Oesophageal emergencies

Anatomy

• Upper oesophageal sphincter
  • Mostly cricopharyngeus muscle with resting pressure 100mmHg
• Lower sphincter
  • Not anatomically discrete
  • Smooth muscle of lower 2cm of oesophagus + diaphragm with resting pressure 25mmHg
• Three anatomic constrictions
  • Cricopharyngeus at C6
  • Aortic arch at T4
  • GOJ at T10/11
• Innervation mirrors the heart

Dysphagia

• Most patients with dysphagia have an organic cause
• Transfer dysphagia
  • Oropharyngeal difficulty initiating swallowing
  • Neuromuscular disorder in 80% e.g. CVA, polymyositis, dermatomyositis, scleroderma, myaesthenia gravis, tetanus, Parkinson’s, botulism, lead, thyroid disease
  • Localised disease e.g. pharyngitis, aphthous ulcer, candida, abscess, Zenker’s diverticulum, cervical osteophytes, cricopharyngeal bar
  • Inadequate lubrication – Scleroderma
• Transport dysphagia
  • Impaired movement of bolus down oesophagus and through the lower sphincter
  • Perceived later in swallowing process (2-4 seconds at least)
  • Perception of getting stuck
  • Obstructive disease (85%) e.g. foreign body, carcinoma, webs, strictures, thyroid enlargement, diverticulum, large-vessel abnormalities
  • Motor disorder – achalasia, peristaltic dysfunction, oesophageal spasm, scleroderma
• Motility issues usually intermittent and variable
• Mechanical/obstructive issues typically progressive (solids then liquids)

Dysphagia

• History
  • Intermittent, progressive, previous symptoms
  • Solids only – mechanical
  • Solids and liquids – severe mechanical or motility disorders
  • Food bolus impaction
• Exam
  • Head, neck
  • Neurological
  • Nodes

Diagnosis

• Transfer dysphagia or proximal transport dysphagia – lateral neck X-ray
• Transport dysphagia – CXR
• Barium swallow, manometry and oesophagoscopy are all performed

Neoplasm

• Common cause of both transfer and transport dysphagia
• Mostly SCC
• Risk factors for SCC
  • Alcohol, smoking, achalasia and previous caustic ingestion with lye
• Barrett’s oesophagus predisposes to adenocarcinoma
• Surgery and radiation therapy for head/neck cancer also are risk factors
• Usually rapid progression (<6mo) from solids to liquids
• Bleeding suggests neoplasm
• Assume neoplasia if >40yo

Anatomic

• Oesophageal stricture
  • Usually from GORD scarring
  • Typically distal oesophagus with symptoms progressive over years and only solids
  • Stricture can prevent reflux with improvement in symptoms
• Schatzki ring
  • Most common cause of intermittent dysphagia with solids
  • Stricture near GOJ in up to 15% of population and mostly asymptomatic
  • May form over time in response to GORD
  • Food impaction is a common presenting event
• Oesophageal webs
  • Middle/proximal oesophagus thin structures of mucosa/submucosa
• Diverticulae
  • Pharyngo-oesophageal (Zenker’s) lie just above upper sphincter caused by increased pressure during hypopharyngeal phase of swallowing
  • Symptom onset usually >50yo
  • Present with transfer dysphagia, halitosis and feeling of neck mass

Neuromuscular disorder

• Liquids often more difficult to handle than solids (especially hot/cold)
• Symptoms often intermittent
• Stroke is the most common cause
• Polymyositis and dermatomyositis also relatively common

Motility disorders

• Achalasia
  • Dysmotility disorder of unknown cause and most common motility disorder causing dysphagia
  • Impaired swallowing-induced relaxation of lower sphincter is seen with absence of oesophageal peristalsis
  • Symptoms usually at 20-40yo
  • May be associated with oesophageal spasm and chest pain with odynophagia
  • Can have associated regurgitation and weight loss
  • Dilation can cause obstruction of airway
  • Treated with reduction in lower sphincter tone with oral meds, botulinum toxin injection, dilatations or surgical myotomy

Motility disorders

• Diffuse oesophageal spasm
  • Dysphagia is intermittent and not progressive
  • Chest pain is a common symptom
  • Therapy is control of reflux, smooth muscle relaxants and/or antidepressants
• Oesophageal dysmotility
  • Excessive, uncoordinated contraction with chest pain
  • Usually presents in 50s
  • Pain often at rest, dull/colicky in nature and triggered by hot/cold liquids
  • Acute pain often followed by hours of dull ache
  • Many patients have intermittent dysphagia
  • Pain may respond to GTN

Chest pain of oesophageal origin

• No historical features are predictive enough to differentiate cardiac from oesophageal 
• Incidence of oesophageal disease in patients with chest pain and normal coronary arteries is up to 80%

GORD

• The primary mechanism is intermittent relaxation of the lower sphincter with normal resting tone
• Hiatal hernia, prolonged gastric emptying, agents that decrease lower sphincter tone and impaired oesophageal motility predispose to reflux
• Burning nature of pain is likely due to localised lower oesophageal mucosal inflammation
• Other symptoms include odynophagia, dysphagia, acid reflux and hypersalivation
• Complications
  • Strictures, dysphagia, inflammatory oesphagitis
  • Barrett’s seen in 10%
• Occult presentations
  • Asthma exacerbations, chronic cough, sore throat, dental erosions, vocal cord ulceration, laryngitis, chronic sinusitis and vocal cord granulomas
• Treatment
  • PPI or H2 blockers
  • Avoid caffeine, alcohol, chocolate, fatty foods
  • Avoid eating within 3 hours of bed, sleep head up 30 degrees

GORD

• Decreased lower sphincter tone
  • High-fat food, nicotine, ethanol, caffeine, nitrates, CCB, anticholinergics, progesteron, oestrogen, pregnancy
• Decreased oesophageal motility
  • Achalasia
  • Scleroderma
  • Presbyoesophagus
  • Diabetes mellitus
• Prolonged gastric emptying
  • Anticholinergics
  • Outlet obstruction
  • Diabetic gastroparesis
  • High-fat foods

Oesophagitis

• Prolonged chest pain and odynophagia
• Inflammatory
  • GORD with subsequent ulcerations, scarring and stricture formation
  • Reflux-induced oesophagitis warrants aggressive acid-suppression +- Nissen fundoplication
  • Ingested medications can also cause oesophagitis due to prolonged contact with mucosa e.g. NSAID, potassium chloride, doxycycline, clindamycin
  • Risk factors for pill oesophagitis include swallowing position, fluid intake, capsule size, and age
• Eosinophilic oesophagitis
  • Chronic allergy-mediated inflammation diagnosed by endoscopy and managed with avoidance of allergens and swallowed liquid corticosteroids
• Infectious
  • Need to rule out immunosuppression
  • Candida with dysphagia, HSV, CMV, fungi, mycobacteria, VZV, EBV

Oesophageal perforation

• Iatrogenic most common
  • Dilatation of strictures increases risk significantly
• Boerhaave’s (10-15%)
  • Full-thickness perforation after sudden rise in pressure
  • Usually distal oesophagus left side and anterior
• Blunt or penetrating neck trauma
  • Oesophagography and oesophagoscopy both used
• Foreign body ingestion or food impaction
• Proximal less severe than distal
• Presentation
  • Severe, unrelenting pain, often radiating to the back
  • Abdominal rigidity with hypotension and fever often occurs early
  • Mediastinal emphysema takes time and is less commonly seen clinically or on CXR in distal perforations – absence does not rule out perforation
  • Hamman’s crunch may be heard
  • Pleural effusions develop in 50% of intrathoracic perforations (can be sympathetic to mediastinitis or direct contamination)
• Diagnosis
  • CXR +- CT confirms diagnosis
• Treatment
  • Resuscitate, broad-spec Ab’s, urgent surgical consult

Boerhaave’s

• CXR normal in up to 30% of cases
  • Most common finding is left pleural effusion
  • May also see PTX, subcut emphysema, pneumomediastinum
• Mackler’s triad
  • Chest pain, vomiting and subcut emphysema
• Also may get hoarse voice, neck vein distension
• Swallowing may exacerbate pain or induce coughing due to connection of GI tract with pleural space
• Haematemesis is NOT typical
• Mortality 20-90%

Swallowed foreign bodies

• Once past pylorus, usually continues on its way
  • If >2.5cm wide, irregular/sharp edges or >6cm long – may become lodged at pylorus
• Clinical presentation
  • Accurate localisation in adults in upper third of oesophagus
  • If unable to swallow secretions – aspiration risk
  • In children, may present with refusal to eat/drink, vomiting, gagging, choking, stridor, neck or throat pain, drooling
    • High degree of suspicion if <2yo
• Diagnosis
  • Plain films (unless food impaction)
  • CT is highest yield for oesophageal FB and can diagnose perforation

Swallowed foreign bodies

• Urgent endoscopy
  • Ingestion of sharp or elongated objects e.g. toothpicks, soda can tabs
  • Ingestion of multiple FB
  • Ingestion of button batteries
  • Evidence of perforation
  • Coin at level of cricopharyngeus in child
  • Airway compromise
  • Presence of FB >24 hours
• Laryngoscopy
  • Indirect or nasendoscopy may allow visualiation and/or removal in very proximal objects
• Expectant treatment
  • If distal to pylorus, has benign shape and nature, and pt is comfortable and tolerating oral intake, treatment is expectant
  • If worrisome and more distal, may require surgical consult
• Glucagon
  • For distal oesophageal objects, 1-2mg IV glucagon may relax the lower sphincter to allow passage
  • Success rates are low generally and may not be any better than watchful waiting

Food impaction

• Meat most commonly
• If complete oesophageal obstruction or food with bony fragments – urgent scope
• Uncomplicated impaction can be watched for up to 24 hours
• Proteolytic enzymes are contraindicated due to potential for mucosal damage and perforation
• Can trial glucagon 1-2mg IV q20min x 2

Button battery

• Lodgement in oesophagus is true emergency
• Perforation can occur within 6 hours of ingestion
• Lithium cells herald worse prognosis due to higher voltage
• If in stomach, can manage expectantly
• Repeat films at 48 hours to ensure passes pylorus (may not occur if large battery or <6yo)

Sharp objects

• If in oesophagus, need immediate removal
• Intestinal perforation from sharp objects that pass distal to stomach is common
  • Therefore, recommended to remove while in stomach or duodenum
• If intestinal perforation does occur, it is usually at ileocaecal valve
• If distal to duodenum at presentation, and patient is asymptomatic, should document passage with daily AXR
• Surgical removal should be considered if 3 days elapse without passage

Narcotics ingestion (body packers)

• Endoscopy contraindicated due to risk of iatrogenic packet rupture
• If packet appears to be transiting, then watchful waiting is advised until reaches rectum
• Some authors advocate whole bowel irrigation in this situation

Last Updated on October 28, 2020 by Andrew Crofton