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General Surgery · CHAPTER 6. BLOOD TRANSFUSION

Massive transfusion syndrome

Massive transfusion syndrome is a severe clinical condition that develops when a patient is transfused with a volume of donor blood exceeding 40–50% of the circulating blood volume (CBV). On average, this critical threshold is 2–3 liters provided the material is administered within a short timeframe (up to 24 hours). The risk of developing this pathology increases manifold if blood from a large number of different donors or long-stored material is used.

Critical volumeAdministration of more than 40–50% of CBV (about 2–3 liters) in less than 24 hours.
Target hemoglobinAn Hb level of 75–80 g/L is sufficient to ensure tissue oxygenation.
Plasma toxicityRisk of intoxication with potassium, ammonia, and high doses of sodium citrate.
HemodynamicsMassive fluid administration can cause cardiovascular system overload.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Key pathogenetic factors

The development of the syndrome is caused by a complex of adverse effects on the recipient's body. The key triggers are:

  • The effect of low temperatures during the administration of refrigerated (cooled) blood.
  • The toxic effect of high doses of the preservative — sodium citrate entering the systemic circulation.
  • The accumulation of cell breakdown products (primarily potassium and ammonia) in the plasma of the donor material.
  • Acute overload of the cardiovascular system due to the rapid influx of massive fluid volumes into the vascular bed.

Homologous blood syndrome

One of the severe manifestations of massive transfusion is homologous blood syndrome. Its pathogenesis is based on profound microcirculatory disorders.

The pathological chain includes:

  1. The occurrence of erythrocyte stasis in the capillary bed.
  2. The formation of multiple microthrombioses.
  3. Pathological blood pooling (exclusion of significant volumes from active circulation).
  4. A marked change in blood clotting time.
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Tactics and target indicators

Strict accounting of the CBV deficit is necessary to prevent complications. The main rule of modern surgery: one should not strive for full restoration of normal hemoglobin concentration.

  • An Hb level of 75–80 g/L is quite sufficient for the adequate performance of oxygen transport function.
  • The entire missing volume of CBV is replenished not with blood components, but with blood substitutes.

The basis of prevention is combination therapy. Donor blood is combined with hemodynamic (antishock) blood substitute fluids. Dextrans (drugs with an average molecular weight of 50,000–70,000 and 30,000–40,000) are most commonly used. They provide the effect of hemodilution (dilution of formed elements), which leads to a decrease in blood viscosity, improvement of its rheological properties (flowability), and normalization of microcirculation.

Methods of complication prevention

To minimize the risks associated with the transfusion of foreign material, the following approaches are used:

  • Autotransfusion — transfusion of the patient's own blood or plasma. This is an absolutely compatible transfusion medium that does not cause immune and metabolic conflicts.
  • The use of specially prepared media — thawed and washed erythrocytes cleared of plasma containing toxic breakdown products.

Briefly: answers to topical questions

Which clinical symptoms indicate the development of citrate intoxication in the recipient?

Clinical symptoms of citrate intoxication in the recipient include a complex of neurological and cardiovascular disorders. The main manifestations include:

  • Tremor and convulsions.
  • Paresthesias of the lips, tongue, and fingertips.
  • Tachycardia, arrhythmia, and decreased blood pressure.

In severe cases, pupil dilation, as well as pulmonary and cerebral edema, are observed.

Which drugs must be administered to prevent citrate intoxication during massive transfusion?

For the prevention of citrate intoxication during massive transfusion of stored blood, calcium preparations are administered:

  • Calcium chloride — 5 ml of a 10% solution per 500 ml of stored blood.
  • Calcium gluconate — 5 ml of a 10% solution per 500 ml of stored blood.

What specific blood coagulation disorders occur during massive transfusion?

During massive transfusion, the following coagulation disorders and related changes may occur:

  • Change in blood clotting time.
  • Microthrombosis and microcirculatory disorders.
  • DIC syndrome: formation of multiple thrombi with depletion of coagulation factors, development of hypocoagulation, and bleeding.
  • Thrombocytopenia with hemorrhagic syndrome during massive transfusions for acute blood loss.
  • During massive infusions, the development of dilutional coagulopathy is possible, manifested by a decrease in plasma clotting factors.

Which ECG changes indicate potassium intoxication after massive transfusion?

Specific changes on the electrocardiogram indicate the development of potassium intoxication (hyperkalemia) after massive transfusion. The main ECG signs include:

  • Hyperacute tall T wave (peaked T wave).
  • PR interval prolongation.
  • Disappearance of the P wave.
  • QRS complex widening.

These changes reflect conduction disturbances and may be accompanied by bradycardia.

Class and exam questions

What transfusion volume is considered a massive blood transfusion?

This is the administration of donor blood in an amount exceeding 40–50% of the patient's CBV (usually 2–3 liters) over a period of up to 24 hours.

Is it necessary to raise hemoglobin to normal levels in massive blood loss?

No, one should not strive for full restoration of the concentration. The target indicator is an Hb of 75–80 g/L; this is sufficient to maintain the oxygen transport function.

How do dextrans help in massive blood transfusion?

Dextrans act as hemodynamic blood substitutes. They cause hemodilution, reduce blood viscosity, and improve its flowability, which helps combat microcirculatory disorders.

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What else to study on this topic

  • Mechanism of the toxic effect of sodium citrate on the recipient's body
  • Pathophysiology of the development of microthrombosis in homologous blood syndrome
  • Properties and pharmacokinetics of dextrans with various molecular weights
  • Technology for the production and use of thawed washed erythrocytes
  • Indications and methods of autotransfusion in elective surgery

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