BENIGN GASTRIC OUTLET BENIGN GASTRIC OUTLET OBSTRUCTIONOBSTRUCTION

ByDr E.Aravind

Under Guidance of Dr DSVL Narasimham

MS Dr R Hemanthi MS

Dr P Sitaram MS

Gastric outlet obstruction (GOO) represents a clinical and pathophysiological consequence of any disease process which produces mechanical impediment to gastric emptying.

Classification 2 groups

Benign causes Malignant

causes

EpidemiologyEpidemiologyUntil the late 1970s benign

disease was responsible for a majority of cases

Recent decades 50 to 80 percent cases have been attributed to malignancy.

Incidence of GOO has been reported to be less than 5% in patients with peptic ulcer disease (PUD), which was earlier the leading benign cause

ETIOLOGYETIOLOGY

PEPTIC ULCER DISEASEPEPTIC ULCER DISEASE

Most common cause previously Decline after discovery of Helicobacter

pylori and proton pump inhibitorsOccurs both in acute and chronic ulcersAcute ulcers inflammation induced

edema, spasm, tissue deformation and pyloric dysmotility

Chronic ulcers scarring and tissue remodeling

Commonly associated with Duodenal Ulcers

GOO associated with Chronic PUDIt includes pathologic entities

such as: -Chronic PUD with active

edematous ulcer; -Chronic PUD with antral

cicatrisation; -Chronic PUD with Pyloric stenosis; -Hour glass stomach; -Teapot stomach

Corrosive injuryCorrosive injuryIngestion of both

acid and alkaliAntral or pyloric

scarring

DrugsDrugsMostly NSAIDs and

Opium productsNSAIDs cause GOO

by diminishing the levels of prostaglandin E2 causing pyloric edema and scarring and increasing histamine release leading to increased gastric secretion, reduction of mucosal absorption, and gastric motility disturbances.

Inflammatory causesInflammatory causesCrohn’s diseaseTuberculosis Chronic pancreatitisAnnular pancreasDuodenal obstruction common

due to pancreatic and biliary duct strictures

Rare causesRare causesGastric bezoarsLarge gastric

polypsGastric vovlulusBouveret’s

syndromeAmyloidosis

PathogenesisPathogenesisIntrinsic or extrinsic obstruction

of the pyloric channel or duodenum

Depends upon the underlying etiology

Obstruction of the stomach

Hypertrophy of the stomach

Dilatation

Gastritis & depressed acid secretion

Complications /Effects Complications /Effects Malnourishment – weight loss Iron deficiency anaemia Vomiting of gastric content resulting

in:- dehydration - shock - electrolyte imbalance( Na, Cl, K)- metabolic alkalosis-paradoxic aciduria - acute kidney injury

Clinical PresentationClinical Presentation

HistoryHistoryAGE:20-45 years with peak 30-35 years

Known or suspected case of chronic PUD

Epigastric and Lt hypochondrial pain :-relieved by alkali, food.-gnawing/biting-periodic (spontaneous

healing)-association with food and

time of day-radiates to the back -Generalized

Anorexia, nausea.

Easy satiety

Vomiting: -characteristic unpleasant

-copious-projectile-Non bilious-Food taken several

days ago.

Feeling of unwell

Appetite is maintained but fear of pain often prevent patient from eating

Weight loss.

Abdominal swelling

General examinationGeneral examinationWasted

Dehydrated

Pallor

Shock

Epigastric / Rt hypochondrial tenderness

Distended abdomen

Visible gastric peristalsis

Succussion splash

Goldstein saline load test

Investigationsnvestigations

Hemoglobin Serum ElectrolytesECGBlood GasesUrine analysis Serum Gastrin levels

Detection of H.pyloriNon invasive:

serologycarbon labelled urea breath test

Invasive:◦Rapid urease test,histology and

culture.

Plain x-ray of abdomen - shows marked gastric air bubble (black arrows) and a downward shift of transverse colon (white arrows)

Barium meal:-markedly

dilated stomach with a lot of residue

-presence of an ulcer crater

-filling defect at the duodenal cap.

-trifoliate duodenum

CT Abdomen – shows dilated stomach, any other extrinsic pathology

Endoscopy Endoscopy To establish the

diagnosisIdentify a specific

causeTherapeutic benefitEndoscopic

biopsies to identify H. pylori and to exclude malignant conditions causing GOO

ManagementManagement

Symptomatic GOO needs hospitalization.

Fluid resuscitationManagement of Metabolic alkalosisNasogastric decompressionTotal parental nutritionDefinitive management can be

instituted after establishment of diagnosis and correction of underlying metabolic abnormalities

Endoscopic balloon dilatation (EBD)Safe and effective

alternative in the management in surgically unfit patients.

A through-the-scope (TTS) 5 mm balloon with a 150 cm long catheter is used.

Balloons are available from 6 mm to 20 mm

The procedure is repeated 1-2 weekly until adequate dilatation of 15-18 mm is achieved

Complications of EBD - Self limiting pain - Bleeding - PerforationEradication of H. pyloriProton pump InhibitorsTuberculosis, Crohn’s disease, and

pancreatitis causing GOO also respond to EBD they have more recurrences unless the basic disease is managed and adequately treated

Intralesional steroids like Triamcinolone and endoscopic incision along with Endoscopic balloon dilatation increase the efficacy of EBD

Placement of biodegradable stents mainly in caustic injury

Surgery for Benign GOOSurgery for Benign GOOSurgery forms the final option for

patients presenting with refractory GOO

A jejunostomy tube should be placed along with surgery

Goal of surgery for ulcer - Reduce gastric acid secretions

Achieved by - Vagotomy – decrease stimulus

- Anterectomy – decrease gastrin secretion

Vagotomy, antrectomy and gastrojejunostomy

Gastrojejunostomy can be Billroths I or II

some times Rouxen- Y Gastrojejunostomy

Vagotomy

Truncal Vagotomy – need a drainage procedure Finneys pyloroplasty or Heineke-Mikulicz pyloroplasty

Selective Vagotomy

Highly Selective Vagotomy

Billroth I Gastrojejuostomy

Billroth II Gastrojejunostomy

Rouxen- Y Gastrojejunostomy

High Selective Vagotomy with Gastrojejunostomy is the recommended procedure

Truncal Vagotomy and gastrojejunostomy most commonly done surgery

Post Vagotomy testsPost Vagotomy tests

i)Pentagastrin test -Peak acid output reduction of >/50% is indicative of completeness.

ii)Insulin (Hollander’s) test - Prognostic Done 1week post vagotomy. If positve in a short time, recurrence risk is high.

ComplicationsComplicationsEarly complications - Haemorahage - Injury to surrounding organs like

spleen, liver, pancreas, thoracic duct

- Anesthetic complications

Post Gasterectomy Post Gasterectomy SyndromesSyndromesDumping Syndrome - Rapid passage of high osmolarity food from

stomach to small intestine leading to rapid shift of fluid - luminal distension - autonomic responses

- Gastrointestinal and Cardiovascular complaints

- 20-30 after intake of meals - Nausea vomittings epigastric fullness

cramping abdominal pain and explosive diarrhoea

- Cardiovascular symptoms- flushing, diaphoresis, palpitations,dizziness, fainting,blurring of vision

Management - Spontaneous relief. - Dietary - Long acting Octreotide

Metabolic Disturbances - Iron deficiency Anaemia - Impairment of Vitamin B12

metabolism - Decreased absorption of

calcium leading to osteomalicia and osteoporosis

Afferent loop Syndrome - Blockage of afferent limb of loop

causes the bile and pancreatic secretions to collect in the afferent limb with increasing pressure these enter the stomach.

- Causing projectile bilious vomiting not containing food and relieves symptoms

- Investigate with UGIE and Radio nucleotide scan

Management - A surgical emergency - A high index of suspicion. - Convert Billroth II to I. - Enteroenterostomy (e.g Braun,

easier) below the stoma. - Creation of a Roux-en-Y

Efferent loop syndrome - Quite rare - Usullay from herniation of limb

behind anastomosis (R-L fashion). - Upper quadrant pain colicky in

nature, bilious vomiting and abdominal distension

- Investigation – CECT Abdomen - Management -Reduce retroanastomosis hernia -Close retroanastomosis space.

Duodenal Blow out: -Usually occurs 4-

5th postop day. -Leak from

Duodenal stump -Life threatening. -Management

Control fistula and sepsis

-Enteroenterostomy later.

Postvagotomy diarrhea -Occurs in >30% of patients as

part of Dumping synd. Usually disappears after 3-4 months.

-Management-self limiting -Cholestyramine(4g tds).

Postvagotomy Gastroparesis - Occurs in both TV&SV, not in

HSV. - Paresis allows liquid(loss of

receptive relaxation) not solid(dependent on antral pump mechanism)

- Management - Prokinetics

Alkaline Reflux Gastritis - Severe epigastric pain with bilious

vomiting and weight loss. Usually after Billroth II.

- Diagnosis largely clinical but HIDA scan shows bile reflux into stomach/esoph endoscopy show beefy red ,friable mucosa.

-Management-Billroth II to a Roux-en-Y GJ.

Blind Loop syndrome Bacterial overgrowth in static loop

causing bind with B12 and deconjugate bile acid which results in deficiency of Vitamin B12 and Megaloblastic anemia.

Retained Antrum syndrome From retained terminal antrum in

the duodenal stump continually bathed in alkaline secretion - increased gastrin release - increased acid secretion - recurrent ulcer.

Follow UpFollow Up

i-H.Pylori Eradicationii-H.pylori screening(to document

eradication)-serology -13C blood urea testiii-BAO output monitoringiv-Yearly upper GI endoscopy+biopsy.v-Nutritional supplementation.vi-Life style

modification(alcohol,smoking)

PrognosisPrognosisAgeH pylori reserveDurationCo morbiditiesPrevious surgeriesPrevious failed Medical therapy

for H.pyloriOverall prognosis is good with

improved surgical and medical therapy

CONCLUSIONCONCLUSION Though PUD is largely medically

managed with the place of the surgeon gradually being relegated to the background following improved medical therapy.

However, considering high proportion of people being of low socioeconomic status in our country the surgeon’s place can not be overemphasized.

Thank YouThank You