Pharynx and Oesophagus

Normal oesophageal wall </= 3mm.

Barium Swallow and Meal


  • NBM 4 hours prior
  • Videofluoroscopy if suspect aspiration.
  • PA and R lateral control then swallow at 2 frames/sec pharynx/upper oesophagus. Puff out cheeks.
  • Give gas effervescent agent
  • Erect 30° LPO lower 1/2 oesophagus and GOJ 3-phase (Ba, gas, contracted).
  • Lie down, rotate patient 360° to the left ± repeat to coat stomach.
  • Supine double contrast gastric body; single contrast fundus, antrum, duodenal cap; DJ flexure.
  • Roll onto LPO ± give 20mg Buscopan (hyoscine) IV to efface rugae.
  • LPO double contrast duodenal cap, antrum, open pylorus ± tilt table 45° and rotate/tilt XII
  • Reflux and hiatus hernia provocation – Few° RPO sip water with straw, Ba column against GOJ.
  • Prone swallow lower oesophagus for 1°, 2° and 3°contractions (under fluoro).
  • Erect double contrast fundus ± duodenal cap.
  • PA barium marshmallow for oesophageal narrowing (if ‘food sticking’ and otherwise normal study), ask if symptoms are reproduced.


  • Reflux oesophagitis – Nodularity, thickened folds, erosions, segmental narrowing from spasm/inflammation/stricture.
  • Oesophageal Ca – Sessile polyps/depressed lesion -> infiltrating (narrowing with shoulder), polypoid (intraluminal mass), ulcerative (irregular ridge), varicoid (tortuous filling defects).
  • Feline oesophagus – Contraction of longitudinal fibres creasting multiple regular transverse folds ~1mm thick, may be early sign of oesophagitis or dysmotility.
  • Glycogenic acanthosis – Degenerative small oesophageal nodules.
  • Heterotropic gastric mucosa – Angular filling defects in bulb of duodenum, uncertain clinical significance.
  • Duodenal pseudolesion = flexural fallacy – Infolding mucosa and superior duodenal flexure.
  • Papilla of Vater with longitudinal and hooding folds.



  • Oral phase – Soft palate elevates, tongue pushes bolus back and down into oropharynx.
  • Pharyngeal phase – Larynx rises (breathing expires and halts), vestibule closes, epiglottis and aryepiglottic folds close forcing bolus into piriform fossae then oesophagus.
  • Oesophageal phase – Upper oesophageal sphincter (UES, cricopharyngeus) opens, peristalsis through tubular oesophagus. Primary peristalsis – rapid wave opening sphincters then slow contraction (outer longitudinal then inner circular) from top to bottom moving bolus, normally clears oesophagus completely. Secondary peristalsis starts in oesophagus at level of distended lumen spreading up and down. Tertiary waves (nutcracker oesophagus) – nonproductive irregular contractions associated with dysmotility disorder from top to bottom, causing a corkscrew/beaded appearance. Lower oesophageal sphincter (LES) opens with swallowing, primary peristalsis and proximal oesophageal distention. Expiration continues.

Abnormal oral/pharyngeal swallowing causes difficulty initiating, globus sensation, cervical dysphagia, nasal regurgitation, hoarseness, coughing, choking. Abnormal oesophageal swallowing causes heartburn, dysphagia (awareness of swallowing difficulty), ‘indigestion’, chest pain.

Motility Disorders

Pharyngeal dysfunction

  • Pharyngeal stasis – Impaired pharyngeal transport, residual volume in valleculae and piriform sinuses.
  • Laryngeal penetration – Into laryngeal vestibule above vocal cords.
  • (Tracheobronchial) aspiration – Below vocal cords.
  • Nasal regurgitation – Poor seal of soft palate against posterior pharyngeal wall, caused by neurological impairment, msucular dystrophy, structural palate defect.

Causes of pharyngeal dysfunction include:

  • Aging (primary presbyphagia)
  • Neurological disease – CVA, parkinsons, Alzheimer’s, MS, CNS neoplasm, post-traumatic CNS injury, CNS infection.
  • Muscular disease – Affects pharynx and proximal 1/3 (striated muscle portion) of oesophagus. Muscular dystrophies, myastenia gravis, dermatomyositis.
  • Structural abnormality – Pharyngeal webs, Zenker diverticulum, tumour.
  • Medication
  • Radiation
  • GOR
  • Trauma, postsurgery
  • Malignancy – Oral, pharyngeal or laryngeal.

Cricopharyngeal Spasm

(Crichopharyngeal achalasia). Failure of UES relaxation causing dysphagia, aspiration. Shelf-like cricopharyngeal bar (cricopharyngeus at level of C5-6) with proximal pharyngeal distension. Dysphagia if cricopharyngeus narrows lumen by >50%, associated with neuromuscular disorders.

Oesophageal Achalasia

Increased tone of LES, impaired LES relaxation and aperistalsis of the oesophagus. Absent peristalsis of oesophageal body, marked increase in LES resting pressure, failure of LES to relax. Uniform oesophageal dilatation with air-fluid level, absent peristalsis with tertiary waves, tapered beak at LES.

  • Primary/idiopathic achalasia – Failed oesophageal inhibitory neurons (Auerbachs plexus). Insidious onset at 30-50yo.
  • Secondary chalasia – Chagas diseaes with destruction of ganglion cells by neurotoxin of protozoa Trypanosoma cruzi, endemic to Brazil. Associated with cardiomyopathy, megaduodenum, megaureter, megacolon. Increased risk of epiphrenic diverticula and oesophageal carcinoma. Tx balloon dilatation or Heller myotomy.


  • Diabetic autonomic neuropathy.
  • Carcinoma of the GEJ – Longer and more irregular segment of distal oesophageal narrowing.
  • Scleroderma with secondary reflux stricture.
  • Peptic strictures – Usually has primary peristalsis.

Diffuse Oesophageal Spasm

Unknown aetiology, middle aged, causes functional obstruction. Multiple tertiary contractions, thickened oesophgeal wall. Primary peristalsis usually present, but infrequent. LES dysfunctional. Increased stress may cause small deverticulae to form (pseudo-diverticulae as they lack a true muscularis).


Unknown aetiology. F>M, 20-40yo. Progressive atrophy of smooth muscle and progressive fibrosis. Oesophagus prodominantly affected (in 75-80%) with weak/absent peristalsis of distal 2/3 (smooth muscle), delayed emptying, stiff dilated oesophagus, wide-gaping LES with free GOR (but tight strictures uncommon), Barretts. Also caues gastroparesis, reduced contraction of the bowel with bacterial overgrowth, hide-bound sign in the small bowel (short spacing between thinned valvulae conniventes), wide-mouthed squared-shaped pseudo-diverticula on the antimesenteric wall (but rarely diverticulitis).


True diverticulae contain all 3 wall layers, with a complete muscularis propria.

  • Lateral pharyngeal diverticula – Mucosa through weakened lateral pharyngeal wall, most at tonsillar fossa and thyrohyoid membrane. From increased intrapharygneal pressure, wind instrument players.
  • Zenker diverticulum (pharyngeal pouch, pharyngoesophageal diverticulum)) – Just proximal to UES in posterior midline at cleavage plane (Killian dehiscence) between circular and oblique cricopharyngeus. Small neck above the sac.
  • Midoesophageal diverticula – Pulsion diverticula from disordered peristalsis. Traction diverticula from adjacent LN fibrous inflammatory reaction. Most have large mouths and empty well, asymptomatic.
  • Epiphrenic diverticula – Just above LES, usually on the right. Rare, usually associated with motility disorders. Small neck higher than sac.
  • Sacculations – Small outpouchings usually from severe oesophagitis. Healing and scarring of ulcerations. Change size and shape during fluoroscopy, smooth contours.
  • Intramural pseudodiverticula – Dilated extretory ducts of deep mucous glands. Flask-shaped from lumen or lines/flecks outside wall, tend to occur in clusters. Aassociated with chronic ulcers/strictures. Linear intramural tracking may bridge adjacent glands.

Oesophagitis and Strictures

Imaging will detect <50% of mild cases, but most moderate/severe cases. Thickened (>3mm) folds, wall thickening >5mm, limited distensibility (asymmetrical flattening), abnormal motility, mucosal plaques and nodules, erosions and ulcerations, strictures, pseudo-diverticulosis, CT target sign (hypodense wall with dense enhancing mucosa). Small <10mm ulcers with reflux oesophagitis, herpes, radiation, drugs, benign mucous membrane pemphigoid. Large >10mm ulcers from CMV, HIV, Barretts, carcinoma. May have ectopic gastric or less likely pancreatic tissue in upper 1/3 oesophagus causing dsyphagia, oesophagitis. Crohn disease rarely causes discrete aphthous ulcers, must also have bowel disease.

Radiation oesophagitis, if acute causes shallow/deep ulcers, later fibrosis with interupted peristalsis, long smooth tapered strictures confined to radiation field. Increased inflammation with simultaneous doxorubicin.

Strictures form from by fibrosis due to inflammation or neoplasm. Benign strictures tend to have smooth tapering, concentric narrowing; malignant tend to be abrupt, asymmetric, ecentric, irregular, nodular; but difficult to distinguish between hence both require endoscopy. Distal strictures from GORD, scleroderma, prolonged NGT. Upper/middle oesophageal strictures from Barrets, radiation, caustic ingestion, pemphigoid, erythema multiforme, epidermolysis bullosa dystrophica. DDx extrinsic compression from lung cancer, lymphoma, mediastinal nodes, TB, histoplasmosis.

Gastro-Oesophageal Reflux (GORD)

Incompetent LES (reduced tone or increased abdominal pressure), more common with alochol, smoking, obesity, CNS depressants, pregnancy, hiatus hernia, delayed gastric emptying, increased gastric volume. Most >40yo. Normal stratified squamous epithelium is resistant to abrasion, but sensitive to acid. Cx include reflux oesophagitis, stricture, Barrett oesophagus. 20% of normal show spontaneous reflux on barium swallow, and those with GORD may not demonstrate reflux without provocation. 24h oesophagael pH monitoring is definitive. Hyperaemia, eosinophils, basal zone hyperplasia.

  • Reflux oesophagitis (RE) – Severity depends on concentration of acid, pepsin, bile salts, caffeine, alcohol, aspirin and duration of contact. More prominent distally. Mucosal oedema (granular/nodular pattern), ulcers (discrete linear/punctate/irregular collections usually surrounded by radiolucent mound of oedema), pseudo-diverticula, poorly defined plaques and nodules (cf Candida), sacculations. Inflammatory exudates and psudomembranes may mimic Candida.
  • Reflux strictures – Most common stricture, usually confined to distal oesophagus, tapered, smooth, circumferential, may be asymmetric and irregular. Small smooth sacculation, fixed transvere folds from scarring. May have Schatzki ring (thickened B ring).
  • Barrett oesophagus – Progressive columnar metaplasia (intestinal type epithelium) of distal oesophagus due to chronic GORD. In 10% of GORD, 40% of scleroderma, typically white males 40-60yo. Premalignant with 15%/40x risk of adenocarcinoma. Reticular/lace-like mucosal pattern (resembles areae gastricae). Barium does not adhere well due to mucous secretions. Confirmed with endoscopy and biopsy. Tongues/patches of red velvety mucosa, alternating with smooth pale squamous mucosa. Short segment <30mm, long segment >30mm. Goblet cells (mucous vacuoles). Barrett strictures tend to be higher in mid-oesophagus (at displaced squamocolumnar junction), smooth and tapered or ring/web-like.

Infectious Oesophagitis

Most commonly immunocompromised.

  • Candida albicans – Increased risk with immunocompromise (AIDS, elderly, diabetic, malignancy, radiation, chemotherapy, steroids). Usually associated with oropharyngeal thrush. Odynophagia. Discrete plaque-like lesions with ‘shaggy’ serrated mucosa (characteristic), cobblestoning (longitudinal linear/irregular filling defects etched in white with normal intervening mucosa), may be tiny/nodular or giant and coalescent in pseudomembranes. Small <10mm ulcers that are punctate, round, oval or linear. Fulminant disease -> ‘foamy oesophagus’ with tiny bubbles at top of barium column.
  • Herpes simplex – Esp young males with sexual contact, painful. Discrete vesicles, rupture to form diamond-shaped/round ulcers with charactersitic lucent halo. Mid-oesophagus with background of normal mucosa. Nodules and plaques are usually absent.
  • CMV – Fulminant with one/more large flat mucosal ulcers.
  • HIV – Giant flat ulcers usually mid-oesophagus. Severe odynophagia.
  • TB – Least common site in GIT to be involved. Ulceration, stricture, sinus tracts, abscesses.

Chemical Oesophagitis

  • Drug-induced (pill) oesophagitis – Focal inflammation in areas of mucosal contact (eg sites of strictures). From tetracycline, doxycycline, quinine, aspirin, indomethacin, ascorbic acid, KCl, theophylline. Discrete ulcers separated by normal mucosa in mid-oesophagus. Healing occurs in 7-10 days of discontinuation.
  • Alkalines (eg liquid lye) – Cause deep full-thickness coagulation necrosis.
  • Acids cause – More superficial injury.

Cx ulceration, perforation, mediastinitis, later fibrosis, long/multiple strictures.

Eosinophilic Oesophagitis

Food impaction, dysphagia similar to GORD. Large numbers of intra-epithelial eosinophils. Most patients are atopic. Tx dietary restriction to prevent food allergins.


SCC in 85% (wordwide), others include adenocarcinoma in Barrett oesophagus (increasing in incidence), undifferentiated or miscellaneous cell types. Irregular, ulcerated, circumferential narowing with shouldering. Infiltrative tumours may cause smooth, rigid narrowing without a clear zone of transition; mucosa might not be altered until significant spread. Oesophagus has no serosa, hence rapid spread and poor prognosis of 5% 5yr. 60% incurable at presentation.

Endoscopic ultrasound layers include inner echogenic mucosa, hypoechoic muscularis mucosae, echogenic submucosa, hypoechoic muscularis propria then echogenic serosa (in stomach).

Tracheobronchial-oesophageal fistula is almost malignant in origin. Usually to trachea or left main bronchus.

Squamous Cell Carcinoma (SCC)

Risk factors include males, >45yo, smoking & alcohol (synergistic), corrosive ingestion, H&N carcinoma, poverty, achalasia, Plummer-Vinson syndrome, frequent consumption of very hot beverages, previous radiotherapy, HPV infection. Insidious dysphagia, odynophagia, obstruction; patients subconsciously adjust diet from solid to liquid foods. Approximately equal distribution throughout the oesophagus. Patterns include annular constricting (irregular, ulcerated stricture), polypoid (intraluminal filling defect), infiltrative (growing along submucosa) and ulcerated mass. Irregular thickening of wall with shouldered margins, eccentric narrowing of lumen, proximal dilatation. Obliteration of fat plane with aorta is high suggestive of invasion. Neck, mediastinal or subdiaphragmatic nodes (depending on location), metastases to lung, liver, adrenals. Varicoid carcinoma – thick, tortuous, longitudinal folds resembling varices, but are rigid and persistent.

Most pharyngeal SCC from base of tongue, palatine tonsil, posterior pharygneal wall or piriform sinus. Intraluminal mass with filling defect, abnormal luminal contour, focal increased density, mucosal irregularity (ulceration, elevations), asymmetric distensibility.


Typically on background of Barrett oesophagus and longstanding GORD. Stepwise genetic changes from Berrett metaplasia, dysplasia and invasive carcinoma. Increased risk with smoking, obesity, previous radiotherapy. M:F 7:1, Western countries. Rapid increase in incidence (now ~50% of US carcinomas). Usually distal 1/3 oesophagus, may invade adjacent cardia. Most produce mucin. Most have advanced stage at diagnosis.


In pharynx is large, bulky tumour of lingual or palatine tonsil. May infiltrate submucosa of oesophagus with thickening folds.


Rare. Most asymptomatic, incidental, benign, M~30yo. Smooth, well-defined in wall but may be pedunculated/polypoid, homogeneous, eccentric wall thickenieng. Occasional coarse calcifications (very suggestive). Rarely ulcerates.

Leiomyosarcomas are very rare, tend to be heterogeneous with large exophytic component.


Perforation and Trauma

Oesophageal tear/laceration – 50% from instrumentation. May cause copious haematemasis. Tends to heal rapidly.

  • Mallory-Weiss tear – Only involves mucosa, from violent retching (commonly after acute alcohol intoxication). ?Failed reflex relaxation of LES, with increased pressure causing oesophageal stretch and tear. Longitudinally orientated ~10-40mm in distal oesophagus, usually crossing the GOJ.

Oesophageal perforation/rupture – Subcutaneous, cervical and mediastinal emphysema, widened mediastinum, pleural effusion, hydropneumothorax. Initial studies should be water-soluble before barium (if negative). CT non-contrast then water-soluble contrast. CXR normal in 10%. Mortality 20-60%.

  • Iatrogenic (60%)
  • Boerhaave syndrome (15%) – Rupture from forceful vomiting. Almost always left posterior wall near left diaphragmatic crus.
  • Foreign body impaction (15%) – In adults usually bones or boluses of meat, in children may be any foreign object. Bones usually lodge in pharynx near cricopharyngeus. Meat impacts in distal/mid-oesophagus. Perforation in ~1%, but risk increases if persists >24hrs. Tx removal via Foley catheter, wire basket or gaseous distension of oesophagus with gas-producing crystals.

Mucosal Web

Uncommon, ledge-like protrusions, usually asymptomatic incidental but may cause obstruction. Unkonwn aetiology, most women >40yo. Hyperkeratotic squamous epithelium. Semicircumferential, eccentric, 2-4mm thick, protruding <5mm into lumen, commonly multiple. Pharyngeal webs most common anterior wall hypopharynx. Oesophageal webs anywhere, but most in cervical just distal to cricopharyngeus. May be associated with iron deficiency anaemia (Plummer-Vinson syndrome with triad of dysphagia, oesophagitis and iron deficiency anaemia), GOR, chronic GVHD, bistering skin diseases. High risk of malignancy.

Schatzki Rings

(Oesophageal rings). Circumferential thickening including mucosa, submucosa and occasionally hypertrophic muscularis propria. A rings are above the GOJ covered by squamous mucosa; B rings are at the squamocolumnar junction.

Oesophageal Varices

Serpiginous filling defects, changing in size with intrathoracic pressure and change in patient position, collapse with peristalsis and distension. Best seen on mucosal relief views. Uphill varices are portosystemic collaterals, coronary vein -> gastrooeosphageal varices -> azygous system; usually only present in distal oesophagus. Downhill varices from obstructed SVC -> portal vein, usually predominently upper oesophagus.


Rare, fibroepithelial or fibrovascular. Large ovoid or elongated intraluminal in upper oesophagus.

Duplication Cyst

Congenital, usually incidental. 60% in lower oesophagus. Well-defined cystic mass. DDx bronchogenic or neuroenteric cyst.

Aberrant RSCA

Arises distal to left SCA, crosses behind oesophagus causing upward-slanting linear defect in posterior wall.

Intramural Haematoma

From anticoagulation or endoscopy. Smooth long narrowing, smooth shoulders top and bottom, semi-circumferential. Tx conservative management, reversal of anticoagulation.