GP beware - upper GI symptoms
Dr Sean Preston discusses three initially simple presentations of ‘reflux’ that were more serious than first thought
Mr Y, a 23-year-old student, presented to his GP with an increase in his ‘reflux’. This had been present since the start of university three years ago, but more problematic in the preceding four months. He often experienced small volumes of undigested food passing back in to his mouth, but was also noting solid food sticking more frequently, particularly bread and roasted meats, although there was no typical heartburn, together with pain on swallowing. He had no significant medical history, but had childhood asthma and hay fever. A once daily PPI was prescribed, with only mild improvement in his regurgitation, but not his difficulty in swallowing.
Three weeks later he had an episode of complete dysphagia while eating steak and presented to A&E. An emergency gastroscopy was performed and the endoscopist removed a large chunk of meat. The endoscopist noted that the oesophageal lining was ‘ringed’ and took biopsies that confirmed the suspected diagnosis. Mr Y’s swallowing significantly improved after four weeks of swallowed beclomethasone.
Eosinophilic oesophagitis (EOO)
Dysphagia should never be attributed to gastro-oesophageal reflux and necessitates a gastroscopy in a patient of any age. Mr Y did not have typical heartburn and dysphagia to solids implies more of a physical, than a functional disorder. His chronic, progressive symptoms together with his personal history of atopy are suggestive of EOO. The diagnosis of gastro-oesophageal reflux should be questioned if symptoms fail to respond to PPIs.
Making a diagnosis of an EOO in primary care is not easy, particularly as the disease is rare, but it is becoming more prevalent. A diagnosis can be made if the pathology is considered in all patients with dysphagia, particularly in the young and middle aged, but especially in those with a personal or family history of atopy. If there is a history of food bolus obstruction, cancer and EOO must be excluded, which means the endoscopist should always take oesophageal biopsies, even in a normal-looking oesophagus.
Mr X, a 60-year-old, presented to his GP with refractory heartburn over three months. He had suffered with this since his mid-40s, but it was always controlled with once daily PPI, unless he exceeded his usual four pints of cider per evening. After a particularly bad week, when he was having to sleep in a chair to prevent nocturnal symptoms, the PPI was prescribed twice daily with some improvement, but not resolution of the heartburn. He had no dysphagia, but no longer felt like eating, had lost 4kg in weight and had a chronic cough, which he attributed to a 40-pack-year history of smoking cigarettes.
One month later he was admitted under the acute medical take, as he was more short of breath and unable to climb the stairs to his bedroom. He was diagnosed with community-acquired pneumonia and underwent a gastroscopy, as it was thought he may have aspirated.
At endoscopy he was found to have a long segment of Barrett’s oesophagus, in addition to an oesophagitis. Biopsies were taken of a worrying nodule just above the gastro-oesophageal junction.
Oesophageal adenocarcinoma on a background of Barrett’s oesophagus
Heartburn is a very common symptom, but usually resolves with twice-daily PPI. Weight loss is often rationalised by patients as caused by either a change in diet, or a more active lifestyle, but this should always be questioned.
Barrett’s oesophagus is present in fewer than 10% of people with heartburn, but is more common in males, Caucasians, the over-50s and those whose heartburn has been present over five years. Population screening is not of benefit – 70% of people having a gastroscopy for heartburn will have a normal-looking oesophagus – but gastroscopy in those of high risk is recommended.
If Mr X had been referred for a gastroscopy earlier, his reflux could have been treated more aggressively, he would have greater reason to modify his lifestyle and his Barrett’s oesophagus could have been surveyed with regular gastroscopies with pre-malignant lesions treated endoscopically. He was not an ideal candidate for neo-adjuvant chemotherapy and a total oesophagectomy.
Mrs Z was 48 and a PADI certified dive master, who spent most of her holidays in a wetsuit. She was becoming increasingly frustrated at having to empty her regulator of small volumes of ‘reflux’. She had seen her GP after six months and was prescribed once, then twice daily PPI, for presumed GORD, likely across a hiatus hernia.
She was no better four weeks later and after considering the recent MRHA warning, domperidone was added to her regular medications, again with little improvement. Within the same time period she had also begun to experience episodes of chest pain, which were becoming more severe. She had no heartburn, but had noted that her meals were taking longer to eat and she was drinking more water with each meal.
She called an ambulance after severe chest pain woke her from her sleep and went to A&E, where she felt better after SC morphine. The admitting doctor thought she had severe oesophagitis and scheduled a gastroscopy the following morning. The endoscopist found the oesophagus to be filled with the previous day’s evening meal. After some time spent emptying the oesophagus, the gastro-oesophageal junction was passed; there was a degree of resistance, but no mass seen. Upper GI physiological testing of the oesophagus was requested, as a motility disorder was suspected.
Mrs Z did not experience heartburn, but ‘silent’ reflux is common. Some 40% of people who have an erosive oesophagitis diagnosed on endoscopy do not have any corresponding symptoms. The lengthening of meal time and her reliance on fluid to wash it down should raise the possibility of oesophageal dysmotility or an obstructing lesion. Pain can be a function of achalasia, but may also be secondary to GORD, but in the former can be excruciating and will not respond to antacids.
Oesophageal dysmotility is more common than once thought and with the advent of high resolution manometry is becoming better classified, with more tailored treatment. It may be either primary (achalasia) or secondary, so it is important to consider in the context of certain systemic disease (scleroderma, diabetes).
As mentioned in the first two cases, twice daily PPIs are very likely to have all but resolved her ‘reflux’ if it was secondary to GORD. Failure of response should prompt a search for an alternative diagnosis. There is little evidence for promotility agents in the treatment of gastro-oesophageal reflux.
A referral for gastroscopy should be made if the ‘reflux’ has worrying features with the endoscopist noting anything consistent with a motility disorder (there is often none) and referring for GI physiological testing when appropriate.
Dr Sean Preston is a consultant gastroenterologist at Barts Health NHS Trust and The London Clinic