Mrs H, an overweight 52-year-old schoolteacher, presented to her local GP, Dr W, with symptoms of nausea, fatty food intolerance and epigastric discomfort. It had started six weeks before, while she was on holiday, and was now getting worse, usually occurring when she tried to eat spicy or fried meals.

Mrs H said that sometimes she would get heartburn and take antacids, but they had made little difference. While she had been on holiday she had a brief attack of diarrhoea, which had now settled, but she thought she might have been infected by a “parasite”. She also mentioned stress that she was experiencing due to work. She was an occasional smoker and drank two to three glasses of wine per night with her evening meals.

Dr W recorded Mrs H’s BMI as 39, examined her abdomen and noted her history and his findings of a mildly tender epigastric/right upper quadrant area, with no fever, guarding, or signs of jaundice, and a temperature of 36.7. He recorded no family history of significance. He provided smoking cessation advice, asked her to reduce her alcohol intake and encouraged exercise. Dr W also prescribed a proton pump inhibitor for Mrs H and arranged for an ultrasound of her liver, a full blood count and amylase and liver function tests, as he suspected she had gallstones and might have been experiencing biliary colic.

Dr W advised Mrs H that he would contact her if the results were abnormal and that she should come back in a month if her symptoms persisted. The ultrasound and blood tests were normal and three months later Mrs H returned, to say that the treatment had initially helped but that now she was once again experiencing intermittent nausea; and when she had stopped the PPI, her dyspepsia had returned. She had successfully stopped smoking and reduced her alcohol intake. Dr W examined her again, noting similar findings to the initial consultation. Rectal examination was normal. He increased the dose of her PPI and recorded that a referral for gastroscopy should be considered if things didn’t improve after a further month’s treatment. He checked another full blood count, and amylase and liver function tests, all of which were once again normal.

Two months later, Mrs H presented with 5kg weight loss and worsening nausea and dyspepsia. The abdominal discomfort had not changed and examination showed a soft abdomen with no palpable masses.

Dr W repeated her blood tests and made a red flag referral for her to the local gastroenterologist. An urgent gastroscopy was arranged, which found a gastric carcinoma. A CT scan showed evidence of metastatic spread to Mrs H’s liver and mesenteric nodes.

Mrs H commenced a course of chemotherapy but died six weeks later. Her husband complained to the Medical Council that her diagnosis was delayed through negligence on the part of Dr W and that if she had been referred earlier for investigations, her death could have been avoided.

The Medical Council produced a critical expert report which supported this. Dr W, it stated, should have taken into consideration the patient’s age, risk factors for gastric cancer and made a red flag referral her on the second visit. Medical Protection challenged this account, citing the comprehensive records made by Dr W displaying his adherence to national guidelines and the case was dismissed.

Learning points

Dr W made clear notes of his findings and plan for further management if it was required. His clinical decisions based on his findings at the time were transparent and appropriate, and he made arrangements for ‘safety netting’ with the patient. He referred to local and national guidelines for the treatment of dyspepsia.

Risk factors for gastric cancer include, amongst others, a positive family history, smoking and excessive alcohol consumption. In this case the only relevant risk factors were smoking and alcohol (and the possibility of H. pylori infection, given the dyspeptic symptoms).

Clinical presentation of patients with gastric cancer is often vague and non-specific. Symptoms include nausea and dyspepsia as in this case, and weight loss is often indicative of late stage disease.