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Hiatus Hernia Peptic Ulcer Gallbladder Disease
1. Hiatus hernia, duodenal ulcer and gallstones
The three commonest upper gastrointestinal diseases are hiatus hernia, peptic ulcer which includes stomach or gastric ulcer, and gallbladder diseases of which the commonest are gallstones or cholecystitis. Their diagnosis is used as an endpoint for treatment. This may not be correct because the symptoms associated are not specific, they overlap with these pathological diagnoses and many patients, especially those seen in general practice, have symptoms but negative investigations. However, they need symptomatic treatment by doctors for their patho-physiological abnormalities even if they have no diagnosable pathology.
The original endpoint was the radiological diagnosis of the anatomical defect of hiatus hernia associated with heartburn and acid reflux which allowed a generation of thoracic surgeons to perform life time operation series of 1,000 to 2,000 patients. The best operation choice was controversial and I did my surgical thesis on the repair of hiatus hernia in dogs. This did not convince any of the senior surgeons to change their choice of operative procedure. But it did allow me to clarify the evidence provided by better and more accurate investigations using manometry, pH intraoesophageal recording of acid reflux and analyse the different thresholds for diagnosis of these abnormalities. Later studies investigated the pain of duodenal ulcer (15, 29) and gallstones (53)
The problem remains-which is the endpoint? The important step forward is to move from a purely pathological concept of disease to a pathophysiological approach based on understanding gastrointestinal physiology.
The diagnosis of an anatomical pathological defect of a displaced lower gastrooesophageal sphincter is called a hiatus hernia, which is best diagnosed by radiology. Using manometry the diagnostic threshold is lower and more sensitive so it increases the number diagnosed.
Gastrooesophageal reflux can be diagnosed by radiology and screening of barium reflux into the lower oesophagus. A more sensitive test is to use manometry and pH acid measurement.
The mucosal damage in the lower 10 cm of the oesophagus is called oesophagitis. The word includes both the macroscopic naked eye appearance as well as the microscopic histopathological findings. They are not the same and microscopy is more sensitive, but what does it actual mean?
• Are these three endpoints separate diseases?
Bernstein reproduced heartburn by pouring 200-300 ml 0.1N hydrochloric acid through a tube into the lower oesophagus, which confirmed that it arose from the lower oesophagus. Placing acid in the stomach itself was an unreliable and mainly negative way of producing the same heartburn symptoms (37). Bernstein did have a few hiatus hernia patients with heartburn which spread to the upper abdomen – the epigastrium.
The epigastric pain reproduction test (15, 29, 107) was a refined development of the Bernstein test for heartburn. The epigastric pain test dripped 20-30 ml in 4 min of the same strength acid directly and specifically onto the lower 10 cm of the oesophagus under manometric control. It was 100 % accurate if the patient had been awoken by such pain during the night before. Curiously if 200-300 ml of acid were placed directly in the stomach such pain was not reproduced. The author could have become worried because such research was against all textbook teaching, in spite of repeated warnings later under such headings as “Dogma Disputed” in the Lancet (83).
The pain of duodenal ulcer patients can be divided into those with epigastric pain and those with other sites for their abdominal pain (49). There is a third group without any pain but they have an ulcer in the duodenum which is silent; they often present as emergencies with a perforated ulcer or bleeding, never having had pain. This needs an explanation.
Manometrically the duodenal ulcer patients with epigastric pain have weaker sphincters and more reflux than those with non-epigastric pain; they are more likely to have heartburn (27, 32). When studied months after truncal vagotomy and pyloroplasty some patients had a positive epigastric pain reproduction test even though they had had no pain for months. Did they have a hypersensitive lower oesophageal mucosa which was stimulated at lower levels of acid reflux?
Gastrin and cholecystokinin are two gastrointestinal hormones which increase the sphincteric pressure of the isolated perfused canine gastrooesophageal sphincter. Both are secretomotor hormones. Gastrin produced from the antrum cause gastric acid secretion from the body of the stomach. Cholecystokinin causes the gallbladder to contract.
Secretin and glucagon are also secretomotor and both reduce gastrooesophageal sphincter pressures as a secondary effect. Secretin’s main effect is to cause pancreatic secretion. Glucagon’s main effect, as its name implies, is to raise blood sugar levels. It counteracts the effect of insulin but is probably the most potent hormone for reducing gastrooesophageal sphincteric pressures.
Work was done at the Royal London Hospital by Paul Thomas on these hormones experimentally in dogs and was thought to be an important promising field for later research (35). Clearly all these hormones had influence on both delayed gastric emptying and gastrooesophageal reflux through a weak sphincter together with bile reflux backwards from the duodenum into the stomach.
In the 1950s and 60s gastric acid was considered to be the main factor in the causation of peptic ulcers. Pentagastrin induced gastric secretion tests were done routinely in most of the professorial university surgical centres. The accepted expert was Jeremy Hugh Baron who wrote Clinical Tests of Gastric Function in 1978. He pointed out that although as a group acid secretion in duodenal ulcer patients was higher than normal, in fact one-third were normal, one-third subnormal and it was only the final third of high levels which pushed the group as a whole into high secretors. Analysis by Earlam confirmed Baron’s work that for the individual the results of pentagastrin tests did not contribute anything to help decision taking for surgery in duodenal ulcer patients (85).
An attempt was made to quantitate the amount of pain suffered by a duodenal ulcer patient by measuring his antacid relief tablet intake to neutralise his pain (54). This seemed a good quantitative measure of symptoms.
By itself bile in the duodenum does not damage the mucosa. But if it refluxes into the stomach so that the biliary reflux joining the gastric hydrochloric acid causes damage, it can lead to gastritis and gastric ulcer. When this mixed acid/bile fluid refluxes into the lower oesophagus the epithelium is also damaged and can cause heartburn. Studies were made of the surgical procedures of partial gastrectomy and Roux en Y anastomosis, where the bile fluid is diverted in a Y shaped anastomosis at least 10 inches (25 cm) below the stomach (53, 75).
Synchronously in the 1970s, together with these manometric and physiological studies, the importance of symptoms became clear because to the patient they were far more important than the original anatomical/pathological diagnosis of hiatus hernia or peptic ulcer or the subsidiary pathophysiological abnormalities.
A huge data base of 319 patients with a radiologically abnormal duodenum was gradually gathered (47, 55). This was done in the early days of computerisation with IBM punch cards combining a) a long symptom analysis, b) pentagastrin gastric acid secretion test results, c) radiological appearances of stomach, duodenum and oesophagus and d) the decision by several different surgeons as to whether to operate or not.
From this data base it was simple to change the endpoints and obtain a computer print out of all the data available to any one given surgeon or clinician. Examples were:
1. a comparison between epigastric and non-epigastric pain duodenal ulcers in regard to reflux symptoms, etc (47).
It became increasingly apparent that the endpoints of hiatus hernia, duodenal ulcer or gallstones were actually confusing because their presence alone did not act as an indication for surgery and inevitably should have been qualified by an analysis of symptoms. This led to the realisation that there were two groups one at each end of the spectrum.
A. Those patients with the old style pathological endpoints who had never ever had any symptoms, eg, asymptomatic gallstones.
The results inevitably lead to questions about the expense and inconvenience spent in trying to find an expected or requisite endpoint radiologically, endoscopically or histologically. But nobody seemed interested in this problem as an intellectual exercise. They may have been far more interested in the money generated by all the unnecessary tests and investigations.
In the middle between the tails of the bell-shaped Gaussian curve lay the majority of hospital patients with a mixture of varying pathological endpoints (HH, duodenal ulcer, gallstones), an assortment of investigations including gastric secretion and emptying, oesophageal motility, pH measurement, histology and finally endoscopy. Did the patients have a disease, a symptom complex, helicobacter pylori or just indigestion or dyspepsia? How could you assess it, measure it, investigate or diagnose? In the end the patient needed treatment while the doctors scratched their heads in doubt.
(b) The gastro-oesophageal junction in duodenal ulcer after operation.
(b) Proceedings: The effects of gastrin and glucagon on gastro-oesophageal function in the isolated perfused canine stomach and oesophagus.
54. An antacid preparation in the treatment of duodenal ulceration. [PDF]
81. Histological appearances of oesophagus, antrum and duodenum and their correlation with duodenal ulcer symptoms. [PDF]