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After abdominal surgery, intestinal function is often impaired. Complex regulatory mechanisms play a role here. Simple therapy can help.

The surgeon and patient were satisfied with the course of the operation. The minimally invasive procedure to repair an inguinal hernia only took 40 minutes. After the anesthesia wore off, the patient was able to move normally again, and a tablet made him forget the pain caused by the operation. Only a slight feeling of fullness was unpleasant. However, during the night the pressure in the abdomen increased, and the next morning a balloon-like distention showed that excessive intestinal gas had accumulated. It wasn't until three days after the operation that the wind gradually disappeared and the intestinal function returned to normal.


Common problem

“Even after minimally invasive abdominal surgery, around half of the patients complain of a temporary bloated stomach,” says Michael Scheruhn, director of the department for visceral surgery at a medium-sized hospital in northern Germany. However, it is not known how this happens and what distinguishes those affected from patients without intestinal disorders.


What is certain is that every surgical procedure in the abdominal cavity - no matter how gentle it is, as in the case of a minimally invasive operation - represents a trauma for the organism, to which it reacts by releasing stress hormones and changing nerve impulses. In the best case scenario, the consequences are a temporary indigestion with a bloated stomach and constipation. What is feared, however, is the clinical picture of postoperative ileus (intestinal paralysis), a serious dysfunction of the entire digestive tract: the intestinal wall muscles, which normally periodically contract in spirals to transport chyme and intestinal gases towards the rectum, are literally paralyzed.


The consequences of this are obvious. Ingested food is not digested, stool accumulates, and wind does not pass. In extreme cases, the patient vomits, the water and mineral balance becomes disordered, and - without timely treatment - circulatory shock with multi-organ failure can develop. Especially in major abdominal operations, postoperative ileus delays healing and causes additional treatment costs.


So it's no wonder that surgeons around the world are looking for ways to prevent the undesirable consequences of surgery. We know from basic research that postoperative intestinal paralysis is a complex disease process. The original assumption that it was a purely neural miscontrol (in the sense of overactivity of the so-called sympathetic nerve cord) was shelved. Apparently several tax systems are derailing at the same time.


Passive hose

As soon as the surgeon cuts through the skin, manipulates an abdominal organ or, during a minimally invasive procedure, pressure is exerted on the intestine by the carbon dioxide blown into the abdominal cavity, the sympathetic nerve cord interrupts communication between the brain, the (autonomic) nerve plexuses present in the intestine and the intestinal wall muscles. The consequence: Within a few hours, an active hollow organ that is constantly changing in form and function becomes a passive piece of tube.


At the same time, the body reacts to the pain stimuli caused by the operation by releasing the body's own opiates (endorphins). This is intended to suppress the perception of pain in the brain. However, opiates also block certain receptors in the intestinal muscle cells and thereby also paralyze intestinal activity. The neural dysregulation and endorphin release usually return to normal after two to three days.


Marked inflammation

However, the immune system associated with the intestinal wall also becomes unbalanced. As the working group led by Jörg Kalff from the Department of Surgery at the University Hospital in Bonn discovered, a pronounced inflammatory reaction in the intestinal wall develops just four hours after an abdominal operation.¹ White blood cells migrate to the intestinal mucosa and activate there in “stand-by mode”. located macrophages, dendrite cells and mast cells. These highly specialized immune cells then produce a wide range of inflammatory messenger substances such as interferon-gamma, tumor necrosis factor-alpha, interleukin-1 and interleukin-6.

At the same time, so-called nitric oxide radicals are released, extremely aggressive chemical compounds that also fuel the inflammatory reaction. The intestine reacts to the massive release of inflammatory mediators by paralyzing its activities, initially locally limited. Genetic differences in the release of inflammatory substances may explain why some patients only develop a bloated stomach, while others suffer from intestinal paralysis for days.


As Kalff and his colleagues were able to show in a series of experiments, the inflammatory reaction spreads throughout the entire digestive tract within hours. After activation by messenger substances, a special group of T lymphocytes leaves the original site of inflammation - typically the site of the intestinal wall where surgery or pressure was applied. The immune cells migrate via lymphatic vessels and the bloodstream to still-functioning sections of the intestine, where they penetrate the intestinal wall and also set off an inflammatory cascade. This is how a generalized inflammation of the intestine develops, with the consequence that the originally limited passage disruption leads to an ileus.


Chewing gum therapy

All drug approaches developed to date to prevent such intestinal motility disorders have been disappointing. For example, attempts to reverse the inhibitory effect of endorphins during the operation by administering opiate antagonists or to stop the transmission of pain to the brain using a special form of “spinal anesthesia” did not show any notable success.² This is hardly surprising, but it was only ever trying to get one component of the derailed tax system back on track. Chewing gum, which is recommended by many surgeons, performs better. In many places this is actually prescribed to the patient after the anesthesia has worn off - as much and for as long as he can.


As an analysis of studies conducted on this topic recently showed, chewing gum does not completely prevent intestinal transit disorders. But it significantly reduces their intensity and duration.³ The time until the first discharge of wind and measurable intestinal contractions was on average twelve hours shorter than in patients without chewing gum therapy. The patients also got back on their feet more quickly and were able to be discharged from the hospital on average a day earlier.


According to the British Vanessa Short, the lead author of the meta-analysis, there is a simple explanation for the success of chewing gum: “When the chewing muscles are moved and the flow of saliva is stimulated, the body thinks that food will soon be delivered to the gastrointestinal tract », writes the researcher from Bristol. As a result, the digestive organs began to work and the complex regulatory system found its balance. So it is a false pretense that brings the disturbed tax system back into line.


¹ Langenbeck's Archive of Surgery 397, 591–601, 2014; ² Clinical and Experimental Pharmacology and Physiology 41, 358–370, 2014; ³ The Cochrane Library, Issue 2, 1–217, 2015.äge-1.18522024

Article to download

From a bloated stomach to intestinal obstruction

When abdominal operations affect the digestive organ

NZZ, April 15, 2015

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