Therapy of gastrointestinal bleeding

Definition gastrointestinal bleeding

A gastrointestinal bleeding is a bleeding of the gastrointestinal tract that is visible from the outside. Blood is either vomited or excreted with the bowel movement. The appearance of the blood allows conclusions to be drawn about the source of the bleeding.

Therapy gastrointestinal bleeding

The therapy gastrointestinal bleeding initially focuses on stabilizing the circulation, since the loss of volume can lead to the danger of acute shock symptoms. For this purpose, foreign blood is transfused or plasma expanders are administered. The latter are also known as plasma substitutes and can be given as the body’s own protein solutions or as artificially produced, modified starch solutions (so-called dextranes).

Synthetic solutions, also known as colloidal solutions, are used if the blood loss does not exceed 20% and no intolerance reactions are to be expected. The name “colloid solution” refers to the volume-increasing mechanism of action of these substances: Due to the high protein content, a high suction, known as “colloid osmotic pressure” is built up in the blood vessels, which leads to the influx of fluid from the surrounding tissue into the vessels. If the patient’s circulation is stable, extensive diagnostics (see above) can be performed prior to e.g. surgical intervention to find the intensity and exact origin of the source of bleeding.

Surgical treatment is not necessary for known esophageal varices (varicose veins of the esophagus): these are preferably treated non-surgically by sealing bleeding vessels with rubber bands. In this treatment method introduced by Goff and Stiegmann, also known as “ligation”, the varices (varicose veins) are aspirated under endoscopic view and tied to the base with rubber band clips. The method of choice today, however, is the so-called sclerotherapy (from sclerosing = obliterating).

By injecting a sclerosing agent, which includes, for example, polidocanol containing many unsaturated fatty acids, an artificial inflammation is caused in the vessel, the tissue swells and the vessel is permanently closed. Thus, a first hemostasis can be achieved. The same method of overmoulding vessels is also used in the treatment of varicose veins.

The mortality rate of esophageal varicose vein bleeding can be reduced most effectively by sclerotherapy:The parameter for evaluating the effectiveness of medical measures, also known medically as the mortality rate, drops from about 50 to 70% to 20 to 30% when sclerosing bleeding varices compared to conventional surgical therapy. Nevertheless, potentially fatal complications can still occur: The wall of the esophagus may tear during aspiration (medical: rupture of the esophagus), parts of the walls of the muscle tube may die (medical: necrosis) or deep, bleeding mucosal lesions (ulcerations) may develop. However, the justification for this intervention, which is associated with complications in about 10% of patients, is a comparatively large therapeutic benefit in an overall very threatening disease, whose mortality risk is many times higher without or with other treatment methods (about one third of patients die from the first bleeding; see above).

The recurrence rate of esophageal varices, i.e. the proportion of relapses, should not be underestimated: even with successful treatment, varices (varicose veins) reappear in 70% of patients. It may be possible to improve the outcome of sclerotherapy and rubber band ligation by inserting a balloon known as a Linton Nachlas probe, which can bring about primary hemostasis by compressing the vessels in the stomach or esophagus. If all of the above measures do not lead to success, the esophageal varicose vein bleeding must be treated surgically, e.g. by opening the chest (medically: transthoracic), cutting the esophagus and removing the bleeding veins (this procedure, which is only rarely used and is used as the ultima ratio, is called “sperm surgery”).

Immediate surgery is required for injecting arterial bleeding (classified as Forrest 1a, see above) and for heavily bleeding defects of the back wall of the stomach due to its proximity to large arteries. Frequently used are electrical and laser coagulation and the placement of metal clips (so-called hemoclips) to achieve initial hemostasis.If a venous oozing bleeding classified as 1b according to Forrest is present, there is a high 80% chance that the bleeding stops by itself. Otherwise, the already mentioned methods of laser coagulation (laser sclerotherapy) and sclerotherapy are also used here.

If this is not possible, the (statistically seen somewhat less successful) electrical coagulation (sclerotherapy) with a so-called Electro-Hydro-Thermo Probe) can also be performed. In all cases, the additional administration of haemostatic drugs, such as secretin and somatostatin, which inhibits hormone production in many glands of the body, is attempted to support primary (direct) haemostasis. Drugs to prevent acid production reduce the frequency of early recurrence of bleeding (so-called H2 receptor antagonists, the “H” stands for histamine, a messenger substance that promotes the production of stomach acid; an H2 receptor antagonist thus blocks the effect of histamine.

Alternatively, the proton pump inhibitors omeprazole or pantoprazole are widely used today to inhibit the production of gastric acid. In addition, treatment is usually carried out to eliminate existing ulcers or to prevent their formation: The germ Helicobacter pylori, which is now proven to be the main cause, can be successfully eliminated by a two-week combination therapy with various antibiotics. )You can find more information on this topic at Gastric ulcer In case of lower gastrointestinal bleeding, e.g. due to bleeding Meckel’s diverticula, these must be surgically removed.

There are various treatment methods available for the treatment of vascular malformations known as angiodysplasias: These can either also be surgically removed, electrically coagulated (sclerosed) or closed by arterial embolization (by clot formation in the vessel). The principle of the latter method is to administer liquid plastic or plastic beads into the vessel by means of a catheter in order to achieve complete closure. The examination with an endoscope (tube camera) allows a classification of the gastrointestinal bleeding into three groups, according to whose classification the further treatment depends.

The basis of the so-called “bleeding” is the activity of the bleeding:

  • Forrest type 1 active bleeding: Forrest type 1a is an injecting arterial bleeding Forrest type 1b is a venous oozing bleeding
  • Forrest type 2 bleeding that has already been stopped Forrest type 2a: the previously bleeding vessel is endoscopically visible within the injured area Forrest type 2b: there is a mucous membrane injury covered with coagulated blood Forrest type 2c: the endoscopy shows an injury covered with hydrochloric acid coagulated blood – i.e. hematin)
  • Forrest type 2a: the previously bleeding vessel is endoscopically visible within the injured area
  • Forrest type 2b: there is a mucosal injury covered with coagulated blood
  • Forrest type 2c: the endoscopy shows an injury covered with hydrochloric acid coagulated blood – i.e. hematin)
  • Forrest type 3 lesions of the stomach or intestinal mucosa, the severity of which is insufficient for classification in one of the above categories and from which no bleeding has (yet) been detected.
  • Forrest type 2a: the previously bleeding vessel is endoscopically visible within the injured area
  • Forrest type 2b: there is a mucosal injury covered with coagulated blood
  • Forrest type 2c: the endoscopy shows an injury covered with hydrochloric acid coagulated blood – i.e. hematin)