PROBLEM

• CORRELATING PATHOPYSIOLOGY, CLINICAL

HISTORY, RADIOLOGICAL ANATOMY AND
MANIFESTATIONS, FOR BETTER DIAGNOSIS
OF GASTRO ENTERIC PATHOLOGIES.
 Achalasia cardia

Achalasia is a motor disorder of the

oesophagus generally occurring in
the 35-50 year age group.
• Achalasia is a motor disorder of the
oesophagus generally occurring in the 35-50
year age group.
PATHOPYSIOLOGY
• It is caused by degeneration of neurones of
Auerbach's plexus, which is situated between
the longitudinal and circular muscle coats.
• Primary and secondary peristalsis initially fails,
tertiary contractions develop, and there is a
failure of relaxation of the lower oesophageal
sphincter.
 Clinical signs
• Achalasia causes dysphagia for both solids and liquids.
• If the patient presents early, pronounced tertiary
contractions may be seen with only modest dilatation,
and the patient may complain of severe chest pains
identical to those of patients with diffuse oesophageal
spasm.
• These two conditions have been considered to be at
different ends of the same disease spectrum, and
sometimes diffuse oesophageal spasm maybe
observed progress to achalasia
 Radiological findings
• A barium swallow will show gastro-oesophageal junction failing
to open fully and tapering to a rat tail or bird beak appearance.
• Intact mucosal folds can be traced through this narrowed
segment, which at times opens briefly to allow a little barium to
spurt into the stomach.
• With time, the oesophagus dilates, lengthens and becomes
tortuous.
• The dilatation may involve the entire length of the oesophagus
and can sometimes be appreciated on a plain chest film where
there is a small or absent gastric fundal air bubble, the fluid-
filled oesophagus widens
 Complications of achalasia cardia
• Recurrent episodes of aspiration pneumonia may
complicate achalasia and lead to the development
of bronchiectasis, lung abscesses or an empyema.
• Repeated aspiration may also cause basal
pulmonary fibrosis.
• Prolonged food stasis may cause oesophagitis,
with an and narrow the trachea to produce stridor.
• Massive oesophageal dilatation has resulted in
sudden death from asphyxiation.
 Peptic ulcer

Peptic ulcer is a sore on the lining of

the stomach, small intestines or
oesophagus.
Radiological anatomy of stomach
• Benign gastric ulcers most frequently occur
along the lesser curve of the stomach and the
adjacent part of the posterior wall
• Giant ulcers are also caused by aspirin and
non-steroidal anti-inflammatory drugs, in
which case they tend to develop on the
dependent part of the greater curve because
gravity deposits tablets at this site
• If the ulcer crater is very shallow, a thin layer of
barium coating results in a ring shadow.
• A benign ulcer in profile protrudes outside the
expected line of the stomach wall.
• whereas a malignant ulcer at the apex of a
protruding tumour mass will lie within the outline
of the stomach . Irregular folds merging into a
mound of polypoid tissue around the crater
suggest a malignancy.
• Fundal ulcers above the level of the cardia are
usually malignant.
 Imaging Findings
Classic signs of benignancy include:
I. Penetration,
II. Hampton line,
III. ulcer collar,
IV. ulcer mound, and
V. radiation of smooth, slender mucosal folds to
the edge of the crater.
Three characteristic of gastric ulcer
• A: benign, projecting. Lesser
curvature ulcer with collar
(broken lines)

• B: malignant, intraluminal
ulcer with irregular nodular
tumour rim.

• C: non-projecting benign
greater curvature ulcer
Punctate collection of barium and “halo” sign
 Benign gastric ulcer
Benign gastric ulceration. Healed benign gastric ulcer.
Small posterior wall ulcer.
 Complication: Perforating ulcer:

• Radiographic signs include the presence of

free air under the diaphragm, as seen with an
erect abdomen radiograph.
• If untreated, this ulcer may lead to peritonitis
and eventual death.
 Duodenum ulcer

The majority of duodenal ulcers

occur within the cap
Radiology anatomy of Duodenum
 Duodenal ulcer
• Duodenal ulcers involve the anterior and posterior walls
with equal frequency.
• As in the stomach, an ulcer on the dependent wall fills
with barium and shows radiating folds, which stop short
of the margin if there is a rim of oedema.
• An ulcer on the non-dependent wall is etched by barium
and appears as a ring.
• It can be difficult to coat the anterior wall of the
duodenum and prone or erect compression views of the
duodenal cap should therefore be obtained.
• Ulcers are generally round, but as with gastric ulcers may
be linear, especially when healing.
• Ulcer craters are seen as well-defined round
or ovoid pools of barium, surrounded by a
symmetrical mound of edematous mucosa.
Adjacent radiating mucosal folds converge to
the edge of the crater.
• Healed ulcer leads to deformity of the bulb.
 Anterior wall duodenal ulcer

Supine projection . The ulcer,

Prone projection. The ulcer is on the non-dependent wall of
dependent, and so fill with the cap, is outlined with a ring
barium of barium
 Deformity of the
Stricture is noted at the duodenal cap .These
junction of first and findings are secondary to
second part of the healed bulbar (A) and post
duodenum bulbar duodenal ulcers
Scarring of the duodenal cap Giant duodenal ulcer replacing
resulting from a chronic the duodenal cap.
duodenal ulcer
Perforated duodenal ulcer
• An unexpected, silent
perforation localised to the
right sub-phrenic and sub-
hepatic space.
key
• S = stomach,
• D = duodenum
• B = leaked barium
 References
• Sutton – textbook radiology and imaging
seventh edition volume 2 by David sutton
• Radiology radiopaedia.org
• emedicine;:mesdcape.com
• ZareMehrjardiM.Bariumswallowandbariumme
al:techniquesandinterpretation.2013.doi:10.1
3140/RG.2.2.10543.33449/1.
 COLORECTAL CARCINOMA

Most common cancer of the

gastrointestinal tract and the second most
frequently diagnosed malignancy in adults.
 RISK FACTOR
• Low fiber and high fat and animal protein diet
• Obesity (especially in men)
• Inflammatory bowel disease
1. Chronic ulcerative colitis
2. Crohn disease (in bypassed loops)
• Asbestos workers
• Family history of benign or malignant colorectal tumors
• History of endometrial/breast cancer
• Pelvic irradiation
• Ureterosigmoidostomy
• Colonic adenoma
• Dysplasia of colon within flat mucosa
 CLINICAL PRESENTATION
• Altered bowel habit (constipation and/ or
diarrhea)
• Iron deficiency anemia
• Weight loss
INITIAL MANIFESTATION MAY BE ACUTE:
• Bowel obstruction
• intussusception
• Heavy rectal bleeding
 PATHOLOGY
• 98% of which are adenocarcinomas, arise in the
vast majority of cases from pre-exiting colonic
adenomas, which progressively undergo a
malignant transformation as they accumulate
addition mutations.
• Morphologically cancers can be;
1. Sessile
2. Exophytic
3. Circumferential (apple core)
4. Ulcerated
5. desmoplastic
 LOCATION
Colorectal cancers can be found anywhere
from cecum to the rectum;
• Rectosigmoid: 55%
• Cecum and ascending colon: ~ 20%
Ileocecal valve: 2%
• Transverse colon: ~ 10%
• Descending colon: ~ 5%
 RADIOGRAPHIC FEATURES
• BARIUM ENEMA
• 90 – 95% rate of detection
• Polypoid filling defect
• Annular constricting = apple-core lesion
• Scirrhous Ca – rare infiltrating type which
gives lead-pipe appearance
• Calcifications- rare
• May have retrograde without antegrade
obstruction
 reference
• Learningradiology.com/notes/ginotes/cacolon
page.htm
• www.radiopeadia.org
 MALABSORPTION/SPRUE
• Is the collective term for the malabsorptive
gastrointestinal enteropathies.
• Composed of 2 entities:
Tropical sprue
Non-tropical sprue/celiac sprue
 CAUSES
• Persistent bacterial, viral, amoebal or parasitic
infections.
• Folic acid deficiency.
• Immune reaction to eating gluten
 CLINICAL PRESENTATION
• Diarrhea
• Steatorrhea or fatty stool
• Cramps
• Weight loss
• Fatigue
• Anemia
• osteoporosis
 PATHOPHYSIOLOGY
• An acute intestinal infection leads to jejunal
and ileal mucosa injury; then intestinal
bacterial overgrowth and increased plasma
enteroglucagon results in retardation of small-
intestinal transit.
 RADIOGRAPHIC FEATURES
• Small bowel dilatation: proportional to disease
severity
• Barium flocculation: due to intestinal hypersecretion
• Hidebound-like appearance
• Duodenal nodular changes
• Jejunoileal fold pattern reversal
• Segmentation
• Mucosal atrophy
• Transient non-obstructive intussusception (coiled
spring appearance)
Reversal of jejunoileal fold pattern
Hide – bound sign
 references
• En.m.Wikipedia.org
• Emedicine.Medscape.com/article/182986-
overview#a6
• www.radiopaedia.org
CLINICAL PRESENTATION

• vomiting of gastric contents

-dehydration
-electrolyte imbalance
• Renal failure from dehydration
• Malnutrition and anaemia
 RADIOLOGICAL FEATURES
•  distended gastric air bubbles that do not cross
the midline.
• If the obstruction is large, the small bowel may
not be visualized.
HIATUS HERNIA AND GERD
In GERD,Gastric acid refluxes through the
esophageal sphincter into the lower esophagus.
Initiated by transient collapses of esophageal
sphincter for longer than normal.

Common clinical signs of GERD and hiatus hernia.

• Chest pain.
• Burning sensation in the chest
• Dysphagia
• regurgitation of food.
• Impaired peristalsis
and poor clearance.
• Reflux of barium into
the esophagus
INFLAMMATORY BOWEL DISEASE
&
HIRSCHSPRUNG DISEASE
 Definition
• is a chronic idiopathic disease affecting the gastrointestinal
(GI) tract that is comprised of two separate, but related
intestinal disorders.

• These disorders are: Crohn’s disease (CD)

•  Ulcerative colitis (UC)
 CROHN DISEASE
• Isinflammatory bowel disease an idiopathic  characterized by
widespread discontinuous gastrointestinal tract inflammation.
The terminal ileum and proximal colon are most often
affected.
 Clinical manifestation of CD
• Chronic diarrhea
• Recurrent abdominal pain
• Rectal bleeding
• Fever
• Fatigue
• Athritis
 Pathophsyology
• Crohn disease begins with crypt inflammation and abscesses,
which progress to tiny focal aphthoid ulcers. These mucosal
lesions may develop into deep longitudinal and transverse
ulcers with intervening mucosal edema, creating a
characteristic cobblestoned appearance to the bowel.
• Transmural spread of inflammation leads to lymphedema and
thickening of the bowel wall and mesentery. Mesenteric fat
typically extends onto the serosal surface of the bowel.
Mesenteric lymph nodes often enlarge. Extensive inflammation
may result in hypertrophy of the muscularis mucosae, fibrosis,
and stricture formation, which can lead to bowel obstruction.
Features of crohn’s disease on barium study.

• Mucosal ulcers
– aphthous ulcers initially
– deep ulcers (>3 mm depth)
– longitudinal fissures
– transverse stripes
– when severe leads to cobblestone appearance
– may lead to sinus tracts and fistulae
• Widely separated loops of bowel due to fibrofatty
proliferation (creeping fat) 2
• Thickened folds due to edema
• Pseudodiverticula/pseudosacculation
formation: due to contraction at the site of
ulcer with ballooning of the opposite (usually
antimesenteric) site
• String sign: tubular narrowing due to spasm or
stricture depending on the chronicity
• Partial obstruction
• On control films presence of gallstones, renal
oxalate stones, and sacroiliac joint or
lumbosacral spine changes should be sought
 ULCERATIVE COLITIS
• Predominantly mucosal disease, possible auto-immune
producing crypt abscesses
 Pathophysiology
• Ulcerative colitis usually begins in the rectum. It may remain localized
to the rectum (ulcerative proctitis) or extend proximally, sometimes
involving the entire colon. Rarely, it involves most of the large bowel at
once.
• The inflammation caused by ulcerative colitis affects the mucosa and
submucosa, and there is a sharp border between normal and affected
tissue. Only in severe disease is the muscularis involved. Early in the
disease, the mucous membrane is erythematous, finely granular, and
friable, with loss of the normal vascular pattern and often with
scattered hemorrhagic areas. Large mucosal ulcers with copious
purulent exudate characterize severe disease. Islands of relatively
normal or hyperplastic inflammatory mucosa (pseudopolyps) project
above areas of ulcerated mucosa. Fistulas and abscesses do not occur.
 Clinical manifestation of UC
• Recurrent episodes of bloody diarrhea
• Electrolyte depletion
• Abdominal pain
• Fever
• Periods of exacerbation and remission
• Iritis, erythema nodosum, pyoderma gangrenosum
• Pericholangitis, chronic active hepatitis, sclerosing
cholangitis, fatty liver
• Spondylitis, peripheral arthritis, RA (10-20%)
• Thrombotic complications 
 Radiographic features

• Plain radiograph
Show evidence of mural thickening (more
common), with thumbprinting also seen in
more severe cases.
• Fluoroscopy
• Double contrast barium enema allows for exquisite
detail of the colonic mucosa and also allows the bowel
proximal to strictures to be assessed. It is however
contraindicated if acute severe colitis is present due to
the risk of perforation.
• Mucosal inflammation leads a granular appearance to
the surface of the bowel. As inflammation increases,
the bowel wall and haustra thicken.
• Mucosal ulcers are undermined (button-shaped ulcers
). When most of the mucosa has been lost, islands of
mucosa remain giving it a pseudopolyp appearance.
• In chronic cases, the bowel becomes
featureless with the loss of normal haustral
markings, luminal narrowing and bowel
shortening (lead pipe sign).
• Small islands of residual mucosa can grow into
thin worm-like structures (so-called filiform
polyps)
• Colorectal carcinoma in the setting of
ulcerative colitis is more frequently sessile and
may appear to be a simple stricture.
 Hirschsprung disease

•  Is the most common cause of neonatal colonic obstruction

(15-20%). It is commonly characterized by a short segment of
colonic aganglionosis affecting term neonates. 
 Clinical presentation
• Swollen belly
• Vomiting, including vomiting a green or brown
substance
• Constipation or gas, which might make a
newborn fussy
• Diarrhea
 Pathophysiology
• It's not clear what causes Hirschsprung's
disease. It sometimes occurs in families and
might, in some cases, be associated with a
genetic mutation.
• Hirschsprung's disease occurs when nerve cells
in the colon don't form completely. Nerves in
the colon control the muscle contractions that
move food through the bowels. Without the
contractions, stool stays in the large intestine.
 REFERENCES
• www.radiopedia.com
• www.slideshare.com
• www.medicalpathology.com