Nosebleeds: diagnosis

To diagnose the causes of nasal bleeding, it is necessary to conduct a study of vascular-platelet and coagulation hemostasis, biochemical studies (blood levels of bilirubin, glucose, urea, total protein, lipidogram), general clinical examination, according to indications - radiography or CT of paranasal sinuses.

Physical examination

Vascular hemostasis characterizes the results of samples for the mechanical stability of capillaries, such as a sample of pinch and a cuff test.

Sample pinch. The doctor collects the skin under the collarbone into the fold and makes a pinch. Normally no changes in the skin are detected either immediately after the test, or after 24 hours. If the resistance of the capillaries is impaired, petechiae or bruising appear on the place of the tweezer, especially clearly visible after 24 hours.

A cuff test. Stepping back 1.5-2 cm down from the ulnar fossa, draw a circle with a diameter of 2.5 cm. Apply a cuff of the tonometer to the shoulder and create a pressure of 5O mm Hg. The pressure is maintained at this level for 5 minutes. Remove the cuff and count in the outlined circle the number of petechial elements that appeared. In healthy individuals petechiae are not formed or there are no more than 10. If the resistance of the wall of capillaries to the amount of the petechia increases sharply.

These samples are practically not used in clinical medicine. Usually, they are replaced by patient survey data. Such patients indicate the appearance of bruises or bleeding of mucous membranes with minor traumatization.

Laboratory research

The purpose of laboratory studies is to evaluate the severity of posthemorrhagic anemia and the indices of vascular-platelet and coagulation hemostasis.

When assessing blood levels, it should be remembered that in the first day after the loss of blood, it is impossible to accurately estimate the degree of anemia due to compensatory mechanisms (discharge of blood from the depot, centralization of blood circulation). The degree of hemorrhage is determined by the content of hemoglobin and hematocrit.

In acute hemorrhage, hemoglobin and hematocrit themselves do not serve as a basis for transfusion of blood components, this issue is solved taking into account the clinical manifestations that determine the severity of the anemic syndrome.

Characterization of the platelet component of hemostasis is carried out according to the results of determining the number of platelets in the blood, the duration of bleeding by Duke.

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

Determination of the duration of bleeding by Duke. This indicator reflects the violation of primary hemostasis and depends on the level of platelets in the blood, on the functional consistency of these cells and on the content of the von Willebrand factor, and the norm is 2-3 minutes. The increase in bleeding time in the absence of thrombocytopenia and hereditary hemorrhagic anamnesis serves as an indication for the study of adhesion-aggregation properties of platelets, that is, the evaluation of their function.

Conduct a study of plasma (coagulation) hemostasis. Rough enough diagnostic test, reflecting the violation of the coagulation unit of hemostasis is the determination of the time of blood coagulation. A marked increase in this indicator indicates that the patient has coagulopathy, but which one, while it is impossible to say.

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

The first phase is the formation of prothrombinase. This is a multi-step process and the result of which blood accumulates factors that can turn prothrombin into thrombin. The process of blood coagulation can be initiated along the external and internal pathway for the formation of the main catalyst, acting in this phase, - prothrombinase. With the external pathway for the formation of prothrombinase, the coagulation process is triggered by the formation of factor III (tissue thromboplastin), which is expressed on the surface of cells in the event of tissue damage. The initiation of blood clotting along the internal pathway occurs without the involvement 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, the XII factor is activated when it contacts the subendothelium of the vessels, or by its enzymatic cleavage. Activation of the XII factor triggers a cascade reaction to convert prothrombin to thrombin (second phase).

Diagnosis of violations of coagulation hemostasis is carried out on the basis of a comparison of the results of the test system.

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

The second group of reactions includes the interaction of factors of the external environment of blood coagulation: VII, X, V and tissue thromboplastin. The most common method for evaluating the external system of blood clotting is the test of a single-stage prothrombin time (prothrombin index). Normally, the prothrombin index is 90-105%. Decrease in this indicator is noted with factor II deficiency in normal thrombin time (hereditary hypo- and dysprotrombinemia, hypovitaminosis K, mechanical jaundice, intestinal dysbacteriosis, liver parenchymal involvement, administration of indirect anticoagulants), as well as deficiency of VII, IX, V factors.

Prothrombin time (according to Kviku) is also attributed to the second group of reactions.

The third phase of the process of blood coagulation (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, early fibrinogen degradation products.

The content of fibrinogen in the blood increases with acute inflammatory processes, with chronic DIC syndrome, a sharp decrease in fibrinogen is observed in acute or lightning-fast ICE syncrome.

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

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

To anticoagulant system of blood carry such physiological anticoagulants, as antithrombin III, heparin, protein S, alpha-2-macroglobulin and others. These factors determine, mainly, to identify the risk of thrombosis and the effectiveness of anticoagulant therapy. The factor of hemorrhagic risk is only 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 anticoagulant and indirect action.

Indications for specialist consultations

Nasal bleeding may be due to a variety of 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 resuscitation specialist's consultation is necessary. In detecting thrombocytopenia, signs of coagulopathy, leukemia, with nose bleeding of unclear etiology, consultation of the hematologist is required.

The Dianetic algorithm

All patients perform screening tests, such as:

• general aval of blood with an estimate of the content of platelets, reticulocytes and hematocrit;
• determination of blood clotting time;
• determination of bleeding time;
• study of the content of fibrinogen and soluble fibrin-monomer complexes.

The second stage of the research is the decision-making on drug therapy.

If the data of a general blood test indicate polycithemia, correction of hemorrhagic manifestations should include the administration of antiaggregants and clotting factors (transfusion of freshly frozen donor plasma),

In detecting thrombocytopenia, the DIC syndrome should be excluded (estimate the content of soluble fibrin-monomer complexes in the blood), prescribe glucocorticoids - prednisolone 3 times a day at a daily dose of 1 mg / kg of patient weight (the dose is determined for ingestion, when transferred to intravenous daily the dose calculated for the patient's weight should be increased fivefold); it is possible to administer ethamylate, aminocaproic acid. With extreme severity of hemorrhagic syndrome and the need for traumatic manipulations and operations, transfusions of platelet concentrate are shown.

With an increase in the time of blood clotting, it should be noted that the patient has coagulopathy. In order to exclude congenital and hereditary coagulopathy, acquired disorders, careful collection of anamnesis is needed (to clarify the heredity, previous haemorrhagic abnormalities and the names of medications the patient took before this episode). To detect violations of the internal blood clotting pathway, it is necessary to determine the activated partial thromboplastin time, and to determine the disturbances in the external blood clotting pathway, the prothrombin time is determined. In both cases, first of all, it is necessary to exclude the DIC syndrome (to determine the level of soluble fibrin-monomer complexes in the blood). With a predominant breakdown in the internal blood clotting path, freshly frozen donor plasma is administered at a rate of not less than 2 times a day with a volume of at least 1.0 liters. If there is a violation in the external blood clotting path, in addition to transfusions of fresh frozen plasma, intravenous administration of sodium menadione bisulfite (or ingestion) is indicated. When coagulopathy is necessary, first of all, the exclusion of violations of the liver and kidneys.

If there is an elongation of bleeding time (against a background of a normal platelet count), one can assume thrombocytopathy or Willebrand disease. To exclude the latter, it is necessary to carefully collect the anamnesis (the presence of pure episodes of hemorrhage, weighed heredity, medication). In the absence of data in favor of von Willebrand disease, the aggregation and adhesion functions of platelets are studied. It is also necessary to exclude the DIC syndrome. Correction methods are presented by infusions of etamzilate, aminocaproic acid, fresh frozen plasma.

With a decrease in the level of fibrinogen and blood, hereditary afibrinogenemia (hereditary anamnesis) and DIC-syndrome (to determine the level of soluble fibrin-monomer complexes) should be excluded. The methods of drug correction are the introduction of fibrinogen concentrate, transfusion of fresh frozen plasma.

When an increased level of soluble fibrin-monomer complexes in the blood is made, an unambiguous conclusion is made about the patient's DVS-syndrome. If fibrinogen is low in the blood, then it is an acute DIC syndrome, and if the level of fibrinogen corresponds to the norm or exceeds it, then this is a chronic DIC syndrome. In this case, treatment of DIC-syndrome in full.

[1], [2], [3], [4]