach, while vomiting, one tying to force something up, the other sucked it back. Colic and cold sweat on forehead.

Lycopodium: Pain in liver; recurrent bilious attacks with vomiting of bile. Subject to gall-stone colic.  After Lyc. The attacks come on less frequently, the bilious secretion becomes normal and the gall-stones have a spongy appearance, as though being dissolved. Lyc. patients are always belching: sour erucations like strong acid burning in pharynx. Bloating: obliged to loosen clothes. Worse cold drinks, often > warm drinks. Worse afternoons: 4-8 p.p. aggravation. Generally, craving for sweets.

Hydrastis: Skin yellow; stools white and frequent: fullness and tenderness over hepatic region. Catarrhal inflammation of mucous lining of gall-bladder and biliary ducts. Cutting from liver to right scapula. < lying on back on right side.

Hepar:  LILIENTHAL gives Hepar as one of the remedies of gall-stone colic. It has stitches in region of liver. Hepatitis, stools white or green. Is extremely sensitive mentally and physically. Cannot bear the slightest touch: or pain. Cannot stand draughts: craves vinegar.

Verat. Alb:  Is in Kent’s repertory for gall-stone colic. It has, Hyperaemia of liver, gastric catarrh, putrid taste, disgust for warm food, great pressure on hepatic region with vomiting and diarrhea. In verat cases, there will be profuse sweating; cold sweat on forehead; Hippocratic face. Pain maddening, driving patient to delirium. Typically, cold skin, cold face, cold back, cold hands, feet and legs, cold sweat.

Merc.Sol: Pressing pains; stitching in liver. Cannot lie on right side. Jaundice: violent rush of blood to head: bad taste: tongue moist and furred: soreness hepatic region: from gall-stones.

Violent stitches in hepatic region, could not breathe or eructate. Worse night: worse warm in bed: worse for the profuse sweat. Foulness of mouth and sweat. Merc loves bread and butter.

Phosphorus:  Probably more important for the treatment of liver, leading to gall-stones, then  for the acute attack? Great tenderness liver region. Craving for ice-cold drinks, vomited when warm, vomiting followed by great thirst. Worse lying on left side. Anxious and restless in the dark.

REFERENCES

1. Krishnadas KV. Text book of Medicine. 5TH ed. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2008.
2. Shroyens F. Repertorium Homoeopathicum Syntheticum. 9.1 edition. New Delhi: B Jain publishers; 2011.
3. Murphey R. Homoeopathic Medical Repertory. 3rd revised. New Delhi: B Jain publishers; 2014.
4. Boger CM. Boenninghausen’s characteristics materia medica and repertory with word index. New Delhi: B Jain publishers; 2007.
5. Boericke’s new manual of Homoeopathic Materia medica with Repertory. 3rd revised and augmented edition. New Delhi: B Jain publishers; 2016.
6. Zandvoort RV. The Complete Repertory.
7. Phatak SR. A concise Repertory of Homoeopathic medicines. 4th edition revised and corrected. New Delhi: B Jain publishers; 2005.
8. Allen’s keynotes rearranged and classified with leading remedies of the Materia medica and bowel nosodes. 10th edition. New Delhi: B Jain publishers;
9. Lippe AV. Keynotes and red line symptoms of the materia medica. Reprint. New Delhi: B Jain publishers; 1998.
10. Kent JT. Lectures on materia medica. Reprint. New Delhi: B Jain publishers;
11. Lesser O. Textbook of Homoeopathic Materia Medica. B. Jain Publishers; 2015.  992 p.
12. Phatak SR. Materia Medica of Homoeopathic Medicines. B. Jain Publishers; 2002. 792 p.
13. Farrington MEA. Lectures on Clinical Materia Medica in Family Order. B Jain Publishers Pvt Limited; 2010. 1040 p.