GIT

Lets talk about ba examination

Radiology of G.I.TRadiological investigations1- Contrast examination Barium study  Ba. Swallow, Ba. Meal, Ba. Follow through & Ba enema 2-Endoscopic Ultrasound .3- CT & MRI.4-Nuclear medicine (FDG-PET): flurodeoxyglucose positron emission tomography

THE OESOPHAGUSBarium Swallow:1. Conventional2. Double contrast (DC)3. Flouroscopy + spot films

Technique

1.Patient will need to be NPO after midnight before the exam 2.The patient will have to swallow a contrast agent: Barium or Gastrograffin May also swallow sodium bicarbonate for double contrast barium swallow 3.X-ray tech will have the patient perform various maneuvers so that the barium can coat the GI tract

Indications

Odynaphagia Dysphagia Hematemesis Abdominal pain Unexplained weight loss


The Normal Anatomy: *Long tubular structure * Length 25-30 cm* Start at level of C5 ( Crico-pharengeal)* End – Cardiac sphincter* Three portions Cervical Thoracic Abdominal* Normal Mucosal pattern (DC) thin regular longitudinal Parallel Numbers of lines ( 4-5 )

Areas of normal Narrowings- body of the cervical vertebra - AA- LT atrium- diaphragmatic hiatus

On the Hypo pharyngeal part Common structures that we can visualize are: Epiglottis Post cricoid impression
lateral pharyngeal pouches
Crico pharyngeal muscle impression



LEFT: Lateral view: Epiglottis (red arrow). Post cricoid impression (yellow arrows). Crico pharyngeous impression (white arrow).RIGHT: AP-view: Small lateral pharyngeal pouches (arrows)


The esophageal wall is composed of: Mucosa Musculature Inner circular layer Outer longitudinal layer: Upper 1/3 striated muscle Middle 1/3 striated and smooth muscle Lower 1/3 smooth muscle
No serosa

Esophagus mucosa: normal thin, parallel, uniform mucosal folds 3-4 in no.in double contrast examination

Esophageal peristalsis Normal: Primary contraction: Propels bolus through the esophagus Secondary contraction: Follows primary contraction and propels any remaining bolus from thoracic esophagus


Abnormal contraction : Tertiary contractions, Diffuse esophageal spasm crock screw o. ))Nutcracker esophagus Decreased peristalsis resulting from achalasia, scleroderma, dermatomyositis, polymyositis, esophagitis, and secondary to many other diseases

tertiary contractions

Diffuse esophageal spasm Diffuse esophageal spasm produces intermittent contractions of the mid and distal esophageal smooth muscle, associated with chest symptoms



Congenital Anomalies 1- Artesia with or with out tracheo-oesophageal fistula (TEF). 2- Congenital Short oesophagus. 3- Congenital Duplication ( Neuro-enteric cyst ) ATRESIA: - Complete blockage of the lumen . - The diagnosis is suggested after birth by in ability of infant to feed or by choking during swallowing . - The blocked segment is mostly seen at level of thoracic inlet

Types of Fistula

Acquired Lesions
DYSPHAGIA difficulty in swallowing causes 1- Carcinoma ( Malignant stricture). 2-Benign Stricture (Corrosive ). 3-Achalasia Cardia. 4-forgien body 5-osophagitis .

Malignant stricture

CA esophagus is the cause for the malignant stricture The most common types of esophageal carcinoma are squamous cell carcinoma and adenocarcinoma . esophagography is unique among esophageal studies for assessing both morphology and motility. Barium esophagography remains the study of choice for characterization of esophageal strictures. Esophageal carcinoma may demonstrate a variety of appearances on barium esophagrams.

Annular Carcinoma

Narrowing : 1-Constant. 2-Irrigular . 3-Variable length. 4- Shouldering sign. 5-Fistula (double tract). 6-Soft tissue shadow of the mass

Computed Tomography

Contrast-enhanced CT plays an important role in the 1.staging of esophageal carcinoma. to 2.determining the extent of the local tumor; 3.invasion of mediastinal structures; 4.involvement of supra clavicular, mediastinal, or upper abdominal lymph nodes 5. Assessment of the distant metastases

examination should extend from the thoracic inlet through the liver Routine oral contrast material such as (gastrographine) or a negative intra luminal contrast medium, such as water. +/ - IV contrast injection CT essential in the Dx & staging of the CA

CT finding of esophageal malignancy

1.Eccentric or circumferential wall thickening is greater than 5 mm. 2.Peri-esophageal soft tissue and fat stranding may be demonstrated. 3.A dilated fluid- and debris-filled esophageal lumen is proximal to an obstructing lesion. 4.Aortic invasion . 5.Osophageal CA is often metastatic at the time of presentation ( look for the LN & distal metastasis ) .

Benign Stricture

Causes : Peptic esophagitis Corrosive Traumatic Ba. swallow : 1-Constant narrowing. 2- Long length (lower third). 3-Smooth and regular. 4-Mild proximal dilatation. 5-No shouldering sign. 6-Smooth tapering ( funnel shape).


Inflammation and InfectionGastroesophageal reflux (GERD) is the most common cause of esophagitis.

Infectious esophagitis Candida esophagitis in patient with an infectious esophagitis due to candida , the barium shows numerous fine erosions & plaques causing shaggy outline of the osophagus due to Candida albicans in immunocompromised patient.

middle year old female with a past medical history significant for HIV/AIDS comes in with complaint of loosing their weight over the past 2 weeks with pain & difficulty on swallowing …. Also feels like food is getting stuck in her throat What is your diagnosis ??????????

A chalasia Cardia

Achalasia Presentation: Equal M:F incidence, most common in middle-age Slow progression of dysphasia to start with to solid material then to solid & water Increased incidence of carcinoma Etiology: Unknown ??? absent or reduced esophageal ganglion cells at their distal lower sphincter Incomplete or absent relaxation of LES with swallowing Absent primary peristaltic waves

A chalasia Cardia

A : Absence Chalasia : Relaxation Narrowing : 1-the narrowing is Constant Short length (confined to cardia). 2-Regular and smooth. 3- No shouldering sign. 4-Tapering (Tip of pencil , cigar shape) Under left dome of diaphragm.

Achalasia continue

5. DILATATION (Sac like in proximal part ) 6-Undulating or spiky out line due to sluggish peristalsis. 7 Non- homogeneity of Barium due to food particles. 8-Air Barium level. 9- CXR shows widening of mediastinum. 10-Absence of fundal gas shadow. 7-Basal fibrosis in lungs due to repeated aspiration pneumonia .



LEFT: Dilated esophagus (arrows) appears as long, well-defined structure paralleling heart RIGHT: Dilated esophagus usually deviates to right. Narrowing (arrow) at hiatus.


LEFT: CT shows dilated esophagus (arrow) that led to esophagram.RIGHT: Esophagram shows narrowing (arrow) at level of hiatus.


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PULSION DIVERTICULUM
Due to raised intra-luminal tension 2- Chocking after meal . 3- In cervical portion at level of C5 4- Posteriorly (Killience dehiscent) 5- Lateral view show increased pre-vertebral space with air fluid level. 6- Confirmed by Ba. Swallow.

TRACTION DIVERTICULUM

Out pouching of lumen laterally due to fibrosis & adhesions ( post-Tb.) 2-In the middle third at level of hilum 3- Up ward direction of diverticulum 4- Irregular base


On the far left a traction diverticulum (arrow) due to hilar granulomatous disease. Calcified adenopathy (asterisk). In the middle a pulsion diverticulum (arrow) due to high intra luminal pressure.On the right multiple pulsion diverticula (arrows)

CONGENITAL DIVERTICULUM

1-Asymtomatic unless complicated. 2-At lower part of esophagus above the diaphragm (Epi-phrenic) 3- Lateral or posterior in position.



Sliding herniaOn the left initially, GE junction is below the esophageal hiatus. Later, stomach protrudes through hiatus

Para esophageal hernia

On the far left gas filled gastric funds (asterisk) protrudes through hiatus but GE junction (arrow) is below diaphragm


Thin mucosal fold (membrane) 2- Arise from anterior wall and extend Posteriorly . 3- Lateral view Ba. Swallow show self like filling defect with proximal dilatation. 4-Single or multiple.
ESOPHAGEAL WEB


10% incidence at autopsy Can be congenital or acquired Most in hypopharynx and proximal esophagus Majority protrude from anterior esophageal wall Symptoms if lumen > 50% compromised Sideropenic dysphagia (Plummer-Vinson syndrome) Iron deficiency anemia Esophageal web with dysphagia Increased incidence of carcinoma Validity of syndrome debatable

1-Dilatation of venous plexus in the wall of the esophagus due to increased pressure ( portal H.T.). 2-Important cause of Hematemesis . 3-Early changes seen in the mucosa (D.C.) loss of parallelism with thick and tortuous folds. 4-Later multiple small filling defects (fine cobble stone). 5-In advanced stage large filling defects ( coarse cobble stone ) . 6- More advanced stage elongated and worm like filling defect . 7-The changes are seen at lower third and gastric fundus.
Esophageal Varieces

Stomach & duodenum

Barium meal Fluoroscopy + spot films Preparation

The Normal Anatomy of Stomach1- Shape.2-Size.3-Site.4-Anatomical parts.5-Mucosal pattern.

Normal Anatomy of DuodenumDuodenal cap.Duodenal loop

Congenital Hypertrophic pyloric stenosisCause:A. Congenital typeB.Adult type

Congenital pyloric stenosis. The abnormal narrowing of the opening of the pylorus causes episodes of projectile vomiting
Congenital hypertrophic pyloric stenosis, hypertrophic pyloric stenosis GI disease A narrowing of the gastric outlet into the duodenum due to thickening of pyloric muscle, which controls gastric flow to the duodenum; PS is more common in ♂; Sex appear shortly after birth.


Barium meal image of a case of corrosive-induced gastric outlet obstruction benign narrowing
GASTRIC CA


PEPTIC ULCERGU, DU and IU.The Ba. meal findings are :1-Direct signs : * Ulcer crater ( nitch): Either in enface or in profile * Associated signs: I. Spasm II. Radiated mucosal folds. III. Edema (Hampton's line).2- Indirect signs : I. Hyper peristaltic waves. II. Companion B sign. III. Thick mucosal folds & hyper peristaltic stomach  (angry mucosa)

Questions?