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Indicators of hematological tests and hemostasis as predictors of hemorrhagic complications in children...
Table 1. - Indicators of the layer thickness of the side wall of the atria of the heart of the control animals, in microns (M ± m), mm, n = 10
Time trials Left atrium Right atrium
Total Endocardium Epicardium Myocardium Total Endocardium Epicardium Myocardium
Newborns 67.03 ± 1.9 9.7 ± 0.4 48.43 ± 1.6 8.6 ± 0.4 33.5 ± 1.45 8.5 ± 0.6 17.5 ± 1.12 7.5 ± 0.5
6 days 69.9 ± 2.87 11.4 ± 0.23 49.7 ± 2.54 8.8 ± 0.23 37.5 ± 0.68 9.6 ± 0.21 19.6 ± 0.76 8.3 ± 0.22
11 days 84.7 ± 2.67* 13.5 ± 0.32 60.8 ± 2.64* 10.4 ± 0.43 42.8 ± 1.76 11.4 ± 0.43* 21.6 ± 0.18 9.8 ± 0.12
16 days 96.4 ± 2.44 14.7 ± 0.16 70.1 ± 1.76* 11.6 ± 0.13 50.7 ± 1.54 12.8 ± 0.14 27.2 ± 0.14* 10.7 ± 0.14
22 days 116.5 ± 3.24* 17.5 ± 0.43 85.6 ± 2.43 13.5 ± 0.13 60.4 ± 2.34 14.9 ± 0.12* 32.9 ± 0.27 12.6 ± 0.06
Note: * — P < 0.01 the accuracy in comparison with the previous period.
Table 2. - Indicators of side wall layer thickness ventricular control animals in microns (M ± m), mm, n = 10
Time trials The ventricle The upper part Of the lower part
Total Endocardium Epicardium Myocardium Total Endocardium Epicardium Myocardium
Newborns The left 675.9 ± 12.23 14.8 ± 0.74 645.5 ± 12.4 15.6 ± 0.14 918.7 ± 14.8 43.6 ± 1.8 885.1 ± 12.9 15.2 ± 0.23
The right 320.5 ± 7.54 15.4 ± 0.53 290.3 ± 7.44 14.8 ± 0.62 385.65 ± 6.78 16.15 ± 0.61 355.25 ± 7.23 14.25 ± 0.54
6 days The left 862.6 ± 5.84 17.1 ± 1.10 828.2 ± 6.63 17.3 ± 0.72 1046.53 ± 1.13 20.9 ± 1.13 1008.91 ± 1.14 16.72 ± 1.1
The right 383.2 ± 7.08 17.9 ± 1.03 349.2 ± 7.29 16.2 ± 0.42 431.89 ± 1.12 18.24 ± 1.2 397.88 ± 1.12 15.77 ± 1.1
11 days The left 990.6 ± 5.6* 19.6 ± 1.06 952.1 ± 5.3 19.0 ± 0.75 1278.7 ± 1.22 24.7 ± 1.18 1234.24 ± 1.22 19.76 ± 1.18
The right 425.7 ± 3.7* 20.3 ± 0.5* 387.7 ± 3.3 17.7 ± 0.85 519.36 ± 1.23 21.66 ± 1.15 479.08 ± 1.20* 18.62 ± 1.18
16 days The left 1209.8 ± 10.75 22.0 ± 0.71 1167.3 ± 11.42* 20.5 ± 0.84 1473 ± 1.15* 27.93 ± 1.13 1423.03 ± 1.15* 22.04 ± 1.11
The right 493.2 ± 12.38 23.4 ± 0.85 450.7 ± 12.4 19.2 ± 1.04 596.81 ± 1.14* 24.32 ± 1.12 552.16 ± 1.15* 20.33 ± 1.09
22 days The left 1468.3 ± 9.23 24.9 ± 0.57 1421.0 ± 8.56 22.4 ± 0.89 1796.58 ± 33.24 ± 1.19 1737.68 ± 1.22 25.65 ± 1.16
The right 574.3 ± 20.38 26.8 ± 0.82 523.7 ± 20.25 23.8 ± 1.37 718.98 ± 1.20 28.31 ± 1.16 667.87 ± 1.21* 22.8 ± 1.12
Note: * — P < 0.01 the accuracy in comparison with the previous period.
References:
1. Akhmedov S. M. Morphological characteristics of the heart wall rats//Science and world. - 2015. - 1(7): 85-87.
2. Bokeria O. L., Ahobekov A. A. Sudden cardiac death: mechanisms of occurrence and risk stratification//Annals arrhythmology. -2012. - 3: 5-13.
3. Boldueva S. A., Shabrov A. V., Lebedev D. S. et al. Prediction and prevention of sudden cardiac death in patients after myocardial infarc-tion//Cardiovascular therapy and prevention. - 2008. - 7(3): 56-62.
4. Gorbunov A. A. Connective tissue infarction component: a new stage in the study oflong-standing problem//Morfolog. - 2007. - 4: 6-12.
5. Kurbanov R. D., Mullabaeva G. U., Kilichev A. A., Kevorkova Y. G., Sayfitdinova N. B. The effectiveness of ivabradine in treating patients with Q-wave myocardial infarction//Cardiology Uzbekistan. - 2014. - 3: 11-16.
6. Lebedynets A. N., Voloshin N. A., Chugin S. V. The dynamics of the structural components of the heart in rats in the postnatal period following intrauterine exposure to antigens of different nature//Patologiya. - 2011. - 2: 43-45.
7. Chirkov E. N. Cardiac morphology and internal structures of different ecological groups of mammals (thesis). - Orenburg, 2009.
8. Michela N. F. Inform the Heart: Control of Cardiomyocyte Cycling and Size by Age-Dependent Paracrine Signals//Developmental Cell. - 2009. - 16: 161.
Babakhanova Nargiza Nusratullayevna, Hematologist, Research Institute of Hematology and Blood Transfusion
of the Ministry of Health of Uzbekistan
Karimov Khamid Yakubovich, MD, Professor
Shodibekova Oksana Borisovna,
Assesorova Yuliana Yurevna, PhD E-mail: [email protected]
Indicators of hematological tests and hemostasis as predictors of hemorrhagic complications in children with acute lymphoblastic leukemia
Abstract: The trial analyzed the significance of hemostatic parameters and blood analyses as prognostic markers for the development of hemorrhagic complications in children with Acute Lymphoblastic Leukemia (ALL) at the early onset of disease.
Section 6. Medical science
In addition to that the research identifies the correlation between the amount of fibrinogen, blasts, immature white blood cells and the level of thrombocytopenia (p < 0.05). It was established that in the early grades of disease in children with ALL indexes of hematological and hemostasis tests poorly correlate with the degree of thrombocytopenia and hemorrhagic syndrome cannot serve as a marker of risk of hemorrhagic complications development.
Keywords: acute lymphoblastic leukemia, children, hemostasis, hemorrhagic complications.
Relevance
Acute leukemia is the most common form of neoplastic diseases in children: in the structure of malignant tumors, acute leukemia account for about 32 %. Among all forms of leukemia, acute lymphoblastic leukemia (ALL) is the most prevalent, and constitutes 75-80 % of cases. The use of modern treatment protocols have drastically changed the outcomes of acute leukemia, until recently it was considered as fatal disease: nowadays long-term event-free survival can be achieved in 70-95 % of children with newly diagnosed ALL [3; 5; 10]. However, a protocol of intensive chemotherapy, as well as the neoplastic process itself, often leads to the development of severe complications that hinder to full treatment, and requires high-quality and expensive supportive therapy [4; 5; 7; 9].
Along with infectious, septic and organ-toxic complications, negative impact on the results of treatment of patients with ALL, have complications that are associated with disorders of the hemostatic system. The risk of these complications is caused by inhibition of normal hematopoiesis and the development of thrombocytopenia, accompanied by the acute leukemia, starting with the early grades of the disease [1; 6]. Severe multidirectional abnormalities in the hemostatic system that prevail to perform polychemotherapy (PCT) within the strictly defined terms, developed in 43.5 % patients with ALL. Symptomatic manifestations of hemostatic disorders in cases ofALL ranged from localized thrombosis to hemorrhagic syndrome of different severity. The genesis of hemorrhagic syndrome in hematologic malignancies in children is complicated as it has a direct relationship with the primary malignancy and with its complications.
Prevention and treatment of hemorrhagic syndrome in children with ALL involves a differentiated correction for disorders of coagulation and anticoagulant part of hemostasis, diagnosing of which is necessary before starting treatment and during treatment. However, the literature suggests untimely and inadequate diagnosis of hemostasis disorders and their correction in children with ALL [6].
Timely prevention of complications caused by hemostasis disorders requires the use of reliable markers capable of indicating the links in the chain of the imbalance of coagulation and anticoagulation mechanisms and identifying violations of the hemostatic system even before their clinical manifestation.
Objective
To study the significance of the indicators of hemostasis and hematological tests, as markers of risk of hemorrhagic complications development, in children with acute lymphoblastic leukemia.
Materials and Methods
Study included assessment of the main laboratory parameters of blood and hemostasis in 25 children aged from 6 months to 15 years with newly diagnosed acute lymphoblastic leukemia (primary patients). Patients were divided depending on the severity of the hemorrhagic syndrome (HS) (group 1 with 0 and I grade of HS — 17 patients; group 2 with II and III grade of HS — 8 patients) and severity of thrombocytopenia (group 1 — mild and moderate degree of thrombocytopenia — 7 patients; group 2 — severe degree of thrombocytopenia — 18 patients).
The hemostatic system was assessed by determining the following parameters: activated partial thromboplastin time (APTT), prothrombin time (PTT), thrombin time (TT), level of fibrinogen,
Hageman factor — dependent fibrinolysis (HF-DF) by means of the orthophenanthroline method, amount of soluble fibrin monomer complexes (SFMC) and D-dimers. In addition to them, indicators of physiological anticoagulants — activity of the protein C (PrC) and the activity of antithrombin III (AT III) were assessed [1; 2; 8].
Statistical treatment
The statistical analysis was performed using the standard software package of Microsoft Office Excel, STATISTICS 6.0. Comparison of groups of patients for categorical attributes was performed using T-Students' criteria. We evaluated the confidence level p, the differences between groups were considered for statistically significant at a significance level of p < 0.05.
Result and discussion
The results of our research of the hemostatic system in children with ALL at the midst of clinical manifestations showed the presence of differently directed shifts depending on the severity of the hemorrhagic syndrome and the severity of thrombocytopenia, according to this, patients were divided into groups. In groups of patients with ALL, that was ranked according to the grade ofhemorrhagic syndrome (group 1 — without HS or with I grade of HS, group 2 — with HS of II and III grade) a comparative intergroup analysis showed no significant changes in basic hematologic parameters of blood (Table 1). The study of hemostasis revealed, that such biochemical parameters of coagulation and fibrinolytic system as: activated partial thromboplastin time (APTT), prothrombin time (PTT), thrombin time (TT), fibrinogen level, Hagemann-dependent lysis time, (XIIa - dependent lysis time), the rate of soluble fibrin-monomeric complexes (SFMC), activity of protein C (PrC) and antithrombin III (AT III) had no significant value between the first and second groups of patients (Table 2).
APTT characterizes the internal way of activation of blood coagulation under standard conditions of contact activation, and evaluates the involvement of coagulation factors in forming of tenase and prothrombinase complexes without affecting platelet phospholipids of the patient. This figure depends on the level of high molecular weight of kininogen, prekallikrein and clotting factors XII, XI, VIII, IX and less sensitive to change of factors X, V, prothrombin and fibrinogen. Lengthening of APTT is observed in the decrease of the activity of next factors: VIII, IX, XI, XII, and may be associated with an increased risk of hemorrhagic complications. In the study of coagulation parameters in children with ALL the activated partial thromboplastin time in HS 0 and I level was 33.9 ± 5.2 seconds, while in the group with HS II and III grade it constituted — 29.6 ± 2.1 seconds (N — 21.1-36.5 sec.).
The prothrombin time (Quick prothrombin), describes the external coagulation cascade and the second phase of plasma hemostasis (prothrombine and thrombine formation) and reflects the activity of prothrombin complex factors (factors VII, V X and II). By reducing, the activity of prothrombin complex factors VII, V X, II the time of clot formation in plasma is slowed down and, accordingly, prolongs the prothrombin time. The lengthening of the PTT demonstrates the tendency to hypocoagulation, shortening — tendency to hypercoagulation. Regardless of the severity of HS PTT indicator (Quick prothrombin), in patients with ALL was in the range close to and within the normal range (76.7 ± 5.8 % - 78.8 ± 5.0 %, N — 70-120 %).
Indicators of hematological tests and hemostasis as predictors of hemorrhagic complications in children.
Fibrinogen — blood coagulation factor I, which is produced in the liver. Under the action ofthrombin it is converted to fibrin, which participates in the formation of a blood clot. Fibrinogen deficiency characterized the violation of a stable thrombus formation and bleeding disorders and the excess — the tendency to thrombosis. In addition, concentration of fibrinogen in blood increases while diseases involving tissue injury and inflammation. Evaluation of fibrinogen level in children with various forms ofhemorrhagic syndrome in ALL showed that the values of the indicator in HS of 0-I grade is made up 0.6 ± 4.3 g/l, while HS of II-III grade — 4.5 ± 0.8 g/l, which exceeds the normal rate borders (N — 1.8-4.0 g/l).
Thrombin time is a screening coagulation time of the final grade of blood clotting — rate of transformation of fibrinogen to fibrin. It depends on the content of fibrinogen and inhibitors that block the action of thrombin and the conversion of fibrinogen to fibrin. Patients with HS of 0-I grade had the normal range (N — 9-14 sec.) ofTT indexes was and made up about 12.2 ± 0.74 seconds. Children with HS of II-III grade TT also did not exceed the normal rate (1.28 ± 1.26; p > 0.05). Patients who have an elongated clotting time, the conversion of fibrinogen to fibrin slowed, which increases the risk of bleeding. In our monitoring, children with AL in a debut of disease TT index did not correlate with the degree of hemorrhagic syndrome severity.
Antithrombin III — specific protein of blood coagulation system, main function is to inactivate key coagulation factors, including thrombin, f. Xa, IXa and Xia, also to restrict increased thrombocyte formation. Manifestation of ATIII deficiency is relapsing arterial and venous thrombosis. The process of thrombin generation is also interrupted with plasma protein C in the presence of its cofactor — protein S. The levels of physiological anticoagulants ATIII and PrC between the groups were not statistically different and were within the normal range (ATIII — 81.5-84.7 %, N — 72-124 (134) % PrC — 1.2-1.7 units, N — 0.7-1.3 units). The study of blood fibrinolytic system parameters has shown that the Hageman — dependent lysis time had no significant difference between the groups and was 12.06 ± 1.27 minutes in the subgroup of HS in 0-I grades and 10.14 ± 2.52 min. in other group with HS of II-III grades (N — 5.5-12.0 min). Increasing the rate of SFMC — thrombinemia markers — also had no statistically significant difference between the groups, however, in both cases it exceeded the reference values (6.1-6.8 mg/l, N — 0-3.38 g/L).
D-dimers are formed during clot lysis and under the influence of plasmin and other proteolithic enzymes. Their concentration is proportional to the activity offibrinolysis in the blood and the number oflysed fibrin, which gives an indication ofthe intensity of the processes offor-mation and destruction of fibrin clots. The qualitative test for D-dimers showed that in the subgroup with HS 0-I grade 12.5 % ofpatients had positive results that are above the reference level of D-dimers (normal concentration ofD-dimer is not more than 400-500 ng/ml fibrinogen equivalent units — FEU) and reactive fibrinolysis. In other 87.5 % of patients with HS 0-I grade and 100 % ofpatients with HS II-III grade, D-dimer level were negative in qualitative test, indicating that the activation of intravascular coagulation and fibrinolysis is absent.
Depending on the severity of thrombocytopenia patients were divided into 2 groups: group 1 — patients with mild and moderate degree of thrombocytopenia; group 2 — patients with severe degree of thrombocytopenia. In the group with severe degree of thrombocytopenia 38.9 % of the patients had clinical manifestations like disorders in hemostasis, such as petechiae, bruising after the injection, hematomas, bleeding at the injection site, gingival bleeding. In the group of children with mild to moderate degree of thrombocytopenia clinical manifestations and violations in hemostasis were not observed.
Level ofhemoglobin in mild and moderate thrombocytopenia was by 25 % higher in comparison with thrombocytopenia of severe degree (90.71 ± 5.47 g/l vs. 68.0 ± 4.14 g/l; t=2.56; р < 0.05). With the development of severe thrombocytopenia was noted almost eleven times higher rate of total white blood cells, but the significance was not reliable because of the importance of a substantial parametric variation in the samples. Moreover, in patients with mild to moderate thrombocytopenia compared to patients with severe thrombocytopenia by 72.7 % and 65.5 %, respectively, parameters of stab neutrophiles (1.43 ± 0.42 % versus 0.39 ± 0.13 %; t = 2.36; p < 0.05) were higher and segmented neutrophils (24 57 ± 5.47 % versus 8.39 ± 2.46 %; t = 2.70; p < 0.05). The significant factor in these subgroups was also changes in the number ofblasts. The amount of blasts in the blood of patients with severe thrombocytopenia increased by 58.7 % in comparison with the group of mild to moderate thrombocytopenia level (37.4 ± 6.02 ± 9.20 vs. 15.43 %; t = 2.0; p < 0.05) (Table 1). However, it should be noted that the increasing blasts and immature leukocytes in the leukemia related to inhibition of normal hematopoiesis, which is a cause of disease but not a consequence of thrombocytopenia. Finally, in both groups revealed an inverse relationship between number of platelets and leukocytes, as well as between platelet and blast cells, which indicates a decrease in the number of thrombocytes due to their lack offormation: if degree of leukocytosis would be high, the normal myelopoiesis — more suppressed. Our research revealed a direct correlation between the decrease in the number of platelets and proportion of mature differentiated leukocytes — stab and segmented, which is also a consequence of the inhibition of normal hematopoiesis. A similar results in leukemia also was found and by other researchers [1].
Comparative evaluation of hemostasis in the groups among the patients with severe degree ofthrombocytopenia, and patients with mild to moderate degree of thrombocytopenia revealed a tendency to reduce the APTT (28.3 %) and PTT (12.6 %), whereas increasing degree of thrombocytopenia takes place. However, these changes did not have significant difference (p > 0.05), which may be related to the spread of the individual values of the studied parameters within the study groups. Noticeable deviation was observed in the content offibrinogen, which increased by 47 % while burdening the degree of thrombocytopenia (from 2.67 ± 0.56 to 5.04 ± 0.52 g/L; t = 3.12; p < 0.05). Inaccurately increased the rates of physiological anticoagulants ATIII with the development of severe thrombocytopenia. There were not significant modifications in the blood indexes of fibrinolitic system, HF-DF and SFMC between compared groups. In the subgroup of patients with mild to moderate degree of throm-bocytopenia, 6.0 % of patients had positive result on the D-dimers, which indicating reactive fibrinolysis.
In 94.0 % of patients with mild to moderate degree of thrombocytopenia and 100 % of patients with severe thrombocytopenia, D-dimers had a negative result in a qualitative analysis (Table 2).
Thus, conducted in Uzbekistan study revealed that the development of acute lymphoblastic leukemia in children affects the state of coagulation and anticoagulation system of blood and shows relevant clinical symptoms and changes in biochemical indices of hemostasis. However, these symptoms do not occur in all patients and have a variable range ofvalues. In addition, parameters ofhemostasis and hematological analyzes correlate poorly with the degree of thrombocytopenia and hemorrhagic syndrome and thus may not be a predictor markers of hemostatic disorders in children with acute lymphoblastic leukemia in early grades of development. Prevention of hemorrhagic complications in acute leukemia in children requires finding for new reliable markers that allow to forecast the risk of the hemostatic system disorders prior of their clinical manifestation.
Table 1. - Indicators of blood elements in children with ALL depending on the degree of hemorrhagic syndrome and thrombocytopenia
Group n Hemoglobin Erythrocytes ESR Total leuko-cytes Lymphocytes Blasts Myelocytes Metamyelocytes Band neutrophil Segmented neutrophil Eosinophil Monocytes
depending on the degree of hemorrhagic syndrome
1st group. 0 and I grade ofHS 17 77.5 ±5.4 2.9 ±0.2 20.0 ±5.8 70.7 ±38.1 49.1 ±6.5 32.8 ±6.9 0.13 ±0.07 0.13 ±0.07 0.7 ±0.2 12.3 ±3.1 0.6 ±0.1 3.7 ±1.0
2nd group. II and III grade of HS 8 66.6 ±6.9 2.7 ±0.3 16.1 ±6.4 22.4 ±12.7 54.9 ±10.2 31.1 ±9.5 0.12±0.12 0 0.5 ±0.2 9.7 ±2.5 0.5 ±0.2 3.0 ±0.6
Student t-test 25 1.24 1.67 0.45 1.20 0.47 0.14 0.07 0 0.36 0.65 0.34 0.58
depending on the degree of thrombocytopenia
Mild and moderate degree of thrombocytopenia 7 90.7 ±7.8 3.2 ±0.3 18.9 ±8.6 5.9 ±3.1 52.7 ±9.1 15.4 ±9.3 0.14±0.14 0.14±0.14 1.4 ±0.4 24.6 ±5.5 0.9 ±0.3 4.9 ±2.0
Severe degree of thrombocytopenia 18 68.0 ±4.4 6.4 ±2.3 17.4 ±5.1 66.9 ±33.1 49.8 ±5.8 37.4 ±6.0 0.11 ±0.06 0.06 ±0.06 0.4 ±0.1 8.4 ±2.5 0.4 ±0.1 2.9 ±0.4
Student t-test 25 2.56; p < 0.05 1.41 0.14 1.83 0.27 2.00 0.20 0.53 2.36; p < 0.05 2.70; p < 0.05 1.35 1.04
Table 2. - Indicators of the endothelium and hemostasis in children with ALL depending on the degree of hemorrhagic syndrome and thrombocytopenia
Groups n Indicators of the coagulation system Indicators of the fibrinolytic blood system Physiological anticoagulants Level of D-dimers
APTT (sec) PTT (%) TT (sec) Fibrinogen (g/D HF-DF (min) SFMC (mkg/ml) Protein C AT III (%)
depending on the degree of hemorrhagic syndrome
1st group. 0 and I grade of HS 17 33.9 ±5.24 78.8 ±5.03 12.20 ±0.74 4.3 ±0.56 12.06 ±1.27 6.1 ±0.50 1.2 ± 0.18 81.5 ±7.72 87.5% — negative 12.5% — positive
2nd group. II and III grade of HS 8 29.6 ±2.11 76.7 ±5.83 11.28 ±1.26 4.5 ±0.79 10.14±2.52 6.8± 1.12 1.7 ±0.20 84.7 ±8.96 100% — negative
Student t-test 24 0.76 0.27 0.63 0.21 0.68 0.62 1.92 0.27
depending on the degree of thrombocytopenia
Mild and moderate degree of thrombocytopenia 7 41.14±9.82 85.28 ±5.47 11.53 ±0.67 2.67 ±0.56 10.94 ±1.22 5.33 ±0.84 1.10±0.28 77.0 ±4.84 100% — negative
Severe degree of thrombocytopenia 18 29.50 ±1.23 74.55 ±4.40 12.50± 1.61 5.04 ±0.52 10.29 ±2.52 6.63 ±0.58 1.42 ±0.13 86.18 ±8.32 94% — negative 6% — positive
Student t-test 25 1.18 1.53 0.56 3.12; p<0.05 0.23 1.27 1.03 0.95
Prevention of intestinal failure syndrome in patients with acute intestinal obstruction
References:
1. Vladimirova S. G., Tarasova L. N., Skolskaya O. U. The indicators of hemostasis in patients with acute myeloid leukemia during manifestation of the disease//Hematology. - 2012. - № 2. - P. 36 -41.
2. Dolgov V. V., Svirin P. V. Laboratory diagnosis ofhemostatic disorders. - M.-Tver: LLC "Triad" Publisher, 2005. - P. 227.
3. Kaznacheev К. S., Burshtein E. S., Zlobina V. D., etc. Outcomes of treatment of acute lymphoblastic leukemia in children of Novosibirsk Region//Vestnik NGU. Series: Biology, clinical medicine. -2008. - T. 6, Vol. 2. - P. 141-144.
4. Mayakova S. А., Nemirovchenko V. S., Popa А. V. Clinical guidelines for the diagnosis and treatment of children with acute leukemia. -Moscow, 2014. - P. 9.
5. Roschik A. S., Kolesnikova O., Fedorov A. V. Hemorrhagic syndrome and hemostasis in acute lymphoblastic leukemia in children//Ba-sic Research. -2009. - № 4. - P. 75 -79.
6. Roschik А. S., Kolesnikova О. I., Fedorov А. V., Voloskova N. I. Correction of hemostasis in children with acute lymphoblastic leuke-mia//Hematology. - 2010. - № 2. - P. 36 -39.
7. Rumyancev U. V., Karachunsky A. I. Optimizing the treatment of acute lymphoblastic leukemia in children in Russia and Belarus: strategy Moscow - Berlin//Questions of Hematology/Oncology and immunopathology in pediatrics. - 2007. - T. 6, № 4. - P. 13.
8. Fischbach F. T., Dunning M. B. A Manual of Laboratory and Diagnostic Tests, 8th ed. Lippincott Williams & Wilkins, 2008. -1344 p.
9. Hagag A. A., Abdel-LateefA. E., Aly R. Prognostic value of plasma levels of thrombomodulin and von Willebrand factor in Egyptian children with acute lymphoblastic leukemia//J Oncol Pharm Pract. - 2014, Oct. - 20(5). - Р. 356 -361.
10. Pui C. H., Campana D., Pei D., et al. Treating childhood acute lymphoblastic leukemia without cranial irradiation//N Engl J Med.-2009, Jun 25. - 360 (26). - P. 2730-2741. - doi: 10.1056/NEJMoa0900386.
Karimov Shavkat Ibragimovich, PhD, MD, Professor of department of faculty and hospital surgery of Tashkent medical academy, Uzbekistan
Baymakov Sayfiddin Risbaevich, PhD, docent of department of faculty and hospital surgery E-mail: [email protected],
Asrarov Askarkhon Asrarovich, PhD, MD, professor of department of faculty and hospital surgery
E-mail: [email protected]
Prevention of intestinal failure syndrome in patients with acute intestinal obstruction
Abstract: There were analyzed the results of investigation and treatment of119 patients with acute intestinal obstruction. Timely and adequate enteral treatment measures were an important stage of complex treatment of patients with intestinal obstruction (especially complicated with peritonitis) and, preventing the development of functional intestinal insufficiency, favored treatment outcomes. The studies allowed the rate of postoperative complications to be reduced from 33.9 % to 12.7 %, lethal outcome from 7.1 % to 3.2 %.
Keywords: acute intestinal obstruction, intestinal insufficiency syndrome, enteral measures, enterosorption, multiple organ failure.
The initial symptoms of intestinal failure syndrome (IFS) in acute intestinal obstruction (AIO), especially mechanical etiology, reflecting primarily pronounced inhibition of motor activity of the intestine may be the result of a reflex earlier-onset disease process. Surgical intervention against this background that becomes another factor contributing to the inhibition of intestinal motility.
Simultaneous local action and reflex factors leads to acute intestinal function failure [7; 9; 11]. Stretching increases the secretion of intestinal loops and extravasation liquid in the lumen of the gut, that the disorder causes a suction further hyperextension of the loop and a reflex inhibition of motility. These changes lead to an increase in intra-abdominal pressure, reduction of the diaphragm excursion and result in respiratory failure, causing a buildup of tissue hypoxia and weighing condition of patients [12; 13].
Consequently, the initial intestinal dysmotility contribute to the development of the IFS, which is the initial link ofsevere pathological
processes causing growing dramatically with the development of metabolic changes in this background of multiple organ failure (MOF) and leading to the death of the patient [12; 16]. Therefore, after the elimination of the causes ofAIO, especially when complication peritonitis, the complex treatment should include prevention of IFS and endogenous intoxication syndrome (EIS), starting with a powerful detoxification therapy, drainage of the abdominal cavity, intubation bowel nasointestinal probes and ending intra-abdominal (lavage or dialysis), and also performing in the early postoperative enteral treatment measures: bowel decompression (BD), intestinal lavage (IL), enterosorption, etc. [2; 3; 6; 15; 16]. Different using methods are often not effective without the implementation of the stimulation of the intestine [5; 8].
In this context, the aim of this study was to improve the results of treatment ofpatients with AIO by developing and improving enteral treatment measures: BD, IL and enterosorption.
