GALLSTONES

Pathogenesis of GALLSTONES

Physiochemical factors

ysioreased hepatic cholesterol secretion and chronic supersaturation of bile

enhanced cholesterol crystal nucleation in gallbladder bile

Motility defects

Gallbladder motility defects

Gallbladder stasis

• Intestinal motility defects. Prolonged intestinal transit, longer migrating motor cycles and disrupted motilin release

Risk factors for gallstones

Cholesterol stones

Older age

• Female sex
• Obesity
• GI motility disorders
• Parenteral nutrition (reduces gallbladder motility)
• Pregnancy and sex hormones
• Drugs: Octreotide, Ceftriaxone
• Diabetes mellitus, cystic fibrosis
• Surgery (e.g. vagotomy, biliopancreatic bypass)
• Pigment stones
• Cirrhosis
• Diseases of terminal ileum

Clinical features of gallstones and complications:

A. In the gallbladder

1. No symptoms (Silent gallstones)
2. Biliary colic due to contraction of gallbladder against a stone impacted in common bile duct. This gives rise to midline or right hypochondrial pain, at times associated with vomiting but generally without fever or systemic upset. Upper abdominal tenderness may be present.
3. Acute cholecystitis SYMPTOMS (a) Pain Type: Distension pain giving rise to a deep, central poorly localized pain. Peritoneal pain with overlying skin tenderness and muscle rigidity in the right hypochondrium. Referred pain radiating to right scapular region. Digestive tract pain causing abdominal colic, nausea, and flatulence without vomiting. SIGNS

(i)General-include fever with often chills at onset and tachycardia.

(ii) Local-(a) Tenderness and muscle guarding

in right upper quadrant. (b) Palpable mass – of globular shape below right costal margin and moving on inspiration may be felt. (c) Murphy’s sign Patient complains of pain on taking a deep breath while the examiner’s hand is pressed below the right costal margin. (d) Abdominal distension -may occur and if marked simulates intestinal obstruction. (e) Boas’s sign – Area of hyperaesthesia over right subscapular region.

INVESTIGATIONS:

1. Leucocyte count – raised with increased polymorphs.
2. Radiograph-Plain film of the abdomen may reveal radio-opaque gallstones or soft tissue mass in region of GB.
3. Ultrasonography is the most common used method of detecting stones
4. Oral cholecystography identifies radiolucent stones. It is useful in determining gallbladder contraction and cystic duct patency, and identifying anatomical abnormalities of the gallbladder.
5. CT is more sensitive in identifying gallstone calcification than plain radiology.

It is required in selection of patients for non-surgical therapy.

6. Other investigations used in compli-cated gallstone disease include ERCP for common bile duct stones, LFTs for acute choecystitis, serum amylase levels for acute pancreatitis.

MANAGEMENT:

1. Diet Nothing by mouth for first 24 hours, or till nausea and vomiting have abated.
2. Broad spectrum antibiotics – Parenter-ally to prevent peritonitis, cholangitis and septicemia.
3. Special measures (a) Local heat to abdomen. (b) 5% glucose saline intrave-nously. (c) TPR 2 hourly. (d) Examine abdomen every 2 hours to follow changes in tenderness, rigidity, and character of

any palpable mass. (e) Total and differ-ential WBC count. (f) Gastric suction if persistent vomiting.

4. Surgery Cholecystectomy within

2-3 days of the onset of symptoms shortens total hospital stay and avoids incidence of repeated attacks of waiting period of delayed ‘cold’ cholecystectomy.

4. Chronic cholecystitis may follow

repeated attacks of biliary colic or present with abdominal distension or epigastric discomfort sometimes relieved by belching, nausea triggered by fatty food and a dull ache in right hypochondrium, epigastrium and right subscapular region. There is localised tenderness in right hypochondrium and positive Murphy’s sign.

B. In bile ducts

1. Biliary colic with transient jaundice due to migration of small stones into the common bile duct and ejection through the papilla of Vater.
2. Acute pancreatitis – due to probably reflux of bile into pancreatic duct through a common channel in ampulla of Vater.
3. Obstructive jaundice from impaction of stone in common bile duct.
4. Cholangitis –

(a) Pyogenic cholangitis Acute suppurative or non-suppurative inflammatory process in biliary system associated with biliary obstruction. Charcot’s triad of jaundice, upper abdominal pain and high fever with rigors. Added presence of bacteremia and mental stupor constitute Reynold’s pentad.

(b) Chronic recurrent cholangitis – May occur in presence of incomplete bile duct stictures and result in secondary biliary cirrhosis and portal hypertension.

Management of gallstones

Surgical treatment – Laparoscopic or open cholecystectomy is the only radical procedure for symptomatic gallstones.

Non-surgical treatment

1. Oral litholytic treatment Bile acids Chenodeoxycholic acid 10-12 mg/kg/day, and Urodeoxycholic acid 10-12 mg/kg/day, alone

or in combination (using one half of the dose of each) is suitable for small stones (<10mm in diameter). The whole dose should preferably be taken at bed time. Side effects Chenodeoxycholic acid: diarrhoea and hypertransaminasemia. Urodesoxycholic acid: gallstone calcification resulting in treatment failure.

2. Contact dissolution treatment – Precutaneous trans-hepatic gallbladder puncture followed by application of methyl-butyl ether (pow-erful cholesterol solvent) directly to the stones. Any number and size of stones can be treated. Complete dissolution is usually achieved within a few hours. Side-effects -Post-puncture severe abdominal pain and nasuea, erosive duodenitis and biliary peri-tonitis.
3. Extracorporeal shockwave lithotripsy (ESWL) Fragments the stones using focussed sound waves; the fragments are subsequently dissolved by bile acid therapy. The procedure is suitable for patients with up to three stones of diameter 10-30mm. Side-effects- Biliary colic, hemobilia and pancreatitis.

Recurrent stones

are radiolucent and smaller, and can be redissolved with bile acids if detected early.