Nosebleed - Diagnosis.

To diagnose the causes of nosebleeds, it is necessary to conduct a study of vascular-platelet and coagulation hemostasis, biochemical studies (blood bilirubin, glucose, urea, total protein, lipidogram), a general clinical examination, and, if indicated, an X-ray or CT scan of the paranasal sinuses.

Physical examination

Vascular hemostasis is characterized by the results of tests for the mechanical stability of capillaries, such as the pinch test and the cuff test.

Pinch test. The doctor gathers the skin under the collarbone into a fold and makes a pinch. Normally, no changes in the skin are detected either immediately after the test or after 24 hours. If the capillary resistance is impaired, petechiae or bruises appear at the pinch site, especially clearly visible after 24 hours.

Cuff test. Stepping back 1.5-2 cm from the elbow fossa, draw a circle with a diameter of 2.5 cm. Place the cuff of the tonometer on the shoulder and create a pressure of 50 mm Hg. Maintain the pressure at the specified level for 5 minutes. Remove the cuff and count the number of petechial elements that appear in the drawn circle. In healthy individuals, petechiae do not form or there are no more than 10 of them. If the resistance of the capillary wall is impaired, the number of petechiae increases sharply.

The above tests are practically not used in clinical medicine. They are usually replaced by patient survey data. Such patients report the appearance of bruises or bleeding of mucous membranes with minor trauma.

Laboratory research

The purpose of laboratory tests is to assess the severity of posthemorrhagic anemia and indicators of vascular-platelet and coagulation hemostasis.

When assessing blood parameters, it should be remembered that in the first 24 hours after blood loss, it is impossible to accurately assess the degree of anemia due to compensatory mechanisms (release of blood from the depot, centralization of blood circulation). The degree of blood loss is determined by the hemoglobin content and hematocrit.

In case of acute blood loss, hemoglobin and hematocrit values alone do not serve as a basis for transfusion of blood components; this issue is decided taking into account the clinical manifestations that determine the severity of the anemic syndrome.

The characteristics of the platelet component of hemostasis are carried out based on the results of determining the number of platelets in the blood and the duration of bleeding according to Duke.

Determination of the number of platelets. Normally, the number of platelets in the peripheral blood is 180-320x10 ⁹ /l. A decrease in the number of platelets to a level below 160x10 ⁹ /l is considered thrombocytopenia.

Determination of the duration of bleeding according to Duke. This indicator reflects the violation of primary hemostasis and depends on the level of platelets in the blood, on the functional viability of these cells and on the content of the von Willebrand factor, and is normally 2-3 minutes. An increase in bleeding time in the absence of thrombocytopenia and hereditary hemorrhagic history serves as an indication for studying the adhesive-aggregation properties of platelets, that is, assessing their function.

A study of plasma (coagulation) hemostasis is conducted. A fairly crude diagnostic test reflecting a violation of the coagulation link of hemostasis is the determination of blood clotting time. A noticeable increase in this indicator indicates the presence of coagulopathy in the patient, but it is impossible to say what kind.

The process of plasma hemostasis can be conditionally divided into three phases.

The first phase is the formation of prothrombinase. This is a multi-stage process, as a result of which factors capable of converting prothrombin into thrombin accumulate in the blood. The blood clotting process can be initiated by the external and internal pathways of formation of the main catalyst acting in this phase - prothrombinase. With the external pathway of prothrombinase formation, the clotting process is triggered by the formation of factor III (tissue thromboplastin), which is expressed on the cell surface during tissue damage. Initiation of blood clotting by the internal pathway occurs without the participation of tissue thromboplastin, that is, without external tissue damage. In these cases, thrombus formation is provoked by damage to the vascular endothelium by circulating immune complexes, and as a result of which factor XII is activated upon its contact with the vascular subendothelium, or by its enzymatic cleavage. Activation of factor XII triggers a cascade reaction of prothrombin conversion to thrombin (second phase).

Diagnosis of coagulation hemostasis disorders is carried out based on a comparison of the results of a system of tests.

The first group of reactions, known as the intrinsic system, includes the interaction of factors XII, XI, IX, VIII and platelet phospholipids and ends with the activation of factor X. The intrinsic blood coagulation system is characterized by the following tests: plasma recalcification time, activated partial thromboplastin time - APTT (or APTT).

The second group of reactions includes the interaction of external blood coagulation factors: VII, X, V and tissue thromboplastin. The most common method for assessing the external blood coagulation system is the one-stage prothrombin time test (prothrombin index). Normally, the prothrombin index is 90-105%. A decrease in this indicator is observed with a deficiency of factor II with normal thrombin time (hereditary hypo- and dysprothrombinemia, hypovitaminosis K, mechanical jaundice, intestinal dysbacteriosis, liver parenchyma damage, administration of indirect anticoagulants), as well as with a deficiency of factors VII, IX, V.

Prothrombin time (according to Quick) is also classified as the second group of reactions.

The third phase of the blood coagulation process (the transition of fibrinogen to fibrin) is also characterized by a group of reactions. This group includes the determination of thrombin time, fibrinogen concentration, soluble fibrin-monomer complexes, and early fibrinogen degradation products.

The fibrinogen content in the blood increases during acute inflammatory processes, during chronic DIC syndrome, a sharp decrease in fibrinogen is observed during acute or fulminant DIC syndrome.

Soluble fibrin-monomer complexes in blood serum are normally not determined (using a qualitative reaction) or are present within the normal range determined by the set of reagents used in a quantitative test. A significant increase in the content of soluble fibrin-monomer complexes is observed in disseminated or massive local intravascular blood coagulation, accompanied by lysis of the formed fibrin, in tumors, thromboembolism, malignant liver lesions, hemolytic anemias and serves as the main laboratory diagnostic criterion for DIC syndrome.

Early fibrinogen degradation products are normally not detected (qualitative reaction) or are within normal limits. A significant increase in their blood is noted in the same situations as with an increase in soluble fibrin-monomer complexes.

The anticoagulant system of blood includes such physiological anticoagulants as antithrombin III, heparin, protein S, alpha-2-macroglobulin and others. These factors are determined mainly to identify the risk of thrombosis and the effectiveness of anticoagulant therapy. The only hemorrhagic risk factor is an increase in the level of antithrombin III (normally 80-120%), which is observed in viral hepatitis, cholestasis, severe acute pancreatitis, pancreatic cancer, vitamin K deficiency. When taking anticoagulants and indirect action.

Indications for specialist consultations

Nosebleeds can be caused by various somatic pathologies. In this regard, each patient should be examined by a therapist. In case of a serious condition of the patient, massive blood loss, signs of hemorrhagic or traumatic shock, a consultation with a resuscitator is necessary. If thrombocytopenia, signs of coagulopathy, leukemia, or nosebleeds of unclear etiology are detected, a consultation with a hematologist is required.

Diagnostic algorithm

All patients undergo screening tests such as:

• general blood test with assessment of platelet, reticulocyte and hematocrit levels;
• determination of blood clotting time;
• determination of bleeding time;
• study of the content of fibrinogen and soluble fibrin-monomer complexes.

The second stage of research is making a decision about drug therapy.

If the general blood test data indicate polycythemia, then correction of hemorrhagic manifestations should include the introduction of antiplatelet agents and blood clotting factors (transfusions of fresh frozen donor plasma),

If thrombocytopenia is detected, DIC syndrome should be excluded (the content of soluble fibrin-monomer complexes in the blood should be assessed), glucocorticoids should be prescribed - prednisolone 3 times a day at a daily dose of 1 mg/kg of the patient's weight (the dose is determined for oral administration, when switching to intravenous administration, the daily dose calculated for the patient's weight should be increased fivefold); it is possible to administer etamsylate, aminocaproic acid. In case of extreme severity of hemorrhagic syndrome and the need to perform traumatic manipulations and operations, transfusions of platelet concentrate are indicated.

If the blood clotting time increases, it is necessary to establish the presence of coagulopathy in the patient. In order to exclude congenital and hereditary coagulopathies, acquired disorders, a thorough anamnesis must be collected (specify heredity, previously occurring hemorrhagic disorders and the names of drugs that the patient took before this episode). To identify disorders in the intrinsic pathway of blood clotting, it is necessary to determine the activated partial thromboplastin time, and to determine disorders in the extrinsic pathway of blood clotting, it is necessary to determine the prothrombin time. In both cases, first of all, it is necessary to exclude DIC syndrome (determine the level of soluble fibrin-monomer complexes in the blood). In case of a predominant breakdown in the intrinsic pathway of blood clotting, fresh frozen donor plasma is administered at a frequency of at least 2 times a day in a volume of at least 1.0 l. In case of disturbances in the extrinsic blood coagulation pathway, in addition to transfusions of fresh frozen plasma, intravenous administration of menadione sodium bisulfite (or oral administration) is indicated. In case of coagulopathies, it is necessary first of all to exclude disturbances of liver and kidney function.

If bleeding time is prolonged (with normal platelet levels), thrombocytopathy or von Willebrand disease may be suspected. To exclude the latter, a thorough medical history must be taken (presence of pure bleeding episodes, burdened heredity, medication intake). In the absence of data in favor of von Willebrand disease, studies of platelet aggregation and adhesive functions are conducted. In this case, DIC syndrome must also be excluded. Correction methods include etamsylate, aminocaproic acid, and fresh frozen plasma infusions.

If the fibrinogen and blood levels decrease, it is necessary to exclude hereditary afibrinogenemia (hereditary history) and DIC syndrome (determine the level of soluble fibrin-monomer complexes). Methods of drug correction include the introduction of fibrinogen concentrate, transfusion of fresh frozen plasma.

If an elevated level of soluble fibrin-monomer complexes is detected in the blood, an unambiguous conclusion is made about the presence of DIC syndrome in the patient. If fibrinogen in the blood is low, then we are talking about acute DIC syndrome, and if the fibrinogen level is normal or exceeds it, then this is chronic DIC syndrome. In this case, DIC syndrome is treated in full.

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