RT 304 Midterm PDF

Gastrointestinal System The Digestive Tract of the body contains all the Organs, Ducts and components to start and complete the...

Gastrointestinal System The Digestive Tract of the body contains all the Organs, Ducts and components to start and complete the Digestive Process:  Mastication (Chewing): mechanical breakdown of food.  Deglutition: complex process. Coordination of Head, Neck and Esophageal Sphincters. Esophagus: vertical tube about 10 inches long.  Extends from C6 - T11. Inferior of Pharynx to the Stomach. Stomach: large inflatable sac that is located in the Left Upper Quadrant of the Abdomen.  Most Dilated Portion of Digestive Tract; it can hold almost 1.5 quarts (qt) of food and liquid. Small Bowel (Intestines): measures 18 - 23 feet. From the Pyloric Sphincter to the Cecum.  Small Bowel because its Lumen is smaller than large bowel.  3 Divisions: Duodenum, Jejunum, and Ileum. Large Bowel (Intestines): average 5 - 6 feet in length. It extends from Cecum to Anus.  Divisions: Ascending, Transverse, Descending, & Sigmoid Colon, Rectum, Anal Canal. Pathology: Esophagus – Congenital Anomaly 1. Atresia  Esophageal Atresia: refers to an Absence in the Continuity of the Esophagus.  Inappropriate division of the Primitive Foregut into the Trachea and Esophagus.  Most Common Congenital Anomaly of the Esophagus. Clinical Manifestation: - Esophageal Atresia: may be suspected in the Neonate.  1. Inability to swallow Saliva or Milk.  2. Aspiration during early feedings.  3. Failure to pass a Nasogastric Tube into the stomach successfully. Digestive System  Digestive System: alters the Chemical and Physical Composition of food so that it can be Absorbed and Used by Body Cells. 2. Tracheoesophageal Fistula (Passageway) Pathology: Esophagus – Acquired Type  Failure of Esophageal Lumen to develop separately from the Trachea. 1. Esophagitis Reflux (GERD – Gastroesophageal Reflux Disease)  Congenital Esophageal Atresia: lack of the development of the Esophageal Lumen resulting in a Blind Pouch.  Spectrum of disease that occurs when Gastric Acid refluxes from Stomach to Lower Esophagus across the Lower Esophageal Sphincter.  Esophageal Atresia & TE fistulas: often associated with other Congenital Malformations  Alcohol, Chocolate, Caffeine, and Fatty Food: tend to decrease the involving the Skeleton, Cardiovascular System, and GI Tract. pressure of the Esophageal Sphincter, allowing reflux to occur. Radiographic Features  Difficulty in radiographic diagnosis of GERD: presence of Spontaneous Reflux on Upper GI Examination in 20% of normal individuals.  Pathologic Gastro-Esophageal Reflux Disease: present with Reflux after provocative maneuvers such as Valsalva, Leg Raising, and Coughing. Appearance  Superficial Ulcerations or Erosion.  Streaks or Dots of Barium Superimposed on Flat Mucosa of Distal Esophagus. 2. Barrett’s Esophagus Types of Findings for Tracheoesophageal (TE) Fistula  Condition related to Severe Reflux Esophagitis.  Normal Squamous Lining of the Lower Esophagus is destroyed & replaced by Columnar Congenital TE Fistula Epithelium similar to the Stomach. Type 1: 2nd most common.  Unusually high susceptibility in developing Malignancy in Columnar Cell-Lined Portion.  These tumors are almost always Adenocarcinoma which are otherwise very Rare in the  Pure Esophageal Atresia – Upper and Lower Esophagus blind pouches. Esophagus (5% of Esophageal Cancer). Type 2  Upper Esophagus communicates with Trachea; Lower segment blind pouch. Type 3: Most common.  Upper Esophagus forms blind pouch (Esophageal Atresia) with a Distal Esophagus communicating with the Trachea. Type 4: 3rd most common.  Upper and Lower Esophageal segments blind pouches. Both connected to Bronchial Tree.  H Fistula: is a connection at the mid-Esophagus and Trachea. 3. Candida and Herpes Virus Acquired TE Fistula  Candida (Fungal) & Herpes Virus: organisms most responsible for Infectious Esophagitis. Fistula caused by:  Usually occurs in patients with Widespread Malignancy who are receiving Radiation Therapy, Chemotherapy, Corticosteroids, or Immunosuppressive Agents and 1. Mediastinal Malignancy 2. Infection Process 3. Trauma Antibiotics (Tetracycline).  Candida Esophagitis Herpes Esophagitis 5. Esophageal Cancer  Uncommon Tumor that occurs within the Esophagus of affected individuals.  Symptoms: Increasing Dysphagia that progress from Solid Foods to Liquids. Appearance Clinical Manifestation:  Irregular Cobblestone Pattern with a Shaggy (Hairy) Marginal Contour of the Esophagus.  Caused by Deep Ulceration and Sloughing of the Mucosa.  1. Increasing Dysphagia  Candida Infection: manifests as Plaques & Nodules; from Superficial Collection of Fungi.  2. Worsening Reflux  Herpetic Esophagitis: include Small Mucosal Ulcers or Plaques.  3. Hoarseness and Cough 4. Ingestion of Corrosive Agents Radiographic Appearance  Alkaline & Acidic Corrosive Agents: produce acute inflammatory changes in esophagus.  Barium Swallow Double Contrast: Flat Plaque like Lesion, Infiltrating Lesion, (Irregular  Strong Alkaline Agents: causes Deeper Lesions than ingestion of strong acids, and only Wall) and Polypoid Mass (Deep Ulceration). half of those who ingest an Acid suffer severe injury.  CT Scan with Contrast: Wall Thickening Greater than 3 – 5 mm. Appearance  Alkaline: Deeper Ulceration and Stricture Formation.  Acidic: Superficial Minimal Ulceration and Stricture Formation. Alkali Sodium Hydroxide Potassium Hydroxide Oven Cleaners, Liquid Agents, Liquid Drain Cleaners, Disk Batteries Calcium Hydroxide Hair Relaxers Lithium Hydroxide Hair Relaxers Ammonia Household Cleaners Dishwater Detergents Acid Sulfuric Acid Hydrochloric Acid Toilet Bowl, and Swimming Pool Cleaners, Rust Removers Nitric Acid Bleaches / Caustics Hypochlorous Acid Bleach – neutral pH commercially Peroxide Mildew Remover 6. Esophageal Diverticula (Outpouching)  Esophageal diverticula found in the Top Part or Area of the Esophagus.  Abnormal Tightening of Upper Esophageal Sphincter. Low Pharynx & Upper Esophagus.  Traction or True Diverticula: Common Lesions that either contain all Layers of the wall.  This causes a Bulge to form, and over time pressure will cause a Diverticulum to develop.  Pulsion or False Diverticula: Mucosa & Submucosa herniating through the muscular layer.  Most Common type of Esophageal Diverticulum.  Small Diverticula: do not retain food or secretions and are Asymptomatic.  Occurs in older women.  Aspiration Pneumonia: when a diverticulum fills with food or secretions.  Posteriorly at Site of Killian’s Dehiscence: superior boundary is Thyropharyngeal Muscle and inferior boundary is Cricopharyngeal Muscle.  Pulsion Diverticulum  False Diverticulum: Herniation of Mucosa and Submucosa through Muscular Layer. 7. Esophageal Varices  Dilated Veins in the wall of Esophagus.  Increased Pressure in Portal Venous System (Portal Hypertension) – Liver Cirrhosis.  Infrequently demonstrated in the Absence of Portal Hypertension. Esophageal Diverticulum: 2 Types of Esophageal Varices:  Pouch or Sac that Protrudes Outwards from the wall of the Esophagus.  Uphill Esophageal Varices: most common form, caused by Portal Hypertension, as a  Sacs appear anywhere on the Esophagus. Collateral Pathway between the Portal Vein and the Superior Vena Cava.  Most commonly found in Middle-Aged or Older People.  Downhill Esophageal Varices: relatively rare, typically caused by Superior Vena Cava  Develops in 3 Variations: Traction Diverticula, Pulsion Diverticula & Zenker’s Diverticulum. Obstruction, as part of Superior Vena Cava Syndrome, as a Collateral Pathway between  Occur when Muscles involved in Digestion stop working properly. the Superior Vena Cava into the Portal Circulation and/or the Inferior Vena Cava.  Most people don’t receive Treatment but Surgery can happen in severe cases. Appearance Esophageal Diverticula are classified differently based on where they are Located:  Serpiginous (Wavy Border) Thickening of Folds which appear as; Traction Diverticula or Mid-esophageal Diverticula  Round Oval Filling Defects resembling the Bead of Rosary.  Pouches most commonly occur in the Middle Area of the Esophagus.  Occurs when there is an External Force on the wall of Esophagus that creates the Pouch.  Formed in response to Pull from Fibrous Adhesions following Lymph Node Infection (TB)  True Diverticulum: contains all 3 Esophageal Layers.  May form from Increased Intraluminal Pressure and be Pulsion Diverticula. Pulsion Diverticula or Epiphrenic / Epiphanic Diverticula  Pouches occur at the Base or Lower Part of the Esophagus.  Esophagus is Pushed due to Incoordination of Sphincter Muscle in Lower Esophagus.  Sphincter: is a Ring made of Muscle that helps connect the Esophagus with the Stomach. 8. Hiatal Hernia  Location is usually in Distal Esophagus on Lateral Esophageal Wall, right > left.  Often associated with Hiatal Hernia.  Occurs in about half of the population over age 50 years.  Pulsion Diverticulum.  Early Stages: a hiatal hernia is Reducible.  False Diverticulum.  Chronic Herniation: may be associated with GERD. Zenker's Diverticulum  Patients with Hiatus Hernia are Asymptomatic, and it is an Incidental Finding.  Symptoms: Epigastric or Chest Pain, Postprandial Fullness, Nausea and Vomiting. There are 2 Main Types of Hiatus Hernia (although they may co-exist):  1. Sliding Hiatal Hernia: 90% most common.  2. Rolling Hiatal Hernia: Paraesophageal Hiatal Hernia. Radiographic Appearance  Plain Radiograph: Retrocardiac Mass with or without an Air-Fluid Level.  Schatzki Ring: Sliding Hiatal Hernia (Trendelenburg Position). Radiographic Appearance  Fluoroscopy: Numerous Coarse Thick Gastric Folds within the Suprahiatal Pouch Tortuous Esophagus with an Eccentric Gastro-Esophageal Junction.  Perforation that extends throughout the Entire Esophageal Wall can lead to Free Air in the Mediastinum or Peri-Esophageal Soft Tissues.  Radiopaque Contrast demonstrate Extravasation through the Perforation or an Intramural Dissection Channel separated by Intervening Lucent Line from Normal Esophageal Lumen. Summary of Findings for the Esophagus Congenital Tracheoesophageal Fistula Location: 9. Achalasia  Blind Pouch Superiorly  Failure of Peristalsis to pass food to esophagus and Failure of Relaxation of the Cardia.  Blind Pouch Distally or Tracheal Fistula  Failure of Esophageal Peristalsis that causes Impaired Relaxation of the Lower Esophageal Imaging Appearance: Sphincter, resulting in food stasis and marked dilatation of the Esophagus.  Blind Pouch filled with Contrast Agent or NG Tube Radiographic Features  Fistula Track (if one exists), NG Tube Injection  CT: demonstrates Fistula location and Size for Presurgical Planning  Achalasia: involves a Short Segment (less than 3.5 cm in length) of the Distal Esophagus. Tracheoesophageal Fistula – Acquired Appearance: Rat Tail or Bird Beak Sign. Location: Usually at level of the Carina or more Proximal. Imaging Appearance: Demonstration of connection between Esophagus and Tracheobronchial Tree Reflux Esophagitis Location: Distal Esophagus. Imaging Appearance: Streaks or Dots Superimposed on Flat Mucosa. Barrett’s Esophagus 10. Esophageal Perforation Location: Middle to Lower Esophagus.  Complication of esophagitis, peptic ulcer, neoplasm, external trauma, & instrumentation Imaging Appearance: Smooth Tapered Strictures.  Severe Vomiting (most common cause) or Coughing - Dietary / Alcoholic Recklessness Candida (Fungal) and Herpesvirus Esophagitis  Mallory-Weiss Syndrome: refers to a Tear or Laceration of the Mucous Membrane, most commonly at the point where the Esophagus and the Stomach meet. Location: Entire Esophagus. Imaging Appearance: Imaging Appearance:  Cobblestone Pattern.  CT: an Outpouching at the Pharyngoesophageal Junction.  Shaggy Marginal Contour. Esophageal Varices  Small Mucosal Ulcers or Plaques. Ingestion of Corrosive Agents Location: Distal Esophagus and Stomach. Location: Alkaline Ingestion. Imaging Appearance: Imaging Appearance:  Esophagram: Serpiginous Thickening of Folds – resembles Rosary Beads.  Endoscopic Ultrasound: Compressible Hypoechoic mass in Outer or Submucosal Layer.  Deeper Ulceration. Hiatal Hernia  Stricture Formation. Location: Acidic Ingestion. Location: Esophagogastric Region. Imaging Appearance: Imaging Appearance:  Superficial Minimal Ulceration.  GI Series: Numerous Thicker Folds of the Stomach above the Diaphragm.  Stricture Formation. Achalasia: Functional Obstruction Esophageal Cancer Location: Distal Esophagus with Proximal Dilation. Location: Imaging Appearance:  Distal Esophagus.  Chest Radiograph: Dilated Esophagus.  Esophagogastric Junction.  GI Series: Narrowing of Distal Esophageal Segment. Imaging Appearance: Foreign Bodies: Food Bolus or Non-Opaque Objects Double-contrast Barium Swallow Study: Location: Any region of the Esophagus.  Flat Plaque-Like Lesion. Imaging Appearance:  Infiltrating Lesion (Irregular Wall).  Polypoid Mass (Deep Ulceration).  Barium Swallow: to demonstrate the level of Impaction causing the Obstruction. CT with Contrast Enhancement: Wall Thickening Greater Than 3-5 mm. Foreign Bodies: Non-Food-Related (Coin) or Opaque Esophageal Diverticula Location: Any region of the Esophagus. Location: Imaging Appearance: Intraluminal Filling Defect with an Irregular Surface.  Traction: all Layers of the wall. Esophageal Perforation: inflammatory, neoplastic, or traumatic. Imaging Appearance: Location: Any region of the Esophagus.  Esophagram: an Outpouching or Pocket Filling with Barium. Imaging Appearance: Location:  Perforation Through Entire Wall – Air in the Mediastinum.  Extravasation of Contrast Material through Perforation.  Epiphrenic: Distal Portion of the Esophagus. Stomach: Pathology Radiographic Appearance 1. Gastritis  Ultrasound: modality of choice. High Sensitivity & Specificity. Accuracy approach 100%  Thickened Pyloric Muscle (width >3 mm) and;  Inflammation of Stomach.  Elongated Pyloric Canal (>1.2 cm) on the Longitudinal Sonogram.  Result of irritants like Alcohol, Corrosive Agents, & Infection.  Palpable Olive appears as a “Doughnut” or “Target” Sign in the Cross-Sectional Image.  Gastritis: changes the Normal Surface Pattern of the Gastric Mucosa.  3 Types: Alcoholic, Corrosive, Bacteria (Phlegmonous) Gastritis. Radiographic Appearance  1. Alcoholic Gastritis: Thickening of Gastric Folds & Multiple Superficial Gastric Erosions.  2. Corrosive Gastritis: Acute Inflammatory Reaction heals by Fibrosis and Scarring, which Result in Severe Narrowing of the Antrum and may cause Gastric Outlet Obstruction.  3. Bacterial (Phlegmonous) Gastritis: Inflammatory Thickening of the Gastric Wall causes Narrowing of the Stomach that may mimic Gastric Cancer.  Infectious Gastritis Diagnosis: can be made if there is evidence of Gas Bubbles (produced 3. Peptic Ulcer Disease by the Bacteria) in the Stomach Wall.  Group of Inflammatory Processes involving the Stomach and Duodenum. Gastritis Emphysematous Gastritis  Caused by Action of Acid & Enzyme Pepsin from Stomach. Occurs on Lesser Curvature.  Peptic Ulcer Disease: involves Ulceration of the Stomach or Duodenal Lining caused by an imbalance between Digestive Fluids in the Stomach and the Protective Lining.  Acute Upper GI Bleeding: most commonly caused by Peptic Ulcer Disease.  Pneumoperitoneum with Peritonitis: most commonly caused by Free Perforation of a Peptic Ulcer located in the Anterior Wall of the Stomach or Duodenum.  Gastric Outlet Obstruction: most commonly caused by Narrowing of the Lumen of the Distal Stomach or Duodenal Bulb caused by Peptic Ulcer Disease. 4 Types of Peptic Ulcer Disease and Radiographic Appearance 1. Inflammation Process 2. Duodenal Ulcer: Most Common Manifestation of Peptic Ulcer Disease.  More than 95% of Duodenal Ulcers occur in the 1st Portion of Duodenum (Duodenal Bulb).  Healed with Scarring: well-defined collection of barium in ulcer crater –cloverleaf deformity  Chronic Duodenal Ulcer Disease: typical Cloverleaf Deformity is visible.  Duodenal Ulcer: Rounded Collection of Barium surrounded by Lucent Edema. 2. Pyloric Stenosis  Infantile Hypertrophic Pyloric Stenosis (IHPS).  2 Muscular Layers of Pylorus become Hyperplastic and Hypertrophic.  Environmental and Hereditary Factors: cause in 2 - 4 per 1000 live births (0.02 – 0.04%). 3. Gastric Ulcers: another form of Peptic Ulcer Disease, occurs on Stomach’s Lesser Curvature. 2 Common Types of Stomach Cancer:  Duodenal Ulcers are virtually always Benign, up to 5% of Gastric Ulcers are Malignant.  1. Gastric Wall Infiltration (Linitis Plastica): Diffuse Infiltration of the Stomach Wall by  Barium-Filled Ulcer Crater along the Lesser Curvature or Posterior Wall of the Stomach, with Cancer Cells, causing Thickening and Loss of Elasticity. surrounding Mucosal Edema “Radiating Folds” around Gastric Ulcers.  2. Polypoid Mass: Protruding Mass that develop from Inner Lining of Stomach - Malignant.  Benign Gastric Ulcer: small, slender folds extending to the edge of crater. Radiographic Appearance  Malignant Gastric Ulcer: thick folds radiate to an irregular mound of tissue around ulcer.  Gastric Wall Infiltration (Linitis Plastica): Rigid, non-distensible stomach with Loss of Rugal Folds. “Leather Bottle Stomach” Appearance.  Polypoid Mass: Large, Lobulated Filling Defect within the Stomach, sometimes with Central Ulceration on a Barium study. Benign Gastric Ulcer  On en face projection: Prominent Radiating Folds extend directly to the Ulcer.  Inflammatory Mass Effect: Lucency around the Ulcer. Summary of Findings for the Stomach  Edema at the Base of Ulcer Crater: Penetration of Contrast outside Normal, Barium-Filled Gastric Lumen with a Thin, Sharply Demarcated, Lucent Line with Parallel Straight Margins. Gastritis Location:  Alcohol: Gastric Folds. Imaging Appearance:  Thickened Gastric Folds.  Gastric Outlet Obstruction. Location:  Corrosive: Narrowing of Antrum. 4. Superficial Gastric Erosions: Small and Shallow Ulcerations that Location: are rarely demonstrated on Single-Contrast Upper GI Examinations.  Bacterial or Infectious: Gastric Wall.  Double-Contrast Techniques: Superficial Gastric Erosion typically appears radiographically as a Tiny Fleck of Barium, Imaging Appearance: Thickened Gastric Wall causing narrowing of Stomach & Gas in Stomach Wall which represents the Erosion, surrounded by a Radiolucent Halo, which represents a Mound of Edematous Mucosa. Location: 4. Cancer of the Stomach  Chronic Atrophic: Mucosal Folds.  Malignant Growth of Cells in the Stomach Lining, which may present in various forms. Imaging Appearance: Thinning and Absence of Mucosal Folds (Bald). Pyloric Stenosis Small Bowel (Intestine): Pathology Location: Two Muscular Layers of the Pylorus. Imaging Appearance:  US: Thickened Pyloric Muscle (> 3 mm width) and Elongated Pyloric Canal (> 1.2 cm) on Longitudinal Sonogram.  UGI: demonstrate Shouldering caused by Filling Defect at the Antrum. Peptic Ulcer Location: Inflammatory Process. 1. Crohn’s Disease (Regional Enteritis) Imaging Appearance: Small Shallow Erosions to Perforations – Bleeding Ulcer.  Chronic Inflammatory Disorder of Unknown Cause. Location: Duodenal Ulcer.  Most often involves the Terminal Area of the Ileum but can affect any part of the GI tract. Imaging Appearance:  Although it can occur at any age, Crohn’s disease is most common in Young Adults.  Stress or Emotional Upsets are frequently related to the Onset or Relapse of the disease.  CT: Irregular Collection of Contrast Material in the Gastric Wall.  Rounded / Linear Collection of Contrast surrounded by Lucent Folds that Radiate to Crater. Radiographic Appearance Location: Gastric Ulcer. Irregular Thickening & Distortion of Mucosal Folds; by Submucosal Inflammation & Edema. Imaging Appearance:  String Sign: Narrowing of the Terminal Ileum due to Chronic Inflammation and Fibrosis.  Skip Lesions: Patchy Areas of Inflammation separated by Normal Bowel Segments SBS  Benign: Mucosal Folds are Smooth and Slender and extend to the edge of the Crater.  Cobblestone Appearance: due to Ulcerations and Submucosal Edema.  Malignant: Irregular Folds merge to a Mound of Polypoid Tissue around the Crater.  Fistulas: Abnormal Connections between Bowel Loops, visible on Contrast Studies. Location: Superficial Gastric Erosions. Cobblestone Appearance: Transverse and Longitudinal Ulcerations separating islands of Imaging Appearance: Fleck of Barium with Radiolucent Halo. Thickened Mucosa and Submucosa. Cancer Location: Gastric Wall Infiltration. Imaging Appearance: Diffuse Thickening, Narrowing, and Fixation of Stomach Wall. Location: Polypoid Mass. Imaging Appearance: Irregularity and Ulceration suggest Malignancy. 2. Small Bowel Obstruction  CT: o Stage 1: Intraluminal Mass without Wall Thickening. Imaging Appearance o Stage 2: Wall Thickening < 1 cm without invasion outside the organ.  Distended Loops of Small Bowel containing Gas and Fluid can usually be recognized o Stage 3: Thickened Wall with Extension into adjacent organs. radiographically within 3 - 5 hours of the Onset of Complete Obstruction. o Stage 4: Wall Thickening and Obliteration of Perigastric Fat.  Endoscopic Ultrasound: Increased Echogenicity of Gastric Mucosa with Vertical Invasion. Almost all Gas proximal to a Small Bowel Obstruction represents Swallowed Air.   Upright or Lateral Decubitus Projections: the interface between Gas and Fluid forms a Radiographic Appearance Straight Horizontal Margin.  Supine & Upright Projections: large amounts of Gas in dilated loops of small bowel.  Uniformly Dilated Loops of Bowel (both Small and Large Bowel).  Upright Position & Horizontal Beam: Multiple Prominent Air–Fluid Levels.  No Air-Fluid Levels, as there is No Active Peristalsis.  Diffuse Gas Pattern throughout the Abdomen with No Point of Transition. 3. Intussusception  Is a condition where one segment of the intestine Telescopes into an adjacent segment.  Leading to Obstruction and Compromised Blood Flow.  Children: Intussusception is most common in the region of the Ileocecal Valve. Radiographic Appearance  Barium Enema or Ultrasound: Coiled Spring or Target Sign, represent Bowel Telescoping 1. Adynamic Ileus  Contrast Studies: Cupped Filling Defect can be seen in the Intestine.  Ultrasound: show a Doughnut or Target Sign, which is characteristic of Intussusception.  Lack of Intestinal Peristalsis, results in Functional Obstruction without Physical Blockage.  Adynamic Ileus: occurs in almost every patient who undergoes Abdominal Surgery.  Other causes of Adynamic Ileus: are Peritonitis, Medications that decrease Intestinal Peristalsis (with an Atropine-like effect), Electrolyte & Metabolic Disorders, and Trauma. Imaging Appearance  Retention of Large Amounts of Gas and Fluid in loops of Dilated Small and Large Bowel.  Entire Small and Large Bowel, appears almost Uniformly Dilated with no Obstruction. There are 2 Major Variants of Adynamic Ileus:  Localized Ileus: Isolated Distended Loop of small and large bowel (the Sentinel Loop), Imaging Appearance which is often associated with an adjacent Acute Inflammatory Process.  Radiographic: Coiled-Spring Appearance of trapped Barium.  Colonic Ileus: refers to Selective or Disproportionate Gaseous Distention of the Large Bowel  Barium Enema Examination: Reduction of a Colonic Intussusception. Great care must be without an Obstruction. exercised to prevent Excessive Intraluminal Pressure, that leads to Perforation of Colon.  CT Images: Intussusception appears as 3 Concentric Circles forming a Soft Tissue Mass. 4. Malabsorption Disorder  Defective Absorption of Carbohydrates, Proteins, and Fats from the Small Bowel.  Steatorrhea: passage of Bulky, Foul-Smelling, High-Fat-Content Stools that Float. Imaging Appearance – The 2 Major Radiographic Appearances:  Many of the diseases that cause Malabsorption produce radiographic abnormalities in the 2. Mechanical Ileus Small Bowel, although Malabsorption can exist without detectable Small Bowel changes.  1. Small Bowel Dilation with Normal Folds.  Blockage caused by a Physical Obstruction, such as Tumors, Adhesions, Hernias.  2. Pattern of Generalized, Irregular, Distorted Small Bowel Folds. Sprue: Diffuse Dilation of entire Small Bowel with Excessive Intraluminal Fluid in Patient with Adynamic Ileus Malabsorption. Location: Loss of Motility in Small Bowel. Whipple’s Disease: Diffuse, Irregular Thickening of Small Bowel Folds in a Patient with Malabsorption. Appearance: Large amounts of Gas and Fluid in Small and Large Bowel. Atrophy of Folds: Reversal of the Fold Pattern with more Prominent Folds in the Ileum and Intussusception Featureless Bald Appearance of the Jejunum. Location:  Children: Ileocecal Valve. Appearance:  Radiograph: Coiled Spring Appearance on Contrast Enema.  CT: 3 Concentric Circles forming a Soft Tissue Mass.  Ultrasound: Doughnut-shaped Lesion. Malabsorption Disorders Location: Throughout Small Bowel. Summary of Findings for the Small Bowel Appearance: Crohn’s Disease (Regional Enteritis)  Dilation with Normal Folds. Location: Most often in Terminal Ileum.  Irregular Distorted Folds. Appearance:  Small Bowel Series: o Irregular Thickened Mucosal Folds. o Cobblestone Appearance. o String Sign and Skip Lesions.  CT: Thick Mucosal Walls and “Dirty Fat” Mesenteric Appearance.  CT Enterography: Subtle Wall Thickening and Mucosal Vascular Changes.  Ulcerations: Fistula Formation. Small Bowel Obstruction Location: Mechanical Appearance:  Abdomen: o Caliber of Air-filled bowel appears as dilated proximal bowel & collapsed distal bowel. o Stepladder Appearance.  CT: Herniation illustrated as a “Target Sign” as a result of Slight Wall Thickening with Mesenteric Engorgement. Large Bowel (Intestine): Pathology 1. Acute Appendicitis  Neck of the Appendix becomes Blocked by a Fecalith or by Post Inflammatory Scarring that creates a Closed-Loop Obstruction within the organ.  Inadequate Drainage: Fluid accumulates in Obstruction – Breeding Ground for Bacteria.  High Intraluminal Pressure: causes Distention and Thinning of the Appendix distal to the Obstruction, which interferes with Circulation and may lead to Gangrene and Perforation.  Appendicitis: occurs in all age groups but is more common in Children and Adolescents. Diverticulosis: Sawtoothed Configuration is produced by Thickened Circular Muscle and is associated with Multiple Diverticula. Imaging Appearance Imaging Appearance  Colonic Diverticula: Radiograph - Round or Oval Outpouchings of Barium projecting  Plain Abdominal Radiograph: Round or Oval, Laminated Calcified Fecalith -Appendicolith beyond the confines of the Lumen.  CT Scan of Upper Pelvis: Enlarged Thickened Wall indicating Inflammation.  Vary in size from Barely Visible Dimples to Saclike Structures 2 cm or more in Diameter.  Giant Sigmoid Diverticula: up to 25 cm in Diameter – Chronic Diverticular Abscesses.  May appear as: Large, Well-Circumscribed, Lucent Cystic Structures in Lower Abdomen 2. Colonic Diverticula Diverticulitis: Necrosing Inflammation in the Diverticula.  Outpouchings that represent Acquired Herniations of Mucosa and Submucosa through the Muscular Layers at points of Weakness in the Bowel Wall.  Complication of Diverticular Disease of Colon, especially in the Sigmoid Region.  Incidence of Colonic Diverticulosis increases with Age.  Intense Adjacent Inflammation: Severe Spasm of the Sigmoid Colon.  Rare in persons younger than 30 years.  Peridiverticular Abscess: develops from Perforation of a Diverticulum.  Diverticula: can be demonstrated in up to half of persons older than 60 years. 3. Ulcerative Colitis  Diverticular Disease: is presumed to occur in individuals who frequently exert High Pressures in the Lumen while straining to pass a large bulk of Stool.  Idiopathic Inflammatory Condition of the Colon.   Results in Diffuse Friability and Superficial Erosions on the Colonic Wall and Bleeding. 5. Ischemic Colitis  Irregular Mucosa with Loss of Normal Haustral Markings.  Abrupt Onset of Lower Abdominal Pain and Rectal Bleeding.  Main Symptoms: Bloody Diarrhea, Abdominal Pain, Fever, and Weight Loss.  Physical Examination: Diarrhea is common, as is Abdominal Tenderness.  Most patients are older than 50 years, and have a history of prior Cardiovascular Disease. Imaging Appearance  Initial radiographic appearance of ischemic colitis is Fine Superficial Ulceration caused by Inflammatory Edema of the Mucosa.  As the disease progresses, Deep Penetrating Ulcers, Pseudopolyps, and characteristic Thumbprinting can be demonstrated.  Thumbprinting: refers to Sharply Defined, Finger-Like Indentations 4. Crohn’s Colitis along the margins of the colon wall.  Earliest radiographic findings are seen on Double-Contrast Examinations. Soft Tissue Polypoid Densities: protrude into the Lumen of the Descending  Isolated Tiny, Discrete Erosions (Aphthous Ulcers) appear as Punctate Collections of Colon in a patient with Acute Abdominal Pain and Rectal Bleeding. Barium with a Thin Halo of Edema around them. 6. Colon Cancer  Aphthous Ulcers: Patchy Distribution against a background of Normal Mucosa, unlike the blanket of Abnormal Granular Mucosa in Ulcerative Colitis.  Malignant Tumor of the Colon, often arising from Adenomatous Polyps.  Diffuse Aphthous Ulcers in early Crohn’s Colitis.  Causes Bowel Obstruction, Bleeding, or Perforation.  Long Intramural Fistula in the Transverse Colon. Radiographic Appearance  Barium Enema: Apple-Core or Napkin-Ring Lesion, a Constricted Segment of the Bowel.  CT Scan: Irregular, Annular Narrowing of the Colon with Thickened Walls, possible Lymph Node Enlargement, and Distant Metastases.  Colonoscopy: Direct visualization of Polypoid or Ulcerative Mass. Annular Carcinoma (described as Apple-Core or Napkin-Ring Carcinoma) is one of the most typical forms of Primary Colonic Malignancy. Summary of Findings for Inflammatory Disease – Colitis Ulcerative  Location: Rectal Involvement in 95% of cases; moves Proximally.  Involvement: Continuous  Layers: Only in Mucosal Layer Crohn’s 7. Volvulus  Location: Proximal Colon (Terminal Ileum in 80% of cases)  Involvement: Patchy  Twisting of Bowel on itself that leads to Intestinal Obstruction.  Layers: All Intestinal Wall Layers (Mucosal through Serosal Layer) Cecal Volvulus  KUB: Appendicolith  US: Noncompressible 7 mm or Larger Outer Diameter.  Distended Cecum tends to be displaced upward & to left.  CT: Round or Oval Mass, possibly containing Gas; Dilated Lumen with Thickened,  Found anywhere within the abdomen. Circumferentially Enhancing Wall.  Pathognomonic Sign is a Kidney-Shaped Mass (representing the Twisted Cecum).  Twisted and Thickening Mesentery mimicking the Renal Pelvis. Diverticulosis Sigmoid Volvulus Location: Most Common in Sigmoid.  Barium Enema: Obstruction to Contrast flow at Volvulus and Distention of the Rectum. Appearance: Round or Oval Outpouching projecting beyond Lumen; usually Multiple.  Bird’s-Beak Appearance: Lumen of the Sigmoid tapers toward the site of Stenosis. Diverticulitis 8. Hemorrhoids Location: Inflammation of Diverticula.  Swollen Veins in Lower Rectum or Anus that causes Discomfort, Bleeding, and Itching. Appearance: Radiographic Appearance  Diverticular Perforation with possible Abscess.  Imaging (rarely needed): Hemorrhoids are not usually diagnosed via Radiology, but on;  US: Hypoechoic Projection surrounded by Inflamed Fat.  Colonoscopy: Swollen, Dilated Veins in the Rectum or Anus.  CT: Nonspecific Wall Thickening with a Narrowed Bowel Lumen.  Ultrasound or Doppler: Dilated Venous Structures in severe cases. Ulcerative Colitis Location: Superficial & Acute; beginning in Rectosigmoid Area with continuous involvement to Colon. Appearance:  KUB: Deep Ulcers with Intraluminal Gas or Polypoid Changes, Loss of Haustral Markings.  BE (Double Contrast): Fine Granularity of Mucosa; Submucosa with broad-based Ulcers 9. Hirschsprung Disease or Congenital Aganglionic Megacolon having a Collar-Button Appearance. Crohn's Disease  Hirschsprung Disease: is a Congenital Condition characterized by the Absence of Ganglion Cells in the Distal Colon, leading to a Functional Bowel Obstruction. Location: Terminal Ileum and Proximal Colon most often.  Aganglionic Segment: cannot relax properly. Severe Constipation or Intestinal Blockage. Appearance: Barium Enema  BE (Double Contrast): Patchy Distribution, Noncontiguous Segments (Skip Lesions).  Reduced Caliber Rectum and Sigmoid with a Saw-Tooth Appearance to the Wall.  CT: Colonic Wall Thickening and Abscess Formation.  Rectum is smaller than the Descending Colon.  Transition Point is seen at the junction between Sigmoid and Descending Colon. Ischemic Colitis Summary of Findings of the Colon Location: Entire Colon. Appendicitis Appearance: Location: Appendix  Fine Superficial Ulceration.  Characteristic "Thumbprinting". Appearance:  Tubular Narrowing and a Smooth Stricture. Irritable Bowel Syndrome Hepatobiliary System Location: Alteration of Intestinal Motility. Appearance:  No specific findings.  Rule out other disorders. Cancer Location: 50% in Rectum and Sigmoid Region. Appearance:  Sessile Lesion: Irregular, Lobulated Surface.  CT: Larger than 2 cm, "Apple-Core" or "Napkin-Ring” Appearance. o Circumferential Bowel Wall Thickening, Metastasis, Lymphadenopathy. o Virtual Colonoscopy demonstrates 8 - to 10 - mm Lesions.  US: Transrectal; depth of Tumor Invasion into Bowel Wall.  PET: detection of Distant Nodular Metastasis.  Fusion (PET/CT) imaging: provides the most specific detail. Large Bowel Obstruction Location: Large Bowel. Appearance:  Ileocecal Valve Competent: large dilated Colon, thin-walled Cecum, little small-bowel Gas. Gallbladder  Ileocecal Valve Incompetent: gas-filled loops of Colon and of Small bowel. Functions of the Gallbladder Volvulus  Concentrates Bile through the Gallbladder Epithelium. Location: Cecal or Sigmoid Colon.  Stores Concentrated Bile. Appearance:  Contracts to Release Bile.  Distended Cecum, displaced Upward and to the Left. Gallbladder Divisions  Distended Rectum, devoid of Haustral markings, and a Sausage or Balloon shape.  1. Fundus  Bird's-Beak appearance.  2. Body Hemorrhoids  3. Neck Location: Distal Rectum. Gallbladder Location Appearance:  Intraperitoneal.  Located in the Gallbladder Fossa on the Posterior Surface of the Gallbladder.  Single or Multiple Rectal Filling Defects simulating Polyps.  Lateral to the Inferior Vena Cava, Anterior and Medial to the Right Kidney. Gallbladder Anatomical Variants Reasons for Non-Visualization of the Gallbladder Hartmann Pouch Junctional Fold Phrygian Cap  Non-Fasting Patient.  Surgically Absent.  Obliteration of the Gallbladder Lumen by Intestinal Air or Gallstone.  Patient Body Habitus.  Ectopic Location.  Agenesis. Non-Inflammatory Causes of Gallbladder Wall Thickening Non-Fasting Patient. Congestive Heart Failure Ascites Hypoalbuminemia Cirrhosis Acute Hepatitis Gallbladder Size Enlarged (Distended) Gallbladder  Normal Fasting Adult Gallbladder: 8-10 in length and 3-5 cm in diameter.  Dehydrated Sonographic Appearance  Low Fat Diet Normal Fasting Gallbladder  Intravenous Nutrition  Ellipsoid Anechoic Structure in the Gallbladder Fossa with Posterior Acoustic Enhancement. If there is no Contraction, search for:  Demonstrates Smooth Hyperechoic Walls 3 mm or less.  Gallstone or Obstruction in the Common Bile Duct.  Located in the Inferior Medial Aspect of the Liver.  Empyema: if the Gallbladder is distended with thickened walls & filled with fluid. Abnormal Fasting Gallbladder  Mucocele: if the Gallbladder is distended with thin walls and filled with fluid.  Transverse diameter above 5 cm. Schedules are made at the beginning of the patient’s day:  Thick Edematous Wall exceeding 3 mm in Thickness.  Decreases the amount of Intestinal Air.  Irregular Wall Contour.  Patient is Fasting.  Intraluminal Focus or Echoes.  Acoustic Shadowing Posterior to the Gallbladder Fossa. Pathology 1. Pneumobilia  Presence of Gas in the Biliary System.  Etiology: Surgical Procedure, Trauma, and Infection.  Clinical Findings: Asymptomatic, RUQ Pain. Sonographic Appearance:  Hyperechoic Focus in the Intrahepatic Bile Ducts.  Comet Tail Artifact often Centrally located. 2. Biliary Ascariasis 4. Adenomyomatosis  Living Worms that colonize the Intestinal Tract may go to the Biliary Tree & Gallbladder.  Hyperplasia of the Epithelial and Muscle Layers of the Gallbladder Wall.  Causes: Cholangitis, Cholecystitis, and Pancreatitis, with High Mortality.  Clinical Findings: Asymptomatic, Dull RUQ Pain, Intolerance to Fatty Foods.  Worms are seen in USD as Moving Tubular Echogenic Structures with an Echolucent Core. Sonographic Appearance:  Etiology: ingestion of Contaminated Water or Food.  Clinical Findings: RUQ Pain, Fever, Leukocytosis.  Echogenic Intraluminal Focus. Sonographic Appearance:  Diffuse Comet Tail Artifact.  Immobile.  Spaghetti-like, Moving Tubular Echogenic Structure with an Echolucent Core within Bile Duct.  Non-Shadowing.  Posterior Acoustic Enhancement. 5. Echogenic Bile  Bile becomes Echogenic when it is Highly Concentrated and Cholesterol Crystals and 3. Gallbladder Polyp Calcium Bilirubinate Granules precipitate as Sludge.  Sludge: commonly layers in the Gallbladder and may become quite Viscous and form  Appear as Echogenic Non-Shadowing Nodules that extend from the Gallbladder Wall. Sludge Balls or Tumefactive Sludge.  Cholesterol Polyps: mostly, which are smaller than 1 cm and are commonly Multiple.  Sludge Balls: usually move within the Gallbladder but do not cast acoustic shadows.  Adenomatous Polyps: are rare and indistinguishable from Cholesterol Polyps.  Mixture of Particulate Solids that have Precipitated from Bile.  Benign Epithelial Tumor.  Etiology: Long Fasting, Biliary Stasis, Biliary Obstruction, Cholecystitis, Sickle Cell Anemia.  Clinical Findings: Asymptomatic, Dull RUQ Pain, Intolerance to Fatty Foods.  Clinical Findings: Asymptomatic, RUQ Pain, Nausea, Vomiting. Sonographic Appearance: Sonographic Appearance:  Echogenic Intraluminal Focus.  Non-Shadowing Low Amplitude Echoes layering in the dependent portion of Gallbladder.  Immobile.  Echoes move slowly with position change, may fill the entire organ.  Non-shadowing.  Thickening of the Gallbladder Wall. 6. Cholelithiasis 1. Cholesterol Stones: Bile that Supersaturated with Cholesterol and decreased amounts of Bile Acids and Lecithin. Cholelithiasis 2. Pigment Stones: composed of Calcium Bilirubinate (Black or Brown).  USD is the imaging method of choice for detection of Gallstones with sensitivity of > 90%.  Gallstones appear within the Gallbladder Lumen as Echogenic objects that cast Acoustic Black Stones: Bilirubin, Polymers, Calcium Phosphate and Carbonate. Shadows and move with changes in patient position.  Etiology: Abnormal Bile Composition, Bile Stasis, Infection.  Common in Patients with Chronic Hemolytic Anemia, Cirrhosis.  Risk Factors: Family History, Obesity, Pregnancy, Diabetes, Female Prevalence 4:1. Brown Stones: often Laminated and consist of alternating layers of Calcium Bilirubinate and  Clinical Findings: Asymptomatic, RUQ Pain, Epigastric Pain, Chest/Shoulder Pain, elevated Cholesterol admixed with Calcium Soaps. Liver function tests, Nausea, Post Prandial Pain, Fatty Food Intolerance.  Common in Patients with Biliary Infections or Liver Flukes Infestation. Sonographic Appearance  Hyperechoic Intraluminal Focus.  Posterior Acoustic Shadowing.  Mobile  WES (Wall, Echo, Shadow) 7. Chronic Cholecystitis  Recurrent Inflammation secondary to Infection, Obstruction or Metabolic Disorders.  Clinical Findings: Asymptomatic, vague RUQ Pain, Heartburn, Fatty Food Intolerance, Intermittent Nausea, mild increase in Aspartate Aminotransferase and Alanine Aminotransferase, possible increase in Alkaline Phosphatase and Bilirubin. Shadowing Hyperechoic / Echogenic foci Cholelithiases. Sonographic Appearance: 10. Porcelain Gallbladder  Small Contracted Gallbladder  Decrease in the Vascular Supply to the Gallbladder.  Thick Hyperechoic Walls  Clinical Findings: Asymtomatic, Vague RUQ Pain.  Cholelithiasis, 90% of cases  Calcification of the Gallbladder Wall complicating Chronic Cholecystitis.  Posterior Acoustic Shadowing  US demonstrates a highly Echogenic Wall with Acoustic Shadowing.  Sludge  Porcelain Gallbladder is a predisposing condition to Gallbladder Carcinoma. Sonographic Appearance:  Gallstones 95%, Hyperchoic Wall, marked Posterior Acoustic Shadowing.  Extensive Mural Calcification around the perimeter of the Gallbladder. 8. Acute Cholecystitis  Etiology: Obstruction of the Cystic Duct, Infection, Idiopathic. e  Clinical Findings: Severe Epigastric Pain, RUQ Pain, Biliary Colic, Positive Murphy Sign, Nausea, Vomiting, Jaundice, Elevated AST, Bilirubin, and Alkaline Phosphatase. 11. Wall-Echo-Shadow Sonographic Appearance  When the Gallbladder is filled with Gallstones, diagnosis becomes more  Thick Edematous Gallbladder Wall. difficult because the Gallbladder resembles an Air-Filled Loop of Bowel.  Impacted Stone in the Cystic Duct.  WES sign: is definitive evidence of a Stone-Filled Gallbladder.  Cholelithiasis, 90%  Gallstones produce a clean dark shadow.  Pericholecystic Fluid.  Air in the bowel produces a dirty brighter shadow.  Positive Murphy Sign.  Sludge 12. Gallbladder Hydrops 9. Mirrizi Syndrome  Etiology: Cystic Duct Obstruction, Biliary Stasis, Surgery, Hepatitis, Gastroenteritis, Diabetes  Clinical Findings: Asymptomatic, RUQ Pain, Epigastric Pain, Palpable Mass.  Etiology: impacted Stone in Gallbladder Neck / Cystic Duct, obstruction of CHD, Jaundice.  Clinical Finding: RUQ Pain, Jaundice, High Bilirubin, Alkaline Phosphatase, High ALT, AST Sonographic Appearance: Sonographic Appearance:  Enlargement, Gallbladder diameter exceeding 5 cm, Thin Hyperechoic Walls.  Immobile Calculus in the Cystic Duct or Neck of the Gallbladder.  Dilatation of the Intrahepatic and CHD, normal CBD. Pancreas Duct of Santorini  Retroperitoneal and Elongated organ lying Transverse and Obliquely in the Epigastric  Secondary Secretory Duct draining the Upper Anterior Portion of the Pancreas. and Hypochondriac regions of the body.  Enters the Duodenum at the Minor Papilla 2 cm Proximal to the Ampulla of Vater. Functions of the Pancreas Normal Pancreatic Size Exocrine Head: 2.0 – 3.0 cm Body: 1.0 – 3.0 cm Neck: 1.0 – 2.0 cm Tail: 2.0 – 3.0 cm  Amylase: breaks down Carbohydrates.  Lipase: breaks down Fats.  Trypsin: breaks down Proteins into Amino Acids. Sonographic Appearance  Cholecystokinin: stimulates secretion of Pancreatic Enzymes & Gallbladder Contraction. Normal Pancreas  Gastrin: stimulates secretion of Gastric Acids.  Secretin: stimulates secretion of Bicarbonate.  Smooth Homogenous Parenchyma.  Adult Pancreas is either Isoechoic or Hyperechoic when compared to normal Liver. Endocrine: Secrete hormones directly into the bloodstream.  Young Children: Hypoechoic.  Alpha Cells: secrete Glucagon.  Adults: Hyperechoic.  Beta Cells: secrete Insulin.  Delta Cells: secrete Somatostatin. Pancreas Division and Location Tail: Most Superior portion of the Pancreas.  Anterior and Parallel with Splenic Vein.  Anterior to the Upper Pole of Left Kidney, Posterior to Stomach, Lateral to the Spine.  Extends toward the Splenic Hilum. Abnormal Pancreas Body: Largest, most Anterior aspect.  Irregular or Heterogenous Parenchyma. Calcifications  Anterior to the Aorta, Superior Mesenteric Artery, Splenic Vein, Left Renal Vein and Spine.  Posterior to the Antrum of the Stomach. Normal Pancreatic Duct Head  Anechoic Non-Vascular Tubular Structure.  Smooth Parallel Hyperechoic Walls