Types of Post-Operative Hemorrhage

Post-operative hemorrhage refers to bleeding that occurs after a surgical procedure. It can be classified based on the timing, source, and clinical presentation. Understanding these types is crucial for prompt diagnosis and management. Here are the main types:

1. Timing-Based Classification

• Primary Hemorrhage

  • Occurs immediately during or after surgery, typically within 24 hours.

  • Causes: surgical technique, inadequate hemostasis, injury to blood vessels during surgery.

• Reactionary Hemorrhage

  • Occurs within 24-48 hours post-surgery.

  • Causes: rise in blood pressure after anesthesia wears off, slipping of a ligature, reopening of a clot.

• Secondary Hemorrhage

  • Occurs after 48 hours post-surgery, often within 7-10 days.

  • Causes: infection, erosion of a vessel by a spreading infection, dislodgement of clots due to increased activity.

2. Source-Based Classification

• Arterial Hemorrhage

  • Characterized by bright red, pulsatile bleeding.

  • Often severe and requires urgent intervention.

• Venous Hemorrhage

  • Dark red blood, steady flow.

  • Less pressure than arterial, but can still be significant.

• Capillary Hemorrhage

  • Oozing of blood from small vessels.

  • Often seen in areas with rich capillary networks.

• Mixed Hemorrhage

  • Combination of arterial, venous, and capillary bleeding.

  • Common in complex surgical sites.

3. Clinical Presentation-Based Classification

• External Hemorrhage

  • Bleeding visible outside the body.

  • Common in surgeries involving skin incisions or accessible body cavities.

• Internal Hemorrhage

  • Bleeding occurs within the body cavities or tissues.

  • Often harder to detect, may present with signs like swelling, pain, and hematoma formation.

• Concealed Hemorrhage

  • Bleeding into a closed space (e.g., retroperitoneal space).

  • Can be difficult to diagnose; may present with signs of shock without obvious external bleeding.

Haemorrhage/ hypovolemic shock:

Caused by loss of whole blood (haemorrhage), plasma ( burns), or interstitial fluid (diaphoresis, diabetes, diuresis) in large amounts.

1. Loss of whole blood or plasma causes hypovolemia directly. Loss of interstitial fluid causes an indirect ‘relative’ hypovolemia by promoting diffusion of plasma from the intravascular to the extravascular space.

2. Hypovolemic shock begins to develop when intravascular volume has decreased by about 15%. Hypovolemic is offset initially by compensatory mechanisms. Heart rate and vasoconstriction increase as a result of catecholamine release by the adrenals. This boosts cardiac output and tissue perfusion pressures. Compelled by a decrease in capillary hydrostatic pressures, interstitial fluid moves into the vascular compartment.

3. The liver and spleen add to blood volume by disgorging stored red blood cells and plasma. In the kidneys, renin (through several intermediaries) stimulates aldosterone release and the retention of sodium (and water).

4. Eventually, hypovolemic shock results in extreme vasoconstriction and increased systemic vascular resistance and afterload in order to improve blood pressure and perfusion to core organs.

5. These compensatory mechanisms are, however, finite. If the initial fluid or blood loss is great or if loss continues, compensation fails, resulting in decreased tissue perfusion. Nutrient delivery to the cells is impaired, and cellular metabolism fails.

6. Fluid replacement is important.

7. Signs and symptoms:

   • Increased HR

   • Tachypnoea

   • Decreased blood pressure

   • Prolonged capillary refill time

   • Pallor and cool and clammy extremities

   • Increased thirst

   • Oliguria

Treatment:----IV fluids/ volume replacement Maintain airway Control Oxygen Blood transfusion (packed RBC, plasma and platelets)