Blood loss

Classification and types

Bleeding can be external (into the external environment) and internal (into body cavities or the lumen of hollow organs). If the escaped blood accumulates in surrounding tissues, it is called a hemorrhage. In isolated hemorrhage, systemic hemodynamics is usually not compromised due to the small volume of lost blood.

Types of tissue hemorrhage:

• Hematoma — accompanied by disruption of tissue integrity and the formation of a cavity filled with blood.
• Hemorrhagic impregnation (infiltration) — tissue structure is preserved. Manifests on the skin and mucous membranes as petechiae (diameter less than 3 mm) and ecchymoses (greater than 3 mm).

Based on the source, bleeding is classified as arterial, venous, capillary, and mixed. Based on the time of onset — primary (immediately after trauma) and secondary (delayed).

The severity of the condition directly depends on the proportion of lost circulating blood volume (CBV):

1. Mild degree: up to 20–25% of CBV. Usually not dangerous and resolved by emergency mechanisms.
2. Moderate degree: 25–35% of CBV. Causes significant disturbances in central hemodynamics and microcirculation.
3. Severe degree: more than 35–40% of CBV.

Reactivity factors

The course of the pathological process depends on the patient's individual characteristics. It has been proven that women and adults tolerate blood loss better than men and children.

The current state of the body also plays a critical role. Extreme temperature exposures (hypothermia or overheating), as well as deep anesthesia, suppress compensatory mechanisms and exacerbate vital activity disorders. In addition, a decrease in the level of clotting factors or hyperactivation of the fibrinolytic system increases the rate and final volume of blood loss.

Compensation mechanisms

To eliminate the consequences of hypovolemia, the body activates four groups of mechanisms. They are activated at different times, but work in parallel, reinforcing each other.

1. Cardiovascular stage (first seconds) Emergency stimulation of heart function occurs: heart rate and stroke volume increase. Blood flow centralization develops — a selective change in vascular tone. Arterioles of peripheral tissues (skin, muscles, kidneys) constrict, while vessels of vital organs (brain, heart) dilate. Due to arteriolar spasm, pooled blood is squeezed into the bloodstream, maintaining CBV.

2. Hydremic stage (first minutes) Aims to shift fluid from tissues into blood vessels. The decrease in CBV is detected by baroreceptors, triggering the secretion of ADH (vasopressin).

• ADH stimulates aquaporins-2 in the kidneys, enhancing water reabsorption.
• Simultaneously, ADH constricts the afferent arterioles of the kidneys. This causes ischemia of the juxtaglomerular apparatus (JGA) and activates the renin-angiotensin-aldosterone system (RAAS).
• Angiotensin II increases vascular tone and stimulates the release of aldosterone, which retains sodium. Plasma hyperosmolality additionally boosts ADH production.

Fluid shifts along an osmotic gradient from cells to the interstitium, then into lymph and blood. By days 2–3, oligocythemic hypo- or normovolemia is formed.

3. Protein stage (after several hours) Proteosynthesis is activated in the liver. The protein composition of plasma is restored and procoagulants are produced to thrombose the vascular defect. Signs of increased synthesis persist for up to 1.5–3 weeks.

4. Bone marrow stage Triggered in response to mixed hypoxia: hemic (low red blood cells), circulatory (impaired blood flow), and respiratory (reduced pulmonary perfusion). Activation of hematopoiesis eliminates the deficiency of formed elements.

Principles of therapy

Treatment is based on two main principles:

• Etiotropic: elimination of the cause. Includes surgical hemostasis (restoring the integrity of the vessel wall) and medical enhancement of blood clotting.
• Pathogenetic: blockade of pathogenesis links (the main principle of treatment).
• Restoration of CBV to eliminate macrocirculation disorders. Blood transfusion, plasma, and medium-molecular dextrans (Polyglyukin, Hemodez) are used.
• Normalization of transcapillary exchange to eliminate microcirculation disorders. Low-molecular dextrans (Rheopolyglucukin), gelatin, and isotonic solution are used.
• Correction of homeostasis — elimination of water, ion, and protein imbalance.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• The role of the renin-angiotensin-aldosterone system (RAAS) in hydremic compensation
• Mechanisms of hemic, circulatory, and respiratory hypoxia development in blood loss
• Differences in the mechanisms of action of Polyglucin and Rheopolyglucin
• Pathogenesis of microcirculation disorders upon loss of more than 30% of BCC
• The effect of deep anesthesia on compensatory reactions in trauma

Other topics in "Chapter 21. Typical Pathology Forms of the Blood System"

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