FEATURES OF LABORATORY DIAGNOSTICS OF CRITICAL STATES IN PATIENTS WITH POLYTRAUMA Ustyantseva I.M., Khokhlova O.I.
Laboratory diagnostics in polytrauma is primarily oriented to evaluation of state of a patient, the compensatory abilities of his or her body, prediction of posttraumatic period course, development of complications and outcomes, as well as to evaluation of efficiency of treatment. One of the necessary conditions is fast quick acquisition of results of studies. For this purpose a clinician should have either bedside techniques of analysis (point of care tests, POCT), or the laboratory has to be in territorial proximity to intensive care units and operating rooms, with tuned inverse relation between laboratory specialists and clinicians.
In evaluation of patient’s state the great importance is related to the choice of optimal range of examinations with maximal information capacity for definite period of a disease. At that, it is necessary to use the principles of evidentiary medicine presented in the clinical guidelines (recommendations) of the international medical associations [5]. So, the practical recommendations of the American National Academy of Clinical Biochemistry (NACB) present the evidentiary information about intensive medicine administration of blood arterial gases, co-oxycometry (hemoglobin and its derivates), glucose, lactate, magnesium, natrium, potassium, chloride, ionized calcium, and in assessment of blood clotting ability - prothrombin time, activated partial thromboplastin time, activated clotting time. For assessment of degree of blood loss and shock in patients with polytrauma one can use the European recommendations for management of patients with posttraumatic bleeding which contain hematocrit and lactate as sufficiently proved tests (with IB level of evidence) [42].
Given the fact that polytrauma rarely proceeds without complications, and their presence is the rule rather than the exception [1-3], the important significance for examination of patients with polytrauma is related to timely diagnostics of disorders in functions of different organs and systems, as well as prediction of possible complications.
The algorithm of laboratory investigation for individual patient is determined by his or her state severity, localization and degree of injuries. The main minimal sufficient list of examinations in dependence on their emergency is presented in the table.
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Table | |
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The approximate chart of laboratory examination of patients with polytrauma from a perspective of evidence-based medicine | |
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Indicators |
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Urgent examinations | |
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Degree of blood loss and shock |
Hematocrit, lactate |
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Degree of anemia |
Hemoglobin |
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Blood oxygen status |
Lactate, sO2, pO2, hemoglobin and its derivates, p50 |
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Acid-base balance |
ðÍ, ðÑÎ2, ÍÑÎ3-, BB, BE |
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Examinations which can be temporarily delayed | |
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Water-electrolytic balance |
Kalium, natrium, chloride, calcium, plasma and urine osmolality |
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Hemostasis |
Hypocoagulation – PTT, APTT, thrombocytes, fibrinogen, Antithrombin III |
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Clot formation – D-dimer, SFC | |
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Additional examinations | |
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Functional state of kydneys |
Creatinine, urine, glomerular filtration rate |
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State of liver |
Hepatocyte cytolysis – AAT, GPT, LDH |
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Synthetic ability – total protein, albumin | |
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Detoxication ability – urea, bilirubin | |
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Acute inflammatory response |
Leukocytes, leukogram |
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Course of acute posthemorrhagic anemia |
red blood cells, hemoglobin, reticulocytes, iron, ferritin |
During prescription of laboratory examination one should consider that its quality is negatively influenced by diagnostic and medical procedures, disorders in rules of preparation of patient for examination, rules of taking, marking, primary preparation, storing conditions and transportation of examples of biomaterials from patients to laboratory. Because patients with polytrauma need infusion, hemotransfusion and nutritive support it is necessary to consider the influence of different drugs on test results which able to interact with reagents, to corrupt the reaction path and to result in overvaluation or undervaluation of true outcome. For example, dextran underrates prothrombin time and urea concentration, protects protein level, results in pseudoagglutination in isoserologic test versions [19]. Citrate (in hemotransfusion) decreases blood pH and distorts coagulation tests. That’s why it is not advisable to take blood for laboratory investigation during infusion therapy. For example, the minimal time after introduction of electrolytes, alkaline solutions, amino acids and hydrolized proteins is 1 hour, for fat emulsions – 8 hours [19].
Evaluation of degree of blood loss, anemia and shock
As a rule, polytrauma is accompanied by great blood loss, which can result in hypovolemic shock and development of the so called death triad – coagulopathy, hypothermia and acidosis [11, 14]. Therefore, the laboratory tests come to the fore which can assess blood loss degree and timely to identify its consequences which are dangerous for patient’s life. However, the laboratory values are not informative in the first 2-3 hours. Blood loss degree is evaluated according to clinical data exclusively (hemodynamic parameters – heart rate, arterial pressure, urine output, level of consciousness of patient, as well as localization of injuries) that is difficult in presence of traumatic shock in patient.
According to the European recommendations of management of patients with posttraumatic bleeding, ideally, the blood tests (hematocrit, blood gases and lactate) are to be accessible in addition to primary clinical assessment [42]. At that it is indicated that the single definition of hematocrit at admission has no diagnostic value [51]. However, during series measurement the decrease in hematocrit by 10 % or more can testify ongoing bleeding in injured patients. In massive bleeding series measuring of hematocrit has low diagnostic sensitivity.
During estimation of series measurement of hematocrit one should consider physiologic variations: decrease in the time period between 17.00 and 7.00, after food intake (approximately by 10 %) and in blood sampling in supine position (up to 6 %) [6]. Long-lasting venous stasis in vein puncture can lead to false overestimated result.
The main indicator for orientation of clinician during evaluation of degree of anemia and decision about question of hemotransfusion is the level of hemoglobin. The value of 7-8 g/dL (70-80 g/L) is threshold for decision about packed red cell transfusion for critically ill patients without additional factors of risk of tissue hypoxia [33]. However, tolerance of patient to anemia depends on the range of physiologic factors including increase in cardiac output as main one [20]. As the reserve mechanisms decrease with aging, decrease in blood hemoglobin, which is quite easy tolerable by young people, can be harmful late in life. Therefore, the cutoff value for older people and individuals with risk of myocardial infarction is 100 g/L [20].
During control of acute posthemorrhagic anemia it is desirable not to be limited to assessment of hematocrit and hemoglobin, but to assess the compensatory abilities of the body (reticulocytes, iron exchange values). So, reticulocytes serve as criteria of erythropoiesis activity, and their number can increase from 3d day after blood loss, achieving the maximum at 4-7 days. If the number of erythrocytes does not decrease in beginning of the second week, it may testify to ongoing bleeding. Hematogenesis activation is accompanied by reserved iron consumption. In great blood loss the sideropenia and the asiderotic anemia develop. However, in massive hemotransfusion the iron overload and development of hemosiderosis of parenchymal organs with their functional disorders are possible. Therefore, after several days after hemotransfusion it is necessary to examine serum iron and ferritin for choice of correct management of a patient.
Assessment of oxygen status of blood
Lactate can be used as one of the most proved parameters for evaluation and monitoring of blood loss and shock degrees [4]. It is shown that lactate level is an indirect measure of oxygen debt, tissue hypoperfusion and severity of hemorrhagic shock [8, 21, 30, 46, 49]. This is the most rapidly changeable laboratory value of hypoxia: in most cases its content increases before appearance of other signs of insufficient oxygen (pH decrease, changes in AP and HR, electrolytic deviances). The clinical significant lactate concentration, defined as moderately increased, is 2.5-4.0 mmol/L, the significant increased one is > 4 mmol/L.
The dynamic examination of lactate levels allows to assess adequacy of drug therapy and can be used as predictive criteria for treatment outcomes. It was proved for patients with hemorrhagic shock [49]. If lactate concentration does not decrease lower than 5 mmol/L, despite of intensive care, the possibility of survival significantly decreases [4].
In venous blood of healthy individuals the lactate level is within 0.9-1.7 mmol/L, and < 1.3 mmol/L in arterial blood. The increase in lactate level can be associated with situations which are not related to hypoxia: aspirin intoxication, adrenalin, ethanol, methanol, glucose, isoniaside, metformin, prednisolone, nalidicsic acid, sodium bicarbonate and hyperventilation. Physical load, tourniquet, fist clenching during blood sampling and food intake are also associated with increase in the concentration of this metabolite (by 20- 50 %) [6]. Morphine has the opposite effect. Therefore, these factors are considered during estimation of results.
In case of impossibility of lactate estimation the index of residual anions (R) or anion interval (AI) can be used with the following formula:
AI = (Na+ + K) – (HCO3- + Cl-) (standard – 10 – 20 mmol/L), or AI = Na+ - (HCO3- + Cl-) (standard – 7-16 mmol/L). However, contents of serum albumin influences on study results [50]. Therefore, in hypoalbuminemia the following formula is recommended:
Corrected AI = observed AI + 2.5 × [normal albumin – measured albumin (g/dL)].
This value correlates with lactate in conditions of oxygen deficit in patients without frank renal insufficiency and without diabetes mellitus [4, 12].
In critically ill patients simultaneously with lactate it is desirable to evaluate blood glucose, which increases almost proportional to lactate increase in conditions of hypoxia that complicates glucose delivery to the cells. Correction of non-diabetic increase of glucose is possible only with improvement of oxygen balance.
Blood gases
The main parameters used in evaluation of oxygenation of arterial blood are pO2, P50, sO2.
Oxygen partial pressure (pO2) of arterial blood in healthy individuals varies within the limits of 83-108 mm Hg. These numbers decrease with aging: pO2 = (- 0.27 × age) + 104 [6]. The level of pO2 < 40 mm Hg gives evidence of hypoxemia; the value < 20 mm Hg often results in death. Increase in pO2 is observed in air breathing enriched with oxygen. In treatment with pure oxygen the arterial blood pO2 can increase up to 640 mm Hg. pO2 values obtained in 37° C are corrected in concordance with body temperature. In case of artificial lung ventilation pO2 is interpreted with consideration of FiO2.
Oxygen partial pressure in half oxygen saturation P50 or pO2 (0.5) is a measure of hemoglobin affinity to oxygen, which defines transition of oxygen to tissues. This value is defined as oxygen partial pressure (with 37° C and pH = 7.40), when hemoglobin is saturated with oxygen by 50 %. The reference in adults is 25-29 mm Hg. Decrease in Hb affinity to oxygen (shift in curve rightwards) is characterized with increase in P50 that possible in hyperthermia, acidosis, hypercapnia, increase of 2,3- diphosphoglyceric acid in blood and appearance of anomal Hb types. And, conversely, increase in Hb affinity to oxygen (shift in curve leftwards) is characterized with decrease in P50 (in hypothermia, acute alcalosis, hypocapnia, decrease of 2,3- diphosphoglyceric acid in blood and presence of several Hb types).
Oxygen saturation (sO2) is calculated as:
sÎ2 = Î2Íb / (Î2Íb + HHb) × 100 %.
Normal arterial blood sÎ2 – 94-98 %, in venous blood – 70-80 %.
Pulseoxymetry gives incorrect results in severe anemia, hypovolemia, hypotonia and arrhythmia, as well as in presence of carboxy-, met- and fetal hemoglobin and angiographic contrasts. For example, in patient with polytrauma as result of methane explosion in an underground mine it is necessary to suppose poisoning with carbon monoxide, which characterized with increased affinity to hemoglobin that is accompanied by formation of carboxyhaemoglobin (HbCO) and decrease in oxygen delivery to tissues. Increased level of HbCO results in decrease in oxygen capacity; dissociation curve shifts to the left that results in errors in calculations of oxygen saturation. Values which are obtained during measurement of arterial blood oxygenation using pulseoxymeter will not reflect the real situation.
Small volumes of HbCO are constant in blood as byproduct of metabolism. The level of HbCO in non-smoking people is within the limits of 0.5-1.5 %, in smokers – up to 8-9 %. The toxic effect of CO appears Hb saturation > 20 %. However, the concentration of HbCO < 10 % can amplify hypoxia manifestations in critically ill patients or in patients with cardiovascular diseases.
Different methemoglobin formers (benzol derivates, aniline dyes, benzocaine, chlorates, isoniaside, lidocaine, metoclopramide, nitrates, nitrites, phenacetin, sulfasalazine, sulfonamides, trimethoprim, smoking etc.) have similar action. In MetHb the haem iron is oxidizes to the form of ferric iron, and it’s not able to combine with oxygen and transfer it. Therefore, it is necessary to assess hemoglobin derivates with gas analyzers equipped with built co-oxymeters, which define oxygen saturation as amount of hemoglobin-bound oxygen compared to amount of oxygen which is possible for transport by hemoglobin (oxygen capacity):
sÎ2 = (% HbO2 / 100 – (% HbÑÎ + % MetHb)) × 100.
Therefore, the general accepted criteria for concordance between oxygen consumption in tissues and their oxygen requirement are oxygen saturation (sO2) and partial pressure (ðÎ2) of arterial and mixed venous blood. The decrease in the above-mentioned parameters indicates the oxygen deficit. However, at the background of intensive care in critically ill patients even the high values do not warrant adequate oxygen balance in the body owing to circulation centralization and presence of toxins complicating oxygen delivery to peripheric tissues. For estimation of the oxygen balance the dynamic examination of lactate concentration is needed, as well as consideration of blood contents of different hemoglobin fractions that is possible with the modern gas and acid-base balance analyzers with built co-oxymeters.
Acid-base balance (ABB) of blood
One of the necessary conditions of the body activity is the constancy of the internal environment reactions which is defined with relation between acids and bases during the metabolism process. It is characterized with so called hydrogen index (pH) and the indicators of buffer systems, particularly hydrocarbonate one as the most labile (the time of the reaction is 30 seconds). The standard arterial blood pH in children aged of more than one day and in adults is within the range of 7.35-7.45, for venous blood – 7.32-7.43. The limits of pH variance compatible with the life are 6.8-7.8. The normal arterial venous difference of pH values is 0.01-0.03; it’s higher in congestive heart failure and shock state. The pH values decrease with temperature increase and conversely. Therefore, the appropriate correction is needed.
Bicarbonate (ÍÑÎ3-) – the greatest fraction in the composition of general dioxide carbon. The standard in adults is 22-26 mmol/L, in children at the age before 2 – 16-24 mmol/L. It increases in compensated respiratory acidosis, metabolic alcalosis and in administration of morphine, barbiturates, corticosteroids, diuretics and in cathartic abuse. It decreases in metabolic acidosis, compensated respiratory alcalosis, methanol and salycylate poisoning (late stage of intoxication).
Standard bicarbonate (SB) – the equilibrium concentration of bicarbonate in whole blood at 38° C, pCO2 = 40 mm Hg and full blood oxygenation, i.e it is defined with concentration of ÍÑÎ3- ions in the blood balanced with the standard gas mixture. The normal values of the arterial blood are 20-27 mmol/L, the venous blood – 22-29 mmol/L.
Buffer bases (BB) – the capacity of buffer systems, i.e. the sum of ions of bicarbonate and anions of proteins in the whole blood. The standard is 40-60 mmol/L.
Alcaline deviation or base deficit (BD) – the difference between the amount of buffer bases and normal buffer bases (the sum of all base components of the buffer systems of the blood taken from patient, but with artificial reduction to the standard conditions: temperature of 38° C, pH = 7.38, pCO2 = 40 mm Hg). The modern analyzers calculate BD. The normal BD in adults is within the range from -2 to +3 mmol/L, in children older 1 year – from -4 to +2, in children younger 1 year – from -7 to -1, in neonates – from -10 to -2.
The European recommendations offer to use BD as another sensitive test for assessment and monitoring of blood loss and shock (the level of evidence 1C) [42]. It is shown that arterial blood BD provides the indirect estimate of tissue acidosis conditioned by disorders in perfusion [49]. However, compared to lactate, the use of this value in patients with polytrauma is limited by absence of large-scale prospective studies.
Partial pressure of CO2 (pCO2).The standard value (arterial blood) in children is 27-41 mm Hg, in women – 32-45, in men – 35-48 mm Hg. Venous blood (in adults) – 46-58 mm Hg. It increases in respiratory acidosis (hypercapnia), metabolic alkalosis (with compensatory hypoventilation). pCO2 decreases in respiratory alcalosis (with compensatory hypoventilation). pCO2 decreases in respiratory alcalosis: increase in alveolar ventilation conditioned by artificial lung ventilation and stimulation of respiratory center as result of impact of one or several factors: hypoxia, salycylates, agitation, hyperthermia, head injury with respiratory center agitation.
For adequate clinical decision it is important to correctly interpret data of ABB examination. At that, the basic parameters are ðÍ, ðÑÎ2 and ÍÑÎ3- [41]. If pH and pCO2 change in one direction, then the main problem is metabolism (metabolic disorders). If pH and pCO2 move in different directions and pCO2 is normal, then the main problem is respiratory disorders. It means that respiratory states influence primarily on pCO2, whereas metabolic disorders originally influence on ÍÑÎ3- ion. If ÍÑÎ3- and pCO2 change in opposite direction, then they are mixed disorders.
In polytrauma, as a rule, the excess of acid products of metabolism is noted. As the response, the level of bicarbonate decreases, and pH stays constant. The shift in the buffer systems is aligned by the means of increased CO2 discharge by the lungs, i.e metabolic acidosis is compensated by respiratory alcalosis. In further accumulation of H+ ions the compensating abilities of the buffer systems run low, pH decreases sharply, and the decompensated metabolic acidosis develops. The laboratory parameters change in one direction during compensation and decompensation. The main difference is pH value: in compensated forms pH remains within the physiologic variations (7.4-7.35), in subcompensated form – 7.34-7.25, in decompensated one – 7.24 and lower. In the case of injuries to the internal organs, which participate in ABB regulation, along with development of complications, the other forms of disorders can be observed.
Oxygen deficit and acidosis conditioned by blood loss are accompanied by shifts in water-electrolytic balance that significantly complicates clinical state of patients, and causes aggravation of degree of disorder of acid base balance. The kidneys play the important role in compensation of these disorders. In case of polytrauma, besides the immediate renal injury, many conditions for their function disorder appear. Any surgical procedure and narcosis increase possibility of development of renal insufficiency [45]. Acute renal injury can appear as result of hypovolemia, rhabdomyolysis, hemolysis, action of nephrotoxic drugs and toxins in combination with different risk factors [9, 10, 18, 29]. That’s’ why renal function examinations (creatinine and blood urea with assessment of glomerular filtration) are very important in patients with polytrauma, as well as values of electrolyte exchange in patients with polytrauma. It is desirable to perform such studies immediately on admission and over time. However, these examinations are not emergent [23].
Accuracy of study of results of ABB and blood gas composition, and their interpretation depend mostly on adherence to the guidelines of blood sampling and storage. The common mistakes are presence of air bubbles in a sample, insufficient or excessive level of anticoagulant, storage of uncooled sample, inadequate mixing [41].
Blood sampling for ABB and gases assessment is preferable to perform with special syringes, with indication of contents of dry electrolyte-balanced heparin and a mark of needed blood volume. Non-compliance of blood/heparin ratio results in mutilation of results of the analysis by means of either clot formation, or sample redilution. Excessive heparin strongly influences on results of pCO2 and electrolytes study. Furthermore, heparin binds to the positive ions (Na+, K+, Ca2+) that results in impossibility of their measurement with ion-selective electrodes [44].
The blood sample analysis is performed during 30 minutes. For samples with high pO2, with increased level of leukocytes or thrombocytes the analysis should be performed during 5 minutes. If longer delay for blood sampling is required it is recommendable to use the syringes preventing air access, with following immediate cooling (placement of a syringe with blood into ice bath). But also the storage of a blood sample at 2-4° C for an hour increases pCO2 by 5 mm Hg.
There is a significant difference between figures received in examination of arterial and peripheric venous blood which depends on skin temperature, duration of blood stasis and muscle load. Therefore, the arterial blood is preferable to use. At the same time, results of study of ABB of arterial blood not always reflect the real situation in peripheric tissues, especially in patients with unstable hemodynamics [50]. There are the data which shows that the arterial blood has normal pH during cardiopulmonary resuscitation, while the venous blood is characterized with expressed acidosis [48].
Assessment of hemocoagulation potential
Life threatening coagulopathy is one of the most serious complications in patients with hypovolemic shock as result of massive bleeding. As a rule, it is predictable at the early stage. Decreased clotting ability of blood or accelerated fibrinolysis, or both are verified in seriously ill victims [24, 27]. It is shown that increase need for transfusion can predict following organ dysfunctions [34, 35, 37], and that coagulopathy is the independent predictive factor of 30-day mortality on admission to ICU [25]. Therefore, it is very important to assess patient’s coagulation status to start appropriate treatment [40].
However, hemostasiology is one of the most problem sections of the laboratory diagnostics in our country. Wide use of old inexact tests with extremely low standardization exists. Capillary blood clotting time assessment with different techniques, venous clotting time according to Lee-White, duration of bleeding and some other methods (for example, fibrinogen concentration assessment with the gravity method according to R.A. Rutberg) are non-informative and can result in incorrect conclusion [7]. The separate issue of provision of quality of hemostasis studies is associated with the problem of the nonstandardized reactives and control materials. Use of automatic coagulometers and commercial assay kits significantly increase reproducibility and reliability of the coagulation tests.
The basic “global” tests with ability of identification of hypocoagulation shifts and tendency to angiostaxis are prothrombin time (PTT), international normalised ratio (INR), activated partial thromboplastin time (APTT), level of fibrinogen, level of thrombocytes. It is shown that significantly prolonged PTT and APTT are associated with the increased risk of lethality from injuries [32]. However, the information exists that these tests present non-full pattern of hemostasis in vivo [16, 28], that they have insufficient predictive ability in relation to clinical bleedings [39], and do not provide sufficient base for rational special hemostatic measures [13, 22, 43]. Furthermore, in absence of active clinical bleeding the attempts of normalization of laboratory indicators have potential danger for development of posttransfusion complications [40].
In recent years thromboelastography and thromboelastometry are considered as the possible point of care tests for assessment of coagulation in massive blood loss. The new generation of devices, such as TEG® (Haemonetics Corp., Niles, IL, USA) and ROTEM® (Tem Innovations GmbH, Munich, Germany), presents information about formation of a clot and its stability after 10 minutes after blood sampling that is important for management of patients with bleeding [17]. It is shown that these viscoelastic technologies are able to identify clinical significant hemostasis disorders in patients with massive bleeding and coagulopathy [13, 26, 36] and can be used for monitoring of treatment of coagulopathy [38]. Nevertheless, one should note that all above mentioned tests are performed, as a rule, during heating of blood samples up to 37° C, and they do not show real state of hemostasis in hypothermia in vivo [31]. Hypothermia leads in changes in functions of thrombocytes, disorders of the coagulation factors (decrease in temperature by 1° C is accompanied by decrease in activity by 10 %), inhibition of fibrinolysis enzymes [15, 47]. The increased body temperature has reverse action on hemostasis. Therefore, during interpretation of results of hemostasis studies it is necessary to consider temperature of patient’s body and clinical picture.
In postagressive period in most patients with polytrauma the disorders of coagulation potential are characterized with hypercoagulation which, on the one hand, is the adaptive reaction of the body oriented to limitation of blood losses and salvation of circulation in the vital organs. But, on other hand, in long-term expression it creates conditions for creation of clot formation and development of complications in view of disseminated intravascular coagulation (DIC) and thromboembolism. Therefore, timely diagnostics of clot formation is important with emphasis not on identification of hyper- and hypocoagulation shift and hypofibrinogenemia, but on identification of high level of thrombinemia markers (D-dimer and fibrin-monomer – SFC). In assessment of DVC syndrome and efficiency of performed therapy the great significance is given to thrombocytopenia and consumption of physiologic anticoagulants (antithrombin III and C protein) [7].
The laboratory examination of hemostatic disorders is sensitive to adherence to the well-known rules of sampling, storage and preparation of blood for a study. Incorrect blood/anticoagulant ratio, insufficient mixing, long time interval from vein puncture to blood study and some other reasons inevitably result in “intra-test tube” clotting and false hypocoagulation in case of anticoagulant overdosage. The standardization of the blood sampling process is provided with using corresponding vacutainers. But, their usage is not always acceptable in significant variations in hematocrit, for example, in anemia in patients with polytrauma, because the plasma/anticoagulant ratio violates, and blood clotting is possible (inversely, false hypocoagulation is observed in high hematocrit). Besides, one should consider the influence of the following factors on the results of examinations: heparinemia (in case of analysis of the blood received with catheter or in heparin therapy), hemodilution, hypercitratemia (observed in hemotransfusion) and a number of plasma substitutes, especially rheopolyglukin [7, 19].
Therefore, the characteristics of the laboratory diagnostics of critical states in polytrauma consist in necessity of understanding of the basic pathologic processes and the principles of evidence-based medicine for choice of optimal range and method of investigation, and interpretation of results. The life of the patient depends on that. The acquisition of reliable results is possible only with adherence to the conditions of standardization of preanalytic and analytic stages. Only collaborative work of laboratory staff and clinical departments may solve problems in examination of patients with polytrauma.