Complications of hemorrhoids

Background and pathogenesis of complications

Hemorrhoids represent varicose dilation of the venous plexuses of the rectum. The upper plexus gives rise to internal nodes (located submucosally), while the lower plexus forms external nodes (localized around the anus). As a rule, external hemorrhoids are not an independent disease, but accompany internal ones.

The development of complications is facilitated by a number of etiological factors causing venous congestion and increased intra-abdominal pressure:

• Chronic constipation and difficulty urinating.
• Heavy lifting, prolonged coughing, as well as standing or sedentary work.
• Compression of pelvic veins (pregnancy, uterine myoma, rectal tumors).
• Portal hypertension (hemorrhoidal veins serve as portacaval anastomoses).
• Congenital connective tissue weakness.

Dynamics of pathological changes:

1. Venous plexuses become engorged with blood and bulge into the lumen of the rectum.
2. The mucous membrane over the enlarged nodes gradually thins out.
3. Mechanical trauma to the nodes by hard fecal masses occurs, which triggers a cascade of complications (up to thrombosis with subsequent canalization of thrombi).

Hemorrhoidal bleeding

Bleeding is often the earliest symptom of the disease and one of its most frequent complications. It occurs due to damage to the thinned mucous membrane over the node at the time of defecation.

Features of bleeding:

• The blood has a bright red color.
• Discharges do not mix with fecal masses (blood remains on the surface of feces or is released in drops at the end of the act of defecation).
• Intensity varies from a few drops or streaks to heavy jet bleeding.

If bleeding becomes chronic, the patient loses a significant volume of red blood cells and iron. This inevitably leads to the development of severe anemia, in which hemoglobin levels can drop critically (down to 2–3 mmol/L).

Inflammation and thrombosis of nodes

Constant trauma to hemorrhoidal cavernous bodies provokes the development of a local inflammatory process and thrombus formation. Thrombosis is a particularly frequent complication specifically of external hemorrhoids.

Clinical picture of inflammation and thrombosis:

• Local temperature rise in the anorectal region.
• Severe, sometimes throbbing pain in the anal area.
• The nodes themselves increase significantly in size, become dense and sharply painful upon palpation.

The inflammatory process can spread to surrounding tissues, causing ulceration of the thinned mucosa.

Strangulation and necrosis

In late stages of the disease, internal hemorrhoidal nodes begin to prolapse outward. Initially, this happens only during heavy physical exertion or defecation, and the nodes reduce independently. Later, they prolapse even during normal walking and require manual reduction.

If the prolapsed node cannot be reduced in time, strangulation may develop. The mechanism of this complication is associated with severe pain irritation, which causes a reflex persistent spasm of the anal sphincter. The sphincter tightly grasps the pedicle of the prolapsed node, completely blocking venous outflow and arterial inflow.

Consequences of strangulation:

• Rapid increase in edema and thrombosis inside the node.
• Formation of deep ulcerations on the mucosal surface.
• Development of ischemic necrosis (death) of the tissues of the strangulated hemorrhoid.

Class and exam questions

What else to study on this topic

• Stages of hemorrhoid development (I-IV) and the clinical picture at each stage.
• Principles of conservative therapy: use of vasoprotectors, suppositories, and ointments.
• Minimally invasive treatment techniques: sclerotherapy, infrared coagulation, rubber band ligation.
• Indications for surgical treatment (hemorrhoidectomy) in late stages.

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.