Differential diagnosis of anemias

1. General anemic syndrome (tissue hypoxia)

The basic manifestations of any anemia are directly related to inadequate oxygen delivery to tissues and the activation of the body's compensatory systems.

• Circulatory changes: to compensate for hypoxia, cardiac output increases. Clinically, this is expressed by tachycardia and functional systolic murmurs (e.g., a "venous hum" over the jugular veins in children). A decrease in blood viscosity and vascular resistance leads to a tendency toward arterial hypotension.
• Respiratory response: shortness of breath (tachypnea) occurs, which sharply increases during physical exertion.
• Neurological manifestations: CNS hypoxia provokes headaches, dizziness, tinnitus, syncopal states, as well as a decrease in cognitive functions, memory, and concentration.
• External signs: pallor of the skin and visible mucous membranes is caused not only by a decrease in hemoglobin levels but also by the centralization of blood circulation.

2. Laboratory and physical differential search

The basis of primary diagnosis is a comprehensive complete blood count (CBC). Evaluation of hemoglobin (Hb), hematocrit (Ht), red blood cell count, erythrocyte indices (MCV, MCH, MCHC), and reticulocytes sets the vector for investigation. For example, a drop in Hb with normal indices (normocytic normochromic anemia) suggests hemoglobinopathies, while a decrease in parameters in a patient with chronic gastritis or a history of ulcers suggests occult blood loss.

During physical examination, it is important to assess for non-hematological anomalies. Thus, the detection of lymphadenopathy, hepatomegaly, or splenomegaly requires the exclusion of hemolytic, infiltrative, or tumor genesis (including hematological malignancies). If constitutional aplastic anemia (AA) is suspected, the physician specifically searches for specific stigmata: facial, dental, and ocular developmental anomalies, nail dystrophy, skin pigmentation, mucosal leukoplakia, hypogonadism, and premature graying.

3. Specific markers of pathogenetic variants

In addition to hypoxia, each anemia has unique clinical features due to its nature:

4. Decompensation and critical states

When hemoglobin drops below 50 g/L, a critical failure of the oxygen-transport function of the blood occurs. Decompensation is often provoked by increased tissue O₂ demand (infections, fever, pain syndrome) or further impairment of gas exchange (pneumonia, acute blood loss).

Early signs of decompensation: pronounced tachypnea with retraction of compliant chest areas (intercostal spaces, suprasternal spaces), abdominal breathing, nasal flaring. With increasing severity, a forced "moaning" expiration appears, depression or agitation of consciousness, weakening of the peripheral pulse, hepatomegaly, and the "white spot" sign (capillary refill time longer than 2 seconds). Such a condition requires emergency therapy and consideration of blood transfusion (approximate indications: Hb < 70 g/L, Ht < 30%).

Class and exam questions

What else to study on this topic

• Constitutional forms of aplastic anemia and the role of non-hematological anomalies in their diagnosis.
• The connection of gastric pathologies (atrophic gastritis, polyps) with the development of pernicious anemia.
• Differential diagnosis of prehepatic jaundice using red blood cell parameters.
• Evaluation of hemostasis and determination of indications for transfusion therapy in the perioperative period.
• Pathogenesis of myocardial dystrophy and ECG changes in long-standing megaloblastic anemias.

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