Anemic syndrome

Anemic syndrome is a pathological condition caused by a decrease in red blood cells and hemoglobin in a unit of circulating blood. True anemic syndrome must be distinguished from hemodilution, which is caused by massive transfusion of blood substitutes and is accompanied by either an absolute decrease in the number of circulating red blood cells or a decrease in their hemoglobin content.

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How does anemic syndrome manifest itself?

Acute anemic syndrome, with the exception of some features, manifests itself in the same way: euphoria or depression of consciousness; pale skin, tachycardia, initial manifestations of hemorrhagic shock, dizziness, flickering spots before the eyes, decreased vision, tinnitus, dyspnea, palpitations; auscultation - a "blowing" systolic murmur at the apex. As anemia increases and compensatory reactions decrease, arterial pressure progressively decreases and tachycardia increases.

According to the classification of I.A. Kassirsky and G.A. Alekseev, there are 3 types of anemic syndrome:

• posthemorrhagic anemic syndrome - due to hemorrhage;
• hemic anemic syndrome - due to a violation of blood formation;
• hemolytic anemic syndrome - due to the destruction of red blood cells.

In addition, a distinction is made between acute, chronic and acute against the background of chronic anemia.

According to the volume of blood loss, it is divided into 3 degrees, which determine its severity: I - up to 15% of the BCC - mild; II - from 15 to 50% - severe; III - over 50% is considered excessive, since with such blood loss, even with immediate replenishment, irreversible changes are formed in the homeostasis system.

The severity of clinical manifestations and the outcome of blood loss are influenced by many factors. The most important are:

1. the age of the patient - children, due to the imperfection of compensation mechanisms, and the elderly, due to their exhaustion, tolerate even minor blood loss very hard;
2. speed - the more powerful the bleeding, the faster the compensation mechanisms are depleted, therefore arterial bleeding is classified as the most dangerous;
3. place of hemorrhage - intracranial hematomas, hemopericardium, pulmonary hemorrhages do not cause significant blood loss, but are the most dangerous due to severe functional disorders;
4. a person's condition before bleeding - anemic conditions, vitamin deficiencies, chronic diseases lead to rapid functional decompensation even with minor blood loss.

Blood loss of up to 500 ml is easily and immediately compensated by minor venous spasm, without causing functional disorders (therefore donation is absolutely safe).

Blood loss of up to a liter (conditionally) causes irritation of the volume receptors of the veins, which leads to their persistent and total spasm. No hemodynamic disorders develop. Blood loss is compensated for in 2-3 days by activating one's own hematopoiesis. Therefore, if there are no special reasons for this, interfering with the bloodstream by transfusing solutions or additionally stimulating hematopoiesis makes no sense.

With blood loss of more than a liter, in addition to irritation of the volume receptors of the veins, the alpha receptors of the arteries are irritated, which are present in all arteries, with the exception of the central ones, providing blood flow to vital organs: the heart, lungs, and brain. The sympathetic nervous system is excited, the function of the adrenal glands is stimulated (neurohumoral reaction) and the adrenal cortex releases a huge amount of catecholamines into the blood: adrenaline - 50-100 times higher than normal, noradrenaline - 5-10 times. As the process increases, this first causes a spasm of the capillaries, then small ones and increasingly larger ones, except for those without alpha receptors. The contractile function of the myocardium is stimulated with the development of tachycardia, the spleen and liver contract with the release of blood from the depot, arteriovenous shunts in the lungs open. All this together is defined as the development of the syndrome of centralization of blood circulation. This compensatory reaction allows maintaining normal blood pressure and hemoglobin levels for some time. They begin to decrease only after 2-3 hours. This time is the most optimal for stopping bleeding and correcting blood loss.

If this does not happen, hypovolemia and hemorrhagic shock develop, the severity of which is determined by the level of arterial pressure, pulse, diuresis and the content of hemoglobin and hematocrit of the blood. This is explained by the depletion of neuroreflex compensation mechanisms: angiospasm is replaced by vasodilation with a decrease in blood flow in the vessels of all levels with erythrocyte stasis, tissue metabolism disorder and the development of metabolic acidosis. The adrenal cortex increases the production of ketosteroids by 3.5 times, which activate the pituitary gland with an increase in the production of aldosterone and antidiuretic hormone.

As a result, not only does the renal vessels spasm, but bypass arteriovenous shunts open, disconnecting the juxtoglomerular apparatus with a sharp decrease in diuresis, up to complete anuria. The kidneys are the first to indicate the presence and severity of blood loss, and the restoration of diuresis is used to judge the effectiveness of blood loss compensation. Hormonal changes block the release of plasma from the bloodstream into the interstitium, which, along with impaired microcirculation, further complicates tissue metabolism, aggravates acidosis and multiple organ failure.

The developing adaptation mechanisms in response to blood loss are not stopped even with immediate restoration of the BCC. After replenishment of blood loss, arterial pressure remains reduced for another 3-6 hours, blood flow in the kidneys - 3-9 hours, in the lungs - 1-2 hours, and microcirculation is restored only on the 4th-7th day. Complete elimination of all disorders occurs only after many days and weeks.

Blood loss of up to 500 ml is considered physiological, and the restoration of the circulating blood volume (CBV) occurs independently. You understand, you won’t transfuse blood to a donor after exfusion.

In case of blood loss up to a liter, this issue is approached differentially. If the patient maintains blood pressure, tachycardia does not exceed 100 per minute, diuresis is normal - it is better not to interfere with the bloodstream and homeostasis system, so as not to disrupt the compensatory-adaptive reaction. Only the development of such conditions, anemic syndrome and hemorrhagic shock, are an indication for intensive therapy.

In such cases, correction begins already at the scene of the incident and during transportation. In addition to assessing the general condition, it is necessary to take into account the blood pressure and pulse rate. If the blood pressure is maintained within 100 mm Hg, there is no need to transfuse anti-shock drugs.

When the BP drops below -90 mm Hg, drip transfusion of colloidal blood substitutes is performed. A decrease in BP below 70 mm Hg is an indication for jet transfusion of solutions. Their volume during transportation should not exceed one liter. It is advisable to use autotransfusion of blood by raising the lower limbs, since they contain up to 18% of the BCC.

When a patient is admitted to a hospital, it is impossible to urgently determine the true volume of blood loss. Therefore, paraclinical methods are used for an approximate assessment of the condition, since they reflect the state of the homeostasis system to a greater extent. A comprehensive assessment is based on the following indicators: blood pressure, pulse, central venous pressure (CVP), hourly diuresis, hematocrit, hemoglobin content, and erythrocytes.

Acute anemic syndrome and hemorrhagic shock are the responsibility of anesthesiologists and resuscitators. It is pointless to start it without stopping the bleeding, moreover, the intensity of bleeding may increase.

The main criteria for replenishing blood loss are: stable arterial pressure at the level of 110/70 mm Hg; pulse within 90 per minute; central venous pressure at the level of 4-5 cm H2O; blood hemoglobin at the level of 110 g/l; diuresis over 601 ml per hour. In this case, diuresis is the most important indicator of the restoration of the BCC. By any means of stimulation: adequate infusion therapy, stimulation with euphyllin and lasix - urine output should be restored within 12 hours. Otherwise, necrosis of the renal tubules occurs with the development of irreversible renal failure. Anemic syndrome is accompanied by hypoxia, forming a hemic form of hypoxic syndrome.

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