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Shapkin Yu.G., Seliverstov P.A.
Saratov State Medical University named after V.I. Razumovskiy, Saratov, Russia
RISK FACTORS AND PROPHYLAXIS OF VENOUS THROMBOEMBOLICCOMPLICATIONS IN POLYTRAUMA WITH SKELETAL INJURIES
Currently, the mortality after polytrauma is still high – 15-24 % even
in the advanced clinics [1, 29]. The improvement in organizational and
anti-shock procedures leads to decreasing mortality in the early phase of
polytrauma, but the relative amount of deaths from late complications [1, 40]. In
10-53 % of patients with polytrauma, despite of timely prevention, venous
thromboembolic complications (VTEC) appear, including deep venous thrombosis
(DVT) and pulmonary embolism (PE) [11, 22, 27, 34, 43, 46]. Skeletal
injuries in polytrauma appear in 70-93 % [4, 40]. Fractures of the lower
extremities and the pelvis prevail in their incidence (60-78 %), significantly
influencing on development of VTEC [4, 27]. The rate of DVT in polytrauma with
fractures of the above-mentioned bones achieves 46-60 % [6, 34, 37]. Venous
thrombosis in polytrauma increases the period of hospital stay and costs for
treatment [17, 44], with increasing incidence of multiple organ dysfunction and
mortality [13, 20, 24]. About 45 % of fatal outcomes of PE are associated with multiple
injuries [48].
Insufficient exploration of multiple risk factors and of features of
VTEC pathophysiology in associated injury hinders the development of prevention
standards and improvement in polytrauma management.
RISK FACTORS OF VTEC IN POLYTRAUMA
Venous thrombosis develops in combination of three factors (Virchow's
triad): bradyhemarrhea, endothelial vascular wall injury and disorders in
hemostasis system (hypercoagulation and fibrinolysis depression).
Bradyhemarrhea in polytrauma is associated with local systemic
hemodynamic disorders which are caused by hypodynamia, traumatic shock and
acute massive blood loss. Systolic arterial pressure below 90 mm Hg [16, 38]
and duration of immobilization and bed rest are the independent risk factors of
VTEC in polytrauma [25, 42, 48].
The high energy mechanism of polytrauma determines the significant
injury to the venous vascular wall. About 70-90 % of patients receive
polytrauma in road traffic accidents or after falling from height [4, 11, 27].
As result, complex fragmented fractures of types B and C (AO/ASIF classification) are identified
in 42-75 % of polytrauma with skeletal injuries, i.e. 2-3 times higher than in
single injuries. 20-27 % of patients demonstrate opened fractures with
extensive soft tissue injuries [4, 40].
Vascular endothelial injuries appear in polytrauma and are mediated by
systemic pathological processes. A systemic inflammatory response appears after
multiple tissue injuries, shock and acute blood loss. Tissue lesions and
release of mitochondrial damage-associated molecular patterns (mtDAMPs) from
injured cells cause the activation of neutrophil leukocytes, which produce
proinflammatory cytokines and strong oxidants. Oxidative stress, tissue
hypoperfusion and hypoxia cause death of endotheliocytes and exposure of the subendothelial
layer, resulting in thrombosis [29]. Systemic disorders of cellular immunity,
leukocytosis and lymphopenia with activation of B- and T-lymphocytes promote
endothelial dysfunction and weakening of clot fixation to the vascular wall.
Floating clots in polytrauma with fractures of the lower extremities and the
pelvis are identified in 25-68 % of patients with DVT, resulting in possible
fatal PE [6, 22, 37].
Shock and massive blood loss in polytrauma cause the significant
disorders in blood-dotting sequence. Posttraumatic coagulopathy has a complex
and non-investigated mechanism of development. The experimental studies with
polytrauma model including the femoral bone fracture showed a relationship
between coagulopathy values and systemic inflammatory response, and regularity
in changes in phases of hyper- and hypocoagulation that are confirmed by
results of clinical studies [10]. The signs of hypercoagulation (according to thromboelastography)
are observed within a week after polytrauma [44]. The hypercoagulation phase is
much more intense in polytrauma with severe skeletal injuries than in single
skeletal injury [47].
Coagulopathy with INR > 1.5 is associated with increasing rate of
VTEC and higher mortality after trauma [26]. The prediction criteria of VTEC in
patients with polytrauma are lymphocytic adhesion, IL-2, D-dimer, activated
partial thromboplastin time, IL10-1082G>A and IL2-303Т>G
gene polymorphism regulating the influence of IL-2 and IL-10 on clot formation
[11, 49]. According to some studies, the thromboelastographic signs of
hypercoagulation are not associated with incidence of VTEC in polytrauma [44].
Another study showed two-fold increase in incidence of DVT in the lower
extremities in patients with hypercoagulation values in thromboelastography
[5].
Metabolic acidosis (pH < 7.2) and hypothermia (< 35 °C) induce and
intensify coagulopathy, consisting “the death triad”. Hyperlactataemia and hyperglycemia
reflect the severe disorders of tissue metabolism and are determined by the
risk factors of VTEC in polytrauma [37, 38]. Massive hemotransfusion in
polytrauma favors the disorders in blood-dotting sequence. Transfusion of four
and more dosages of erythrocytic media in the first day after injury is the
predictor of VTEC [21].
Polytrauma causes the phenomenon of mutual burdening of injuries. This
phenomenon causes progressive increase in the incidence of complications and
lethal outcomes. The mechanisms of increasing rate of VTEC in presence of this
phenomenon cause cumulative increase in shock potential of trauma, development
of more intense systemic inflammatory response and coagulopathy [36, 40].
The phenomenon of mutual burdening of injuries explains the increasing
rate of VTEC with higher ISS [20, 49] and TMPM (Trauma
Mortality Prediction Model) [25]. It testifies that combinations of the most severe injuries exert the
dominating influence on formation of VTEC. In patients with two or more leading
injuries, VTEC develop with higher frequency and are identified in uncommonly
early periods – 7-10 days after polytrauma [40].
Fractures of long bones, of pelvic
bones and of the spine with spinal cord injury [30], traumatic brain injury
(TBI) [16, 49], abdominal and thoracic injuries with AIS (Abbreviated Injury
Scale) > 2 have the highest significance for formation of phenomenon of
mutual burdening of injuries and present the independent predictors of VTEC
[17, 23, 38].
Pelvic, femoral, spinal and leg
fractures significantly increase the incidence of VTEC in polytrauma by means
of high increase in blood loss and shock potential of an injury, with limited
mobility of the patient [16, 21, 37, 49]. The risk of VTEC is highest for
multiple fractures of the pelvis of the lower extremities [6, 14, 42]. Multiple
pelvic injuries with AIS ≥ 3 present the independent risk factor of DVT in
polytrauma [7, 20, 24].
Complex high energy fractures of the
long bones with massive soft tissue injuries after polytrauma are accompanied
by release of high amount of inflammatory mediators and tissue factor which
initiate the processes of blood clotting. The experimental studies show that
systemic inflammatory response is much more intense in combination of a fracture
with extensive soft tissue injury in comparison with single injuries [28].
Severe soft tissue injury in the lower extremities is the independent
predictors of VTEC [25, 38].
TBI severity correlates with
incidence of VTEC. So, GCS (Glasgow Coma Scale) < 8 during 4 hours is the
independent predictor of VTEC [21]. The increasing risk of VTEC in TBI is
explained by disorder of the hematoencephalic barrier and by delivery of tissue
factor, which participates in thrombin formation, into systemic blood flow from
cerebral injury foci [19]. However E.J. Vale et al. (2014) showed that
traumatic brain injury did not increase the incidence of VTEC in polytrauma,
despite presence of more intense signs of hypercoagulation in
thromboelastography [43].
The spinal cord injury significantly
increases the risk of DVT by means of immobility of the patient, disordered
innervation of blood vessels and slow venous flow. The incidence of DVT in
polytrauma with the spinal cord injury show the highest values (about 75 %) [34].
There are some attempts to identify
and to combine the main factors of VTEC risk in polytrauma into the integral
values and the prediction scores [21, 27, 46]. The identification includes the
risk factors of VTEC, like in Military Field Surgery-Injury scale, which
changes during treatment (severity of injuries, age, concurrent diseases) and
the factors relating to condition severity, which changes during treatment
[27]. It allows timely correcting the prevention of VTEC and estimating its
efficiency.
PREVENTION OF VTEC IN POLYTRAUMA
For prevention of VTEC in
polytrauma, first of all, it is necessary to remove the influence of the
factors promoting phlebothrombosis: recovery of circulating blood volume,
hemodynamics normalization, creation of conditions for fast activation of the
patient.
Early (within two days) stable and
functional osteosynthesis of the long bones, the pelvis and the spine with
adherence to Early Total Care (ETC) prevents the progression of local and
systemic responses, allows fast activation of patients and decrease the risk of
VTEC in polytrauma [6, 12, 39].
However traumatic and long-lasting
final internal osteosynthesis, which presents the surgical injury, can cause
the second hit and increase the risk of systemic and thromboembolic complications,
neutralizing the positive moments of early fixation. The duration of surgery
more than two hours is the independent risk factor of VTEC in severe injury
[21].
The second hit phenomenon in
polytrauma develops as result of postsurgical worsening systemic inflammatory
response, hypercoagulation, vascular endothelial damages and disordered venous
flow in narcosis with myorelaxants. The most unfavorable time intervals for
osteosynthesis are the days 3-5, when the intensity of systemic inflammatory response
and hypercoagulation are maximal [39].
The staged surgical management for
long bones and pelvic fractures (Damage Control Orthopedics – DCO) and for thoracic and lumbar
vertebrae (Spine Damage Control – SDC) decreases the risk of the
second hit, incidence of postsurgical complications and mortality in polytrauma
[27, 29, 39, 40, 41, 50].
Other
authors compared the mortality and the incidence of VTEC and did not find any
advantages of temporary external fixation in concordance with DCO before early primary
intramedullary fixation [31] or before skeletal traction during preparation for
final fixation [35]. Moreover, recurrent osteosynthesis in staged treatment
become the risk factors of VTEC [8, 20, 44].
According
to ultrasonography data, the forced attitude of the lower extremity in skeletal
traction caused the deformation of the femoral vein and development of “splint
phlebothrombosis” in 46 % of patients with polytrauma [6].
Closed
locking intramedullary osteosynthesis of the long bones is characterized by low
traumatic potential of the intervention, low intrasurgical blood loss and
appropriate fixation of fragments, resulting in early activation of the
patient. However in case of polytrauma, early intramedullary fixation can
initiate the progression of inflammatory responses and coagulation disorders.
The experimental and clinical studies showed that intramedullary fixation of
femoral and tibial bones, especially with the intramedullary canal drilling,
cause the additional significant increase in IL-6 in the blood and increasing
hypercoagulation within 10 days after surgery [3, 47]. The risk of VTEC and
lethal outcome increases in single-stage intramedullary fixation, particularly
in combination with the chest injury [18].
Objective
estimation of the patient’s condition severity and choice of optimal time of
surgical intervention for polytrauma give the maximal advantages of DCO and ETC
and prevent the second hit phenomenon.
R. Pfeifer и H.C. Pape (2016) developed the
concept of safe definitive surgery for polytrauma on the basis of graduation of
severity of patients’ condition with consideration of acidosis, coagulopathy,
hypothermia, shock and severity of injuries. ETC is allowed for stable
condition of the patient. For borderline or unstable condition, it is
recommended to adhere to DCO staged management [29].
B.R.
Childs et al. (2016) showed the lactate level < 4 mmol/l, pH ≥ 7.25
or base excess ≥ -5.5 mmol/l. VTEC and mortality showed the lowest values in
patients who were operated in presence of the above-mentioned indices within 36
hours after polytrauma [8].
The
Russian clinical recommendations [33], the manual from Eastern Association for the
Surgery of Trauma (EAST) [32] and the guidelines from American
College of Chest Physicians (ACCP) [15] are
considered as the main guidelines for pharmacological, mechanic and surgical
prevention of VTEC after trauma. According to these guidelines, it is optimally
to use preventive doses of low weight molecular heparins, preferably with
intermittent pneumatic compression. Oral anticoagulants can be used in the postsurgical period.
However the mechanical methods of venous thrombosis
prevention are sometimes impossible to use for patients with polytrauma, owing
to frequent damages of the lower extremities. The time intervals for initiation
of anticoagulation pharmacological therapy in TBI with intracranial hemorrhage
and in spinal cord and parenchymal organ injuries are not clear and can be
delayed for 24-72 hours after trauma, to the moment of hemostatis achievement
[32, 33, 45]. Traumatic brain injury without intracranial bleeding, damage of
parenchymal organs and retroperitoneal hematoma in pelvic fractures or full
spinal cord injury without ongoing bleeding are not considered as
contraindications for anticoagulants [33]. For ongoing bleeding it is offered
to use only non-pharmacological preventive measures, with addition of
anticoagulants after disappearance of possibility of bleeding. VTEC prevention
is not recommended to delay or stop because of planned surgical interventions
[15, 33].
The indications for implantation of temporary or
constant cava-filters for prevention of fatal PE in polytrauma are not
standardized, and they vary significantly. Each method is offered to use in
patients with DVT in presence of contraindications to anticoagulant therapy
because of high risk of bleedings or in extensive floating thrombosis of
femoral or iliac veins and in recurrent PE [15, 32, 33]. EAST guidelines extend
the indications for placement of cava-filters for patients without DVT who
cannot receive the anticoagulants because of risk of bleeding or in presence of
one of the following injuries: severe TBI with GCS < 8, partial spinal cord
injury with para- or tetraplegia, a complex fracture of the pelvic bones in
combination with a long bone fracture, multiple fractures of the long bones
[32]. The adherence to EAST would result in implantation of the cava-filter in
25 % of polytrauma cases, but it is really installed not more than in 4 % of
such patients, and without significant increase in incidence of PE [2, 9]. The
prevention technique of PE with implantation of cava-filters is not without
serious complications and to be used in substantiated indications.
The high incidence of symptomless DVT in polytrauma
with skeletal injuries and formation of embologenic floating clots require for
timely diagnosis for correction of management techniques. The gold standard of
diagnosis of DVT in the lower extremities is compression ultrasonography. The
time and periodicity of compression ultrasonography for polytrauma are
disputable and are not clearly determined in the guidelines. Ultrasonic
screening is the most essential for impossibility of anticoagulation therapy,
for presence of spinal cord injuries, fractures of the lower extremities and
the pelvis, and for severe TBI [15, 33]. Ultrasonography is recommended to
conduct at least one time per week, beginning from the days 3-5 from
polytrauma, the days 1-2 before surgery and 2-3 days after surgery [6, 22, 39].
The study is reasonably to repeat before recurrent surgical intervention and
before increase in movement activity [27].
Prevention of VTEC in polytrauma with skeletal
injuries is optimally to continue at least to the moment of restoration of
movement activity – from 4 weeks to 3 months after trauma or surgery [6, 13,
33]. Some studies showed that 50-62 % of all cases of VTC and 54-96 % of deaths
from PE were registered after hospital discharge [4, 25, 48]. It determines the
need for development of clear recommendations for prevention of VTEC in the
period of hospital treatment and in the outpatient phase of rehabilitation.
CONCLUSION
The patients with polytrauma are related to the group
of high risk of VTEC. The factors, which increase the risk of VTEC in
polytrauma, are traumatic shock and acute massive blood loss, multiple
high-energy fractures of bones with extensive soft tissue injuries, systemic
inflammatory response and coagulopathy, the phenomenon of mutual burdening of
complications. The severity and multiplicity of injuries correlate with
intensity of systemic inflammation, hypercoagulation and incidence of VTEC.
Complex pelvic, femoral, leg and spinal fractures, TBI and spinal cord injuries
significantly increase the risk of VTEC.
Polytrauma requires for complex prevention of VTEC.
The important components are anti-shock procedures, maximally early stable
functional osteosynthesis of the long bones, the pelvis and the spine with low
traumatic techniques. Damage Control Orthopedics allows minimizing the risk of
the second hit phenomenon in borderline or unstable patients. Low molecular
weight heparins make the basis of pharmacological prevention, which should be
initiated before hemostasis achievement. Implantation of cava-filters is
indicated for DVT with high risk of fatal PE. The need for implantation of
cava-filters in patients without DVT has the low degree of evidences.
Currently, the clear recommendations for prevention of VTEC in
polytrauma have not been developed and standardized. It is mainly associated
with absence of sufficient evidences, multiple variants of combinations of
injuries and difficulties of pathophysiology of mutual interaction.
Information on financing and conflict of interests
The study was
conducted without sponsorship.
The authors
declare the absence of clear or potential conflicts of interests relating to
publishing this article.
REFERENCES:
1. Agadzhanyan
VV, Kravtsov SA, Shatalin AV, Levchenko TV. Hospital mortality in polytrauma and main directions
for its decrease. Polytrauma. 2015; (1): 6-15. Russian (Агаджанян В.В.,
Кравцов С.А., Шаталин А.В., Левченко Т.В. Госпитальная летальность при
политравме и основные направления ее снижения //Политравма. 2015. № 1. С. 6-15)
2. Berber O, Vasireddy A, Nzeako O, Tavakkolizadeh A. The high-risk polytrauma patient and inferior vena cava filter use. Injury. 2017; 48(7):
1400-1404
3. Blankstein M, Byrick RJ, Nakane M, Bang AK, Freedman J, Garvey MB et al. A
preliminary study of platelet activation after embolization of marrow contents.
J OrthopTrauma. 2012; 26(11): e214-220
4. Bondarenko AV, Gerasimova
OA, Lukyanov VV, Timofeev VV, Kruglykhin IV. Composition, structure of
injuries, mortality and features of rendering assistance for patients during
treatment of polytrauma. Polytrauma. 2014; (1):
15-28. Russian (Бондаренко А.В., Герасимова О.А., Лукьянов В.В., Тимофеев В.В., Круглыхин
И.В. Состав, структура повреждений, летальность и особенности оказания
помощи у пострадавших на этапах лечения политравмы //Политравма. 2014. № 1. С. 15-28)
5. Brill JB, Badiee J, Zander AL, Wallace JD, Lewis PR, Sise MJ et al. The rate of deep vein
thrombosis doubles in trauma patients with hypercoagulablethromboelastography. J Trauma Acute Care Surg. 2017; 83(3): 413-419
6. Byalik
EI, Mezhebitskaya LO, Trofimova EYu, Semenova MN. Algorithm of ultrasound
examination of lower limb veins in patients with fractures of pelvis and lower
extremities in polytrauma. Polytrauma. 2012; (4):
46-51. Russian (Бялик Е.И., Межебицкая Л.О., Трофимова Е.Ю.,
Семёнова М.Н. Алгоритм ультразвукового исследования вен ног у пострадавших с
переломами костей таза и нижних конечностей при политравме //Политравма. 2012. № 4. С. 46-51)
7. Chaari A, Ghadhoune H, Chakroune O, Abid H, Turki O, Bahloul M et al. The use of a low
dose hydrocortisone to prevent pulmonary embolism in patients with multiple trauma. Int J Clin Pharm. 2013; 35(4): 593-599
8. Childs BR, Nahm NJ, Moore TA, Vallier HA. Multiple
procedures in the initial surgical setting: when do the benefits outweigh the
risks in patients with multiple system trauma? J OrthopTrauma. 2016; 30(8):
420-425
9. Cook AD, Gross BW, Osler TM, Rittenhouse KJ, Bradburn EH, Shackford SR et al. Vena cava filter use
in trauma and rates of pulmonary embolism, 2003-2015. JAMA Surg. 2017; 152(8):
724-732
10. Darlington DN, Gonzales MD, Craig T, Dubick MA, Cap AP, Schwacha MG. Trauma-induced
coagulopathy is associated with a complex inflammatory response in the rat. Shock. 2015; 44 Suppl 1:
129-137
11. Dorzheev VV, Miromanov AM, Davydov SO,
Miromanova NA, Vitkovsky YuA. The personalised aspects of development of venous
thromboembolic complications in polytrauma. Polytrauma.2016; (4): 31-39. Russian (Доржеев В.В., Мироманов А.М., Давыдов С.О.,
Мироманова Н.А., Витковский Ю.А. Персонализированные аспекты развития венозных
тромбоэмболических осложнений при политравме //Политравма. 2016. № 4. С. 31-39)
12. Gandhi RR, Overton TL, Haut ER, Lau B, Vallier HA, Rohs T
et al. Optimal
timing of femur fracture stabilization in polytrauma patients: a practice
management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2014; 77(5):
787-795
13. Godat LN, Kobayashi L, Chang DC, Coimbra R. Can we ever stop worrying about venous thromboembolism
after trauma? J Trauma Acute Care Surg. 2015; 78(3): 475-481
14. Godzik J, McAndrew CM, Morshed S, Kandemir U, Kelly MP. Multiple
lower-extremity and pelvic fractures increase pulmonary embolus risk. Orthopedics. 2014; 37(6):
e517-524
15. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ. American college of chest physicians
antithrombotic therapy and prevention of thrombosis panel. Executive summary: antithrombotictherapy and prevention
of thrombosis, 9thed:
Americancollege of chest
physicians evidence-based clinical practice guidelines. Chest. 2012; 141(2 Suppl): 7S-47S
16. Hamada SR, Espina C, Guedj T, Buaron R, Harrois A, Figueiredo S et al. High level of venous thromboembolism in critically
ill trauma patients despite early and well-driven thromboprophylaxis protocol. Ann Intensive Care. 2017; 7(1): 97
17. Kim DY, Kobayashi L, Barmparas G, Fortlage D, Curry T, Coimbra R. Venous
thromboembolism in the elderly: the result of comorbid conditions or a
consequence of injury? J Trauma
Acute Care Surg. 2012; 72(5):
1286-1291
18. Lane MK, Nahm NJ, Vallier HA. Morbidity and mortality of
bilateral femur fractures. Orthopedics. 2015; 38(7):
e588-592
19. Laroche M, Kutcher ME, Huang MC, Cohen MJ, Manley GT. Coagulopathy after traumatic
brain injury. Neurosurgery. 2012; 70(6):
1334-1345
20. Lichte P, Kobbe P, Almahmoud K, Pfeifer R, Andruszkow H, Hildebrand F, et al.
Post-traumatic thrombo-embolic complications in polytrauma
patients. IntOrthop. 2015; 39(5): 947-954
21. Meizoso JP, Karcutskie CA 4th, Ray JJ, Ruiz X, Ginzburg E, Namias N et al. A simplified
stratification system for venous thromboembolism
risk in severely injured trauma patients. J Surg Res. 2017; 207: 138-144
22. Mezhebitskaya
LO, Trofimova EY, Ivanov PA, Kungurtsev EV. Ultrasound diagnosis of venous
thrombosis in the course of prophylactic drug therapy in the acute phase of
trauma. Russian Sklifosovsky Journal «Emergency
Medical Care». 2015; (1): 38-43.
Russian (Межебицкая Л.О., Трофимова Е.Ю.,
Иванов П.А., Кунгурцев Е.В. Ультразвуковая диагностика венозных тромбозов на фоне
медикаментозной профилактики в остром периоде травмы //Журнал им. Н.В. Склифосовского «Неотложная медицинская помощь». 2015. № 1. С. 38-43)
23. Nahm NJ, Como JJ, Vallier HA. The impact of
major operative fractures in blunt abdominal injury. J Trauma Acute Care Surg. 2013; 74(5): 1307-1314
24. Paffrath T, Wafaisade A, Lefering R, Simanski C, Bouillon B, Spanholtz T et al. Venous thromboembolism after severe trauma:
incidence, risk factors and outcome. Injury. 2010; 41(1): 97-101
25. Park MS, Perkins SE, Spears GM, Ashrani AA, Leibson CL, Boos CM et al.Risk factors for venous thromboembolism after
acute trauma: A population-based case-cohort
study. Thromb Res. 2016; 144: 40-45
26. Peltan ID, Vande Vusse LK, Maier RV, Watkins TR. An international normalized
ratio-based definition of acute traumatic coagulopathy is associated with
mortality, venous thromboembolism, and multiple organ failure after. Injury Crit Care Med. 2015; 43(7): 1429-1438
27. Petrov AN, Borisov MB,
Denisenko VV, Ganin EV, Semenov EA, Koskin VS et al. Prevention of acute
thromboembolic events in patients with multistage surgical treatment was
combined skeletal trauma. Emergency
Medical Care. 2016; (2): 42-48. Russian (Петров А.Н., Борисов М.Б., Денисенко В.В., Ганин Е.В.,
Семенов Е.А., Коскин В.С. и др. Профилактика
острых тромбоэмболических осложнений у пострадавших с многоэтапным
хирургическим лечением сочетанной скелетной травмы //Скорая медицинская помощь. 2016. № 2. С. 42-48)
28. Pfeifer R, Darwiche S, Kohut L, Billiar TR, Pape HC. Cumulative effects of bone and soft tissue injury on systemic inflammation: a
pilot study. Clin Orthop Relat Res. 2013; 471(9): 2815-2821
29. Pfeifer R, Pape HC. Diagnostics and treatment
strategies for multiple trauma patients. Chirurg.
2016;
87(2): 165-175
30. Piran S, Schulman S. Incidence and risk factors
for venous thromboembolism in patients with acute
spinal cord injury: a retrospective study. Thromb Res. 2016; 147: 97-101
31. Rixen D, Steinhausen E, Sauerland S, Lefering R, Maegele MG, Bouillon B et al. Randomized, controlled, two-arm,
interventional, multicenter study on risk-adapted damage control orthopedic
surgery of femur shaft fractures in multiple-trauma patients. Trials. 2016; 17: 47
32. Rogers FB, Cipolle MD, Velmahos G, Rozycki G, Luchette FA. Practice management guidelines for the prevention of
venous thromboembolism in trauma patients: the EAST practice management
guidelines work group. J Trauma.
2002; 53(1): 142-164
33. Russian clinical
guidelines for the diagnosis, treatment and prevention of venous thromboembolic
complications (VTEC). Phlebology. 2015; 9(4-2): 2-52. Russian (Российские клинические рекомендации по диагностике,
лечению и профилактике венозных тромбоэмболических осложнений (ВТЭО) //Флебология. 2015.
Т. 9, № 4, выпуск 2. С.
2-52)
34. Samokhvalov IM, Nemchenko NS, Petrov AN, Denisov AV, Golovko KP, Zhirnova NA et al. Pathogenesis and
early diagnosis of deep vein thrombosis in case of polytrauma.
Military
Medical Journal. 2013; 334(8): 25-35. Russian (Самохвалов И.М., Немченко Н.С., Петров А.Н., Денисов
А.В., Головко К.П., Жирнова Н.А. и др. Особенности патогенеза и ранней
диагностики острого тромбоза глубоких вен при политравме //Военно-медицинский
журнал. 2013.
Т. 334, № 8. С. 25-30)
35. Scannell BP, Waldrop NE, Sasser HC, Sing RF, Bosse MJ. Skeletal
traction versus external fixation in the initial
temporization of femoral shaft fractures in
severely injured patients. J Trauma. 2010; 68(3): 633-640
36. Shapkin YuG, Seliverstov PA. Phenomenon of mutual
aggravation of injuries in polytrauma. Perm Medical Journal. 2016; 33(5): 82-94. Russian (Шапкин Ю.Г., Селиверстов П.А. Феномен взаимного отягощения повреждений при
политравме //Пермский медицинский журнал.
2016. Т.
33, № 5. С. 82-94)
37. Shestova
ES, Vlasov SV, Vlasova IV, Ustyantseva IM, Khokhlova OI. Status of patients
with high risk of embolic complications in polytrauma. Polytrauma. 2017; (4): 23-30. Russian (Шестова
Е.С., Власов С.В., Власова И.В, Устьянцева И.М., Хохлова О.И. Статус пациентов
с высоким риском эмболических осложнений при политравме //Политравма. 2017. № 4. С. 23-30)
38. Shuster R, Mathew J, Olaussen A, Gantner D, Varma D, Koukounaras J et al. Variables associated with
pulmonary thromboembolism in injured patients: a
systematic review. Injury. 2018; 49(1): 1-7
39. Sirazitdinov
SD, Pankov IO, Safarov RR. Improving the prognosis and prevention of
thromboembolic complications in emergency and emergency care for victims with
multiple fractures of limb bones. Modern
Problems of Science and Education. 2016; (3). Available
at: http://science-education.ru/ru/article/view?id=24676 (accessed 25.04.2018).
Russian (Сиразитдинов С.Д., Панков И.О., Сафаров Р.Р. Совершенствование
прогнозирования и профилактики тромбоэмболических осложнений при оказании
экстренной и неотложной помощи пострадавшим с множественными переломами костей
конечностей //Современные проблемы науки и образования. 2016. № 3). Режим
доступа: http://science-education.ru/ru/article/view?id=24676 (дата обращения:
25.04.2018)
40. Sokolov
VA, Byalik EI, Shchetkin VA, Sharipov IA, Klopov LG. The organizational and
work experience of the department of concomitant injury. Polytrauma. 2006; (3): 9-14. Russian (Соколов
В.А., Бялик Е.И., Щеткин В.А., Шарипов И.А., Клопов Л.Г. Опыт организации и
работы отделения сочетанной травмы //Политравма. 2006. № 3.С. 9-14)
41. Stahel PF, VanderHeiden T, Flierl MA, Matava B, Gerhardt D, Bolles G et al. The impact of a standardized «spine
damage-control» protocol for unstable thoracic and lumbar spine fractures in
severely injured patients: a prospective cohort study. J Trauma Acute Care Surg. 2013; 74(2): 590-596
42. Tan L, Qi B, Yu T, Wang C. Incidence and risk factors for venous
thromboembolism following surgical treatment of fractures below the hip:
a meta-analysis. Int Wound J. 2016; 13(6): 1359-1371
43. Valle EJ, Van Haren RM, Allen CJ, Jouria JM, Bullock MR, Schulman CI et al. Does traumatic brain
injury increase the risk for venous thromboembolism in polytrauma patients? J Trauma Acute Care Surg. 2014; 77(2): 243-250
44. Van Haren RM, Valle EJ, Thorson CM, Jouria JM, Busko AM, Guarch GA et al. Hypercoagulability and
other risk factors in trauma intensive care unit
patients with venous thromboembolism. J Trauma Acute Care
Surg. 2014; 76(2): 443-449
45. Van PY, Schreiber MA. Contemporary
thromboprophylaxis of trauma patients. Curr Opin Crit Care. 2016; 22(6): 607-612
46. Vlasov SV, Vlasova IV. Prediction of
thromboembolic complications in patients with polytrauma. Polytrauma. 2013; (2): 42-47. Russian (Власов С.В., Власова И.В. Прогнозирование
тромботических осложнений у пациентов с политравмой //Политравма.
2013. №
2. С. 42-47)
47. White AE, Edelman JJ, Lott N, Bannon PG, McElduff P, Curnow JL et al. Characterization
of the hypercoagulable state following severe orthopedic trauma.
J Trauma
Acute Care Surg. 2014; 77(2): 231-237
48. Yakar A, Yakar F, Ziyade N, Yıldız M, Üzün I. Fatal pulmonary thromboembolism. Eur Rev Med
Pharmacol Sci. 2016; 20(7):
1323-1326
49. Yumoto T, Naito H, Yamakawa Y, Iida A, Tsukahara K, Nakao A. Venous
thromboembolism in major trauma patients: a
single-center retrospective cohort study of the epidemiology and utility of
D-dimer for screening. Acute Med Surg. 2017; 4(4): 394-400
50. Zhu TF, Zhao WG, Zheng HL, WuJ X. Application of damage control orthopedics for the treatment of severe
multiple fractures. Zhongguo Gu Shang. 2018; 31(2): 145-149
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