Angina in leukemia

In modern interpretation, leukemia is a tumor of hematopoietic cells, affecting the bone marrow with displacement of normal hematopoietic sprouts, as well as other organs and tissues containing lymphadenoid tissue. Acute and chronic leukemia are distinguished. They are considered as independent polyetiologic diseases, in which the total number of leukocytes can be either increased or normal, or even decreased.

Acute leukemia is characterized by an increase in the number of blast, or leukemic, "young" cells in the bone marrow, spleen, lymph nodes, liver and other internal organs. The lymphadenoid tissue of the pharynx is not indifferent to this pathological process. Depending on the morphological and cytochemical characteristics of the blast cells, several forms of acute leukemia are distinguished: myeloblastic, lymphoblastic, plasmablastic, erythromyelosis, etc.

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Symptoms of angina in leukemia

Angina in leukemia begins with general weakness and mild bone pain. During the full clinical picture, a waxy pallor of the face is noted, general weakness increases sharply, bone pain intensifies, and fever appears. For no apparent reason, small-point hemorrhages appear in the skin, spreading throughout the body. The same hemorrhages are observed on the visible mucous membranes; bleeding gums, nosebleeds, intestinal, uterine bleeding are noted, which can serve as the immediate cause of death. Repeated bleeding quickly leads to hypochromic anemia. Ulcerative-necrotic lesions of the skin and mucous membranes often develop, especially in the oral cavity, pharynx and gastrointestinal tract. Large nodes may appear on the skin of the face and scalp, isolated or merging into conglomerates, which create a picture of a "lion's muzzle". Blast cells are present in the blood in large quantities (30-200) x 10 ⁹ /l and more, the number of platelets and erythrocytes is often reduced, and a high content of blast cells is noted in the bone marrow. The general diagnosis is established based on the clinical picture, and the form of leukemia is determined by the morphological and cytochemical indicators of blast cells.

Anginal manifestations begin with leukemic infiltration of the pharyngeal tonsil, soft palate, posterior pharyngeal wall, tongue and buccal mucosa. These infiltrates soon undergo necrotic decay due to a sharp increase in the virulence of the saprophytic microbiota. Ulcerative-necrotic lesions can spread to the larynx, nasopharynx and nasal cavity. Lesions of the pharyngeal tonsil can occur primarily or as a complication of ulcerative-necrotic stomatitis (in 70-80% of cases). Oro- and pharyngoscopy reveal unusually vivid signs of stomatitis, gingivitis, bleeding gums, which are covered with granulations and purulent-necrotic crusts. The tongue is dry with elements of desquamation, a putrid odor is felt from the mouth. The lesion of the tonsils initially manifests itself as hyperemia and enlargement of the tonsils, then the surface of the tonsils becomes covered with a diphtheroid-like coating. The tonsils reach gigantic sizes, acquiring the appearance of pseudophlegmon, their surface ulcerates. Infection of the decaying tissues of the oral cavity leads to the development of regional (submandibular) lymphadenitis.

The evolution of the disease lasts from 6 weeks to 2 months; there are also fulminant forms. Death occurs as a result of a combination of causes: toxemia, generalization of the angina process, purpura syndrome, internal bleeding, etc.

Diagnosis of angina in leukemia

The diagnosis is not established immediately in almost all cases, since the general and local symptoms of incipient acute leukemia have a certain similarity with many other diseases. The final diagnosis is established based on a bone marrow examination obtained by sternal puncture, which reveals a large number of blast cells.

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Treatment of angina in leukemia

Treatment of angina in leukemia is carried out in specialized hematological departments under the supervision of a dentist, otolaryngologist and internist. Modern cytostatic drugs can lead to long-term remissions or convert acute leukemia into chronic. Treatment for secondary ulcerative-necrotic complications includes all types of local symptomatic treatment (rinsing with antiseptic solutions, applications and spraying with local anesthetics, lubrication and irrigation with oil solutions of vitamins. To prevent secondary infection, broad-spectrum antibiotics are prescribed. To combat bleeding, infusions of fresh citrate blood, direct blood transfusion or UV-irradiated blood, autohemotherapy are performed, administration of platelet mass, calcium preparations, ascorbic acid, immunoprotectors are prescribed.