Carol, aged 58, had been with the practice for many years but I had not met her before. She was registered with my partner but because he was on holiday she came to see me.
She had been taking diclofenac for some back pain, and had noticed some constipation and abdominal distension over a couple of days.
Carol had no nausea, vomiting or abdominal pain. Her weight had been static and she had not had any rectal bleeding. She had taken lactulose, which stimulated passage of some flatus but no faeces.
Examining her, I could not find anything of concern. She was not jaundiced or anaemic, and I could feel no lymph nodes in the supraclavicular fossae, axillae or anywhere else. Her abdomen was slightly bloated but this was consistent with the history of constipation. Bowel sounds were present and I certainly could not demonstrate any shifting dullness that might suggest ascites.
Her liver, spleen and kidneys were all impalpable and no masses were detectable. Digital rectal examination revealed an empty rectum and no masses or other abnormalities. My working diagnosis at this stage was abdominal distension secondary to constipation.
I changed the lactulose to ispaghula husk and asked Carol to come and see me again in a week. However, she gave me her word she would contact me earlier if she had not opened her bowels in a day or two, stopped passing flatus, or developed abdominal pain or vomiting.
Carol dutifully came to see me the following week. She said she felt a bit better, and her bowels had opened a little although she still felt somewhat bloated.
Examining her again, the findings were much the same, but because she showed a recent change in bowel habit I decided to run some tests. I ordered a carcinoembryonic antigen, along with FBC, ESR and LFTs. My working diagnosis at this point was irritable bowel syndrome and I suggested plenty of fruit, vegetables and fibre.
I also added mebeverine to the ispaghula husk that she was taking.
She came back to review the blood test results the following week and I was pleased to tell her they were all normal. Her symptoms were virtually static, as were her examination findings. I suggested we meet again in a month's time, but she understood she could contact me at any time if she had any concerns.
Her husband rang me a couple of weeks later and asked, very apologetically, if they could trouble me for an urgent appointment as she was 'a bit more distended'.
When she walked into the consulting room I was shocked by her appearance.
Her massively swollen abdomen was obvious even before she undressed. It was extremely tight and this time I thought I could detect shifting dullness.
I rang the surgical registrar on call and between us we formed a plan.
I would arrange an urgent ultrasound scan and he would see Carol with the result as soon as it was available.
From that point on, I followed her progress via hospital reports and information from her husband. The scan had shown massive ascites, and the hunt for a presumed carcinoma was on. Colonoscopy and barium enema showed no abnormality.
Numerous imaging studies of the pelvis showed no abnormalities either and she had a thorough assessment by a gynaecologist who could find no signs of ovarian or any other kind of pelvic cancer.
Finally, she was referred to a specialist oncology centre at a London teaching hospital where a peritoneal biopsy was performed.
The biopsy revealed a diagnosis of primary peritoneal cancer.
Primary peritoneal carcinoma is a rare tumour, more common in women than in men. It is often initially mistaken for peritoneal deposits from a primary ovarian, abdominal or breast malignancy.
The differential diagnosis includes peritoneal mesothelioma, granulomatous reaction secondary to intra-abdominal foreign bodies, and fibrosis secondary to generalised fibrosing conditions.
Ultrasound and CT scans are both relatively insensitive and the diagnosis is made via a combination of peritoneal lavage percutaneously or during laparoscopy or laparotomy, and by percutaneous biopsy of the omentum.
The treatment of choice is usually hysterectomy and oophorectomy, with debulking of the tumour, followed by chemotherapy and, sometimes, radiotherapy.
However, all this treatment is palliative and the prognosis is extremely poor. The mortality rate in primary peritoneal carcinoma is 100 per cent and most patients fail to survive beyond two years.
The oncologists at the teaching hospital decided that surgery would not be helpful in Carol's case and she received a combination of chemotherapy and radiotherapy. My role has been to provide palliative care for her and her husband, who was kept fully informed of what the future was likely to hold.
Dr Knott is a GP in Enfield.