Oesophageal Disorders — Written Clinical Reasoning

Model answer — Part A: progressive dysphagia with alarm features

Frame it first. Progressive dysphagia that began with solids, with weight loss and iron-deficiency anaemia, is a mechanical obstruction from malignancy until endoscopy proves otherwise. This combination of alarm features bypasses any empirical PPI trial — the first test is an urgent upper gastrointestinal endoscopy with biopsy of any lesion [1].

Assessment establishes the trajectory and the host: tempo and direction of the dysphagia, regurgitation and aspiration symptoms, performance status and nutrition, cardiorespiratory comorbidity that will shape fitness for neoadjuvant therapy and oesophagectomy, and smoking/alcohol exposure that fits the squamous risk profile [1].

Investigation and staging proceed in layers once biopsy confirms cancer: CT of neck, chest and abdomen for gross spread; PET-CT to exclude occult distant metastases that would convert the intent from curative to palliative; and endoscopic ultrasound for T-depth and regional nodal status in patients who remain potentially resectable. Early intramucosal disease is treated endoscopically; locally advanced disease in a fit patient is not [2].

Curative-intent treatment for locally advanced oesophageal or junctional cancer is neoadjuvant therapy then surgery. The CROSS regimen — weekly carboplatin and paclitaxel for five weeks with 41.4 Gy of concurrent radiotherapy, followed by oesophagectomy — roughly doubled median overall survival (about 49 versus 24 months) against surgery alone, with benefit durable at ten-year follow-up in both squamous and adenocarcinoma histologies. The answer closes with the multidisciplinary frame: nutrition optimisation, smoking cessation, and explicit staging review before any knife [2] [3].

Model answer — Part B: recurrent food boluses in a young atopic patient

Frame it first. Recurrent food bolus obstruction in a young atopic man is eosinophilic oesophagitis until proven otherwise. The discriminating history points away from a fixed mechanical lesion and away from a primary motility disorder: intermittent solids-only dysphagia over years, impactions with fibrous foods, and an atopic background [4].

After disimpaction, the critical step is oesophageal biopsies from multiple levels regardless of mucosal appearance — rings, furrows and exudates may be subtle or absent, and the diagnosis requires at least 15 eosinophils per high-power field with the process isolated to the oesophagus [4].

Stepwise management begins PPI-first: proton pump inhibitor therapy induces clinical and histological remission in roughly half of patients and is the accepted initial step. Non-responders move to dietary elimination therapy or swallowed topical corticosteroid — budesonide orodispersible or viscous preparation, which achieved histological remission in 58 per cent versus none on placebo in the EOS-1 induction trial. Refractory or steroid-dependent disease earns dupilumab, the IL-4/IL-13-blocking biologic that delivered histological remission in about 60 per cent of patients in the LIBERTY programme [5] [6] [7].

Dilation has a defined, cautious place: it is for fixed fibrotic strictures causing persistent dysphagia despite anti-inflammatory control — never first-line, never a substitute for treating the inflammation, and performed gently because the EoE oesophagus tears more readily than a peptic stricture. The consultant close is chronicity: EoE relapses when therapy stops, so a maintenance strategy and follow-up are part of the plan, not an afterthought [4] [6].