Gallstones

Types of gallstones:

• Cholesterol stones
• Pigment (brown/black) stones and
• Mixed stones

Pathogenesis

Cholesterol stone:

Cholesterol is synthesized in liver. Its solubility is determined by relative concentration of cholesterol, bile salts and lecithin. Altered levels of cholesterol, lecithin, and bile salts in bile reduces the micelle concentration in the bile leading to precipitation of insoluble cholesterol, hence the stone formation.

Factors altering the cholesterol to bile salt ratio are obesity, high-calorie diets and certain medications. These increase the secretion of cholesterol and supersaturate the bile, increasing the lithogenicity of bile.

Pigment stone:

Types- black and brown

Black stones- 

composed of insoluble bilirubin pigment polymer mixed with calcium phosphate and calcium bicarbonate. Black stones accompany hemolysis (hereditary spherocytosis or sickle cell disease)

Brown stones-

 composed of calcium bilirubinate, calcium palmitate, calcium stearate and cholesterol. It is rare in gall bladder and usually forms in bile duct and are related to bile stasis and infected bile. Deconjugation of bilirubin deglucuronide by bacterial beta- glucuronidase  causes insoluble unconjugated bilirubinate to precipitate leading to stone formation.

Brown stones are also associated: Foreign body within the bile duct (e.g. endoprosthesis) 

Parasites (like Clonorchis sinensis and Ascaris  lumbricoides)

Cholesterol stone

Pigment stone

Clinical presentation:

Patient may be asymptomatic or presents with features of its complications.

Effects and complications of gallstones

In the gall bladder

Biliary colic

Acute cholecystitis

Chronic cholecystitis

    Empyema of the gall bladder

    Mucocele

    Perforation

b. In the bile ducts

    Biliary obstruction

    Acute cholangitis

    Acute pancreatitis

c. In the intestine: Gallstone ileus ( intestinal obstruction)

Diagnosis:

Based on history, physical examination and confirmatory radiological studies such as transabdominal USG and radionucleide scans.

T/T

Asymptomatic gall stone: observation

If symptomatic or complication of gallstones: cholecystectomy

Prophylactic cholecystectomy is done in:

diabetic pt

those with congenital hemolytic anaemia

those who undergo bariatric surgery for morbid obesity

Acute Cholecystitis

Definition: acute inflammation of the gallbladder, usually caused by cystic duct obstruction by gallstones.

Presentation

Biliary colic: severe right upper quadrant pain associated with nausea and vomiting. Pain may radiate to the chest. Pain is usually severe and last for minutes or several hours. Frequently, pain starts during the night, waking the patient. Dyspeptic symptoms may coexist and be worse after the attack. 

Right upper quadrant (RUQ) tenderness on palpation that is exacerbated during inspiration: Murphy’s Sign.

 Low-grade fever and leukocytosis

Murphy’s sign

Investigations

1. USG: reveals presence or absence of gallstone and thickening of the gall bladder wall

2. Plain X-ray abdomen : 10% of gallstone are radiopaque

3. Blood: Leucocytosis

Moderately elevated liver function

4. Radioisotope scanning

Allows visualisation of biliary tree and gall bladder. GB is visualised within 30min of isotope injection. Non-visualization of GB is suggestive of Acute cholecystitis.

USG findings in Ac. Cholecystitis

Treatment

• After the diagnosis of acute cholecystitis is made, IV fluids, antibiotics, and analgesia should be initiated. 
• Antibiotics should cover gram-negative aerobes as well as anaerobes. 
• Cholecystectomy is the definitive treatment for patients with acute cholecystitis. 
• Early cholecystectomy performed within 2 to 3 days of presentation  (if patients fail initial medical therapy and require surgery during the initial admission)
• If early cholecystectomy not indicated: Interval or delayed cholecystectomy that is performed 6 to 10 weeks after initial medical therapy. 

Cholecystectomy: open or laparoscopic

Complications

i. Empyema of the gall bladder

ii. Gangrene of the gallbladder

iii. Perforation and peritonitis

iv. Fistula formation and gallstone ileus (small bowel obstruction by a large gallstone

Chronic Cholecystitis

Defnition: ongoing chronic inflammation of the gallbladder usually caused by gallstones

Micro: chronic inflammation and Rokitansky-Aschoff sinuses

Late complication: calcification of the gallbladder ("porcelain gallbladder")

T/t: Cholecystectomy

Rokitansky-Aschoff sinuses

Porcelain gallbladder

Acalculous Cholecystitis

• Inflammation of the gall bladder in the absence of the stones.
• Seen particularly in patients recovering from major surgery, trauma and burns.
• Clinical picture similar to calculous cholecystitis.

T/t: Cholecystectomy

Empyema of the gall bladder

Definition: Presence of pus in the gall bladder

Etiology

Sequel of acute cholecystitis

Infected mucoecele

c/f

Fever, toxicity

Pain and tenderness in Rt. Hypochondrium

The wall may become necrotic and perforate with the development of localised peritonitis

Investigation   

1. USG abdomen

2. Blood: leucocytosis

   Treatment

   Drainage and, later, cholecystectomy

Mucocele

A nontender, palpable gall bladder results from complete obstruction of the cystic duct with resbsorption of the intraluminal bile salts and secretion of uninfected mucus by the gall bladder epithelium 

Mucocele of gall bladder

Clinical presentations

• Painless swelling in the right hypochondrium
• O/E: Non tender, smooth, globular, palpable gall bladder
• If infected, can cause empyema gall bladder

Investigation
USG abdomen

T/t: cholecystectomy

Fistula In Ano

• It is a track lined by granulation tissue which connects perianal skin superficially to anal canal or rectum deeply.
  
  
  
  
  
  
  
  
• It usually occurs in a pre-existing anorectal abscess which burst spontaneously.
  
  
  
  
  
  
  

Classification

According to whether the internal opening is below or above the anorectal ring:

• Low-level fistulae- Open into the anal canal below the anorectal ring.
  
  
  
  
  
  
  
• High-level fistulae- open into the anal canal at or above the anorectal ring.
  
  
  
  
  
  
  

Anatomical classification (standard)

• Subcutaneous
  
  
  
  
  
  
• Submucous
  
  
  
  
  
  
• Low anal
  
  
  
  
  
  
• High anal and
  
  
  
  
  
  
• Pelvirectal 
  
  
  
  
  
  

Park’s classification

• Intersphincteric 
  
  
  
  
  
  
• Trans-sphincteric (maybe high or low) and
  
  
  
  
  
  
• Supralevator 
  
  
  
  
  
  

Clinical features

• It presents with seropurulent discharge, along with skin irritation and one or more external opening may be present with induration of the surrounding skin.
  
  
  
  
• Pain is not  a symptom as long as the opening is large enough for the pus to escape. But if the orifice is occluded pain increases until the discharge erupts.
  
  
  
  
• Often it may heal superficially but pus may collect beneath forming an abscess which again discharges through same or new opening. Thus there may be two or more external openings, grouped together on the right or left of the midline, but when both ischiorectal fossas are involved then the opening is seen on each side which often intercommunicates.
  
  
  
  

Fistula In Ano

Goodsall’s rule

• Fistulas with an external opening in relation to the anterior half of the anus is of direct type.
  
  
• Fistulas with external openings in relation to posterior half of the anus, has a curved track may be of horse-shoe type, opens in the midline posteriorly and may present with multiple external opening all connected to a single internal opening.
  
  

Goodsall’s rule

Digital examination:

• Internal opening can be felt as a nodule on the wall of the anal canal.

Proctoscopy:

• May show the internal opening of the fistula.
• A hypertrophied papilla is suggestive that the internal orifice lies within the crypt related to the papilla.

Probing: not advisable
Radiography

Treatment

Low level fistulas:

• Under G/A or spinal anaesthesia
• Probe is passed through external opening up to the internal opening which is felt as an induration.
• Fistula is opened along the probe using a knife.
• Fibrous track along with unhealthy granulation tissue and additional external openings are excised.
• Specimen is then sent to HPE

High level fistulas:

Surgery involves staged procedure:

Initial colostomy followed by definitive procedure. This prevents sepsis ans promotes faster healing.
Later closure of colostomy is done.

• A slik or linen ligature is passed across the fistula and left in place with a tie.
• This allows the fistula to granulate and heal from above and to close completely. 
• Takes longer duration to heal.

CONGENITAL HYPERTROPHIC PYLORIC STENOSIS

• Hypertrophy of the musculature of pyloric antrum, especially the circular muscle fibres, causing failure of pylorus to relax. 
• Duodenum is normal.

Pathophysiology

• Progressive hypertrophy of the circular muscles in the pyloric sphincter.
• Not present at birth but occurs over 3 to 5 weeks.

Clinical Features

• Common in 1st born male child.
• Projectile vomiting (non bile-stained fluid)
• Weight loss, child becomes emaciated and dehydrated.
• Hypertrophied pylorus is palpated in the epigastrium (“olive”). It’s mobile, smooth, firm mass with  well defined borders.
• Visible gastric hyperperistalsis.

Visible gastric hyperperistalsis

Diagnosis

•      Diagnosis can be made with test feed .
•      USG is the investigation of choice- features present in the pyloric canal can be seen.

D/D

•      GERD
•      Feeding problems
•      Raised ICP
•      Duodenal atresia
•      Intestinal obstruction

T/T

At first metabolic abnormalities should be corrected (i.e. dehydration with low Na+,Cl, K+ and metabolic alkalosis) with i.v dextrose, NS and K+.

Surgery

• Ramstedt’s operation:
• Laparotomy is done
• Hypertrophied muscle is cut along the whole length until the mucosa bulges out. Mucosa should not be opened.

Duodenal Atresia

• Atresia is distal to entry of the common bile duct (occurs at the point of fusion between the foregut and midgut)
• Association with Down syndrome

• History of maternal polyhydramnios (cannot reabsorb amniotic fluid)
• Vomiting of bile-stained fluid at birth

     "Double bubble sign": air in stomach and air in proximal duodenum

•      Antenatal diagnosis can be made-USG

T/T

•      Duodenoduodenostomy

Cholecystoses

Cholecystoses are chronic inflammatory conditions of the gallbladder with cholesterol deposits.

Types :

1)Cholesterosis (Strawberry Gallbladder)

Aggregations of cholesterol crystals in the mucosa or submucosa

2)Cholesterol polyposis (Gallbladder polyp)

Cholesterol laden polypoid projections in the mucosa

3)Cholecystitis  glandularis proliferans

Granulomatous thickening and hyperplasia of the gallbladder.

4)Diverticulosis of the gallbladder

Diverticula formation in the wall of the gallbladder

5)Gallbladder wall fistula

Strawberry gallbladder

Cholesterol polyposis (Gallbladder polyp)

Cholecystitis  glandularis proliferans

Clinical features

Features of cholecystitis like positive Murphy’s sign, dyspepsia.

Investigations:

• USG abdomen
• OCG
• Isotope study

Treatment

• Cholecystectomy

Cystic fibrosis

Most common lethal genetic disorder

   

Defect: mutation of the chloride channel protein, cystic fibrosis trans-membrane conductance regulator (CFTR)

Genetics

  

i. CFTR gene is located on chromosome 7

ii. Most common mutation is a deletion in amino acid position 508 (AF508)

Pathogenesis: 

• defective chloride channel protein leads to abnormally thick viscous mucous, which obstructs the ducts of exocrine organs

Distribution of disease

i. Lungs

• Recurrent pulmonary infections with P. aeruginosa and S. aureus . 
• Chronic bronchitis
• Bronchiectasis

ii. Pancreas

•  Plugging of pancreatic ducts results in atrophy and fibrosis
•  Pancreatic insufficiency
•  Fat malabsorption 
•  Malodorous steatorrhea
•  Deficiency of fat-soluble vitamins

iii. Male reproductive system

• Obstruction of the vas deferens and epididymis
• May lead to male infertility

 iv. Liver:

•  plugging of the biliary canaliculi may result in biliary cirrhosis

v. GI tract:

• small intestinal obstruction (meconium ileus)

Diagnosis

i. Sweat test (elevated NaCl)
ii. DNA probes

Treatment

• Chest Physiotherapy
• Antibiotics
• Mucolytics : N-acetylcysteine
• Gene therapy

Prognosis
i. Mean survival: 30 years
ii. Most common cause of death is pulmonary infections

Anal Fissure

It is an ulcer in the longitudinal axis of the lower anal canal.

Location

• Midline posteriorly- most common (more common in males)
• Midline anteriorly- next most common (more common in females)

Causes

• Due to the curvature of the sacrum and rectum, hard fecal matter while passing down causes a tear in the anal valve leading to posterior anal fissure.
• Anterior anal fissure is common in females due to lack of support to the pelvic floor.
• Haemorrhoidectomy
• IBD- esp. chron’s disease
• STD

Pathology

• It can be acute and chronic. Fissure ends above at the dentate line.
• Acute anal fissure
• It is a deep tear in the lower anal skin with  spasm of anal sphincter with little inflammatory induration or edemaof its edges.
• Chronic anal fissure
• It has got inflamed, indurated margin with scar tissue.
• Ulcer at its inferior margin is having a skin tag, which is edematous, acts like a guard-’ Sentinel Pile’
• It can cause repeated infection-fibrosis-abscess foramtion-fistula formation.

Clinical features

• Common in middle aged women, not in elderly.
• Pain is severe in nature in acute type, whereas less severe in chronic.
• Constipation, bleeding and discharge.
• O/E
• In standing cases there may be sentinel skin tag. Sentinel skin tag + typical Hx + tightly closed, puckered anus= pathognomonic. 
• In chronic fissure, ulcer is felt with button like depression, induration and often sentinel pile.
• The lower end of the fissure can be seen by gently parting the margins of anus.
• Digital examination and proctoscopy is not possible in acute fissure in ano. 

Anal fissure

Sentinel pile

Differential Dx

• Carcinoma of anus
• Inflammatory bowel disease
• Venereal diseases
• Anal chancre
• Tuberculous ulcer
• Proctalgia fugax

Treatment

Conservative t/t

• NO- neurotransmitter that induces relaxation of the internal spchicter.
• Glyceryl trinitrate- being nitric acid donor, when applied as an ointment causes relaxation of the sphincter and also improves blood flow- both aids healing. 
• Use of laxatives and xylocaine surface anaesthetic.

Surgical

Gentle dilatation of the sphincter under GA:

• Can be used in young men with high pressure sphincter.
• CI in pts. with weak sphincter.
• If this method is ineffective or if the fissure is chronic with fibrosis, a skin tag or a mucus polyp, then surgery is done under GA(best) or LA.

Lateral anal sphincterotomy:

• Here internal sphincter is divided away from the fissure either in right or left lateral positions.
• Can be done in OPD basis under L/A.
• Healing completes in 3 wks.
• Good result for acute than chronic cases.
• Small risk of incontinence.

Closed and open

Anal advancement flap:

• Here excision of the edges of the fissure and mobilization of a square, full-thickness anal skin flap which is slided forward over the fissure and sutured in place.
• Only little risk of damage to the underlying internal sphincter and incontinence is unlikely.