Anemic syndrome

Clinical presentation

The foundation of all clinical manifestations of the syndrome is tissue hypoxia — oxygen starvation of organs. The severity of symptoms directly depends on how rapidly hemoglobin levels drop and how severely they are reduced.

• Central nervous system: patients complain of syncopal states and frequent dizziness.
• General manifestations: rapid fatigability, pronounced general weakness, and dyspnea are characteristic. Notably, symptoms manifest even against the background of completely insignificant physical exertion. Tolerance to any routine activity decreases.
• Physical examination: inadequate blood supply to peripheral tissues manifests as pronounced pallor of the visible mucous membranes and skin. During an objective examination, the physician should also purposefully look for signs of enlargement of the liver (hepatomegalia), spleen (splenomegalia), and lymph nodes (lymphadenopathia).

If the pathology progresses gradually, the body manages to mobilize internal reserves. In such situations, the patient may not notice a deterioration in well-being for a long time, but a sharp collapse in parameters poses a critical threat to life.

Compensation mechanisms

To survive under conditions of increasing oxygen deficit, the body triggers a number of compensatory reactions. They are divided into hemodynamic and biochemical.

Hemodynamic compensation by the cardiovascular system typically starts when hemoglobin levels drop below 100 g/L:

• Cardiac output increases and heart rate (HR) accelerates.
• Total peripheral vascular resistance (TPVR) decreases. This occurs due to tissue hypoxia itself, as well as the fact that the blood becomes less viscous.
• During cardiac auscultation, a characteristic systolic murmur begins to be heard over the apex. Its genesis is explained by accelerated blood flow and blood thinning.

Biochemical adaptation consists in shifting the oxyhemoglobin dissociation curve. As a result of this process, hemoglobin releases oxygen molecules to the starving peripheral tissues much more easily and rapidly.

Anamnesis collection and causes of development

Since anemia can be a consequence of other concealed illnesses, a thorough patient interview is extremely important. The physician needs to pay attention to:

• External exposure: intake of specific medications, regular contact with toxic substances, dietary features, and regular alcohol consumption.
• Hereditary factor: identification of cases of severe anemia in blood relatives.
• Concomitant pathology: searching for conditions that could have become the source of the problem. A classic example is gastric or duodenal ulcer disease, which produces recurrent occult bleeding.

Globally, the etiology of the syndrome is divided by the rate of development (acute form after massive blood loss or hemolysis versus slowly progressive chronic) and by association with the somatic background. The syndrome frequently accompanies oncology (solid tumors and hemoblastoses), connective tissue disorders, and infectious-inflammatory processes. Excretory organ diseases (chronic kidney disease) and endocrinopathies (hypothyroidism, hyperthyroidism, adrenal insufficiency, hypopituitarism) play a huge role.

Laboratory diagnostics and classification

Diagnostic investigation relies not only on the fact of decreased parameters, but also on a qualitative assessment of blood cells. The mandatory range of tests includes hematocrit, erythrocyte indices (MCV and MCH), reticulocyte count (indicating the bone marrow's regenerative capacity), as well as white blood cells and platelets.

According to morphology and pathogenesis, three key variants are distinguished:

1. Hypochromic microcytic: erythrocytes are small, with low saturation. Iron deficiency, globin synthesis defects (thalassaemia) or porphyrin defects, lead poisoning, and anemia of chronic disease underlie this condition.
2. Normochromic normocytic: normal cells, but low in number. These are hypoproliferative states in endocrine disorders, renal pathology, bone marrow hypoplasia, and myelofibrosis (when myelopoiesis is selectively impaired).
3. Hyperchromic macrocytic: megaloblastic large cells. They arise due to a lack of folic acid, vitamin B12 deficiency, or the toxic effects of medications.

Standing apart are hemolytic anemias, where erythrocytes are actively destroyed. This occurs either due to immunological failures or due to intrinsic genetic cell defects (membranopathies, hemoglobinopathies, congenital enzymopathies).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis and stages of development of iron deficiency anemia
• B12-deficient and folate-deficient anemias: clinical features
• Differential diagnosis of types of hemolytic anemia
• Anemia of chronic disease and the role of renal failure
• Erythrocyte indices (MCV, MCH) in clinical practice

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