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  1. Mucous cells: secrete alkaline mucus that protects the epithelium against acid.
  2. Parietal cells: secrete hydrochloric acid!
  3. Chief cells: secrete pepsin, a proteolytic enzyme
  4. G cells: secrete the hormone gastrin
  5. There are differences in the distribution of these cell types among regions of the stomach: eg, parietal cells are abundant in the glands of the body, but absent in pyloric glands.
  6. The stomach is lined by a layer of mucus, a gelatinous material composed of proteins, glycoproteins and mucopolysaccharides secreted by the surface epithelium and.
  7. The mucus appears to protect the gastric mucosa against surface injury by physical irritants, and to buffer gastric acid under basal conditions, although its effect in buffering stimulated acid secretion is negligible. The mucus layer is also important in allowing colonization by Helicobacter pylori.
  8. The vagus acts on parietal cells to stimulate acid production, and on G cells to stimulate gastrin release, in both cases via the action of acetylcholine.
  9. In addition, acetylcholine potentiates the parietal cell response to other secretagogues. Gastrin is also   released directly by exposure to peptides and amino acids, and by antral distension. 
Benign Gastric Ulcer
  1. Most common site for benign (peptic) gastric is lesser curvature near incisura angularis. (AIIMS June 04)
  2. By far the two most common cause of peptic ulcer are infection with H-pylori & certain drugs.
  3. The classical presentation of benign gastric ulcer with weight loss and indigestion made worse by eating though it is not often seen.
  4. Benign are commonest on the lesser curve away from acid-secreting epithelium.
  5. Barium meal examination showing an ulcer crater with radiating mucosal folds reaching to its rim strongly suggests that the ulcer is benign.
  6. Histologically, the intact gastric mucosa extends to the margins of the ulcer crater, the base of the ulcer consisting mainly of granulation tissue.
  7. With chronicity, fibrosis may completely replace the gastric muscle, seen then only at the margins of the lesion.
  8. Ulcers on the greater curve are more often malignant than ulcers elsewhere in the stomach, but a common benign variant is the sump ulcer, which occurs in the most dependent part of the stomach and is often associated with ingestion of anti-inflammatory drugs.
  9. Juxtapyloric ulcers are invariably benign and can be considered with duodenal ulcers, which they resemble in clinical behaviour.
Extra Edge
  1. Most common complication of chronic gastric ulcer is Massive haematemesis  (AIIMS May 11)
  2. In gastric outlet obstruction in a peptic ulcer patient the site of obstruction in most likely to be first part of duodenum. (AIPG 08, AIIMS May 09)
Gastric ulcer Duodenal ulcer
-  Atrophic gastritis                                                                                
-  H. pylori (75%)                                                                   
- Smoking, Alcohol                                                                 
-  Lower socioeconomic status                                              
-  Altered mucosal barrier function (NSAIDs)       
-  There is either normochlorhydria or achlorhydria
-  Cirrhosis                                                                                              
- Stress, anxiety: 'hurry, worry, curry'   
-  H. pylori (90%)                   
- NSAIDs, steroids                  
-  Blood group O+ve                               
-  Endocrine: Zollinger-Ellison syndrome, MEN-1, Cushing's syndrome, hyperparathyroidism           
- Alcohol, smoking, vitamin deficiency
-  Chronic pancreatitis, Cirrhosis                           
MC Site:                                                                                 
- Lesser curvature along the incisura angularis (Type 1)
MC Site:
- 1st part of duodenum (overall MC site for peptic ulcer)
Clinical features:                                                                    
- Equal in both sexes                                                             
-  Pain in the epigastrium after taking food"; relieved by vomiting
- Pain is uncommon during night                                          
- Hematemesis common                                                      
- Appetite good, but hesitant to eat as eating leads to pain
that results in loss of weight                                                
-  More common in mates                    
-  Pain in early morning, decreases after food (hunger pain)
-  Pain common during night                 
-  Melena common                                
-  Appetite good, eats more frequently and there is weight gain                                        
Features on Barium meal:                                                    
-Niche on lesser curve with notch on greater curve
- Regular/round margin of ulcer create spoke wheel pattern
- Overhanging mucosa at the margins of a benign gastric ulcer projects inwards, towards the ulcer: Hampton's Iine
- Converging mucosal folds at the base of the ulcer
- Deformed or absent duodenal cap (because of spasm)    
-  Appearance of trifoliate duodenum due to secondary duodenal diverticula                              
  1. Complications of peptic ulcer –
    1. Gastrointestinal bleeding- Most common complication of peptic ulcer
      1. Bleeding is more common in duodenal ulcers
      2. It is commonly seen in posterior duodenal ulcers because of erosion of gastroduodenal artery (PGI Dec 2000).
    2. Perforation
      1. It is the second most common complication of peptic ulcer disease.
      2. Perforation occurs commonly in the ulcers located in the anterior part of duodenum.
      3. Duodenal ulcers tend to penetrate into pancreas causing pancreatitis.
      4. Gastric ulcers tend to penetrate into left hepatic lobe.
      5. A posteriorly perforating ulcer in the pyloric antrum of the stomach is most likely to produce initial localized peritonitis or abscess formation in the Omental bursa (lesser sac) (AIPG 03)
    3. Gastric outlet obstruction
      It is the least common ulcer related complication. It is commonly associated with duodenal ulcers. Tea pot stomach is caused due to longitudinal shortening of the gastric ulcer at the lesser curvature of the stomach (it causes the stomach to look like tea pot).
  2. Type of peptic ulcer:
    1. Type I  - Ulcer along lesser curve
    2. Type II – Two ulcer present one gastric one duoden
    3. Type III -  Prepyloric ulcer
    4. Type IV – Proximal gastroesophageal ulcer
    5. Type V – Anywhere along gastric body, NSAID, induced.
Surgical Treatment Recommendations for Complications Related to Peptic Ulcer Disease
Duodenal Ulcer
  1. If the patient is known to be H. pylori–negative, presents with a chronic history, requires NSAID use, or is thought to be at risk for noncompliance with therapy, we recommend adding parietal cell vagotomy.
  2. For all perforated duodenal ulcer patients who are H. pylori–positive, documentation of H. pylori eradication with a urea breath test is mandatory, and it is paramount that the patients are compliant with their medications to treat H. pylori regardless of whether they are managed surgically or nonoperatively.
Intractable: parietal cell vagotomy
Bleeding: truncal vagotomy with pyloroplasty and oversewing of bleeding vessel
Perforation: patch closure with treatment of H. pylori with or without parietal cell vagotomy
Obstruction: rule out malignancy and parietal cell vagotomy with gastrojejunostomy

Gastric Ulcer
Perforated Gastric Ulcer
  1. Because they behave like duodenal ulcers, type II and III gastric ulcers can be simply treated with patch closure with or without truncal vagotomy and pyloroplasty, depending on the medical condition, hemodynamic status, and extent of peritonitis, followed by treatment for H. pylori. Again, this assumes that patients are H. pylori–positive
Gastric Ulcer
 a.  Type I: distal gastrectomy with Billroth I
 b.  Type II or III: distal gastrectomy with truncal vagotomy
 c.  Type I: distal gastrectomy with Billroth I
 d.  Type II or III: distal gastrectomy with truncal vagotomy
 e.   Type I, stable: distal gastrectomy with Billroth I
 f.   Type I, unstable: biopsy, patch, and treatment for H. pylori
 g.  Type II or III: patch closure with treatment of H. pylori
 h.  Obstruction: rule out malignancy and antrectomy with vagotomy
  • Type IV: depends on ulcer size, distance from the gastroesophageal junction, and degree of surrounding inflammation (see text)
  Giant gastric ulcers: distal gastrectomy, with vagotomy reserved for type II and III gastric ulcers

Forest classification for bleeding peptic ulcer
IA  - Active blood spisting
IB  - Oozing
IIA -  Visible vesseti
IIB - adherent clot
IIC - flat, pigmented shop
III - Clean base ulcer

Surgical option in the treatment of duodenal and gastric ulcer disease
Indication Duodenal Gastric
Bleeding 1. Oversewa
2. Oversew, V+D
3. V + A
1. Oversew and biopsya
2. Oversew, biopsy, V+D
3. Distal gastrectomyb
Perforation 1. Patcha
2. Patch, HSVb
3. Patch, V+D
1. Biopsy and patcha
2. Wedge excision, V+D
3. Distal gastrectomyb
Obstruction 1. HSV + GJ
2. V + A
1. Biopsy; HSV + GJ
2. Distal gastrectomyb
Intractability / nonhealing 1. HSVb
2. V+D
3. V+A
1. HSV and wedge excision
2. Distal gastrectomy
aUnless the patient is in shock or moribund, a definitive procedure should be considered.
bOperation of choice in low – risk patint.

GJ - gastrojejunostomy ; HSV = highly- selective vagotomy; V + A = vagotomy and antrectomy; V+D = vagotomy  and drainage.

Ref: Schwartz's Principles of Surgery 9th Edition Ch 26
Types of Vagotomy
Highly selective vagotomy Vagotomy and drainage Vagotomy and Antrectomy
• Procedure of choice of chronic or intractable duodenal ulcers.
• Nerves of Latarjet supplying the antrum are preserved (and hence gastric motility)
• TV is performed by division of left and right vagus nerves above the hepatic and celiac branches just above the GE junction • Procedure of choice for recurrent duodenal ulcers
• Lowest recurrence rate
  Secondary to Gastric Resection   Secondary to Gastric Reconstruction   Post-Vagotomy Syndrome
· Dumping syndrome · Afferent loop syndrome · Post-vagotomy diarrhea
· Metabolic disturbances · Efferent loop obstruction · Post-vagotomy gastric atony
    · Alkaline reflux gastritis · Incomplete vagal transection
    · Retained antrum? syndrome    

Metabolic Complications After Gastrectomy
  • Metabolic complications are more common and serious after partial gastrectomy than after vagotomy.
  • More common in Billroth II >Billroth I procedure
  • Severity is directly related to the extent of gastric resection
  • Me metabolic defect appearing after gastrectomy: Anemia
  • Me metabolic defect appearing after gastrectomy: Anemia
  • Iron deficiency anemia (IDA) is more common than vitamin B12 deficiency anemia.


Gastritis - inflammation of the gastric mucosa - has 3 basic patterns - acute, chronic, and special.
  1. Acute Gastritis
    1. Acute gastritis is often the result of toxic injury by drugs such as nonsteroidal anti-inflammatory agents or alcohol, and is frequently seen in the seriously ill patient.
    2. The most important clinical feature is gastrointestinal haemorrhage, which may be both generalized and profuse.
    3. Radiology is helpful only if a double contrast technique is used; it may then show small, shallow erosions in which a central pit of barium is surrounded by a lucent halo.
    4. Endoscopically, lesions appear as multiple haemorrhagic spots with small superficial erosions against a background of hyperaemia.
    5. Acute gastritis can be broken down into the following additional categories: erosive (eg, hemorrhagic  erosions, superficial erosions, deep erosions) and nonerosive (generally caused by H pylori).
    6. Acute gastritis has a number of causes, including certain drugs (Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen, and naproxen); alcohol; bacterial (H pylori gastritis typically starts in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa.
    7. It is also responsible for as many as 80% of gastric ulcers and is associated with a transient increase in gastric acid secretion), viral (Cytomegalovirus can cause gastritis in immunocompromised, who have had a transplant, and even in immunocompetent.
    8. Gastric-fold thickening may be confined to the antrum), and fungal infections(Candida albicans and histoplasmosis. C albicans rarely involves the gastric mucosa); acute stress (shock); radiation; and direct trauma.
  • Important Components and Mediators of Mucosal Defenses in the Stomach
  1. Mucosal defense
  1. Mucous barrier                                                   
  2. Bicarbonate secretion
  3. Epithelial barrier                                                 
  4. Hydrophobic phospholipids
  5. Tight junctions                                                     
  6. Restitution
  7. Microcirculation (reactive hyperemia)                           
  8. Afferent sensory neuro
  1. Mediators
    1. Prostaglandins                                                                     
    2. Nitric oxide
    3. Epidermal growth factor                                                    
    4. Calcitonin gene-related peptide
    5. Hepatocyte growth factor                                
    6. Histamine
    7. Gastrin-releasing peptide
  • Indication of CX:-
  1. To deal with complication                                                 
  2. Obstruction that fails to respond to drug
  3. Two or more major episodes of bleeding or recur.     
  4. Gastric ulcer suspected of being conscious
    Ref: Schwartz's Principles of Surgery 9th Edition Ch 26
  • Treatment: Medical Care:
  1. Treatment is dependent on the pathology and cause of gastritis.
  2. No specific therapy is indicated. Discontinue use of drugs known to cause gastritis, eg, NSAIDs and  alcohol.
  3. Surgical Care: Surgical intervention is rarely needed for phlegmonous gastritis.
  1. Chronic Gastritis
    1. Chronic atrophic gastritis, which usually spares the antrum, is associated with parietal cell antibodies, reduced secretion of acid and intrinsic factor, and hence with pernicious anaemia and other autoimmune disorders.
    2. By contrast, in chronic gastritis associated with Helicobacter pylori infection, activity is maximal in the antrum, acid secretion is not much affected, and B12 malabsorption is not found.
  2. Special forms of Gastritis
    1. Eosinophilic gastritis affects the distal stomach. Dyspepsia is common, and thickened antral folds may cause pyloric obstruction. Bleeding, protein-losing enteropathy, and eosinophilic ascites are also described. Other sites in the gastrointestinal tract may also be affected, and peripheral eosinophilia is usually present.
    2. The diagnosis is generally made from gastric histology; the changes are most marked in the antrum, where there is submucosal oedema and a variable eosinophilic infiltrate.
    3. Granulomatous gastritis is a diagnosis of exclusion. Macroscopically there may be ulceration, infiltration, and thickening of the mucosa responsible for pyloric narrowing, or changes resembling linitis plastica.
    4. Giant-cell granulomas within the mucosa - with or without an associated gastritis - are seen histologically. 

NIH Consensus Panel Recommendations for Helicobacter pylori Treatment
Patients with active peptic ulcer disease who are H. pylori positive
   Use of nonsteroidal anti-inflammatory drugs should not alter treatment.
Document eradication in those with complications.
Ulcer patients in remission who are H. pylori positive, including patients on maintenance H2-receptor antagonist therapy
H. pylori–positive patients with mucosa-associated lymphoid tissue (MALT) lymphoma
Controversial issues in H. pylori–positive patients
First-degree relatives of gastric cancer patients
Immigrants from countries with high prevalence of gastric cancer
Individuals with gastric cancer precursor lesions (intestinal metaplasia)
Non–ulcer dyspepsia patients who insist on eradication (benefit vs. risk)
Patients on long-term antisecretory therapy for reflux disease
Ref: Sabiston Textbook of Surgery, 18th Edition Ch 47

Gastric Polyps
  1. Gastric polyps may be hamartomatous and, regenerative or hyperplastic, or true neoplasms (adenomas).
  2. It is probably only the adenoma that have malignant potential, with a higher risk when multiple and diameter exceeds 2cm.
  3. Barium studies demonstrate apparently translucent filling defects.
  4. Endoscopy, adenomatous polyps are more obviously distinct from surrounding mucosa than the commoner hyperplastic type.
  5. Polyps in the duodenum are common in familial adenomatous polyposis, but unusual proximal to the ampulla of Vater.
Important Most Common Sites
· Gastric ulcer  Lesser curvature (near incisura angularis)
· Peptic ulcer  1st  part of duodenum
· Gastric outlet obstruction  
· Small bowel adenocarcinoma  Duodenum
· Atresia  
· Polyps in PJS  Jejunum
· Pneumatosis intestinalis  
Menetrier's Disease (Hypoproteinemic Hypertrophic Gastropathy)
  • A rare, acquired, premalignant disease, of unknown cause
  • Characterized by massive gastric folds in the fundus and corpus of the stomach, giving the mucosa a cobblestone or cerebriform appearances.
  • Associated with CMV infection in children and H. pylori infection in adults.
  • Foveolar hyperplasia (expansion of surface mucous cells) with absent parietal cells.
  • Increased TGF-alpha has been noted in the gastric mucosa - Associated with protein loss from the stomach, excessive mucus production, and hypochlorhydria or achlorhydria. 
Clinical Features:
  • Epigastric pain, vomiting, weight loss, anorexia, and peripheral edema.
  • Typical gastric mucosal changes can be detected by radiographic or endoscopic examination.
  • Biopsy should be performed to rule out gastric carcinoma or lymphoma,
  • Twenty-four-hour pH monitoring reveals hypochlorhydria or achlorhydria
  • Chromium-labeled albumin test reveals increased GI protein 10ss.
  • Medical treatment is limited to albumin replacement and maintenance of adequate nutrition, acid suppression, octreotide and H. pylori eradication,
  • Total gastrectomy for bleeding, severe hypoproteinemia or cancers.
Gastric Carcinoma
  1. About 85% of stomach cancers are adenocarcinomas, with 15% due to lymphomas and gastrointestinal stromal tumors (GIST) and leiomyosarcomas.
  2. 30% of gastric cancers originate in the distal stomach, ~20% arise in the midportion of the stomach, and ~37% originate in the proximal third of the stomach. The remaining 13% involve the entire stomach.
  3. Primary lymphoma of the stomach is relatively uncommon, accounting for <15% of gastric malignancies and ~2% of all lymphomas.
  4. The stomach is, however, the most frequent extranodal site for lymphoma, and gastric lymphoma has increased in frequency during the past 30 years.
  5. Gastric cancer is the second most common cause of cancer-related death in the world.
  6. The site of the lesion is classified based on the long axis of the stomach.
  7. Gastric cancer afflicts slightly more men than women.
  8. The median age at diagnosis is 65 years (range 40-70 y).
  9. Genetic factor – 10% familial,  Mutation in E-cadherin gene detected in 50% of diffuse type gastric cancer
  10. Clinical features:-
    1. Most common presentation asymptomatic or non specific symptoms
    2. All physical signs are late events. Signs may include a palpable enlarged stomach with succussion splash; primary mass (rare); and enlarged liver, Virchow node's (ie, left supraclavicular), Sister Mary Joseph's node, and Blumer's shelf, Left anterior axillarylymph node (Irish node)
    3. Some patients have weight loss. Other patients may have pallor from bleeding and anemia.
    4. Pareneo plastic syndrome – Dermatomyositis, a cantharis nigricans, peripheral thrombophlebitis, 
Extra Edge:
Carcinoma Stomach
  • H. pylori infection increases risk of gastric cancer by causing chronic gastritis, loss of gastric acidity and bacterial growth in stomach.
  • Gastrectomy can be total or subtotal in D2 gastrectomy .
  • Patient with incurable disease are not subjected to radical surgery. Treatment is palliative systemic chemotherapy.
  • After gastrectomy, there is loss of parietal cell mass leads to vitamin B'2 deficiency and replacement should be given routinely.
  • MC symptom of carcinoma stomach is abdominal pain >weight loss.
  • Hematemesis is very rare in carcinoma stomach.
Risk factors Precursor states
Diet low in Vitamin C
Blood group A (Controversial)
Pernicious anaemia
Post gastrectomy
Radiation expensive &  Obesity
Helicobacter pylori infection - strongest risk factor
    Atrophic gastritis
Intestinal metaplasia
Gastric dysplasia
Gastric polyps

Micro angioplastic hemolytic anemia.

Lauren’s classification
  1. Intestinal type I
    Epidemic type associated with chronic   
    Little massiveness
    Sharp margin
    Better prognosis
    No familial history
  2. Diffuse type II(Associated with genetic, younger age)
    Endemic cancer atrophic gastritis
    Scaffered cell cluster with poor deferential
    Dangerously decipher margin
    Invade larger area of stomach (so called limitis plestica or leather bottle appearance
    More prevalent in women
    Poor pragnosis
Differentiating points between:
  Intestinal Type Diffuse Type
1 Environmental Familial
2 Gastric atrophy, intestinal metaplasia Blood type A
3 Men >women Women >men
4 Increasing incidence with age Younger age group
5 Gland formation Poorly differentiated, signet ring cells
6 Hematogenous spread Transmural/lymphatic spread
7 Microsatellite instability Decreased E-cadherin
8 APC gene mutations  -
9 p53, p16 inactivation p53, p16 inactivation
  1. The Borrmann classification system was developed in 1926 and remains useful today for the description of endoscopic findings.
  2. The Borrmann system divides gastric carcinoma into five types depending on the lesion's macroscopic appearance.
  3. Borrmann type 1 represents polypoid or fungating lesions; type 2, ulcerating lesions surrounded by elevated borders; type 3, ulcerating lesions with infiltration into the gastric wall; type 4, diffusely infiltrating lesions; and type 5, lesions that do not fit into any of the other categories. Linitis plastica is the term to describe type 4 carcinoma when it involves the entire stomach.
Gastric Carcinogenesis

  1. Causes:
    Several factors are implicated in the development of gastric cancer, including diet, Helicobacter pylori infection (Helicobacter pylori infection is associated with chronic atrophic gastritis, and patients with a history of prolonged gastritishave a 6-fold increase in their risk of developing gastric cancer), previous gastric surgery, pernicious anemia, adenomatous polyps, chronic atrophic gastritis, genetic factors, and previous radiation therapy.
  2. Imaging Studies:
    1. Esophagastroduodenoscopy and biopsy is investigation of choice:
    2. Double-contrast upper GI series: An upper gastrointestinal barium swallow detects large primary tumors but only occasionally detects their spread to the esophagus and duodenum (particularly if the tumor is small and submucosal).
    3. Chest radiograph evaluates for metastatic lesions.
    4. CE CT is the radiological investigation of choice.
    5. Endoscopic ultrasound – allows most precise assessment of the T stage of tumor or deapth of lesion (More sensitive and specific than CE CT).
    6. PET CT – Most sensitive and specific radiological investigation for gastric cancer staging.
    7. Staging of Gastric – best done by Laproscopy (Most sensitive and specific for peritoneal and omental deposit)
    8. CEA is increased iv 45 – 50%      
  3. Histologic Findings:
    Adenocarcinoma of the stomach comprises between 90-95% of all gastric malignancies. The second most common malignancies are lymphomas. Leiomyosarcomas (2%), carcinoids (1%), adenoacanthomas (1%), and squamous cell carcinomas (1%) are the remaining histologies. 
  1. Factor Biomarkers for diagnosis & prognosis of gastric cancer
    1. CEA
    2. CA – 125, CA 19 – 9, Alpha – Jehimoter
    3. Serum pepsinogen I (Predictor of stomach cancer)
    4. Proteases (Pepsinogenic, plasminogen ochvotor)
    5. Cathedrin, mucin, CD-44 (related to invesion / metastosis)
  2. Prognostic factor
    1. Two important factor are deptic of invasion and presence or absence of regional LN
    2. Linitions plastina
    3. Margins pusitive associated with poor prognosis.
      Staging: 1997 TNM classification system (AJCC) for staging gastric carcinoma.
Primary tumor Regional lymph nodes Distant metastasis
TX = primary tumor (T) cannot be assessed
T0 = no evidence of primary tumor
Tis = carcinoma in situ, intraepithelial tumor without invasion of lamina propria
T1 = tumor invades lamina propria or submucosa
T2 = tumor invades the muscularis propria or subserosa
T3 = tumor penetrates serosa (ie, visceral peritoneum) without invasion of adjacent structures
T4 = tumor invades adjacent structures
NX = regional lymph nodes (N) cannot be assessed
N0 = no regional lymph node metastases
N1 = metastasis in 1-6 regional lymph nodes
N2 = metastasis in 7-15 regional lymph nodes
N3 = metastasis in more than 15 regional lymph nodes
MX = distant metastasis (M) cannot be assessed
M0 = no distant metastasis
M1 = distant metastasis
Stage T N M
0 Tis N0 M0
IA T1 N0 M0
T1 N1 M0
T2 N0 M0
T1 N2 M0
T2 N1 M0
T3 N0 M0
T2 N2 M0
T3 N1 M0
T4 N0 M0
T4 N1–3 M0
T1–3 N3 M0
Any T Any N M1

Tis Carcinoma in situ; Intraepithelial tumor without invasion of lamina propria
Ref: Schwartz's Principles of Surgery 9th Edition
  1. Treatment:
    1. Surgery is the only prospective of cure
    2. Extent of resection is to maintain a 5 cm margin proximally & 2 cm distally to primary lesion.
    3. Subtotal gastrectomy for tumors of distal esophagogactrectomy for tumors of cardia & GE total gastrectomy (if required for negative margin, finites plasma with pervious aeremia)
    4. A tumour is considered resectable if confined to stomach or N1 or N2 nodes involved Nodes less than 3 cm from tumour = N1 nodes
    5. Nodes along hepatic artery asplenic left gastric & celier artery)
      1. If tumour and N1 nodes resected = D1 gastrectomy
      2. If tumour and N2 nodes resected = D2 gastrectomy
    6. Evidence to support the use of D2 gastrectomy is incomplete & D2 gastrectomy associated with increased post-operative mortality and complications
    7. Even in patients with incurable disease surgery may palliate symptoms
    8. Results from adjuvant chemotherapy post surgery are disappointing though Chemoradiotherapy may reduce relapse and improve survival
Recent Advances
  1. Oral fluoro pyrimidine S-1 alone & with cisplatin
  2. S-1 with tegafur (Prodrug of 5-FU)
  3. Oxiliplatin and irinotecan gave promising result
  4. BEVACIZUMAB, monoclonal antibody is currently bens evaluated
  5. Phase III performed with demonstrable survival benefit associated with post operative chemo radio therapy.
  6. Patients with I3 or N+ adenocarcinoma who received adjuvant chemo radio demonstrated improved disease free survival & overall & survival rate.
  7. Adjuvant therapy
    1. The pattern of failure prompted a number of investigations into adjuvant therapy. The rationale behind radiotherapy is to provide additional local-regional tumor control. Adjuvant chemotherapy is used either as a radiosensitizer or as definitive treatment for presumed systemic metastases.
    2. Adjuvant radiotherapy
      1. Moertel and colleagues randomized postoperative patients with advanced gastric cancer to 40 Gy radiotherapy or 40 Gy radiotherapy with 5-FU as a radiosensitizer, and demonstrated improved survival associated with the combined modality therapy.
      2. A series from the Mayo Clinic randomized patients to postoperative radiotherapy with 5-FU versus surgery alone and demonstrated improved survival in the patients receiving adjuvant therapy (23% vs 4%).
    3. Intraoperative radiotherapy
      1. Some centers suggest that intraoperative radiotherapy (IORT) shows promising results.
      2. The National Cancer Institute randomized patients with grossly resected stage III/IV gastric cancer to either 20 Gy IORT or 50 Gy postoperative external beam.
  8. Chemotherapy
    The most widely studied regimen is 5-fluorouracil, doxorubicin, and mitomycin C.
  9. Survival
    1. Prognosis if generally very poor
    2. Overall 5 year survival is approximately 5%
    3. Survival is 70%, 32%, 10% and 3% for Stages 1,2,3 and 4 respectively
Other gastric tumours
GIST (Leiomyoma and leiomyosarcoma)
  1. Most common site of GIST is stomach.
  2. Originate from C-kit receptor of tyrosin kinase (Intertitial cells of Cazal).
  1. Leiomyoma:
    1. Leiomyomas are the commonest benign tumours of the stomach.
    2. They arise from the gastric smooth muscle, and, because they are submucosal and rarely impinge on the lumen, are frequently asymptomatic though may present with haemorrhage; endoscopic ultrasound is ideal investigation when asymptomatic.
  2. Leiomyosarcoma
    1. Accounts for 2-3% of all gastric tumours
    2. Arises from the smooth muscle of the stomach wall
    3. Lymphatic spread is rare
    4. 75% present with an upper gastrointestinal bleed
    5. 60% have palpable abdominal mass
    6. Diagnosis can be confirmed by endoscopy and biopsy.
    7. If upper GI endoscopy and biopsy is inconclusive than need EUS guided biopsy.
    8. Treatment of choice D1 gastrectomy
    9. Adjuvent treatment or palliative treatment with imatinive.
    10. 5-year survival is approximately 50%
  3. Other Gastric Neoplasms
    1. The stomach is an occasional site for metastatic spread, usually from an adenocarcinoma of origin in the pancreas, ovary or breast. Other, non-epithelial, tumours, such as lipomas, neural sheath tumours, and gastric carcinoids, are also seen.
    2. Gastric involvement with Kaposi's sarcoma is not infrequently seen in AIDS patients (particularly in the homosexual community).
    3. The histological appearance of deep endoscopic biopsies is similar to that of Kaposi's at other gastrointestinal sites.
    4. Ectopic islands of pancreatic tissue may be recognized endoscopically- confusion with neoplasia is readily overcome by biopsy, which reveals normal pancreatic histology.
    5. Gastric xanthoma is unlikely to be confused with more sinister pathology.
  4. Gastric lymphoma
    1. Stomach is the commonest extranodal primary site for non-Hodgkin's lymphoma
    2. Accounts for approximately 1% of gastric malignancies
    3. Clinically presents similar to gastric carcinoma
    4. 70% of tumours are resectable
    5. 5-year survival is approximately 25%
    6. Both adjuvant radiotherapy and chemotherapy may be useful
    7. Gastric lymphoma may be an isolated lesion or part of a disseminated process; it is being seen with increased frequency in AIDS.
      1. Malignant lymphomas of mucosa-associated lymphoid tissue (MALTomas), comprising diffuse sheets of maturing lymphocytes are the most common, but the full range of cytological patterns may occur, including Hodgkin's disease.
      2. A rare form of 'so-called' benign, follicular, lymphoid hyperplasia (pseudolymphoma) has now been shown by immunocytochemistry to be monoclonal and hence a true lymphoma
  • Treatment:
  1. Antibiotic to treat H. pylon regression of 75% MALT lymphomas should be given before surgery, radiation or chemotherapy.
  2. Subtotal gastrectomy followed by combination chemotherapy for localized high grade tumors or gastric outlet obstruction.
  3. Combination chemotherapy is option of choice.
  4. Radiation therapy is a adjuvant treatment.  
  1. Trichobezoars, composed of hair, occur most commonly in pediatric (9 – 12 years), Psychiatric female, who swallow their hair.
  2. Bezoars are concretions of undigestible matter that accumulate in the stomach.
  3. Phytobezoars are composed of vegetable matter and, are usually seen in association with gastroparesis or gastric outlet obstruction.
  4. They also are associated with persimmon ingestion. Most commonly, bezoars produce obstructive symptoms, but they may cause ulceration and bleeding.
  5. Diagnosis is suggested by upper GI series and confirmed by endoscopy. Treatment options include enzyme therapy (papain, cellulase, or acetylcysteine), endoscopic disruption and removal, or surgical removal.
Congenital Hypertrophic Pyloric Stenosis
  1. This condition is second only to inguinal hernia as a reason for surgical intervention during the first year of life.
    Visible gastric contractions occurring from left to right.
  2. Results in hypertrophy and hyperplasia of pyloric sphincter in neonatal period
  3. Mainly affects circular muscle fibres of pylorus
  4. Pylorus becomes elongated and thickened (? Due to failure of nitric oxide synthesis)
  5. Results in gastric outflow obstruction, vomiting and dehydration
  6. Affects 3 per 1000 live births
  7. Male : female 4:1. Most common in first born males
  8. Usually presents between 3 and 6 weeks of age
  9. Child hungry and often feeds immediately after vomiting
  10. Metabolic abnormality a hypochloraemic, hypokalemic metabolic alkalosis with Paradoxical aciduria and kaleuria.
  11. Non-bilious vomiting, associated with weight loss and dehydration, are typical.
  12. The upper abdomen may be distended with visible gastric peristalsis and a palpable lump representing the hypertrophied pylorus (palpation of typical olive in right upper quandeant)
  13. Confirmation of the diagnosis is by ultrasound scanning.  Identification of sausage shaped mass, muscle thickness greater than 4 mm & a length more than 16 mm.
  14. At laparotomy, pyloromyotomy (Ramstedt's operation) procedure of choice (Laproscopy is a preferred option).
  15. Associated anomalies include hiatal & inguinal hernia (most common), other include congenital heart disease, esophageal atresia, TOF, turner syndome.
Gastric Outlet Obstruction
Clinical entities that can result in GOO generally are categorized into 2 groups of causes—benign and malignant.
  1. Etiology:
    1. The major benign causes of GOO are PUD, gastric polyps pyloric stenosis, congenital duodenal   webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars.
    2. Within the pediatric population, pyloric stenosis constitutes the most important cause of GOO.
    3. Pancreatic cancer is the most common malignancy causing GOO (may occur in 10-20% of pancreati carcinoma).
    4. Other tumors that may obstruct the gastric outlet include ampullary cancer, duodenal cancer,  cholangio carcinomas, and gastric cancer.
  2. Clinical Feature:
    1. Nausea and vomiting, usually nonbilious, and it characteristically contains undigested food particles.
    2. Early satiety and epigastric fullness are common. Weight loss is frequent. Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer.
    3. Physical examination demonstrates the presence of chronic dehydration and malnutrition. A dilated stomach may be appreciated as a tympanitic mass in the epigastric area.
    4. Patients with GOO due to benign ulcer disease may be treated medically if results of imaging studies or endoscopy determine that acute inflammation and edema are the principle causes of the outlet obstruction (as opposed to scarring and fibrosis, which may be fixed).
    5. If medical therapy conducted for a reasonable period fails to alleviate the obstruction, then surgical intervention becomes appropriate.
    6. The choice of surgical procedure is vagotomy and antrectomy, against which the efficacy of other procedures should be measured.
Metabolic Effects: The vomiting of hydrochloric acid results in hypochloremic alkolosis.
  1. Diagnostic Procedures:
    1. Upper endoscopy can help visualize the gastric outlet and may provide a tissue diagnosis when the obstruction is intraluminal.
    2. Nuclear gastric emptying studies measure the passage of orally administered radionuclide over time.
    3. Unfortunately, both the nuclear test and saline load test may produce abnormal results in functional states.        
    4. Barium upper GI studies are very helpful because they can delineate the gastric silhouette and demonstrate the site of obstruction.
  2. Treatment
    1.  Medical therapy:
      1. Initial management of GOO should be the same regardless of the primary cause i.e. hydration and correction of electrolyte abnormalities. Sodium chloride solution should be the initial IV fluid of choice.
      2.  Potassium deficits are corrected after repletion of volume status, and after the chloride has been replaced.
    2. Surgical therapy:
      1. Management of benign disease: The most common surgical procedures performed for GOO related to PUD are vagotomy and antrectomy, vagotomy and pyloroplasty, truncal vagotomy and astrojejunostomy, pyloroplasty, and laparoscopic variants of the aforementioned procedures.
      2. Of these, vagotomy and antrectomy with Billroth II reconstruction (gastrojejunostomy) seems to offer the best results.
    3. Management of malignant disease
      1. Of patients with periampullary cancer, 30-50% present with nausea and vomiting at the time of diagnosis.
      2. Most of these tumors are unresectable (approximately 40% of the gastric cancers and 80-90% of the periampullary cancers).
      3. Gastrojejunostomy remains the surgical treatment of choice for GOO secondary to malignancy.
      4. Traditionally an antecolic anastomosis has been performed to prevent further obstruction by advancing tumor growth, recent studies favours retrocolic anastomosis.
Gastric Volvulus
  1. Gastric volvulus is defined as an abnormal rotation of the stomach of more than 180°, creating a closed loop obstruction that can result in incarceration and strangulation.
  2. According to the axis of rotation, gastric volvulus is classified into the following:
    1. Organo-axial: The stomach rotates around an axis that connects the gastroesophageal junction and the pylorus. This is the most common type in both children and adults. It is usually associated with diaphragmatic defects. Strangulation and necrosis occurs commonly with this type and has been reported in 5-28% of cases.
  3. Mesenterico-axial: Here the axis bisects both the lesser and greater curvatures.The antrum rotates anteriorly and superiorly so that the posterior surface of the stomach lies anteriorly. The rotation is usually incomplete and occurs intermittently. Vascular compromise is uncommon. This type usually presents without diaphragmatic defects and usually manifests with chronic symptoms.
  4. Combined: This is a rare form in which the stomach twists both mesentero- and organo-axially and usually is seen in patients with chronic volvulus.
  5. Etiology: According to etiology, gastric volvulus can be classified as either type 1 or 2.
Type 1, or idiopathic:
  1. The most common cause of gastric volvulus in adults is diaphragmatic defects. In cases of paraesophageal hernias, the gastroesophageal junction remains in the abdomen while the stomach ascends adjacent to the esophagus, resulting in an upside-down stomach.
  2. Gastric volvulus is the most common complication of paraesophageal hernias.
Acute gastric volvulus
  1. Intra-abdominal gastric volvulus presents most commonly with the sudden onset of severe epigastric or left upper quadrant pain.
  2. Borchardt’s triad (pain, retching, and inability to pass a nasogastric tube) is diagnostic of acute volvulus and has been reported to occur in 70% of cases.
Chronic gastric volvulus
  1. Intermittent epigastric pain and abdominal fullness following meals.
  2. Early satiety, dyspnea, and chest discomfort.
  3. Dysphagia may occur if the gastroesophageal junction is distorted.
Imaging Studies:
  1. Chest x-ray: A retrocardiac gas-filled viscus in cases of intrathoracic stomach confirms the diagnosis.
  2. Plain abdominal radiograph reveals a massively distended viscus in the upper abdomen.
  3. Barium study may be valuable in chronic volvulus with the stomach lying horizontal or upside down.
  4. CT scan is imaging modality of choice.

Medical therapy: endoscopic reduction can be attempted in selected cases.
  1. Surgicaltherapy:
    Emergent surgical intervention is indicated for acute gastric volvulus. With chronic gastric volvulus, surgery is performed to prevent complications.
  2. The strategy of surgery is as follows:
    1. Reduction of the volvulus
    2. Assessment of gastric viability with resection of the gangrenous portions by segmental, subtotal, or total gastrectomy
    3. Prevention of recurrence by anterior gastropexy, which is most often accomplished with a gastrostomy Tube
  1. Strangulation and necrosis occur most commonly with organo-axial gastric volvulus and occur in 5-28% of cases.
  2. Gastric perforation occurs secondary to ischemia and necrosis. It can also complicate endoscopic reduction.
Gall bladder and bileducts
  1. The common hepatic duct is formed by right and left hepatic ducts at porta hepatis.
  2. The cystic duct joins the common hepatic duct to form the CBD, which enters the 2nd part of duodenum together with the pancreatic duct in the ampulla of Vater.Q
  3. The gall bladder is usually a pear-shaped sac,8-10cm long with a capacity of about 50ml. It is divided into a neck, body and fundus.
  4. The mucosa comprises tall columnar epithelium which is thrown into simple folds.
  5. In the neck of the gall bladder is a small pouch (Hartmann's pouch) which is particularly marked in pathological states, and it is here that stones commonly impact.
  6. The normal gall bladder contracts following fat ingestion. 
  1. Cholelithiasis is the presence of gallstones in the gallbladder.
  2. The spectrum of gallbladder disease ranges from asymptomatic gallstones to gallbladder colic, cholecystitis, choledocholithiasis, and cholangitis. Gallbladder colic is pain caused by a stone temporarily obstructing the cystic duct or common bile duct (CBD).
  3. Cholecystitis is inflammation of the gallbladder from obstruction of the cystic duct or CBD (choledocholithiasis). Cholangitis is infection of the biliary tree.
Risk Factors for Gallstones (Ref: Sabiston Textbook of Surgery, 18th Edition Ch 54)
  1. Obesity (B ml>30)                                      
  2. Rapid weight loss kg/m2                           
  3. Childbearing                                                
  4. Multiparity
  5. Female sex
  6. First-degree relatives
  7. Drugs: ceftriaxone, postmenopausal estrogens, total parenteral nutrition Ileal disease, resection or  bypass
  8. Increasing age
  9. Heal disease, by pass arresection
  10. ethnicity: Native American(Pima Indian),Scandinarian.
  11. hereditary spherocytosis, sickle cell disease,thalessemia.
  1. Pathophysiology
    Three types of gallstones exist. They are
    1. Mixed stones. (commonest)
    2. Cholesterol (commonest in western country)       
    3. Black stone – More common haemolytic anemia.                
    4. Brown stone – Infected stone (Most common E. coli)
      1. Cholesterol stones: Normally, bile acids, lecithin, and phospholipids help to maintain cholesterol as a solute.
      2. When bile is supersaturated with cholesterol, it crystallizes and forms a nidus for stone formation.
      3. Calcium and pigment also may be incorporated in the stone.
      4. Pigment stones: Pigment stones, which comprise 15% of gallstones, are formed by the crystallization of calcium bilirubinate.
      5. Diseases that lead to increased destruction of red blood cells (hemolysis), abnormal metabolism of hemoglobin (cirrhosis), or infections (including parasitic) predispose people to pigment stones. Black stones are found in people with hemolytic disorders.
      6. Brown stones are found in the intrahepatic or extrahepatic duct and are associated with infection in the gallbladder.
      7. History: The 3 clinical stages of gallstones are asymptomatic, symptomatic, and with complications (eg, cholecystitis, choledocholithiasis, cholangitis).
      8. Most gallstones (60-80%) are asymptomatic. A history of epigastric pain with radiation to the shoulder may suggest symptomatic cholelithiasis.
      9. Most patients develop symptoms prior to complications. The best definition of biliary colic is pain that is relatively severe right upper quadrant that lasts 1-5 hours, with radiation to shoulder or back.
      10. Associated symptoms are nausea, vomiting, or referred pain.
  2. Imaging Studies:
    Abdominal ultrasound – Gold standard for GB calculi.
    Asymptomatic gallstones usually are observed incidentally on an x-ray,  or CT scan while imaging for other reasons.
    1. 20% of stones are radiopaque and visible on x-rays. Calcium or pigmented stones are more likely to be observed on x-rays. A porcelain gallbladder is seen on plain films
    2. Investigation of choice is Ultrasound: Ultrasound is 98% sensitive for gallstones. Cholecystitis is diagnosed sonographically by gallbladder wall thickening (> 2-4 mm), gallbladder distention (diameter > 4 cm, length > 10 cm), pericholecystic fluid from perforation or exudate, and sonographic Murphy sign (pain when a probe is pushed directly on the gallbladder).
    3. Most sensitive investigation for cholecystitis is HIDA scan.
  3. Treatment:
    1. In people with symptomatic gallstones, discuss the option of elective surgery with the patient.
    2. Diabetic persons and pregnant women should have close follow-up to determine if they become symptomatic or develop complications.
    3. Patients with a calcified or porcelain gallbladder should consider cholecystectomy due to the increased risk of  carcinoma (25%).
  4. Medication: Dissolution of small gallstones is possible with 6-12 months of therapy; however, recurrence is approximately 50%. Bile acid therapy consists of ursodeoxycholic acid sometimes in combination with chenodeoxycholic acid.
  • Prerequisite for medical therapy
  1. RadioLucent stone <1cm
  2. Functioning gall bladder
  3. Non acute symptoms
Gall Stones
  1. Translucent Stones: Over 80% of gall stones are radiolucent as they contain too little calcium to render  them visible on a plain X-ray. Oral cholecystogram is only successful if the gall bladder function is good enough to concentrate contrast media.
  2. Ultrasound is technique of choice as it is quick, accurate, safe and noninvasive. Stones are diagnosed by the accoustic shadow. ERCP may also be used to demonstrate gallstones, but it is not usually employed unless bile duct calculi are suspected.
  3. Bile Duct Stones: Although valuable as a means of detecting bile duct dilatation, ultrasound is a very much less reliable technique for identifying calculi within the common bile duct.
  4. PTC or ERCP/ MRCP is the preferred techniques. Intravenous cholangiography is no longer recommended for investigating bile duct stones.
Indications of preoperative ERCP
  1. Recent jaundice                                                                  
  2. Abnormal liver function rest
  3. Dilated common bile duct                                                    
  4. USG suspicion of bile duct stones.
  1. Clinical presentations & complication

    1. Acute cholecystitis
    2. Mucocele of gall bladder
    3. Empyema of gall bladder
    4. Perforation of gall bladder
    5. Mirizzi’s syndrome
    6. Obstructive jaundice
    7. Cholangitis
    8. Pancreatitis
    9. Gall stone lens
    10. Carcinoma gall bladder
Extra Edge:  Mercedes benz sign or seaguu sign
The centre of gall stone may contain radiolucent gas in a triradiate or biradiate fissure, this gives rise to characteristic dark shapes on radiograph, the Mercedes Benz sign or Seagull sign.
Extra Edge:
In USA and Europe, 80% are cholesterol or mixed stones, whereas in Asia, 80% are pigment stones
  • MC gall stone: Mixed (90%)
  • MC gall stones in USA and Europe: Cholesterol stones (Mixed, if given in the option)
  • MC gall stones in India (Asia): Pigment stones (80%)
Classification of Gallstones
  Cholesterol Black pigment Brown pigment
Location Gall bladder and bile duct  Gall bladder and bile duct  Bile ducts
Major constituent Cholesterol  Bilirubin pigment polymer  Calcium bilirubinate
Consistency Crystalline with nucleus  Hard  Soft, friable
% Radio-opaque 15%  60%  0%
Effects and Complications of Gall Stones
In Gall Bladder In Bile duct In Intestine
· Silent stones · Obstructive jaundice . Gall stone ileus
· Acute cholecystitis · Cholangitis    
· Chronic cholecystitis · Acute pancreatitis    
· Mucocele        
· Empyema        
· Perforation        
· Gangrene        
· Carcinoma        

Extra Edge:
  1. Bouveret's Syndrome
    • Duodenal obstruction due to gall stones, usually in the bulb is known as Bouveret's syndromes.
    • It is treated by duodenostomy or pyloroplasty.
  2. Gall stone ileus - Most patients in gall stone ileus are unstable to withstand a prolonged operative procedure, so cholecystectomy should not be done in same episode.
  3. Fistula can be addressed at a second laparotomy
  1. Treatment of Gall Stones
    • Laparoscopic cholecystectomy is treatment of choice if in acute cholecystitis if presented within 72 hrs.
    • If presentation after 72 hours of acute cholecystitis managed by conservative treatment followed by laproscopic cholecystectomy after 4-6 week.
Indications for Cholecystectomy Ref: Sabiston Textbook of Surgery, 18th Edition Ch 54
        a. Acute cholecystitis
        b. Emphysematous cholecystitis
        c. Empyema of the gallbladder
        d. Perforation of the gallbladder
        e. Previous choledocholithiasis with endoscopic duct clearance
        a. Biliary dyskinesia
        b. Chronic cholecystitis
        c. Symptomatic cholelithiasis
* Within 24 to 72 hours.

  1. Most common presenting symptom is upper abdominal pain radiating to tip right scapula.
  2. Most commonly associated bacteria with cholecystitis module E. coli & bacteroids
  3. Stones in the gall bladder can cause either acute or chronic cholecystitis. Occasionally, the cystic duct is blocked by a stone, following which the gall bladder is distended by white mucus and gives rise to a mucocoele.
  4. The histological appearances of the gall bladder in acute cholecystitis may range from acute inflammatory changes to widespread haemorrhagic necrosis. In chronic cholecystitis, the gall bladder is thickenedand degree of inflammation is variable.
  5. Cholesterolosis of the gall bladder is an uncommon condition in which yellow flecks are seen over the mucosal surface, giving an appearance known as the strawberry gall bladder.
  6. This is due to large numbers of foamy macrophages in the mucosa andd is a benign asymptomatic abnormality.
Limey Bile and Porcelain' Gall Bladder
  1. An opaque gall bladder is a rare finding on plain abdominal radiograph. But this can occur when the cystic duct is blocked and concentrated residual bile containing calcium is formed within thegall
  2. Bladder Unusually, the wall calcifies, forming the porcelain' gall bladder that appears on the radiograph as an outline of radio-opaque calcium.
Diverticula of the Gall Bladder
  1. Outpouchings of mucosa between the muscle bundles (Aschoff-Rokitansky sinuses) are common.
  2. They increase with age and have many features in common with colonic diverticula. They are most  frequent in the fundus and often become filled with inspissated bile, biliary gravel or cholesterol crystals.
Empyema Gallbladder
  1. Acute cholecystitis in the face of bacteria-containing bile may progress to suppurative infection in which the gallbladder fills with purulent material, a condition referred to as empyema of the gallbladder.
  2. The underlying cause of cholecystitis involves obstruction of the cystic duct; thereby causing the Build up of infected fluid. Systemic antibiotics and urgent drainage or resection are required to reduce the incidence of complications and to avoid or treat associated sepsis.
  3. History: The clinical history is similar to that of a patient with acute cholecystitis. As the disease progresses, severe pain and associated high fever, chills, and even rigors may be reported. Diabetic and immunosuppressed patients may have a paucity of symptoms.
  4. Ultrasound: The finding of an enlarged distended gallbladder and associated pericholecystic fluid points to an acute inflammatory process involving the gallbladder.
  5. Medical Care: Intravenous antibiotic therapy is an adjunct to urgent decompression and/or resection of the gallbladder in cases of suspected empyema.
  6. Surgical Care: Surgical decompression and resection of the affected gallbladder is the criterion standard of therapy.
  7. Empyema of the gallbladder without significant gangrenous changes or perforation may be treated with a laparoscopic procedure.
Acalculous Cholecystopathy
  1. Acalculous cholecystopathy is characterized by biliary colic-type pain in the absence of gallstones.
  2. The exact pathophysiology is unknown but likely is due to abnormal gallbladder motility that possibly causes relative obstruction of the cystic duct. 
Causes of Acalculous Cholecystitis
  Common Causes   Uncommon Causes
· Elderly and critically ill patients after trauma · Vasculitis
· Burns · Obstructing GB adenocarcinoma
· Long term TPN · GB torsion
· Major operations (abdominal aneurysm repair and · Parasitic infestation
  cardiopulmonary bypass) · Unusual bacterial infection:
· Diabetes mellitus · Leptospira
    · Streptococcus
    · Salmonella
    · Vibrio cholera
  1. Ultrasound: Ultrasound is most useful to rule out conditions in the D/D. Ultrasound detects abnormalities of gallbladder, including the presence (or absence) of stones, wall thickening, or pericholecystic fluid.
  2. Hepatobiliary scanning: After the gallbladder fills with the radioisotope, a cholecystokinin analog is administered.  HIDA scan most sensitive modality.
  3. This analog stimulates emptying of the gallbladder, allowing an ejection fraction to be calculated. gallbladder ejection fraction of less than 35% is considered abnormal and suggests that a patient with the appropriate symptom complex may benefit from laparoscopic cholecystectomy.
  4. No imaging study is ideal. Three 3 primary imaging are complimentary with USG, CT and cholescintigraphy.
  5. Medical Care: No effective medical treatment for acalculous cholecystopathy exists.
  6. Visceral ischemia is also common in patients with acute acalculous cholecystitis and may explain the high incidence of gallbladder gangrene.
  7. Patients may also present with only unexplained fever, leukocytosis, and hyperamylasemia without right upper quadrant tenderness. If untreated, rapid progression to gangrene and perforation may occur.
  8. It has a more fulminant course than acute calculous cholecystitis and more commonly progresses to gangrene, empyema, or perforation.
T/TUltrasound guided per cutaneous cholecystostomy is the treatment of choice and 90% of the patient recover. Only 10% need electic laproscopic cholecystectomy. 

Emphysematous Cholecystitis
  1. Emphysematous cholecystitis is an acute infection of the gall bladder wall caused by gas-forming organisms.
  2. Four pathogenetic factors are proposed in the development of emphysematous cholecystitis: Vascular compromise of the gall bladder, Gallstones,  Impaired immune protection, Infection with gas-forming organisms (E-coli (Most common) clostridial species, Escherichia coli, and Klebsiella species and less frequently, enterococci and anaerobic streptococci) 
  3. History: The typical patient is a male older than 60 years, often with type II diabetes mellitus. Otherwise, the clinical scenario does not differ significantly from that observed in acute cholecystitis.
  4. Abdominal radiographs: Abdominal radiographs show the classic picture of a gallbladder wall containing gas.
  5. Abdominal ultrasound: Obfuscation of the gallbladder by high-level echoes occurs when gas accumulates in the wall and lumen of the gallbladder.Curvilinear gaseous artifacts in the gallbladder, the so-called "ring-down effect" or "comet tail" are diagnostic of emphysematous cholecystitis.
  6. Computerized tomography of the abdomen: CT scan demonstrates emphysematous changes in the gallbladder wall that are diagnostic of this condition.CT scan may also demonstrate possible extension into the pericholecystic tissues and the hepatic ducts.
  7. Treatment; Medical Care:
    1. Intravenous antibiotics of choice are those that have beta-lactamase inhibitor activity or combinations that provide coverage for anaerobic and gram-negative organisms. Fluid replacement and correction of electrolyte deficits should be initiated to prepare the patient for surgery.
    2. Surgical Care: Management of emphysematous cholecystitis is surgical (lap or open cholecystectomy) 

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