How anastomoses heal and why they sometimes don’t heal

Anastomotic leakage is the result of an abnormal healing process. The pathophysiology of wound healing should allow us to understand the anastomotic dehiscence.  There are three phases in the healing process: inflammation, proliferation and remodeling.

During normal blood flow, red cells, neutrophils, lymphocytes, platelets and macrophages circulate in the center of the vessels. An injury disturbs this flow and these cells come to the surface. They come into contact with endothelial cells and their adhesion molecules which allow them to escape to the extravascular compartment when the permeability increases. It is a difficult process for neutrophils, which requires special skills, such as locomotion, priming and degranulation. All of this requires oxygen, and therefore a good blood flow. Lymphocytes will regulate the process and start the proliferative phase, when collagen is produced.

Days later the remodeling phase starts, requiring a perfect balance between the production and degradation of matrix products.

Wound healing in the colon is different than in the skin. The cells that destroy the matrix are found in a larger amount in the microflora. But the pathophysiology underlying the anastomotic healing process is the same that we find in wound healing. So factors such as age, medications, sex hormones or diseases like diabetes or immune alterations, as well as hypoxia and the kind of microflora in the colon, have a direct effect on the healing process.

In 1955 Dr. Cohn from New Orleans published a paper in Annals of Surgery suggesting that colon bacteria had something to do with the results of the anastomoses performed in elective surgery, proposing preoperative colon preparation to improve them.

Gut microbiota is composed of one hundred trillion bacteria. Most of them are harmless but 1% of them, including Enterococcus, Pseudomonas and Escherichia, are potentially very harmful in the presence of a wound or an anastomosis. Bacteria come into contact with the enterocyte when an injury occurs. They are able to produce matrix proteases, enzymes that destroy the extracellular matrix and therefore the anastomosis.

There is likely a link between bacteria and the blood flow, causing an anastomotic leak when found together.

In conclusion, the fate of an anastomosis depends on good technique as well as on good microflora and a good blood flow. But, Dr. Berho wonders, what would the best way to evaluate the blood flow in an anastomosis be?