Hemorrhage and bleeding

Classification and terminology

Bleeding is divided into external (blood escapes into the environment) and internal (blood accumulates in body cavities or the lumens of hollow organs).

Depending on the source, arterial, venous, arteriovenous, capillary, parenchymal, and cardiac bleeding are distinguished.

Special terminology is used to denote the accumulation of blood in specific areas:

• Hemothorax — in the pleural cavity.
• Hemopericardium — in the pericardial cavity.
• Hemoperitoneum — in the abdominal cavity.
• Hemarthrosis — in the joint cavity.
• Melena — intestinal bleeding.
• Metrorrhagia — uterine bleeding not associated with the normal menstrual cycle.

Types of Hemorrhages

Hemorrhage is a specific type of bleeding. Depending on the nature of tissue damage, several types are distinguished:

1. Hematoma — accompanied by disruption of tissue integrity and the formation of a pathological cavity filled with coagulated or liquid blood.
2. Hemorrhagic impregnation (infiltration) — the tissue structure is preserved; it is merely infiltrated with erythrocytes.
3. Bruise (ecchymoma) — a flat accumulation of blood in the skin, subcutaneous tissue, or mucous membranes. If the diameter of the bruise exceeds 2 cm, it is called an ecchymosis.
4. Petechiae — small, punctate hemorrhages. Multiple petechiae that merge into larger foci form hemorrhagic purpura.

Mechanisms of development

The escape of blood outside a vessel occurs via one of three main mechanisms:

• Rupture (haemorragia per rhexin). Occurs due to mechanical trauma, wall necrosis (e.g., myocardial rupture in myocardial infarction), inflammation (syphilitic mesaortitis), or aneurysm rupture.
• Erosion (haemorragia per diabrosin). Arrosive bleeding in which the entire thickness of the vessel wall is destroyed by a pathological process. Causes: purulent inflammation, malignant tumor breakdown, caseous necrosis (in the wall of a tuberculous cavity), exposure to chemical agents (gastric juice in a peptic ulcer), or invasion by chorionic villi (in ectopic pregnancy).
• Diapedesis (haemorragia per diapedesin). The oozing of blood through intact microcirculatory vessels due to increased permeability. Observed in severe hypoxia, intoxications, systemic vasculitis, leukemias, uremia, and hypertensive crises.

Etiology and Hemorrhagic Diathesis

Hemorrhagic diathesis is a pathological tendency to spontaneous bleeding in response to minor trauma. It is based on the following causes:

1. Increased vascular fragility: congenital defects, hypovitaminoses, infections, and the effects of steroid therapy.
2. Platelet defects: reduced count (thrombocytopenia), impaired adhesion (von Willebrand disease, Bernard–Soulier syndrome), or weakened aggregation.
3. Coagulation factor deficiency: congenital (hemophilia A — factor VIII deficiency, hemophilia B — factor IX deficiency) or acquired (liver diseases, vitamin K deficiency).
4. Excessive intravascular coagulation: characteristic of disseminated intravascular coagulation (DIC).

Plasmorrhagia

Plasmorrhagia is the leakage of blood plasma from the vessel lumen followed by the imbibition of surrounding tissues. The process is associated with vascular intima damage and altered blood properties.

Mechanisms of plasma extravasation (predominantly transendothelial):

• Ultrafiltration through basement membrane pores during pressure surges.
• Diffusion along the concentration gradient.
• Microvesicular transport (micropinocytosis).
• Interendothelial leakage (rarely occurs under normal conditions).

On light microscopy, the microvessel wall appears thickened and homogeneous. Electron microscopy reveals endothelial cell swelling, fenestration, and loosening of the basement membrane. In mild cases, plasmorrhagia results in hyalinosis of the vascular wall, while severe cases lead to fibrinoid necrosis.

Outcomes and clinical significance

The clinical significance of bleeding depends on its type, volume, duration, and, above all, localization.

• Acute bleeding: arterial bleeding threatens massive blood loss and death from acute anemia. Cardiac rupture leads to hemopericardium—even 100–200 ml of blood can cause fatal cardiac tamponade.
• Chronic bleeding: prolonged loss of small volumes of blood (e.g., from a gastric ulcer) leads to chronic posthemorrhagic anemia.
• Localization of hemorrhages: a massive subcutaneous hematoma is not life-threatening, whereas even a tiny hemorrhage in the brain can cause edema and death.

Outcomes of hemorrhages can be favorable (resorption, organization, encapsulation) and unfavorable (suppuration upon infection). In the brain, a "rusty" cyst often forms at the site of a hematoma, its color resulting from the accumulation of the pigment hemosiderin.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis and stages of DIC
• Morphology of chronic posthemorrhagic anemia
• Hereditary coagulopathies: hemophilia and von Willebrand disease
• Ultrastructural endothelial changes in plasmorrhagia
• Hemoglobin metabolism and hemosiderin formation at the hemorrhage site

Other topics in the section "Disorders of Blood and Lymph Circulation"

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