In this section you find information about the partial or total gastric resection.
The partial or total gastric resection (gastrectomy) firstly involves a defect in the continuity of the upper gastrointestinal tract and secondly involves a loss in the reservoir function of the stomach. These changes can cause a considerable impairment of the secretion transport digestion function and lead to the known complex syndrome after a gastrectomy (postgastrectomy syndrome, early and late dumping syndrome).
Motility changes are caused partly by the loss of the gastric pacemaker in the antrum due to the truncal vagotomy, and also by the loss of the lower oesophageal sphincter and of the pylorus.
In addition, following a gastrectomy there are complex changes in the balance of gastrointestinal hormones. These changes are firstly due to the fact that the stomach itself secretes gastrointestinal hormones (e.g. gastrin, somatostatin, vasoactive intestinal polypeptide). Secondly, there is an influence on the regulation of gastrointestinal hormones due to the altered food passage time, the altered pH environment and the lack of direct alimentary stimulation in the event of the removal of the duodenal passage. Overall, following a gastrectomy, under stimulation conditions, a strong increase can be observed in the gastrointestinal hormones gastrointestinal polypeptide (GIP) and cholecystokinin (CCK), whereas gastrin, pancreatic polypeptide (PP), motilin and secretin decrease. Insulin secretion is reduced following a gastrectomy and the removal of the duodenal passage, which leads to a pathological glucose tolerance with up to 30% higher postprandial blood sugar concentration. Otherwise, if the duodenal passage is kept then there is increased insulin secretion.
The increase of CCK with the simultaneous drop in the secretin level can result in a post-operative exocrine pancreatic insufficiency in the event of a gastrectomy. This is responsible for the maldigestion and weight loss in many patients. For this reason, gastrectomy patients should regularly be given pancreas enzymes after the operation. In addition, CCK restricts the appetite via central mechanisms and creates a feeling of fullness, which is accompanied by reduced consumption of food. In the event of the removal of the duodenal passage (pancreatico-cibal asynchrony) in particular, there is frequently steatorrhoea with relevant fat losses and a resulting deficiency in fat-soluble vitamins.
While around 10–20% of patients become underweight following gastric resection, this figure is around 60% in the event of gastrectomy patients. The causes are inadequate nutrient intake and the occurrence of malassimilation (among other things as a result of exocrine pancreatic insufficiency). For example, this means that in the first months after a gastrectomy, less than half of the usual meal portions will be tolerated, meaning that the energy and nutrients requirements can only be met by consuming 7–10 meals per day. The tolerable meal size increases individually during the further progression.
Both after replacement stomach formation and after oesophagojejunostomy, a pathologically increased stool fat content may occur in up to 90% of patients, followed by energy and nutrient losses of calcium, magnesium, fat-soluble vitamins, zinc.
This means that the following are decisive for adequate energy and nutrient supply: