Acute and chronic bleeding

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BLEEDING = haemorrhagia, escape of whole blood outside the vessels

Haemostasis – plays a key role in population mortality and morbidity; its failure corresponds to organ failure. It consists of the endothelium + coagulation factors + platelets.

Causes of bleeding

• Acquired (AF – warfarin, dabigatran)
• Congenital (AD – hemophilia, von Willebrand disease, vasculopathies)
• Surgical, post-traumatic, coagulopathies, thrombocytic, vascular

We must understand bleeding as any clinical symptom. Whether it is isolated or part of another finding; spontaneous or induced; fresh or recurrent; in common locations (gynecology) or unexpected sites (perianal, urinary tract), cutaneous or mucosal.

Laboratory approach

Platelets (primary haemostasis, aggregation/adhesion)

150–450 × 10⁹/L, 6 fl, fragments of megakaryocytes; adhesive and aggregating abilities; granules

Thrombocytopenia = numerical deficit

• decreased production in BM (tumor, drug-induced, HIV, congenital)
• increased degradation (AIO – ITP, angiopathies, DIC, hypersplenism)

Thrombocytopathy = functional deficit (membrane GP defects, granule defects – congenital; NSAIDs)

Pseudothrombocytopenia = false thrombocytopenia, caused by increased platelet aggregability; patients have no bleeding symptoms (aspirin, heparin, organ failure, paraneoplastic – acquired)

Blood coagulation system (secondary haemostasis, fibrin clot)

The goal of haemostasis is not to block a vessel, but preservation of vessel integrity (repair and recanalisation → fibrinolytic system).

Coagulopathies

• congenital – hemophilia VIII, IX, XI (<2% severe, >5% mild), von Willebrand disease
• vitamin K deficiency (cofactor for coagulation factors), liver cirrhosis + bleeding from esophageal varices

Inhibitors of coagulation

• Antithrobine III
• Protein C
• Protein S

Factor V mutation (binding site for these inhibitors) = Leiden mutation → thrombophilic state

Fibrinolytic system (tertiary haemostasis, tPA, plasminogen, plasmin)

D-dimers – degradation products of fibrin

Classification of bleeding

1. According to location

External – directly through the skin to the surface, but also into organs communicating with the exterior (bronchi, GIT, urinary tract, female genital tract)

Internal – into body cavities, soft tissues → hematoma, joints

2. Traumatic vs. non-traumatic

Traumatic (due to injury)

Non-traumatic (gynecological, ruptured aneurysm, esophageal varices, etc.)

3. According to vessel type

Arterial – bright red blood, spurting

Venous – dark red blood, flowing

Capillary – oozing

4. According to pathogenesis

Per rhexin – rupture of a vessel (trauma, aneurysm rupture)

Per diabrosin – erosion of a vessel by a pathological process (tumor, ulcer)

Per diapedesin – leakage of blood through widened endothelial pores (toxic capillary damage, venous stasis)

5. According to timing

Primary – occurs immediately after injury

Secondary – later in the course after injury (dislodged thrombus, rupture of necrotic vessel wall, two-stage rupture of the spleen)

6. Macroscopic classification

Petechiae – pinpoint hemorrhages in skin

Ecchymosis – on mucosae, serous membranes

Purpura – confluent petechiae

Sugillation – superficial bleeding into skin and subcutis (bruise) or mucosa

Suffusion – larger area of extravasation (large bruise)

Hematoma – compact accumulation of blood compressing surrounding tissue, elevating the skin surface

Other terms:

Apoplexy – massive destructive hemorrhage (e.g., apoplexia cerebri)

Hematocephalus – hemorrhage into cerebral ventricles

Hematomyelia – spinal cord hemorrhage

Hemorhachis – epidural spinal canal hemorrhage

Epistaxis – nosebleed

Hemoptysis – blood in sputum

Hemoptoe – coughing/choking up blood

Hematemesis – vomiting of blood (red – esophageal varices; digested – gastric or duodenal ulcer, tumor)

Enterorrhagia – fresh red blood in stool (tumor, ulcer, lower GIT)

Melena – black, tarry stool due to digested blood (upper GIT)

Hematuria – blood in urine (glomerulonephritis)

Metrorrhagia – uterine bleeding outside cycle (tumor)

Menorrhagia – abnormally heavy menstruation

Hematometra – blood in the uterus

Hemosalpinx – blood in the fallopian tube

Hemoperitoneum (hemascos) – blood in the peritoneal cavity

Hemothorax – blood in pleural cavity

Hemopericardium – blood in the pericardial sac

Hemarthrosis – blood in a joint (injury, hemophilia)

Acute bleeding

Leads to oligaemia (decreased blood volume).

Circulatory failure results from sudden loss of approx. 1/3 of blood volume (≈ 1.5–2 L in adults).

Clinical signs: tachycardia, ↓ blood pressure, thready pulse, cold extremities, dyspnea (due to insufficient O₂ transport). After restoring intravascular volume, typical signs of anemia may appear (fatigue, dyspnea, pallor, tachycardia).

In CBC, anemia appears after several hours, when fluid shifts from interstitium into the intravascular space. The anemia is normocytic normochromic (post-hemorrhagic). Later → increased reticulocytes.

Treatment: stop the bleeding; replace lost volume depending on severity using plasma substitutes (colloids), plasma, or whole blood.

Chronic bleeding

Most common causes:

• GIT (peptic ulcer disease, tumors, hemorrhoids)

• urogenital (metrorrhagia, renal or bladder bleeding)

Anemia results from iron deficiency due to increased losses → iron-deficiency anemia (sideropenic anemia). Losses as little as 2–4 ml/day may cause deficiency. CBC shows microcytic hypochromic anemia.

Anemias due to increased erythrocyte loss: post-hemorrhagic anemia or hemolytic anemia.