Caustic Ingestion

Section: UGI Sub-section: Gastric and Oesophagus Curriculum: Curriculum, page 94

Aetiology and Incidence

• Uncommon but devastating
  • Children (accidental) > Adults (usually more deliberate)
• Commonly available acids
  • Toilet cleaners (Hydrochloric acid)
  • Battery fluid (Sulphuric acid)
  • Metal working (Phosphoric and Hydrofluoric acids)
    • NB: Hydrofluoric acid also has metabolic effects on calcium and can cause associated refractory cardiac arrhythmias
• Common Alkalis
  • Cleaners and bleaches
  • Drain cleaner
  • NB: Most household items are only mild caustic agents

Pathophysiology

• Severe alkali injury more common because acid immediately causes pain in the mouth
• Injury points above main constricting points due to hold-up
  • Cricopharyngeus
    • C6, cricoid cartilage, 15cm from incisors (narrowest point)
  • Aortic arch
  • Left main bronchi; T4, angle of Louis, 25cm from incisors
  • Diaphragm hiatus
    • T10, 38cm

Mechanism of the injury

• Alkali – Liquefactive Necrosis
• Acid – Coagulative Necrosis

Alkali

• Liquefactive necrosis
  • Dissolves tissue by Liquefactive necrosis (hydrolytic enzymes)
  • Deeply penetrating injury, within seconds goes through mucosa and wall of oesophagus
    • Slowed by tissue fluids buffering the alkali
  • Causes extensive transmural tissue necrosis
    • Phase 1 – Acute liquefactive necrosis 1-4 days
      • Coagulation of IC proteins = cell necrosis. Surrounding inflammation
    • Phase 2 – Ulceration & granulation – up to day 12
      • Oesophagus weakest and thinnest
    • Phase 3 – Cicatrisation & scarring ~ 3weeks post-injury
  • Gastric injury less extensive due to buffering by gastric acids
  • Duodenal injury rarer, but can be as severe as oesophageal injury

Acid

• Coagulative necrosis
  • Ischemic eschar formed
  • Full-thickness rare
  • Acids tend to be less viscous than alkali substances, so pass into stomach faster
    • Acid in stomach causes pyloric spasm, therefore sits in stomach
    • Stomach damage proportionally greater than oesophageal damage
  • Full extent of injury known at about 48 hours
  • Therefore acids tend to cause more damage to the stomach, and alkali the oesophagus and duodenum
  • Studies have shown that overall ingestion of strong acid is worse than strong alkali, with greater perforation rates and mortality

Determinants of Severity

• Corrosive properties (pH) of ingested substance
• Concentration and amount ingested
• Physical from of the agent (solid or liquid)
• Duration of contact with the mucosa

Clinical Presentation

• Varied and can be confusing
• Oral or substernal pain, hypersalivation, odynophagia, dysphagia, hematemesis, vomiting, facial oedema, stridor
  • Then dysphagia.
  • Refusal to eat in children
• Fever may indicate perforation
  • Pain in back or chest - thoracic perforation
  • Abdominal pain – abdominal perforation
• Look out for respiratory signs
• 2nd/3rd degree injuries present like any burn
  • Massive fluid shifts, renal failure, and sepsis
  • NB: Cannot rely on seeing oral burns
    • May have passed quickly through oropharynx

Initial Evaluation

• Aim to distinguish life threatening injury from mild injury (and not requiring urgent operative management)
• History and Exam
  • Type and amount of agent
  • Time from ingestion
  • ? Co-ingestion of other drugs
  • Inspect oro-and hypo-pharynx
  • Evaluate for respiratory distress
  • Evaluate for peritonism or signs of perforation (subcut emphysema)
• Basic bloods and toxicology
  • May initially be normal
  • Predictors of transmural necrosis
    • High WCC and CRP
    • Severe acidosis
    • Renal failure
    • Deranged LFTs
    • Thrombocytopenia
• CXR
  • Assess respiratory symptoms, rule out other aetiologies
  • Assess for oesophageal or gastric perforation
• CT chest/abdomen
  • Determine depth of necrosis
  • Oesophageal wall blurring, peri-oesophageal fat blurring, absence of wall enhancement
  • Grading system

CT Grading of Caustic Ingestion

1	No oesophageal wall oedema
2	Oesophageal wall oedema
3	2 + peri-oesophageal soft tissue infiltration
4	3 + loss of tissue interface OR fluid collection around oesophagus/desc aorta

Endoscopic Evaluation

• Accurately predicts risk of stricture formation
  • Should be performed within 24hrs
  • Can delay to 48hrs if haemodynamically unstable
  • Contraindicated if perforation
• Graded similar to burns
  • Zargar Classification
    • Grade 0 – Normal
  • Low grade
    • Grade 1 – Mucosal oedema, hyperaemia and haemorrhage
    • Grade 2A – Superficial localized ulcers, bleeding, exudates
  • High Grade
    • Grade 2B – Deep focal or circumferential ulcers
    • Grade 3A – Focal necrosis with multiple and deep ulcerations and small scattered areas of necrosis
    • Grade 3B – Extensive necrosis

Management

• If asymptomatic without significant ingestion
  • No oral burns, low volume (<200mLs), accidental ingestion of low concentration acid or alkali
  • Observe and discharge when tolerating PO intake, and cleared by psychiatry
  • Don’t need endoscopy if asymptomatic and low risk
• If symptomatic, or significant ingestion, patients at high risk of oesophageal injury
  • Oral burns
  • High concentration
  • High volume (> 200ml) of low concentration
• Admit all patients for observation
  • Basic supportive cares
• If transmural necrosis or perforation
  • Emergency surgery
• If don’t require immediate surgery
  • Early endoscopic evaluation to grade injuries
• Subsequent Management
  • Low grade injuries
  • High grade injuries

Basic Supportive Cares

• Immediate priority is ABC’s (do with initial assessment)
  • Airway support and 02
    • Laryngotracheal burns or airway compromise consider intubation
  • Fluid resuscitation
  • Pain relief
• ICU/HDU management
• NBM until endoscopic evaluation
• PPI to protect against Stress ulcers
  • IV abx only if perforation suspected (don’t forget antifungals)
• DO NOT USE:
  • Induced emesis
    • Vomiting re-exposes oesophagus and oropharynx to caustic agent, aggravates injury
  • Gastric lavage or NG aspiration
    • May induce vomiting, compounding injuries or cause perforation
  • Neutralising chemicals
    • Do not work - damage is instantaneous and already done
    • Neutralisation releases heat, adds thermal injury to already injured tissue

Emergency Surgery

• Indicated if clinical signs of perforation and CT evidence of transmural necrosis
• Generally extensive gastric and oesophageal damage
  • All obvious transmural necrotic injuries should be resected
• Most commonly, oesophagogastrectomy through combined abdominal and cervical approach performed
  • Cervical spit fistula, duodenum defunctioned, and Feeding jejunostomy
• 20% have concomitant injuries to surrounding organs needing resection
  • Spleen, colon, small bowel, duodenum, pancreas
  • High morbidity (but death is the only alternative)
• If necrosis limited to stomach, can do total gastrectomy and retain native oesophagus
  • Exclude oesophagus and do delayed anastomosis
• Don’t do partial gastrectomy or oesophagectomy with gastric preservation
  • Stomach likely to be too injured to preserve

Subsequent Management of Low-Grade Injuries

• Endoscopy grade 1 or 2a, CT grade 1
• Supportive care
  • Analgesia
  • Initiate liquid diet, moving to regular diet in 24-48hrs
  • Still need long-term endoscopic surveillance for malignancy

Subsequent Management of High-Grade Injuries

• Endoscopy grade 2b or 3, CT grade 2 or 4
• Inpatient monitoring for clinical signs of perforation over at least one week
• If concerning signs, re-CT and surgery as appropriate
• Optimal timing of reintroducing diet not known
  • Usually PO liquids after 48hrs if swallowing saliva
  • If not tolerating, consider enteral (NJ or jejunostomy) or TPN feeding
  • Routine imaging not required
• Endoscopy if new symptoms arise or at 8 weeks to evaluate healing

Complications of Caustic Ingestion

• GI bleed
• Strictures
• Fistulae
• Oesophageal SCC

Strictures

• Develop in 5-50% of patients
  • 70-100% of Zargar Classification grade 2B, 3A or 3B
• 95% are distal
  • Most can be managed by serial endoscopic dilatation
  • Prevention
  • Surgical Reconstruction
• Pharyngo-oesophageal strictures
• Gastric Strictures

Endoscopic Management of Caustic Strictures

• Usually wait 3-6 weeks before attempting dilatation
  • Dilate slowly to minimise perforation risk
  • Perforation rates much higher for caustic strictures than benign
    • 4-17% vs 0.1-0.4%
• Use Savary-Gilliard Bougie dilatation
  • NB: May need PPI’s or anti-reflux surgery after dilatation

Prevention of Caustic Strictures

• Stenting not routinely recommended
  • Not enough literature to support
• Systematic reviews have failed to demonstrate benefit of steroids in preventing strictures
  • Although 1x RCT may have shown benefit
  • Steroids in initial phase may mask clinical symptoms and add to perforation risk

Surgical Reconstruction of Caustic Strictures

• Should wait at least 6 months
• Indicated if
  • Multiple failed attempts at endoscopic dilatation
  • Young patients with long, severe strictures
  • High lifetime risk from repeated dilatations and malignancy
• Options
  • Bypass
    • May avoid mediastinal dissection, but retaining native oesophagus means on-going SCC risk, secretion problems, and bacterial overgrowth
  • Resection –preferred approach
    • Using colonic conduit or stomach (rare, only if no stomach damage)
  • Stricturoplasty – not used commonly

Pharyngo-oesophageal Strictures

• Management more complex
  • Site of injury
  • Possible associated laryngeal injury
  • Possible other downstream strictures
• Usually retrograde dilatation (mini-laparotomy and gastrotomy) or surgical reconstruction with colonic interposition required

Oesophageal SCC after Caustic Injury

• Squamous malignant transformation in around 16-30%
  • 1000x risk of general population
• Long latent period (15-40 years)
• UTD recommends 2-3yrly endoscopic surveillance beginning 10-20yrs after injury
• Carcinoma at site of previous injury (scar carcinoma) has better prognosis than usual SCC
  • ? Diagnosed earlier as oesophagus not as distensible, so becomes symptomatic earlier
  • ? Scar tissue makes lymphatic spread and direct tumour extension more difficult
  • Scar carcinoma also responds better to combined surgical/radiation therapy

Prognosis

• Depends upon the extent of oesophageal injury and the underlying medical condition of the patient
• General based on endoscopic grading
  • Grades 1 and 2A
    • Excellent prognosis without significant acute morbidity or subsequent stricture formation
  • Grades 2B and 3A
    • Strictures in 70 to 100% of cases
  • Grade 3B
    • Early mortality rate of 65%