GIT pdf - د. سمير الصفار

Forth stage

Surgery

Lec-5

Dr.Samer

28/2/2016

Stomach & Duodenum

Gross anatomy of stomach

Microscopic anatomy :



The gastric epithelial cells are mucus producing and turned over rapidly



In the pyloric part , mucus secreting glands are found



Parietal cells : Present in the body”acid-secreting” of stomach , Responsible for acid
secretion



Chief cells : Pepsinogen



Endocrine cells :

G cells; in the gastric antrum---gastrin

Enterochromaffin-like (ECL) cells ---Histamine

D cells ---somatostatin

Microscopic anatomy of Duodenum :



Lined by mucus secreting columner epithe



Brunner’s glands



Endocrine cells----cholecystokinin secretin

Physiology :



Storage “reservoir”



Mechanical break up of ingested food



Production of chyme by the actions of acid and pepsin



Programmed passage of contents into duodenum

Gastric acid secretion :

Investigation of stomach and duodenum :

Flexible Endoscopy:



Is more sensitive than conventional radiology in the assessment of the majority of GD
conditions, e.g. peptic ulceration, gastritis, and duodenitis.



Upper GIT bleeding



Early gastric cancer



Diagnostic:
Visual
Biopsy
Endoluminal Ultrasound



Therapeutic:
Control of bleeding, inj. Laser, diathermy
Endoscopic gastro-cystostomy
Endoscopic Gastrostomy
Removal of Foreign bodies



Disadvantages:
Invasive, discomfort
Perforation, of pharynx, oesophagus
Miss-diagnosis,early gastric cancer.

Contrast radiology



Less commonly asked for



Of value in;



Hiatus Hernia specially of the rolling type



Volvulous of stomach



Linitus plastica

Ultrasonography



Conventional US



Detection of large gastric tumor



Metastases to liver



Endoluminal US



Depth of wall invasion” T staging”



Local LN



Liver metastases



Laparoscopic US

CT scan and MRI



CT scan

In Gastric malignancy



Miss smaller lesions



Less accurate in T staging



Less easy to detect small liver metastases



MRI

Higher sensitivity for detection of gastric cancer liver metastases

Laparoscopy



Well used for assessment of patients with gastric cancer



Particularly for detection of peritoneal seedlings

Other investigations



Gastric emptying studies



Angiography



Measurement of gastric acid secretion



Gastric motility



Plasma gastrin

Paediatric Disorders :

1. Hypertrophic pyloric stenosis of infancy



Aetiology:



3:1000 births



4:1 male to female



Familial



Pathology:

Hypertrophy of musculature of pylorus and adjacent antum



Clinical features :



Commonly present at 4 wks of age



Vomiting of milk without bile---2-3 days become forcible and projectile



Immediately after vomiting, the baby is usually hungery



Wt loss---emaciation, dehydration



Diagnosis



Test feed



Imaging:

Ultrasonography Olive mass

Contrast radiology no longer necessary



Differential Diagnosis



Gastro-oesophageal reflux



Feeding problems



UTI



Raised intracranial pressure



Treatment



Correction of dehydration and electrolyte abnormalites; by using Dextrose
saline plus potassium



Followed by Operation “ Ramstedt’s”

2. Duodenal Atresia



Occur at the point of fusion between the foregut and midgut, in the neighbourhood
of the ampulla of Vater.



Other defects



Antenata Dx : US



The child vomits from birth and the vomitus is bile stained



Differential DX. : High intestinal obstruction , Pyloric stenosis



Treatment : Duodenoduodenostomy

3. Helicobacter Pylori



Proved its importance in the aetiology of ch.gastritis, peptic ulceration,and cancer



Waren and Marshal in 1980 proved casual relation between HP and Gastritis



HP is spiral shaped, able to hydrolyse urea to ammonia “a strong alkali”



Spread Feco-oral



Incidence 80 –90 %



Pathogensis

o Antral gastritis---relase of ammonia---decrease in acidity---G cell stimulation--

increase gastrin----increase in HCL

o Disruption of gastric mucosa through a number of cytotoxins



Diagnosis of HP infection

o Brith test

o CLO

o Histological examination of biopsy

o Serological tests



Treatment

Eradication therapy :

o Combination of antibiotics like : Metronidazol + Amoxil or Claithromycin +

Amoxil

o With the use of proton pump inhibitor like : Omerprazol, Lansoprazol

Gastritis

Type A gastritis :

----achlorhydria

----hypergastrinaemia----

Hypertrophy of ELC

Type B gastritis :

Reflux Gastritis:

ectomy

Treatment:

Erosive gastritis:

alcohol.

SAID act as anti inflammatory without affection on gastric

barrier

Stress gastritis

May lead to stress ulceration that may bleed

Treatment: Prevention; routine use of H2 antagonists, + -mucosal barrier agents
like sucralfate

Peptic Ulcer





Not related to pepsin

Can occur in the:

1. 1stpart of duodenum,

2. lesser curve of stomach

3. stoma of gastrojejunostomy,

4. oesophagus,

5. Meckel’s diverticulum

Aetiology:

ollinger-

Ellison syndrome”

Duodenal Ulceration

Incidence

rease in its incidence

Pathology

Penetrates the mucosa and into the muscle coat

Histopatholgy:

uscular coat

Gastric Ulcers

Incidence

ents

Aetiology

Pathology:

Lesser curve of the stomach

Malignancy in gastric ulcers:

il proved otherwise usually by

well targeted multiple biopsis “as many as10”

Clinical features of peptic ulcers

Pain: epigastric, gnawing, may radiate to back, eating may relieve the discomfort,

intermittent

Periodicity:intermittent, spring and autmen

Vomiting:indicates stenosis

Alteration in weight: wt loss or gain may occur ,,, wt loss more with GU

Bleeding: all may bleed; may be: chronic anaemia acute presentation with

hematemesis and melaena

Clinical examination

c tenderness

Investigation :

Treatment of peptic ulceration :

Medical treatment:

except in patients with :

Zollinger-Ellison syndrome

Surgical treatment of uncomplicated DU ulceration :

Operations for duodenal ulcer

1. Truncal vagotomy and drainage

2. Highly selective vagotomy

3. Truncal vagotomy and antrectomy

4. Billroth II gastrectomy

Protocol for GU :

-8 wks later

If un-healed ------Surgery

Operations for gastric ulcer :

1. Billroth I gastrectomy

2. Billroth II gastrectomy

3. Vagotomy, pyloroplasty and ulcer excision

Sequelae of peptic ulcer surgery :

Bile vomiting

Post-vagotomy diarrhoea

Complications of peptic ulceration

Perforated peptic ulcer

Epidemiology:

Pathology:

The ulcers that are liable for perforation are:

Clinical features

Sudden onset of severe generalised abdominal pain

Board like rigidity

Investigations:

Air under the diaphragm in about 50

–70 % of cases

--free peritoneal leak

Treatment:

Laparotomy

Laparoscopy

Upper GIT Bleeding

Haematemesis and Melena

Is a common emergency
A mortality of 5%
Bleeding peptic ulcer, gastric erosions, Mallory-Weiss and oesophageal vavices.
Medical treatment is ineffective



Therapeutic endoscopy

Causes of GIT bleeding

Principles of management:

Bleeding peptic ulcers

Epidemiology;



Affect much older persons



Commonly associated with NSAIDs

Diagnosis:
Endoscopy

Goal of treatment:
1. Control of bleeding
2. Prevention of rebleeding

Options to control bleeding
1- Medical treatment
H2 antagonist
Proton pump inhibitors
Tranexamic acid; fibrinolysis inhibitor
2

Minimal invasive treatment

;

Therapeutic endoscopy:
Injection, epinephrine
Thermal , electrocoagulation
Laser, APC
3- Surgical treatment
Criteria for surgery:
1. Patients who continue to bleed
2. Significat rebleeding
3. A patient who required >6 units of blood / 24h
4. Elderly patients
Certain endoscopic features;



Visible vessel in the ulcer base



Spurting vessel



Clot cover the ulcer

Its Aim is to stop bleeding By Minimal surgery
Definite acid lowering surgery is not required

Mallory-Weiss tear

Longitudinal tear below the gastro-oesophageal junction
Induced by repetitive and strenuous vomiting
Diagnosis by OGD –difficulty and easily missed
Surgery may be needed to stop the bleeding

Dieulafoy

’s disease

Gastric arterial venous malformation
Difficult to diagnose Treatment:
Endoscopic----injection of sclerosant
Surgery—local excision

Tumors

Chronic or acute
Not torrential
Common presentation of gastric smooth muscle tumors

Gastric outlet obstruction

The two most common causes:
Pyloric stenosis
Gastric cancer

Clinical features



In pyloric stenosis

Long history of peptic ulcer disease
Unremitting pain
Unpleasent vomiting that lacking bile
Contain foodstaff taken several hours previously
Loss of wt.

On examination

Dehydrated, loss of wt.
Distended stomach, succussion splash

Metabolic effects:
Hypochloraemic alkalosis
Initially the urine contain low chloride and high HCO3, then dehydration---Na retention
with excessive K and H ions excretion resulting in paradoxical acid urine
Alkalosis-----decrease in ionized Ca---tetany

Management
Diagnosis

: usually by



Endoscopy



Contrast radiology

Treatment:



Correction of dehydration and metabolic abnormalities by using IV isotonic saline with K



Correction of mechanical problem: Usually needs Surgery:



Prior to surgery;

Wide bore NG tube
Gastric antisecretory agents


Surgical treatment:

1. Gastro-enterostomy
2. Vagotomy



Endoscopic treatment by balloon dilatation

Disadvantages:
Applicable for early cases
Repeated courses
Perforation

Gastric polyps

Accidental finding at endoscopy
May be premalignant
Must be biopsied

Types of gastric polyps:



Metaplastic related to H.pylori infection



Inflammatory



Fundic gland polyp; associated with proton pump inhibitors and familial polyposis



Adenoma premalignant

Gastric cancer



Is the major cause of cancer mortality



Poor prognosis



Early detection



The aetiology is multifactorial, but H. pylori is an important factor.

Epidemiology:
The incidence is highest in Japan and some areas of China; >70 per 100000
Men more than female
Incidence increase with age
Increase incidence of tumors affecting the proximal part of stomach
Proximal gastric cancer dose not seem to be associated with H.pylori

Aetiology

Multifactorial disease
H.pylori

Risk factors

Pernicious anaemia and gastric atrophy
Peptic ulcer surgery
Cigarette smoking

Diet, N-nitros compounds, excessive salt intake
Alcohol
Genetic

Clinical features
Early gastric cancer
Advanced gastric cancer
Early gastric cancer:
Non-specfic symptoms; dyspepsia
Liberal use of gastroscopy in patients with dyspepsia (Open access gastroscopy)
Antisecretory agents can improve the symptoms of gastric cancer
Advanced gastric cancer:
Early satiety, bloating, distension and vomiting
Bleeding, mild and chronic
Obstruction,:



proximal---dysphagia



Distal ---------gastric outlet obstruction

Non-metastatic effects:
Thrombophlebitis (Trousseau’s sign)
Deep vein thrombosis

Pathology
Lauren classification: Intestinal gastric cancer



Intestinal metaplasia



Polypoid or ulcer Diffuse gastric cancer



Deep infiltration no obvious mass



Poorer prognosis Mixed



Early gastric cancer (90% five years survival)



Cancer limited to mucosa and submucosa with or with out LN involvement ( T1,any N)



Advanced gastric cancer: ( < 30% five years survival)



Involve the muscularis

Spread of gastric cancer

Direct spread

Penetrates the mucsularis, serosa, and ultimately adjacent organs
Lymphatic spread
Both by permeation and emboli
Distant nodal; supraclavicular (Troisier’s sign)
Blood borne metastases:
First to liver and then other organs like lung and bone
Transperitoneal spread:
Involve anywhere in the peritoneal cavity
Ascites

Krukenberg’s tumours
Tumour shelf
Sister Joseph’s nodule
Laparoscopy and cytology

Gastric cancer

The prognosis of operable cases of gastric carcinoma depends on whether or not there is
histological evidence of regional LN involvement.

International Union Against Cancer (UICC) staging of gastric cancer

 T1 Tumour involves lamina propria

 T2 Tumour invades muscularis or subserosa

 T3 Tumour involves serosa

 T4 Tumour invades adjacent organs

 N0 No lymph nodes

 N1 Metastasis in 1–6 regional nodes

 N2 Metastasis in 7–15 regional nodes

 N3 Metastasis in more than 15 regional nodes

 M0 No distant metastasis

 M1 Distant metastasis (this includes peritoneum and distant lymph nodes)

Staging

 IA T1 N0 M0

 IB T1 N1 M0

 T2 N0 M0

 II T1 N2 M0

 T2 N1 M0

 T3 N0 M0

 IIIA T2 N2 M0

 T3 N1 M0

 T4 N0 M0

 IIIB T3 N2 M0

 IV T4 N1–3 M0

 T1–3 N3 M0

 Any T Any N M1

Diagnosis

 Clinical Signs

 Investigations:

 For Dx.:-----Endoscopy, with biopsy

 For extend and operability “Staging”:

 Ultrasound

Endoluminal

Laparoscopic

Conventional

 CT scan

 For assessment:

Treatment

Surgery:

 Radical

 Palliative

Operability

Radical surgery:

Palliative surgery:

 Partial gastrectomy

 Gastroenterostomy

 Gastric exclusion oesophagojejunostomy

Partial gastrectomy Gastrojejunostomy

Subtotal gastrectomy

Total gastrectomy

Postoperative complications of gastrectomy

 Leakage; from oesophagojejunostomy

 Leakage from duodenal stump

 Biliary peritonitis

 Secndary haemorrhage

Long term complications

 Nutritional deficiencies

 Dumping

 Diarrhoea

Other treatment modalities

 Chemotherapy:



Improvement in the survival of several months



Combination cytotxic chemotherapy

 Radiotherapy:



Disappointing except for bony metastases

Other gastric tumours

GASTROINTESTINAL STROMAL TUMOURS(GIST)

 Previously Called Gastric Leiomyoma and Leiomyosarcoma

 Distniction between them difficult

 Associated with a mutation in the tyrosine kinase c-kit oncogene.

 Peritoneal and liver metastases

 spread to lymph nodes is extremely rare.

 Clinical features



Non specific symptoms



Bleeding



Difficult to detect by endoscopy

 TREATMENT

 wedge excision

 GASTRECTOMY

 lymphadenectomy is not required

 imatinib before operation

Gastric Lymphoma:

 Primary
 Part of generalized lymphoma



Clinical features:

 Similar to gastric cancer

 Diagnosis is by endoscopic biopsy

 Ct scan for staging



Treatment:

 Primary lymphoma: surgery + - chemotherapy

 Systemic lymphoma chemotherapy

GASTRIC OPERATIONS FOR MORBID OBESITY

 Obesity when the BMI of the person is

more than 25

 BMI = (Weight in kg)/(Height in m)

 Normal weight when BMI between 18 –

24.9

 Over weight when BMI 25 – 29.9

 Obesity when BMI > 30

 Morbid obesity when BMI >45

Bariatric Surgical procedures

1. Laparoscopic gastric Band procedure

2. Laparoscopic gastric bypass

3. Laparoscopic sleeve gastrectomy

1-Lap Band procedure

2-Gastric bypass

3-Lap sleeve gastrectomy

Intragastric balloon

Zollinger- Ellison syndrome

 Gastrin producing endocrine tumour

 Head of pancreas

 Duodenal loop

 Effects; persistant peptic ulceration

 Treatment:



Total gastrectomy in the past



Proton pump inhibitor

OTHER GASTRIC CONDITIONS

 Acute gastric dilatation

 Trichobezoar and phytobezoar

 Foreign bodies in the stomach

Gastric volvulous

Total gastrectomy