GASTRIC OUTLET OBSTRUCTION

DEFINITION

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

CausesTwo well-defined groups of causes—

Benign & Malignant

In the past-- peptic ulcer disease  more prevalent, benign causes most common BUT IN RESOURCE CHALLENGED COUNTRIES WHERE IT MAY STILL BE THE COMMONEST CAUSE

Now-- only 37% have benign disease and the remaining have obstruction secondary to malignancy

Etiology Major benign causes of gastric outlet

obstruction (GOO) are---

PUD

gastric polyps

ingestion of caustics

  pyloric stenosis

congenital duodenal webs

gallstone obstruction (Bouveret syndrome)

pancreatic pseudocysts

and bezoars

Etiology(Contd) Pancreatic cancer is the most common malignancy causing

GOO

Outlet obstruction may occur in 10-20%

 Ampullary cancer

Duodenal cancer

 Cholangiocarcinomas

  Gastric cancer

Metastases to the gastric outlet by other primary tumors

Pathogenesis

Intrinsic 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

Metabolic effects Dehydration and electrolyte abnormalities-- Increase in

BUN and creatinine are late features of dehydration

Prolonged vomiting causes loss of hydrochloric acid & produces an increase of bicarbonate in the plasma to compensate for the lost chloride-------hypokalemic hypochloremic metabolic alkalosis

Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum potassium is increased factitiously

With continued vomiting, the renal excretion of potassium increases in order to preserve sodium

The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia

Paradoxically acidic urine

Initially, the urine has a low chloride and high bicarbonate content, reflecting the primary metabolic abnormality

This bicarbonate is excreted along with sodium and so, with time, the patient becomes progressively hyponatraemic and more profoundly dehydrated.

Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference.

This results in the urine becoming paradoxically acidic.

Alkalosis leads to a lowering of the circulating ionised calcium, and tetany can occur.

Clinical features

Nausea and vomiting are the cardinal symptoms

Vomiting -- Nonbilious, and it characteristically contains undigested food particles

Early stages --- vomiting intermittent and usually occurs within 1 hour of a meal

Very often it is possible to recognise foodstuff taken several days previously

Pt. loses weight, appears unwell & dehydrated

Clinical features(Contd)

GOO from a duodenal ulcer or incomplete obstruction typically present with symptoms of-----------

Gastric retention, including early satiety, bloating or epigastric fullness, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss

Frequently malnourished and dehydrated and have a metabolic insufficiency

Weight loss , most significant with malignant disease

Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer

Examination

Chronically ill looking

Wasted

Dehydrated

may be pale due either to a bleeding ulcer, malignancy

Shock

Epigastric / Rt hypochondrial tenderness

Distended abdomen

Visible gastric peristalsis

Succussion splash

PRINCIPLES OF MANAGEMENT .

Guiding Principles lies in the recognition of GOO as an emergency, as such, GOAL of treatment include:

-1)Resuscitation/stabilization.;-2)Relieve obstruction;-3)Patient selection/categorization; - patient related factors-4)Offer definitive curative care; - Lesion related factors-5)Prevent recurrence/Follow up care.

Management Involves

Correcting the metabolic abnormality &

Dealing with the mechanical problem

Rehydrated with i/v isotonic saline with potassium supplementation/ Ringer’s . Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality

investigations

1) Stabilise patient

FBC (anaemia)

SEUCR (hypochloraemia, hypokalaemia,hyponatraemia,elevated Hco3)

BLOOD GASES(metabolic alkalosis)

URINALYSIS (paradoxical aciduria)

investigation

2)To confirm diagnosis

Plain x-ray of abdomen:shows large gastric shadow and a large amount of gastric fluid.

Gastric aspiration:a wide bore stomach tube is placed early in the morning and the stomach is aspirated of resting juice.if >400ml of juice is obtained a presumptive diagnosis of GOO can be made.

investigation

Esophagogastroduodenoscopy + biopsy(histology and bacterioloical investigation).

Aim is to visualise the stomach mucosa and any ulcer.

Barium meal:

-markely dilated stomach with a lot of residue

-presence of an ulcer crater

-trifoil deformity of the duodenal cap.

Indications(Surgery) GOO due to benign ulcer disease may be treated medically

if results of imaging studies or endoscopy determine - acute inflammation and edema are the principle causes (as opposed to scarring and fibrosis, which may be fixed)

If medical therapy -- fails, then surgical

Typically, if resolution or improvement is not seen within 48-72 hours, surgical intervention is necessary

The choice of surgical procedure depends upon the patient's particular circumstances

In cases of malignant obstruction, weigh the extent of surgical intervention for the relief of GOO against the malignancy's type and extent, as well as the patient's anticipated long-term prognosis

As a guiding principle, undertake major tumor resections in the absence of metastatic disease(in fit pts)

In patients with largely metastatic disease, determine the degree of surgical intervention for palliation in light of the patient's realistic prognosis and personal wishes

THE CHALLENGES HERE

The commonest cause is chronic PUD

Diagnostic challenge in terms of a CT scan, though can still be done

Laboratory challenge in determining the metabolic anomalies

Best to use Ringer’s for resuscitation as potassium is not easily available

SUMMARY

In poor resource countries, the best diagnostic modality still remains to be clinical ( non- bilious vomitus within an hour of taking a meal, gastric peristalsis and succution splash)

the availability of PPIs and eradication therapy for H.pyroli has made the incidence of malignancy to be on the rise as the cause of GOO