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Year 2017 Vol. 25 No 6

EXPERIMENTAL SURGERY

O.V. FALKO, N.A. SHEVCHENKO, V.Y. PROKOPYUK, A.A. ROENKO, O.S. PROKOPYUK

COMPARATIVE ANALYSIS OF LIMBS’ TROPHIC ULCERS MODELING METHODS IN MICE

Institute for Problems of Cryobiology and Cryomedicine of NAS of Ukraine, Kharkov, Ukraine

Objective. To compare the existing methods of modeling an ulcerative defect as well as hemodynamics and innervation disorders, and then to develop the model of the lower limbs trophic ulcer in mice.
Methods. Trophic ulcers were simulated in male Balb/Ñ mice. Vascular insufficiency was formed by either ligation (group 1) or electrocoagulation (group 2) of the neurovascular bundle at the site of bifurcation of the common iliac and femoral arteries and veins. The ulcerative defect was formed by intradermal injection of 0.1 ml 10% calcium chloride (groups 3, 5 and 7) and 9% acetic acid (groups 4, 6 and 8). The animals of the groups 5 and 6 were electrocoagulated prior to administration of chemical agents and the animals of the groups 7 and 8 after it. The term of ulceration, ulcer area, period of complete healing and functional status of the limb were determined.
Results. Ligation (group 1) resulted in a mummification of limb tissues and electrocoagulation (group 2) led to a temporary disruption of function without forming ulcerous surface. Dry ulcer had been revealed in the animals of the groups 3 and 5 by the 10th day; the ulcer had been completely healed by the 20th day and the 30th day, respectively. A weeping ulcer was revealed in mice of the groups 4 and 8 to day 3; its healing had been observed by the 15th and the 35th, respectively. No ulcerative defects were observed in the animals of the groups 6 and 7, there was observed necrotic injury of skin and under laying structures. Impaired functional activity of the injured limb was found in all experimental groups. In the animals of the 1st and 7th groups the limb function did not recover up to the end of the experiment.
Conclusions. Intradermal administration of acetic acid and subsequent electrocoagulation of neurovascular bundle allow forming a long-lasting non-healing weeping ulcer and limb dysfunction, which were typical for trophic ulcers. Other studied techniques can be applied when simulating various diseases, related to vascular, nervous and skin damages.

Keywords: trophic ulcer, modeling, mice, electrocoagulation, ligation, acetic acid, calcium chloride
p. 561-566 of the original issue
References
  1. Shval’b PG, Griaznov SV. Miniinvazivnyi metod korrektsii klapannoi nedostatochnosti bedrennoi veny pri razlichnykh prichinakh ee proiskhozhdeniia [Minimally invasive method of correction of valvular insufficiency of the femoral vein for various reasons of its origin]. Angiologiia i Sosud Khirurgiia. 2015;2 (2):84-87.
  2. Kroege K, Storck M, Kujath P, Rabe E, Dissemond J. Prophylaxis of recurrent venous leg ulcer. Zentralbl Chir. 2016;(141):1-5. doi: 10.1055/s-0042-109977.
  3. Stefanov OV, red. Dokl³n³chn³ dosl³dzhennia l³kars’kikh zasob³v: metodichn³ rekomendats³¿ [Preclinical research of medicinal products: methodical recommendations]. Ki¿v, Ukraina: Av³tsena; 2001. 528 p.
  4. Obolenskii VN. Khronicheskaia rana: obzor sovremennykh metodov lecheniia [Chronic wound: an overview of modern methods of treatment]. RMZh. 2013;21(5):282-89.
  5. Diao Y, Lian L, Guo L, Chen H, Chen Y, Song X, et al. A vascular endothelial growth factor activating transcription factor increases the endothelial progenitor cells population and induces therapeutic angiogenesis in a type 1 diabetic mouse with hindlimb ischemia. Chin Med J (Engl). 2014;127(20):3623-29.
  6. Hellingman AA, Bastiaansen AJ, de Vries MR, Seghers L, Lijkwan MA, Löwik CW, et al. Variations in surgical procedures for hind limb ischaemia mouse models result in differences in collateral formation. Eur J Vasc Endovasc Surg. 2010 Dec;40(6):796-803. doi: 10.1016/j.ejvs.2010.07.009.
  7. Semenov DV. Vpliv maz³ z ol³ºiu aron³¿ chornopl³dno¿ na patogenez ranovogo protsesu [Influence of the ointment with aronia oil on the pathogenicity of the wound process]. Kl³n³chna Farmats³ia. 2009; (3): 35-38.
  8. Frolova NI, Mel’nikova TI, Buriakina AV, Vishnevskaia EK, Avenirova EL, Sivak KV i dr. Metodicheskie podkhody k eksperimental’nomu izucheniiu dermatotropnykh sredstv [Methodical approaches to the experimental study of dermatotropic agents]. Eksperim i Klin Farmakologiia. 2009;72(5):56-60.
  9. Plotnikov MB, Ivanov IS, Sidekhmenova AV, Aliev OI, Fomina TI, Ermolaeva LA. Modelirovanie khronicheskoi venoznoi nedostatochnosti nizhnikh konechnostei [Modeling of chronic venous insufficiency of lower extremities]. Biomeditsina. 2013;(1):55-66.
  10. Urakova NA, Urakov AL. Inektsionnaia bolezn’ kozhi [Injectable skin disease]. Sovrem Problemy Nauki i Obrazovaniia [Elektronnyi resurs]. 2013;(1). Rezhim dostupa: https://www.science-education.ru/ru/article/view?id=8171.
Address for correspondence:
61016, Ukraine,
Kharkov, Pereyaslavskaya str., 23,
Institute for Problems of Cryobiology
and Cryomedicine of NAS of Ukraine,
Department of Cryobiology
of the Reproduction Systems,
tel. office.: +38 057 373-59-53,
e-mail: o.v.falko@gmail.com,
Oksana V. Falko
Information about the authors:
Falko O.V., PhD, Researcher of the Department of Cryobiology of the Reproduction Systems for the Institute of Problems of Cryobiology and Cryomedicine of NAS of Ukraine.
Shevchenko N.A., PhD, Senior Researcher of the Department of Cryobiology of the Reproduction Systems of the Institute for Problems of Cryobiology and Cryomedicine of NAS of Ukraine.
Prokopyuk V.Y., PhD, Senior Researcher of the Department of Cryopathophysiology of the Institute for Problems of Cryobiology and Cryomedicine of NAS of Ukraine.
Roenko A.A., Post-Graduate Student of the Department of Cryobiology of the Reproduction Systems of the Institute for Problems of Cryobiology and Cryomedicine of NAS of Ukraine.
Prokopyuk O.S., MD, Professor, Head of the Department of Cryobiology of the Reproduction Systems of the Institute for Problems of Cryobiology and Cryomedicine of NAS of Ukraine.

GENERAL & SPECIAL SURGERY

A.T. SHCHASTNY

CHRONIC PANCREATITIS: CORRELATION BETWEEN PAIN SYNDROME INTENSITY AND PANCREAS NERVE TISSUE CHANGES

Vitebsk State Medical University, Vitebsk
The Republic of Belarus

Objective. To study interrelation between pain syndrome intensity and nerve tissue marker neurofilament (NF) expression in pancreas at chronic pancreatitis.
Methods. The research included 45 patients with chronic pancreatitis who needed surgical intervention because of abdominal pain that could not be stopped by medications. For assessment of a pain syndrome a visual analogue scale (VAS) was used. Involvement of nervous tissue was estimated by a NF expression in the serial histological sections of resected pancreas head stained with Anti-Neurofilament Monoclonal Antibody. Control group for morphological research included 7 pancreas head samples without any pancreas pathology from age comparable people died by accidents.
Results. In patients with chronic pancreatitis the pain syndrome intensity index, estimated by VAS, varied from 2 to 10 points. A «mild pain» (from 1 to 3 points) was noted by 4 (9%), «moderate pain» (4-6 points) – 17 (38%), «severe pain» (7-10 points) – 24 (53%) patients.
Statistical assessment of a pain syndrome intensity and NF expression showed a moderate linear relationship (r=0,3, p=0,04). The research of a pain syndrome intensity and positively NF-expressing nervous elements percent also showed a moderate correlation (r=0,33; p=0,03).
Conclusions. Chronic pancreatitis is associated with a different intensity pain syndrome (from 2 to 10 points). At the same time the intensity of the pain syndrome estimated by visual analogue scale (VAS) was associated with nervous tissue qualitative characteristics changes that was confirmed by high rates of NF expression and percent of NF- positively expressing nervous elements at the severe pain syndrome.

Keywords: chronic pancreatitis, immunohistochemistry, nerve tissue, neurofilament, abdominal pain, visual analog scale
p. 567-573 of the original issue
References
  1. Teo K, Johnson MH, Truter S, Pandanaboyana S, Windsor JA. Pain assessment in chronic pancreatitis: A comparative review of methods. Pancreatology. 2016 Nov-Dec;16(6):931-39. doi: 10.1016/j.pan.2016.09.006.
  2. Talukdar R, Reddy DN. Pain in chronic pancreatitis: managing beyond the pancreatic duct. World J Gastroenterol. 2013 Oct 14; 19(38): 6319-28.Published online 2013 Oct 14. doi: 10.3748/wjg.v19.i38.631.
  3. Toma H, Winston J, Micci MA, Shenoy M, Pasricha PJ. Nerve growth factor expression is up-regulated in the rat model of L-arginine-induced acute pancreatitis. Gastroenterology. 2000 Nov;119(5):1373-81. doi: 10.1053/gast.2000.19264.
  4. Friess H, Zhu ZW, di Mola FF, Kulli C, Graber HU, Andren-Sandberg A, Zimmermann A, Korc M, Reinshagen M, Büchler MW. Nerve growth factor and its high-affinity receptor in chronic pancreatitis. Ann Surg. 1999 Nov;230(5):615-24.
  5. Mascetta G, di Mola FF, Tavano F, Selvaggi F, Giese N, Bassi C, Büchler MW, Friess H, di Sebastiano P. Substance P and neprilysin in chronic pancreatitis. Eur Surg Res. 2012;48(3):131-38. doi: 10.1159/000337869.
  6. Zhu Y, Colak T, Shenoy M, Liu L, Pai R, Li C, Mehta K, Pasricha PJ. Nerve growth factor modulates TRPV1 expression and function and mediates pain in chronic pancreatitis. Gastroenterology. 2011 Jul;141(1):370-77. doi: 10.1053/j.gastro.2011.03.046.
  7. Liu L, Shenoy M, Pasricha PJ. Substance P and calcitonin gene related peptide mediate pain in chronic pancreatitis and their expression is driven by nerve growth factor. JOP. 2011 Jul 8;12(4):389-94. doi: 10.6092/1590-8577/3226.
  8. Michalski CW, Shi X, Reiser C, Fachinger P, Zimmermann A, Büchler MW, Di Sebastiano P, Friess H. Neurokinin-2 receptor levels correlate with intensity, frequency, and duration of pain in chronic pancreatitis. Ann Surg. 2007 Nov;246(5):786-93.
  9. Farkas G Jr, Hofner P, Balog A, Takács T, Szabolcs A, Farkas G, Mándi Y. Relevance of transforming growth factor-beta1, interleukin-8, and tumor necrosis factor-alpha polymorphisms in patients with chronic pancreatitis. Eur Cytokine Netw. 2007 Mar;18(1):31-37.
  10. Wick EC, Hoge SG, Grahn SW, Kim E, Divino LA, Grady EF, Bunnett NW, Kirkwood KS. Transient receptor potential vanilloid 1, calcitonin gene-related peptide, and substance P mediate nociception in acute pancreatitis. Am J Physiol Gastrointest Liver Physiol. 2006 May;290(5):G959-69.
  11. Hutter MM, Wick EC, Day AL, Maa J, Zerega EC, Richmond AC, Jordan TH, Grady EF, Mulvihill SJ, Bunnett NW, Kirkwood KS. Transient receptor potential vanilloid (TRPV-1) promotes neurogenic inflammation in the pancreas via activation of the neurokinin-1 receptor (NK-1R). Pancreas. 2005 Apr;30(3):260-65.
  12. Liddle RA. The role of Transient Receptor Potential Vanilloid 1 (TRPV1) channels in pancreatitis. Biochim Biophys Acta. 2007 Aug;1772(8):869-78.
  13. Breivik H, Borchgrevink PC, Allen SM, Rosseland LA, Romundstad L, Hals EK, Kvarstein G, Stubhaug A. Assessment of pain. Br J Anaesth. 2008 Jul;101(1):17-24. doi: 10.1093/bja/aen103.
  14. Yuan A, Rao MV, Sasaki T, Chen Y, Kumar A, Veeranna, Liem RKH, Eyer J, Peterson AC, Julien JP, Nixon RA. &alfa;-internexin is structurally and functionally associated with the neurofilament triplet proteins in the mature CNS. J Neurosci. 2006;26(39). doi: 10.1523/JNEUROSCI.2580-06.2006.
  15. Gnanapavan S, Grant D, Pryce G, Jackson S, Baker D, Giovannoni G. Neurofilament a biomarker of neurodegeneration in autoimmune encephalomyelitis. Autoimmunity. 2012 Jun;45(4):298-303. doi: 10.3109/08916934.2012.654865.
Address for correspondence:
210023, The Republic of Belarus,
Vitebsk, Frunze ave., 27,
EE “Vitebsk State Medical University”,
Department of Surgery
of the Faculty of Advanced Training and Retraining,
Tel.: +375 29 654-45-99,
E-mail: anatol1961@bk.ru,
Anatoliy T. Shchastny
Information about the authors:
Shchastny A.T., MD., Ass. Professor, Rector of Vitebsk State Medical University

V.N. NIKITIN 1.2, S.G. KLIPACH2

«DIFFICULT» STUMP IN COMPLICATED GIANT PENETRATING PYLORODUODENAL ULCERS

SBEE HPE “Omsk State Medical University” 1,
BME OR “City Emergency Clinical Hospital ¹2” 2, Omsk
The Russian Federation

Objective. To develop a method for treating «difficult» stump of the duodenum during surgery for a complicated giant penetrating pyloroduodenal ulcer.
Methods. The studied group consisted of 18 patients who underwent surgical treatment for the complicated pyloroduodenal giant ulcers. Ulcerations larger than 2.5 cm were referred to pyloroduodenal giant ulcers. One proposed the method of treating «difficult» duodenal stump, implying a longitudinal incision of the anterior wall of the duodenal bulb, affected by a circular ulcerative process. It allows determining the extent of ulcerative stenosis, making exterritorialy ulcer craters with the excision of the remnants of the duodenal bulb mucosa and using stenotically changed postbulbar part as a frame in the formation of the stump. Using a two-level continuous seam permits to evenly distribute the load across the seam and thus to increases the mechanical strength of the place of suturing.
Results. The average duration of the operation amounted to 136,6 minutes (95% CI:125,2; 152,0); duration of hospital treatment: from 7 to 26 days, with an average of 15.7 (95% CI:13,1; 18,2). The complications in the early postoperative period were: a wound infection – 2 (11,1%), pneumonia – 3 cases (16.7%), acute myocardial infarction – 1 (5.5 %), failure of the stump of duodenum in one case (5.5%). Postoperative mortality amounted to 16.7%: two patients – the cause was bilateral lower lobe necrotizing pneumonia (11.2%). The failure of the duodenal stump and abundant serous-fibrinous peritonitis, identified on the 6th day after the operation, occurred in one patient (5,5%). After 1 year 12 patients were examined: during endoscopy in one patient the ulcer of the posterior lip of the gastrojejunal anastomosis was revealed, superficial gastritis of the stump of the stomach was detected in 3 (25%), erosive gastritis of the stomach stump was identified in 1 (8.3%).
Conclusions. The conducted study has confirmed the efficacy of the proposed method of treating of the duodenum stump in therapy of patients with a complicated giant circular pyloroduodenal ulcer by minimizing the probability of the failure.

Keywords: pyloroduodenal ulcer, perforation, bleeding, penetration, stomach resection, the stump of the duodenum
p. 574-582 of the original issue
References
  1. Kubyshkin VA, Petrov DI, Smirnov AV. Metody endoskopicheskogo gemostaza v lechenii iazvennykh gastroduodenal’nykh krovotechenii [Methods of endoscopic hemostasis in the treatment of ulcerative gastroduodenal hemorrhages]. Khirurgiia Zhurn im NI Pirogova. 2013;(9):67-72.
  2. Barkun AN, Bardou M, Kuipers EJ, Sung J, Hunt RH, Martel M, et al. International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010;152(2):101-13. doi: 10.7326/0003-4819-152-2-201001190-00009.
  3. National Institute for Health and Clinical Excellence (NICE). Acute upper gastrointestinal bleeding: management. London, UK: National Institute for Health and Clinical Excellence (NICE); 2012 Jun. 23 p. (Clinical guideline; no. 141).
  4. Kim JJ, Sheibani S, Park S, Buxbaum J, Laine L. Causes of bleeding and outcomes in patients hospitalized with upper gastrointestinal bleeding. J Clin Gastroenterol. 2014 Feb;48(2):113-18. doi: 10.1097/MCG.0b013e318297fb40.
  5. Sazhin VP, Bronshtein PG, Zaitsev OV, Kondrus’ IV, Krivtsov GA, Lobankov VM, i dr. Natsional’nye klinicheskie rekomendatsii «Probodnaia iazva» [National Clinical Recommendations «Perforated Ulcer»] [Elektronnyi resurs]. 37 p. Rezhim dostupa: http://obshchestvo-khirurgov.rf/upload/perforated_ulcer.pdf.
  6. Søreide K, Thorsen K, Søreide JA. Strategies to improve the outcome of emergency surgery for perforated peptic ulcer. Br J Surg. 2014 Jan;101(1):e51-64. doi: 10.1002/bjs.9368.
  7. Cienfuegos JA, Rotellar F, Valentí V, Arredondo J, Baixauli J, Pedano N, et al. Giant duodenal ulcer perforation: a case of innovative repair with an antrum gastric patch. Rev Esp Enferm Dig. 2012 Aug;104(8):436-39. [Article in Spanish]
  8. Krylov NN, Mukhammed MKh. Sushchestvuet li optimal’nyi variant gastroenteroanastomoza posle distal’noi subtotal’noi rezektsii zheludka [Is there an optimal option for gastroenteroanastomosis after distal subtotal resection of the stomach?] Khirurgiia Zhurn im NI Pirogova. 2012;(8):83-86.
  9. Nikitin NA, Korshunova TP, Onuchin MA, Goloviznin AA. Khirurgicheskoe lechenie sochetannykh oslozhnenii iazvennoi bolezni pri piloroduodenal’noi lokalizatsii iazvy [Surgical treatment of combined complications of peptic ulcer with pyloroduodenal ulcer localization]. Med Al’m. 2010;(1):121-25.
  10. Nobori C, Kimura K, Ohira G, Amano R, Yamazoe S, Tanaka H, et al. Giant duodenal ulcers after neurosurgery for brainstem tumors that required reoperation for gastric disconnection: a report of two cases. BMC Surg. 2016 Nov 17;16(1):75.
  11. Buck DL, Vester-Andersen M, Moller MH. Prompt Surgery Is Critical for Survival in Patients With Perforated Peptic Ulcer. Br J Surg. 2013;100:1045-49.
  12. Mukhopadhyay M, Banerjee C, Sarkar S, Roy D, Rahman1 QM. Comparative study between omentopexy and omental plugging for giant duodenal ulcer perforation. Indian J Surg. 2011 Oct; 73(5): 341–45. doi: 10.1007/s12262-011-0320-8.
  13. Vavrinchuk SA, Kosenko PM, Chernyshov DS. Sovremennye aspekty khirurgicheskogo lecheniia perforativnoi iazvy dvenadtsatiperstnoi kishki: monogr [Modern aspects of surgical treatment of perforated duodenal ulcer]. Khabarovsk, RF: IPKSZ; 2013. 241 p.
  14. Tsukanov IT, Nikitin VN, Nikolaichuk AI. Sposob formirovaniia kul’ti dvenadtsatiperstnoi kishki pri gigantskoi tsirkuliarnoi oslozhnennoi iazve [The method of forming the stump of the duodenum with a giant circular complicated ulcer]. Patent RF¹ 2460474. 10.09.2012.
  15. Thorsen K, Søreide JA, Kvaløy JT, Glomsaker T, Søreide K. Epidemiology of perforated peptic ulcer: Age- and gender-adjusted analysis of incidence and mortality. World J Gastroenterol. 2013 Jan 21;19(3):347-54. doi: 10.3748/wjg.v19.i3.347.
  16. Møller MH, Engebjerg MC, Adamsen S, Bendix J, Thomsen RW. The Peptic Ulcer Perforation (PULP) score: a predictor of mortality following peptic ulcer perforation. A cohort study. Acta Anaesthesiol Scand. 2012 May;56(5):655-62. doi: 10.1111/j.1399-6576.2011.02609.x.
Address for correspondence:
644043, Russian Federation,
Omsk, Lenin str., 12,
SBEE HPE “Omsk State Medical University”,
Department of Faculty Surgery
with the Course of Urology,
Tel: +7 3812 35-91-30,
E-mail: nikitin-1966@inbox.ru,
Vyacheslav N. Nikitin
Information about the authors:
Nikitin V.N., PhD, Associate Professor of the Department of Faculty Surgery with the Course of Urology of SBEE HPE “Omsk State Medical University”.
Klipach S.G., Head of Surgery Unit of BME OR “City Emergency Clinical Hospital ¹2”.

V.A. YANUSHKO ², N.A. ROGOVOY ¹, D.V. TURLIUK ², I.P. KLIMCHUK ¹, S.S. KALININ ¹

ENDOVENOUS LASER ABLATION OF GIACOMINI VEIN IN SURGICAL TREATMENT OF VARICOSE VEINS OF LOWER EXTREMITIES

4th N.E. Savchenko City Clinical Hospital ¹,
Republican Scientific and Practical Centre «Cardiology» ², Minsk,
The Republic of Belarus

Objective. To assess the efficacy of endovenous laser ablation (EVLA) in the complex treatment of varicose veins with paradoxical reflux in Giacomini vein.
Methods. In 2014-2016 we have operated 25 patients with paradoxical reflux in Giacomini vein. All EVLA procedures were guided by ultrasound (US). The average energy delivered was 60±6,2 J/cm and power of 10 watts. Men were 8(32%), women – 17(68%).
Results. Evaluation of the treatment results was conducted based on clinical data and US control. Pain during surgical intervention and in the first 5 days after the operation was assessed by visual analogue score. The change in the quality of life was assessed using the CIVIQ-2 questionnaire. Improvement of the quality of life in the postoperative period by 7.0 points was noted. Also, a decrease in the severity of the disease assessed by the VCSS questionnaire was found to be 3 points. Occlusion of the ablated veins was confirmed during surgery and on the follow-up examination at 1, 7 day and 1, 3, 6, 12 months after EVLA.
Conclusions. Ultrasound (US) guided EVLA of Giacomini vein is an effective and safe method of treatment of incompetent Giacomini varicose veins which provides high clinical and cosmetic results. Proposed method enables to operate with Giacomini vein only preserving great and small saphenous veins, which can be used further as prosthesis in arterial bypass grafting.

Keywords: varicose veins, endovenous laser ablation, Giacomini vein, saphenous vein, questionnaires, quality of life
p. 583-588 of the original issue
References
  1. Kirienko AI, Stoiko YM, Bogachev VY. Rossiiskie klinicheskie rekomendatsii po diagnostike i lecheniiu khronicheskikh zabolevanii ven [Russian clinical guidelines for diagnosis and treatment of chronic venous diseases]. Flebologiia. 2013;7(2 vyp 2):6-47.
  2. Giacomini, C. Osservazioni anatomiche per servire allo studio della circolazione venosa delle estremita inferiori (Parte I: Delle vene superficiali dell’arto addominale e principalmente della saphena esterna). Giornale della Reale Accademia di Medicina di Torino. 1873;14:109-15.
  3. Delis KT, Knaggs AL, Khodabakhsh P. Prevalence, anatomic patterns, valvular competence, and clinical significance of the Giacomini vein. J Vasc Surg. 2004 Dec;40(6):1174-83. doi: 10.1016/j.jvs.2004.09.019.
  4. Kosinski C. Observations on the superficial venous system of the lower extremity. J Anat. 1926 Jan;60(Pt 2):131-42.
  5. Theivacumar NS, Dellagrammaticas D, Mavor AI, Gough MJ. Endovenous laser ablation (EVLA) of great saphenous vein to abolish “paradoxical reflux” in the Giacomini vein: a short report. Eur J Vasc Endovasc Surg. 2007 Aug;34(2):229-31.
  6. Oğuzkurt L. Ultrasonographic anatomy of the lower extremity superficial veins. Diagn Interv Radiol. 2012 Jul-Aug;18(4):423-30. doi: 10.4261/1305-3825.DIR.5321-11.1.
  7. Park SW, Lee SA, Hwang JJ, Yun IJ, Kim JS, Chang SH, Chee HK, Chang IS. Early results of endovenous ablation with a 980-nm diode laser for an incompetent vein of Giacomini. Korean J Radiol. 2011 Jul-Aug; 12(4):481-86. Published online 2011 Jul 22. doi: 10.3348/kjr.2011.12.4.481.
  8. Georgiev M, Myers KA, Belcaro G. The thigh extension of the lesser saphenous vein: from Giacomini’s observations to ultrasound scan imaging. J Vasc Surg. 2003 Mar;37(3):558-63. doi: 10.1067/mva.2003.77.
  9. Riabinskaia OS, Osmanov RR. Klassifikatsiia gemodinamicheskikh variantov varikoznoi bolezni maloi podkozhnoi veny (na osnovanii dupleksnykh kharakteristik) [Classification of hemodynamic variants of varicose veins of the small saphenous vein (based on duplex characteristics).] Promeneva D³iagnostika Promeneva Terap³ia. 2011;(3-4):39-42.
  10. Bush RG, Hammond K. Treatment of incompetent vein of Giacomini (thigh extension branch). Ann Vasc Surg. 2007 Mar;21(2):245-48.
  11. Kulikova AN, Gafurova DR. Evoliutsiia khirurgicheskikh i endovazal’nykh metodov korrektsii stvolovogo venoznogo refliuksa u bol’nykh s varikoznoi bolezn’iu nizhnikh konechnostei [Evolution of surgical and endovasal methods of correction of stem venous reflux in patients with varicose disease of lower extremities]. Klin Meditsina. 2013;(7):13-18.
  12. van den BOS RR, de Maeseneer MMG. Endovenousthermal ablation for varicose veins: strengths and weaknesses. Phlebolymphology. 2012;19(4):164-65.
  13. Escribano JM, Juan J, Bofill R, Rodríguez-Mori A, Maeso J, Fuentes JM, Matas M. Haemodynamic strategy for treatment of diastolic anterograde giacomini varicose veins. Eur J Vasc Endovasc Surg. 2005 Jul;30(1):96-101. doi: 10.1016/j.ejvs.2005.03.001.
  14. Atasoy MM, Gümüş B, Caymaz I, Oğuzkurt L. Targeted endovenous treatment of Giacomini vein insufficiency-associated varicose disease: considering the reflux patterns. Diagn Interv Radiol. 2014 Nov;20(6):481-6. doi: 10.5152/dir.2014.14148.
  15. Guzelmansur I, Oguzkurt L, Koca N, Andic C, Gedikoglu M, Ozkan U. Endovenous laser ablation and sclerotherapy for incompetent vein of Giacomini. Phlebology. 2014 Sep;29(8):511-16. doi: 10.1177/0268355513496552.
Address for correspondence:
220036, The Republic of Belarus,
Minsk, Rosa Luxemburg str., 110,
4th N.E. Savchenko City Clinical Hospital,
Department of Vascular Surgery,
Tel.: +375 (17) 286-19-52,
+375 (29) 3852753,
E-mail: kolia_med@mail.ru,
Nikolay A. Rogovoy
Information about the authors:
Yanushko V.A., MD, Professor, Head of the Laboratory of Vessels Surgery of the Republican Scientific and Practical Centre «Cardiology».
Rogovoy N.A., Vascular Surgeon of the Department of Vascular Surgery of the 4th N.E. Savchenko City Clinical Hospital.
Turliuk D.V., PhD, Associate Professor, Leading Researcher of the Laboratory of Vessels Surgery of the Republican Scientific and Practical Centre «Cardiology».
Klimchuk I.P., PhD., Headof the Department of Vascular Surgery of the 4th N.E. Savchenko City Clinical Hospital.
Kalinin S.S, Head of the Department of Vascular Surgery of the 4th N.E. Savchenko City Clinical Hospital.

A.M. KUPCHENKO, V.A. KOSINETS

ETIOLOGICAL STRUCTURE OF DIFFUSE PERITONITIS AT VARIOUS LEVELS OF THE GASTROINTESTINAL TRACT DAMAGE

ÅÅ “Vitebsk State Medical University”, Vitebsk
The Republic of Belarus

Objective. To determine the main causative agents of diffuse peritonitis at various levels of the gastrointestinal tract damage.
Methods. The aerobic and anaerobic microorganisms were identified in the peritoneal exudate of 144 patients with diffuse peritonitis using test systems «ENTER-ID» and «AN-ID»; their sensitivity to antibacterial drugs was determined with the test systems «AB-ENTER», «AB-GRAM(-)», «AB-PSEV», «AB-AN», designed in EE “Vitebsk State Medical University”. Depending on the level of the gastrointestinal tract damage, the following variants of the pathological process were identified: peritonitis as a complication of the stomach and duodenum diseases (1st level – 59 patients); as a complication of the small intestine diseases (2nd level – 23 patients); as a complication of the large intestine diseases (3rd level – 62 patients).
Results. In case of perforation localization on the 3rd level bacterial microflora was determined in all inoculations, on the 1st level the inoculations proved to be sterile in 27,1% of the cases, on the 2nd level – in 8,7%. On the 1st level E. ñoli (34,04%) and gram-positive aerobic microflora were identified in the peritoneal exudate, B. fragilis – only in 20,3%. On the 2nd level in the inoculations gram-negative aerobic microflora prevailed, mainly represented by E.ñoli (65,21%), anaerobic microflora reached 69,6%. In the inoculations on the 3rd level gram-negative aerobic microflora was more often determined: E.ñoli (55,36%) and Klebsiella spp. (16,07%), with the dominance of anaerobic component which reached 88,7%. Imipenem (91,3% sensitive microorganisms), amikacin (88,1%), ciprofloxacin (88,1%), meropenem (84,2%) had maximum antibacterial effect on aerobic component. Anaerobic non-clostridial microflora of the peritoneal exudate was most sensitive to meropenem (98,1%), imipenem (96,1%) and metronidazole (91,3%).
Conclusions. Administration of antimicrobial therapy in the treatment of patients with diffuse peritonitis should be carried out taking into account the level of the gastrointestinal tract damage. The obtained data will contribute to the creation of the modern efficient schemes of empiric antimicrobial therapy in the treatment of this disease.

Keywords: diffuse peritonitis, identification of microorganisms, test systems, gastrointestinal microbiome, sensitivity determination, anti-bacterial agents
p. 589-599 of the original issue
References
  1. Savel’ev VS, Gel’fand BR, red. Abdominal’naia khirurgicheskaia infektsiia: klinika, diagnostika, antimikrobnaia terapiia [Abdominal surgical infection: clinic, diagnosis, antimicrobial therapy: A practical guide]: prakt. rukov. Moscow, RF: Literra; 2006. 168 p.
  2. Chow AW, Evans GA, Nathens AB, Ball CG, Hansen G, Harding G, et al. Canadian practice guidelines for surgical intra-abdominal infections. Can J Infect Dis Med Microbiol. 2010 Spring; 21(1):11-37.
  3. Lopez N, Kobayashi L, Coimbra R. A Comprehensive review of abdominal infections. World J Emerg Surg. 2011 Feb 23;6:7. doi: 10.1186/1749-7922-6-7.
  4. Moore LJ, Moore FA. Epidemiology of sepsis in surgical patients. Surg Clin North Am. 2012 Dec;92(6):1425-43. doi: 10.1016/j.suc.2012.08.009.
  5. Timsit JF, Perner A, Bakker J, Bassetti M, Benoit D, Cecconi M, et al. Year in review in Intensive Care Medicine 2014: III. Severe infections, septic shock, healthcare-associated infections, highly resistant bacteria, invasive fungal infections, severe viral infections, Ebola virus disease and paediatrics. Intensive Care Med. 2015; 41(4): 575-88. doi: 10.1007/s00134-015-3755-8.
  6. Sartelli M. A focus on intra-abdominal infections. World J Emerg Surg. 2010 Mar 19;5:9. doi: 10.1186/1749-7922-5-9.
  7. Rybachkov VV, Kostiuchenko KV, Maevskii SV. Peritonit [Peritonitis]. Iaroslavl’, RF: IarMediaGrup; 2010. 308 p.
  8. Paul JS, Ridolfi TJ. A case study in intra-abdominal sepsis. Surg Clin North Am. 2012 Dec;92(6):1661-77. doi: 10.1016/j.suc.2012.08.014.
  9. Boiko VV, Krivoruchko IA, Teslenko SN, Sivozhelezov AV. Rasprostranennyi gnoinyi peritonit [Genreralized purulent peritonitis]. Khar’kiv, Ukraina: Prapor; 2008. 280 p.
  10. Sukovatykh BS, Blinkov IuIu, Frolova OG. Mekhanizmy razvitiia rasprostranennogo peritonita [Mechanisms of development of generalized peritonitis]. Vestnik Eksperim i Klin Khirurgii. 2012;5(2):469-77
  11. Brook I, Wexler HM, Goldstein EJ. Antianaerobic antimicrobials: spectrum and susceptibility testing. Clin Microbiol Rev. 2013 Jul;26(3):526-46. doi: 10.1128/CMR.00086-12.
  12. Kosinets VA. Identifikatsiia i opredelenie chuvstvitel’nosti k antimikrobnym preparatam osnovnykh vozbuditelei rasprostranennogo gnoinogo peritonita [Identification and determination of susceptibility to antimicrobial agents of the main pathogens of generalized purulent peritonitis]. Novosti Khirurgii. 2012;20(5):62-69.
  13. Chapter 2-5-4. Anaerobic infections (individual fields): intraperitoneal infections (acute peritonitis, hepatobiliary infections, etc.). J Infect Chemother. 2011 Jul;17(Suppl 1):84-91. doi: 10.1007/s10156-010-0146-5.
Address for correspondence:
210023, Republic of Belarus,
Vitebsk, Frunze ave., 27,
EE “Vitebsk State Medical University”,
Department of Operative Surgery
and Topographic Anatomy,
Tel. +375 33 675-48-62,
E-mail: anna.annushka75@mail.ru,
Anna M. Kupchenko
Information about the authors:
Kupchenko A.M., Senior Lecturer of the Department of Operative Surgery and Topographic Anatomy of EE “Vitebsk State Medical University”.
Kosinets V.A., MD, Professor, Professor of the Department of Hospital Surgery with Urology and Pediatric Surgery Courses of EE “Vitebsk State Medical University”.

M.Y. GAIN, S.V. SHAKHRAY, Y.M. GAIN

PILONIDAL SINUS: IS RADICAL OPERATION ALWAYS INDICATED?

SEE “Belarusian Medical Academy of Post-Graduate Education”, Minsk,
The Republic of Belarus

Objective. To study the treatment results of an acute inflammation of the sacrococcygeal region cyst in the distant period.
Methods. The study involved 481 patients suffering from an acute pilonidal sinus in which the abscess opening and draining was performed in 2007-2010. In the group A (250 patients) after the primary operation the second stage of treatment was applied including the radical operation to excise the cyst with the wound suturing by Donati. The group B includes 231 patients in whom the radical excision wasn’t performed. The groups were gender and age comparable. Follow-up was carried out in 2017 – in terms from 7 to 10 years after the primary operation.
Results. The recurrence rate after the radical excision (group A) was 10,8% (27 patients). 234 patients (93.6%) were subject to removal of postoperative sutures in terms up to 10 days. An average term of complete wound healing in the group A was 42 [28 - 57] (Me [25%-75%]) days. In the group B the abscess recurrence and repeated operation (abscess incision) was required in 74 patients (32.03%). In 157 (67.97%) cases, 7-10 years after the primary operation, absence of complaints (asymptomatic sinus, remission) was observed. While comparing two groups by general terms of disability for the period of 7-10 years, the significant advantages of the group B have been revealed: median of 12 days (group B) against 38 (in group A) (p=0.000319). Comparing two groups by the remote recurrence frequency has revealed the following data – 10.8% (group A) against 32.03% (group B) (p = 0.00164).
Conclusions. The research result testifies to the necessity for further discussion concerning a rational surgical tactics, choice of indications for radical excision.

Keywords: pilonidal sinus, sacrococcygeal region, abscess, drainage, wound healing, cysts
p. 600-604 of the original issue
References
  1. Datsenko BM. Ostroe nagnoenie epitelial’nogo kopchikovogo khoda [Acute suppuration of epithelial coccygeal]. Khar’kiv, Ukraina: Prapor; 2006. 165 p.
  2. Shelygin YA, Blagodarnyi LA. Spravochnik po koloproktologii [Handbook of Coloproctology]. Moscow, RF: Litterra; 2012. 596 p.
  3. Gecim IE, Goktug UU, Celasin H. Endoscopic pilonidal sinus treatment combined with crystalized phenol application may preven trecurrence. Dis Colon Rectum. 2017 Apr;60(4):405-407. doi: 10.1097/DCR.0000000000000778.
  4. Dessily M, Charara F, Ralea S, AlléJ JL. Pilonidal sinus destruction with a radial laser probe: technique and first Belgian experience. Acta Chir Belg. 2017 Jan 6:1-8.doi: 10.1080/00015458.2016.1272285.
  5. Isik A, Idiz O, Firat D. Novel approachesin pilonidalsinus treatment. Prague Med Rep. 2016;117(4):145-52. doi: 10.14712/23362936.2016.15.
  6. Harris C, Sibbald RG, Mufti A, Somayaji R. Pilonidal Sinus Disease: 10 Steps to Optimize Care. Adv Skin Wound Care. 2016 Oct;29(10):469-78. doi: 10.1097/01.ASW.0000491324.29246.96.
  7. Iesalnieks I, Ommer A, Petersen S, Doll D, Herold A. German national guideline on the management of pilonidal disease. Langenbecks Arch Surg. 2016 Aug;401(5):599-609. doi: 10.1007/s00423-016-1463-7.
Address for correspondence:
220013, Republic of Belarus,
Minsk, P. Brovki str., 3, b.3,
SEE “Belarusian Medical Academy
of Post-Graduate Education”,
Department of Emergency Surgery;
Tel.: 375-17-225-88-10,
E-mail: mishahain@tut.by,
Michail Y. Gain
Information about the authors:
Gain M.Y., PhD, Senior Lecturer of the Department of Emergency Surgery of SEE “Belarusian Medical Academy of Post-Graduate Education”.
Shakhray S.V., MD, Professor of the Department of Emergency Surgery of SEE “Belarusian Medical Academy of Post-Graduate Education”.
Gain Y.M., MD, Professor, Vice-rector for scientific work of SEE “Belarusian Medical Academy of Post-Graduate Education”.

TRAUMATOLOGY & ORTHOPEDICS

Z.S. NAUMENKO, M.V. CHEPELEVA, N.V. GODOVYKH

CYTOKINES AND MICROBIOCENOSIS IN PREDICTING THE POSTOPERATIVE PERIOD COURSE IN PATIENTS WITH PERIPROSTHETIC INFECTION OF THE HIP JOINT AFTER REMOVAL OF THE INFECTED IMPLANT

FSBE “Russian Ilizarov Scientific Center “Restorative Traumatology and Orthopaedics” of the RF, Ministry of Health, Kurgan,
The Russian Federation

Objective. To study microbiocenosis and the dynamics of the main cytokines in order to predict the postoperative period course after the hip joint implant removing in patients with the periprosthetic infection.
Methods. All the patients underwent debridement of the hip joint with the infected implant removal. The patients were retrospectively divided into two groups: group I included 29 patients with uncomplicated postoperative period course, group II – 20 patients with the infection recurrence in the immediate postoperative period due to hematoma infection in the residual cavity of the femoral medullary canal after the removal of the implant stem. Study of the concentrations of IL-1β, IL-6, IL-10, IL-8, TNF&alfa;, IFNγ was carried out by the enzyme-linked immunosorbent method before the surgery, on the 3, 7, 21, 30 days after surgery. Microbiocenosis was analyzed before the surgery, intraoperatively and postoperatively.
Results. It was found out, that the pathogens represented by monocultures (mainly Staphylococcus aureus, S. epidermidis) prevailed in Group I patients, and mixed infections prevailed in Group II patients. Microbiocenosis of Group II patients was characterized by the increase in the proportion of Gram-negative bacterii (Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter baumanii) postoperatively.
Dynamically, there was a tendency for Group I cytokines to decrease, and for those in Group II – to increase. In Group I statistically significant differences were observed 30 days after surgery, comparing with the preoperative period, for IL-1β, IL-8, IL-10 the concentrations of which decreased. In Group II, IL-1β, IL-6, IL-10 significantly increased at this time. In Group I the complex dynamics of serum cytokines evidenced in favor of infection process stopping, in Group II – in favor of pyoinflammatory complications.
Conclusions. The changes in microbiocenosis structure as well as the comprehensive investigation of cytokine concentrations can be used as additional predictive criteria of infection recurrences in patients with periprosthetic infection after the hip joint implant removal.

Keywords: the hip joint, arthroplasty, periprosthetic infection, Staphylococcus aureus, cytokines, microbiocenosis, recurrence
p. 605-612 of the original issue
References
  1. Slobodskoi AB, Osintsev EI, Lezhnev AG, Voronin IV, Badak IS, Dunaev AG. Faktory riska razvitiia periproteznoi infektsii posle endoprotezirovaniia krupnykh sustavov [Risk factors for periprosthetic infection after endoprosthetics of large joints]. Vestn Travmatologii i Ortopedii im NN Priorova. 2015;(2):13-18.
  2. Darwiche H, Barsoum WK, Klika A, Krebs VE, Molloy R. Retrospective analysis of infection rate after early reoperation in total hip arthroplasty. Clin Orthop Relat Res. 2010 Sep;468(9):2392-96. doi: 10.1007/s11999-010-1325-5.
  3. Petrova NV. Diagnostika implant-assotsiirovannykh infektsii v ortopedii s pozitsii dokazatel’noi meditsiny [Diagnosis of implant-associated infections in orthopedics from the perspective of evidence-based medicine]. Khirurgiia Pozvonochnika. 2012;(1):74-83.
  4. Simbirtsev A.S., Gromova AI. Funktsional’nyi polimorfizm genov reguliatornykh molekul vospaleniia [Functional polymorphism of the genes of regulatory molecules of inflammation]. Tsitokiny i Vospalenie. 2005;4(1):3-10.
  5. Markelova EV, Kostiushko AV, Krasnikov VE. Patogeneticheskaia rol’ narushenii v sisteme tsitokinov pri infektsionno-vospalitel’nykh zabolevaniiakh [Pathogenetic role of disorders in the cytokine system in infectious and inflammatory diseases]. Tikhookean Med Zhurn. 2008;(3):24-29.
  6. Romanova IM, Gintsburg AL. Tsitokiny – vozmozhnye aktivatory rosta patogennykh bakterii [Cytokines are possible activators of growth of pathogenic bacteria]. Vestn RAMN. 2000;(1):13-17.
  7. Berbari E, Mabry T, Tsaras G, Spangehl M, Erwin PJ, Murad MH, et al. Inflammatory blood laboratory levels as markers of prosthetic joint infection: a systematic review and meta-analysis. J Bone Joint Surg Am. 2010 Sep 1;92(11):2102-9. doi: 10.2106/JBJS.I.01199.
  8. Buttaro MA, Tanoira I, Comba F, Piccaluga F. Combining C-reactive protein and interleukin-6 may be useful to detect periprosthetic hip infection. Clin Orthop Relat Res. 2010 Dec;468(12):3263-67. doi: 10.1007/s11999-010-1451-0.
  9. Elgeidi A, Elganainy AE, Abou Elkhier N, Rakha S. Interleukin-6 and other inflammatory markers in diagnosis of periprosthetic joint infection. Int Orthop. 2014 Dec;38(12):2591-95. doi: 10.1007/s00264-014-2475-y.
  10. Jacovides CL, Parvizi J, Adeli B, Jung KA. Molecular markers for diagnosis of periprosthetic joint infection. J Arthroplasty. 2011 Sep;26(6 Suppl):99-103.e1. doi: 10.1016/j.arth.2011.03.025.
  11. Chepeleva MV, Kliushin NM, Ermakov AM, Ababkov IV. Interleikin-6 v prognozirovanii techeniia posleoperatsionnogo perioda u patsientov s periproteznoi infektsiei tazobedrennogo sustava [Interleykin-6 in predicting the course of the postoperative period in patients with periprosthetic hip infection]. Sib Nauch Med Zhurn. 2015;35(4):45-48.
  12. Shipitsyna IV, Osipova EV, Naumenko ZS. Issledovanie faktorov persistentsii: bioplenkoobrazuiushchei sposobnosti i antilizotsimnoi aktivnosti etiologicheskikh agentov khronicheskogo osteomielita [Investigation of persistence factors: biofilm-forming ability and antilizimic activity of etiological agents of chronic osteomyelitis]. Infektsii v Khirurgii. 2014;12(2):40-42.
  13. Liu B, Tikhilov RM, Shubniakov II, Bozhkova SA, Artiukh VA, Denisov AO. Analiz effektivnosti saniruiushchikh operatsii pri paraendoproteznoi infektsii [Analysis of the effectiveness of sanitizing operations with paraendoprosthetic infection]. Travmatologiia i Ortopediia Rossii. 2014;(2):22-29.
  14. Frangiamore SJ, Siqueira MB, Saleh A, Daly T, Higuera CA, Barsoum WK. Erratum to: Synovial Cytokines and the MSIS Criteria Are Not Useful for Determining Infection Resolution After Periprosthetic Joint Infection Explantation. Clin Orthop Relat Res. 2016 Jul; 474(7):1740-41. doi: 10.1007/s11999-016-4824-1.
  15. Frangiamore SJ, Saleh A, Grosso MJ, Farias KM, Zhang X, Daly TM, et al. Neer Award 2015: Analysis of cytokine profiles in the diagnosis of periprosthetic joint infections of the shoulder. J Shoulder Elbow Surg. 2017 Feb;26(Is 2):186-96. doi: 10.1016/j.jse.2016.07.017.
Address for correspondence:
640014, Russian Federation,
Kurgan, M. Ulyanova str., 6,
FSBE “Russian Ilizarov Scientific
Center “Restorative Traumatology
and Orthopaedics”,
Clinical Laboratory of Microbiology
and Immunology,
tel. office: +7 352 2 45-16-54,
e-mail: zinaida_n@inbox.ru,
Zinaida S. Naumenko
Information about the authors:
Naumenko Z.S., PhD, Head of the Scientific and Clinical Laboratory of Microbiology and Immunology of FSBE “Russian Ilizarov Scientific Center “Restorative Traumatology and Orthopaedics”.
Chepeleva M.V., PhD, Senior Researcherof the Scientific and Clinical Laboratory of Microbiology and Immunology of FSBE “Russian Ilizarov Scientific Center “Restorative Traumatology and Orthopaedics”.
Godovykh N.V., Junior Researcher of the Scientific and Clinical Laboratory of Microbiology and Immunology of FSBE “Russian Ilizarov Scientific Center “Restorative Traumatology and Orthopaedics”.

ONCOLOGY

Y.B. RADZISHEVSKA 1,2, L.Y. VASIL’EV 1, V.G. KNIGAVKO 2, N.I. LYKHOVITSKAYA 1

RELATIONSHIPS OF NOSOLOGICAL FORM OF THE PRIMARY AND SECOND NEOPLASMS IN ONCOLOGICAL PATIENTS

SE “Institute of Medical Radiology named after S.P. Grigoriev”
of the National Academy of Medical Sciences of Ukraine 1,
Kharkov National Medical University 2, Kharkov,
Ukraine

Objective. To investigate the relationship between nosological forms of the primary and second neoplasms in patients who have undergone special treatment for cancer, and who have developed second neoplasms three and more years after the end of treatment.
Methods. The study has compared the nosological structure of second neoplasms that developed in 203 patients undergoing treatment for oncological pathology with the official data on the specific weight of 10 major nosological forms of malignant neoplasms in Ukraine. The statistical significance of the obtained results has been estimated using confidence intervals normalized taking into account the specificity of the patients of the clinic where the study was conducted.
Results. In accordance with the specific weight of the nosological forms of the primary neoplasms, conditioned first by the specialization of the clinic, the study groups were divided into 5 nosological subgroups: patients with breast, thyroid, uterine, cervical, ovarian, and subgroup with other forms of cancer. For each of the subgroups, the nosological structure of the second neoplasms was investigated and compared with the overall structure of malignant neoplasms according to the official statistics. It is shown that the frequencies of five allocated nosological forms calculated for the clinic correspond fairly well to the population mean, while for two most representative nosological forms the correspondence is within the expected stochastic variability. Thus, it has been demonstrated that there are no statistically significant differences between the percentage composition of 10 major nosological forms of cancer in Ukraine and the structure of nosological forms of second neoplasms in the study group of patients.
Conclusions. The nosological form of second neoplasms is not a consequence of the primary cancer, but reproduces the overall nosological structure of the incidence of malignant neoplasms.

Keywords: primary neoplasms, second neoplasms, incidence structure of malignant neoplasms, etiology of second cancers
p. 613-620 of the original issue
References
  1. Alberts D. Second cancers are killing us. Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(Is 11): 2019. doi: 10.1158/1055-9965.EPI-06-0417.
  2. Rowland J, Mariotto A, Aziz N, Tesauro G, Feuer EJ, Blackman B, et al. Cancer survivorship–United States, 1971-2001. MMWR Morbid Mortal Wkly Rep. 2004 Jun 25;53(24):526-29.
  3. Berrington de Gonzalez A, Curtis RE, Gilbert E, Berg CD, Smith SA, Stovall M, et al. Second solid cancers after radiotherapy for breast cancer in SEER cancer registries. Br J Cancer. 2010 Jan 5;102(1):220-26. doi: 10.1038/sj.bjc.6605435.
  4. Virtanen A, Pukkala E, Auvinen A. Angiosarcoma after radiotherapy: a cohort study of 332 163 Finnish cancer patients. Br J Cancer. 2007 Jul 2; 97(1): 115-17. doi: 10.1038/sj.bjc.6603805.
  5. Maksimov SI. Pervichno-mnozhestvennye opukholi organov reproduktivnoi sistemy [Primary-multiple tumors of organs of the reproductive system]. Prakt Onkologiia. 2009;10(2):117-23.
  6. Kakinuma S, Shimada Y. Risk of second cancer after radiation therapy. Igaku Butsuri. 2014;34(2):79-84. [Article in Japanese]
  7. Ota T, Takeshima IN., Tabata IT, Hasumi 1K, Takizawa K. Treatment of squamous cell carcinoma of the uterine cervix with radiation therapy alone: long-term survival, late complications, and incidence of second cancers. Br J Cancer. 2007 Oct 22;97(8): 1058-62. doi: 10.1038/sj.bjc.6604005.
  8. Ganz PA. A teachable moment for oncologists: cancer survivors, 10 million strong and growing! J Clin Oncol. 2005 Aug 20;23(24):5458-60.
  9. Vogel VG. Identifying and screening patients at risk of second cancers. Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2027-32.
  10. Lischko AM, Seddon JM, Gragoudas ES, Egan KM, Glynn RJ. Evaluation of prior primary malignancy as a determinant of uveal melanoma. A case-control study. Ophthalmology. 1989 Dec;96(12):1716-21.
  11. Bernshtein LM, red. Gormonal’nyi kantserogenez [Hormonal carcinogenesis]. S-Peterburg, RF: Nauka; 2000. 199 p.
  12. Bokhman IV, Rybin EP, Polineoplazii organov reproduktivnoi sistemy [Polyneoplasia of the organs of the reproductive system]. S.-Peterburg, RF: Neva-Liuks; 2001. 240 p.
  13. Ackerman J, Baunoch DA, Gimotty P, George J, Lane MA, Dawson PJ. The role of p53 mutations in bilateral breast carcinoma. Mod Pathol. 1995 Apr;8(3):244-48.
  14. Birben E, Sahiner UM, Sackesen C, Erzurum S, Kalayci O. Oxidative stress and antioxidant defense. World Allergy Organ J. 2012 Jan;5(1):9-19. doi: 10.1097/WOX.0b013e3182439613.
  15. Abe H, Hanasawa K, Naitoh H, Endo Y, Tani T, Kushima R. Invasive ductal carcinoma within a fibroadenoma of the breast. Int J Clin Oncol. 2004 Aug;9(4):334-38.
  16. Schaapveld M, Aleman BM, van Eggermond AM, Janus CP, Krol AD, van der Maazen RW, et al. Second cancer risk up to 40 years after treatment for Hodgkin’s Lymphoma. N Engl J Med. 2015 Dec 24;373(26):2499-511. doi: 10.1056/NEJMoa1505949.
  17. Grantzau T, Mellemkjær L, Overgaard J. Second primary cancers after adjuvant radiotherapy in early breast cancer patients: a national population based study under the Danish Breast Cancer Cooperative Group (DBCG). Radiother Oncol. 2013 Jan;106(1):42-49. doi: 10.1016/j.radonc.2013.01.002.
Address for correspondence:
61024, Ukraine,
Kharkov, Pushkinskaya str., 82,
SE «Institute of Medical Radiology
named after S.P. Grigoriev»,
Medical Informatics Group,
tel. office: +380 (67) 799-36-63,
e-mail: radzishevska@ukr.net,
Evgeniya B. Radzishevska
Information about the authors:
Radzishevska E.B., PhD, Head of the Medical Informatics Group of SE “Institute of Medical Radiology named after S.P. Grigoriev “of the National Academy of Medical Sciences of Ukraine, Associate Professor of the Department of Medical and Biological Physics and Medical Informatics of Kharkov National Medical University.
Vasil’ev L.Y., PhD, Head Physician of SE “Institute of Medical Radiology named after S.P. Grigoriev “of the National Academy of Medical Sciences of Ukraine.
Knigavko V.G., Doctor of Biological Sciences, Professor, Head of the Department of Medical and Biological Physics and Medical Informatics of Kharkov National Medical University.
Lykhovitskaya N.I., PhD, Researcher of the Nuclear Medicine Department of SE “Institute of Medical Radiology named after S.P. Grigoriev “of the National Academy of Medical Sciences of Ukraine.

REVIEWS

D.A. MOROZOV 1, O.L. MOROZOVA 1, S.A. KLYUEV 2, I.A. BUDNIK 1, L.D. MALTSEVA 1, K.D. MOROZOV 1

INTRA-ABDOMINAL HYPERTENSION SYNDROME IN CHILDREN

FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University) 1,
FSAE National Scientific Center of Children's Health of the Ministry of Health of Russia2, Moscow,
The Russian Federation

Intra-abdominal hypertension (IAH), abdominal compartment syndrome (ACS) are diagnosed in every third critically ill child and lethality in the syndrome of intra-abdominal hypertension (SIAH) is observed in more than half of children. The World Society of the Abdominal Compartment Syndrome (WSACS) consensus definitions and practical guidelines for diagnosis and management of IAH/ACS do not account for age-dependent anatomical and physiological characteristics of pediatric patients and are often ignored by health care professionals. Intra-abdominal pressure measurement is performed in less than half of critically ill patients. When applied in children, currently standard approach to diagnosis and treatment of IAH/ACS delivers unsatisfactory results. Timely abdominal decompression is mandatory for effective prevention of multiple organ failure and poor outcome. This article reviews the most common causes and risk factors, associated with intra-abdominal hypertension in children of different age groups; it discusses the pathophysiology of ACS, summarizes different techniques for intra-abdominal pressure measurement, overviews recent advances in assessment of target organ damage using instrumental and molecular diagnostic techniques, and highlights new treatment options in this patient population.

Keywords: intra-abdominal hypertension, abdominal compartment syndrome, multiple organ failure, congenital malformations, biomarkers of renal damage, monitoring, child
p. 621-631 of the original issue
References
  1. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, et al.Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013 Jul;39(7):1190-206. doi: 10.1007/s00134-013-2906-z.
  2. Kaussen T, Steinau G, Srinivasan PK, Otto J, Sasse M, Staudt F, et al. Recognition and management of abdominal compartment syndrome among German pediatric intensivists: results of a national survey. Ann Intensive Care. 2012 Jul 5;2(Suppl 1):S8. doi: 10.1186/2110-5820-2-S1-S7.
  3. Oda J, Ueyama M, Yamashita K, Inoue T, Noborio M, Ode Y, et al. Hypertonic lactated saline resuscitation reduces the risk of abdominal compartment syndrome in severely burned patients. J Trauma. 2006 Jan;60(1):64-71.
  4. Ure BM, Suempelmann R, Metzelder MM, Kuebler J. Physiological responses to endoscopic surgery in children. Semin Pediatr Surg. 2007 Nov;16(4):217-23.
  5. Sepbaeva AD, Geras’kin AV, Kucherov II, Zhirkova IV, Tepliakova OV, Khamatkhanova EM, i dr. Vliianie povyshennogo vnutribriushnogo davleniia na funktsiiu dykhaniia i gemodinamiku pri pervichnoi plastike perednei briushnoi stenki u novorozhdennykh detei s gastroshizisom i omfalotsele [Influence of increased intra-abdominal pressure on respiratory function and hemodynamics in primary abdominal wall plasty in newborns with gastroschisis and omphalocele]. Det Khirurgiia. 2009;(3):39-41.
  6. Ozbey H. Use of sterile adhesive film and polypropylene mesh in the construction of a temporary silo in the treatment of omphalocele. Surg Today. 2005;35(8):700-2.
  7. Goldkrand JW, Causey TN, Hull EE. The changing face of gastroschisis and omphalocele in southeast Georgia. J Matern Fetal Neonatal Med. 2004 May;15(5):331-35.
  8. Risby K, Jakobsen MS, Qvist N. Congenital Abdominal Wall Defects: Staged closure by Dual Mesh. J Neonatal Surg. 2016 Jan-Mar; 5(1):2.
  9. Kozlov YA, Novozhilov VA, Podkamenev AV, Kovalev VM, Makhov AN, Kupriakov SO. Minimal’no invazivnoe lechenie gastroshizisa [Minimally invasive treatment of gastroschisis]. Det Khirurgiia. 2005;(2):10-11.
  10. Plokhikh D.A. Rezul’taty issledovaniia fiziologicheskikh pokazatelei vnutribriushnogo davleniia u novorozhdennykh detei [Results of the study of physiological indicators of intra-abdominal pressure in newborns] Mat’ i Ditia v Kuzbasse. 2010;(2):30-33.
  11. Mandal KC, Halder P, Barman S, Kumar R, Mukhopadhyay B, Shukla RM. Intragastric pressure: Useful indicator in the management of congenital diaphragmatic hernia. J Indian Assoc Pediatr Surg. 2016 Oct-Dec;21(4):175-77. doi: 10.4103/0971-9261.186547.
  12. Shcherbina VI, Mashkov AE, Tsuman VG, Tarasova OV, Semilov EA, Filiushkin YI. Lechenie nesostoiatel’nosti anastamoza i ego stenozirovaniia posle ezofagoplastiki u novorozhdennykh s atreziei pishchevoda [Treatment of anastomosis failure and its stenosis after esophagoplasty in neonates with esophageal atresia] Det Khirurgiia. 2008;(6):21-24.
  13. Chung PH, Wong KK, Lan LC, Tam PK. Abdominal compartment syndrome after open biopsy in a child with bilateral Wilms’ tumour. Hong Kong Med J. 2009 Apr;15(2):136-38.
  14. Zani A, Eaton S, Puri P, Rintala R, Lukac M, Bagolan P, et al. International survey on the management of necrotizing enterocolitis. Eur J Pediatr Surg. 2015 Feb;25(1):27-33. doi: 10.1055/s-0034-1387942.
  15. Tanriverdi S, Koroglu O, Uygur O, Celik A, Dulger F, Yalaz M, et al. Serial intravesical pressure measurements can predict the presence and the severity of necrotizing enterocolitis. Eur J Pediatr Surg. 2013 Jun;23(3):243-48. doi: 10.1055/s-0032-1329706.
  16. Liang YJ, Huang HM, Yang HL, Xu LL, Zhang LD, Li SP, et al. Controlled peritoneal drainage improves survival in children with abdominal compartment syndrome. Ital J Pediatr. 2015;41:29. doi: 10.1186/s13052-015-0134-6.
  17. Panagiotis H, Panagiotis D, Nikolaos A, Ion B. Abdominal compartment syndrome post-late Bochdalek hernia repair: A case report. Cases J. 2008;1:199. doi: 10.1186/1757-1626-1-199.
  18. Gain IuM, Alekseev SA, Bogdan VG. Sindrom abdominal’noi kompressii v khirurgii [Syndrome of abdominal compression in surgery]. Bel Med Zhurn. 2004;(3):34-37.
  19. Libório A.B., Branco KMPC, Torres de Melo Bezerra C. Acute kidney injury in neonates: from urine output to new biomarkers. Biomed Res Int. 2014;(2014): Article ID 6015. 8 ð. doi: 10.1155/2014/601568.
  20. Tuktamyshev V.S., Kuchumov A.G., Niashin Iu.I., Samartsev V.A., Kasatova E.Iu. Vnutribriushnoe davlenie cheloveka [Human intra-abdominal pressure]. Ros Zhurn Biomekhaniki. 2013;17(1):22-31.
  21. Ricci Z, Ronco C. Neonatal RIFLE. Nephrol Dial Transplant. 2013 Sep;28(9):2211-14. doi: 10.1093/ndt/gft074.
  22. Malbrain ML, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med. 2005 Feb;33(2):315-22.
  23. Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia A, Burch JM. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997 Dec;174(6):667-72; discussion 672-3.
  24. Singhal J, Shanbag P. Measurement of Intra-abdominal Pressure in Critically-ill Children. J Clin Diagn Res. 2014 Dec; 8(12): PC06-PC07. doi: 10.7860/JCDR/2014/10435.5345.
  25. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989 Feb;17(2):118-21.
  26. Morozov DA, Morozova OL, Tsyplakov AA, Mel’nikova IA. Povrezhdenie pochek u novorozhdennykh s sindromom intraabdominal’noi gipertenzii [Kidney damage in newborns with intra-abdominal hypertension syndrome]. Vestn RAMN. 2015;(6):704-9.
  27. Davis PJ, Koottayi S, Taylor A, Butt WW. Comparison of indirect methods of measuring intra-abdominal pressure in children. Intensive Care Med. 2005 Mar;31(3):471-75.
  28. Diaz FJ, Fernandez Sein A, Gotay F. Identification and management of Abdominal Compartment Syndrome in the Pediatric Intensive Care Unit. PR Health Sci J. 2006 Mar;25(1):17-22.
  29. Doty JM, Saggi BH, Blocher CR, Fakhry I, Gehr T, et al. Effects of increased renal parenchymal pressure on renal function. J Trauma. 2000 May;48(5):874-77.
  30. Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. II. Recommendations. Intensive Care Med. 2007 Jun;33(6):951-62.
  31. Tiwari A, Myint F, Hamilton G. Recognition and management of abdominal compartment syndrome in the United Kingdom. Intensive Care Med. 2006 Jun;32(6):906-9.
  32. McGuigan RM, Mullenix PS, Vegunta R, Pearl RH, Sawin R, Azarow KS. Splanchnic perfusion pressure: a better predictor of safe primary closure than intraabdominal pressure in neonatal gastroschisis. J Pediatr Surg. 2006 May;41(5):901-4.
  33. Ejike JC, Mathur M, Moores DC. Abdominal compartment syndrome: focus on the children. Am Surg. 2011 Jul;77(Suppl 1):S72-77.
  34. Suominen PK, Pakarinen MP, Rautiainen P, Mattila I, Sairanen H. Comparison of direct and intravesical measurement of intraabdominal pressure in children. J Pediatr Surg. 2006 Aug;41(8):1381-85.
  35. Ejike JC, Mathur M. Abdominal decompression in children. Crit Care Res Pract. 2012;2012:180797. doi: 10.1155/2012/180797.
  36. Macedo E, Malhotra R, Claure-Del Granado R, Fedullo P, Mehta RL. Defining urine output criterion for acute kidney injury in critically ill patients. Nephrol Dial Transplant. 2011 Feb;26(2):509-15. doi: 10.1093/ndt/gfq332.
  37. Genovese F, Manresa AA, Leeming DJ, Karsdal MA, Boor P. The extracellular matrix in the kidney: a source of novel non-invasive biomarkers of kidney fibrosis? Fibrogenesis Tissue Repair. 2014 Mar 28;7(1):4. doi: 10.1186/1755-1536-7-4.
  38. de Geus HR, Fortrie G, Betjes MG, van Schaik RH, Groeneveld AB. Time of injury affects urinary biomarker predictive values for acute kidney injury in critically ill, non-septic patients. BMC Nephrol. 2013;14:273. doi: 10.1186/1471-2369-14-273.
  39. Bihorac A, Baslanti TO, Cuenca AG, Hobson CE, Ang D, Efron PA, Maier RV, Moore FA, Moldawer LL. Acute kidney injury is associated with early cytokine changes after trauma. J Trauma Acute Care Surg. 2013 Apr;74(4):1005-13. doi: 10.1097/TA.0b013e31828586ec.
  40. Mao S, Huang S. The signaling pathway of hypoxia inducible factor and its role in renal diseases. J Recept Signal Transduct Res. 2013 Dec;33(6):344-8. doi: 10.3109/10799893.2013.830130.
  41. Morozov DA, Morozova OL, Tsyplakov AA, Zakharova NB, Budnik IA. Molekuliarnye markery povrezhdeniia pochek u novorozhdennykh s sindromom intraabdominal’noi gipertenzii [Molecular markers of kidney damage in newborns with intra-abdominal hypertension syndrome]. Pediatriia Zhurn im GN Speranskogo. 2015;94(3):13-19.
  42. Vaidya VS, Ford GM, Waikar SS, Wang Y, Clement MB, Ramirez V, et al. A rapid urine test for early detection of kidney injury. Kidney Int. 2009 Jul;76(1):108-14. doi: 10.1038/ki.2009.96.
  43. Peng H, Mao Y, Fu X, Feng Z, Xu J. Comparison of biomarkers in rat renal ischemia-reperfusion injury. Int J Clin Exp Med. 2015 May 15;8(5):7577-84. eCollection 2015.
  44. Chevalier RL, Thornhill BA, Forbes MS, Kiley SC. Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy. Pediatr Nephrol. 2010 Apr;25(4):687-97. doi: 10.1007/s00467-009-1316-5.
  45. Sugerman HJ, Bloomfield GL, Saggi BW. Multisystem organ failure secondary to increased intraabdominal pressure. Infection. 1999 Jan-Feb;27(1):61-6.
  46. Pearson EG, Rollins MD, Vogler SA, Mills MK, Lehman EL, Jacques E, et al. Decompressive laparotomy for abdominal compartment syndrome in children: before it is too late. J Pediatr Surg. 2010 Jun;45(6):1324-29. doi: 10.1016/j.jpedsurg.2010.02.107.
  47. Gel’fand BR, Protsenko DN, Chubchenko SV, Ignatenko OV. Sindrom intraabdominal’noi gipertenzii u khirurgicheskikh bol’nykh: sostoianie problemy v 2007g [Syndrome of intra-abdominal hypertension in surgical patients: the state of the problem in 2007 yr]. Infektsii v Khirurgii. 2007;5(3):20-29.
  48. Mitanchez D, Walter-Nicolet E, Humblot A, Rousseau V, Revillon Y, Hubert P. Neonatal care in patients with giant ompholocele: arduous management but favorable outcomes. J Pediatr Surg. 2010 Aug;45(8):1727-33. doi: 10.1016/j.jpedsurg.2010.04.011.
  49. Morozov DA, Filippov IV. Ocherki detskoi abdominal’noi khirurgii [Essays on Pediatric abdominal surgery]. Saratov, RF: Izd-vo SGMU; 2008. 140 p.
  50. Ozbey H. Use of sterile adhesive film and polypropylene mesh in the construction of a temporary silo in the treatment of omphalocele. Surg Today. 2005;35(8):700-2.
Address for correspondence:
119991, Russian Federation,
Moscow, Trubetskaya str., 8,
FSAEI HE I.M. Sechenov First Moscow State Medical University Ministry of Healthcare Russian Federation (Sechenov University),
Department of Pathophysiology,
tel. office: 8 (499) 622 96 47,
e-mail: morozova_ol@list.ru,
Olga L. Morozova
Information about the authors:
Morozov D.A., MD, Professor, Head of the Department of Pediatric Surgery, Urology and Andrology of FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University).
Morozova O.L., MD, Professor of the Department of Pathophysiology of FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University).
Klyuev S.A., Pediatric Surgeon, Post-Graduate Student of FSAE National Scientific Center of Children’s Health of the Ministry of Health of Russia.
Budnik I.A., PhD, Associate Professor of the Department of Pathophysiology of FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University).
Maltseva L.D., PhD, Associate Professor of the Department of Pathophysiology of FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University).
Morozov Ê.D., Student of FSAEI HE I.M. Sechenov First Moscow State Medical University MOH Russian Federation (Sechenov University).

V.N. ZASIMOVICH, N.N. IOSKEVICH

REPERFUSION (REOXYGENATION) INJURY AS A PROBLEM OF THE ARTERY RECONSTRUCTIVE SURGERY IN ATHEROSCLEROTIC GENESIS CHRONIC ISCHEMIA OF THE LOWER LIMBS

ME “Brest Regional Hospital”1, Brest
EE “Grodno State Medical University”2, Grodno
The Republic of Belarus

Objective. To perform the analysis of literature sources dedicated to the problem of reperfusion (reoxygenation) injury after revascularization of the lower limbs.
Methods. The native and foreign literature data have been analyzed concerning the investigation stages of the problem, pathogenesis, clinical manifestations of reperfusion (reoxygenation) injury and methods of its prediction, prevention and correction for recent 20 years.
Results. The steady increase in atherosclerosis incidence, quantitative rise of lower limbs revascularization determines an increase in the frequency of reperfusion injury, significantly reducing the effectiveness of surgical interventions, impeding the restoration of function and, often, and preservation of the limb. Post-reperfusion injuries of the organs and systems remote from the lower limbs result in an evident life quality decline and lethality increase. The generalization of data on the studies of various links in the pathogenesis of ischemia-reperfusion and the methods of its correction indicate their fragmentation. The relationship between the severity of reperfusion injuries and the initial degree of the limb ischemia has not been adequately investigated.
Conclusions. Necessity in improvement of the surgical treatment results of chronic lower limb ischemia requires systemic researches on the correlation of disturbances of prooxidant-antioxidant balance, oxygen transport function, electrolyte and energy balance, depending on the degree of ischemia. This will allow developing the criteria for the severity of reperfusion (reoxygenation) injury, algorithms of its prediction, diagnosis, and correction. There is an urgent need to create a practically meaningful classification of ischemia-reperfusion, to determine the laboratory criteria for the degree of its severity, and to develop schemes for its medicinal prevention and treatment.

Keywords: reperfusion injury, revascularization, peripheral artery disease, atherosclerosis, prooxidant-antioxidant balance, oxygen transport function
p. 632-642 of the original issue
References
  1. Kalmykov EL, Skrypnik DA, Vinogradov RA, Gaibov AD. 30-i kongress evropeiskogo obshchestva sosudistykh khirurgov (Kopengagen, Daniia, 28-30 sentiabria 2016g.) [The 30th Congress of the European Society of Vascular Surgeons (Copenhagen, Denmark, September 28-30, 2016)]. Angiologiia i Sosud khirurgiia. 2017;(1):143-47.
  2. Moler III ER, Dzhaff MR, red. Zabolevaniia perifericheskikh arterii [Diseases of peripheral arteries]. Per. s angl. Pisarev MV, red. Moscow, RF: GEOTAR-Media; 2010. 224 p.
  3. Ianushko VA, Ioskevich NN, Lozhko PM, Turliuk DV, Ianushko AV. Khirurgiia aorty i ee vetvei [Surgery of the aorta and its branches]: atlas i ruk. Moscow, RF: Med lit; 2013. 224 p.
  4. Enge I, Edenberg J, Stuland T. Treatment with percutaneous transluminal angioplasty of the popliteal and crural arteries. Tidsskr Nor Laegeforen. 2004 Jan 22;124(2):173-75. [Norwegian]
  5. Wright LB, Matchett WJ, Cruz CP, James CA, Culp WC, Edidt JF. Popliteal artery disease: diagnosis and treatment. Radiographic. 2004 Mar-Apr;24(2):467-79.
  6. Belov IuV, Stepanenko AB. Povtornye rekonstruktivnye operatsii na aorte i magistral’nykh arteriiakh [Repeated reconstructive surgery on the aorta and main arteries]. Moscow, RF: MIA; 2009. 176 p.
  7. Koreiba KA, Kliushkin IV, Maksimov AV, Fatykhov RI, Nasrullaev MN. Reperfuzionnyi sindrom pri sosudistoi rekonstruktsii u bol’nykh s sindromom diabeticheskoi stopy [Reperfusion syndrome in vascular reconstruction in patients with diabetic foot syndrome]. Vestn Sovrem Klin Meditsiny. 2013;6(5):67-70.
  8. Kalinin RE, Pshennikov AS, Suchkov IA. Reperfuzionnoe povrezhdenie tkanei v khirurgii arterii nizhnikh konechnostei [Reperfusion injury of tissues in surgery of arteries of lower extremities]. Novosti Khirurgii. 2015;23(3):348-52.doi: 10.18484/2305-0047.2015.3.348.
  9. Natsional’nye rekomendatsii po vedeniiu patsientov s zabolevaniiami arterii nizhnikh konechnostei [National guidelines for management of patients with lower limb arteries]. Moscow, RF: Meditsina; 2013. 74 p.
  10. Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review. Cardiovasc Surg. 2002 Des;10(6):620-30.
  11. Dick F, Li J, Giraud MN, Kalka C, Schmidli J, Tevaearai H. Basic control of reperfusion effectively protects against reperfusion injury in a realistic rodent model of acute limb ischemia. Ñirculation. 2008 Nov 4;118(19):1920-28.
  12. Kuznetsov MR, Koshkin VM, Komov KV. Sovremennye aspekty diagnostiki, profilaktiki i lecheniia reperfuzionnogo sindroma [Modern aspects of diagnosis, prevention and treatment of reperfusion syndrome]. Angiologiia i Sosud Khirurgiia. 2006;12(1):133-43.
  13. Baines CP. How and when do myocytes die during ischemia and reperfusion: the late phase. J Cardiovasc Pharmacol Ther. 2011 Sep-Dec;16(3-4):239-43.
  14. Coats P, Hillier C. Differential responses in human subcutaneous and skeletal muscle vascular beds to critical limb ischemia. Eur J Vasc Endovasc Surg. 2000 Apr;19(4):387-95.
  15. Edrees WK, Lau LL, Young IS, Smye MG, Gardiner KR, Lee B, et al. The effect of lower limbs ischemia-reperfusion on intestinal permeability and the systemic inflammatory response. Eur J Vasc Surg. 2003 Apr;25(Is 4):330-35.
  16. Gavrilenko AV, Shabaltas ED. Sostoianie mikrotsirkuliatsii pri reperfuzionnom sindrome posle rekonstruktivnykh operatsii na sosudakh nizhnikh konechnostei [The state of microcirculation in reperfusion syndrome after reconstructive operations on the vessels of the lower limbs]. Khirurgiia Zhurn im NI Pirogova. 2003;(2):62-65.
  17. Shval’b PG, Kalinin RE. Antioksidantnaia zashchita i funktsional’noe sostoianie endoteliia u bol’nykh obliteriruiushchim aterosklerozom nizhnikh konechnostei do i posle operativnogo lecheniia [Antioxidant protection and functional state of the endothelium in patients with obliterating atherosclerosis of the lower limbs before and after surgical treatment]. Khirurgiia Zhurn im NI Pirogova. 2009;(1):53-55.
  18. Marshalov DV, Petrenko AP, Glushach IA. Reperfuzionnyi sindrom: poniatie, opredelenie, klassifikatsiia [Reperfusion syndrome: concept, definition, classification]. Patologiia Krovoobrashcheniia i Kardiokhirurgiia. 2008;(3):67-72.
  19. Ioskevich NN. Khirurgiia khronicheskoi ishemii nizhnikh konechnostei ateroskleroticheskogo geneza [Surgery of chronic ischemia of lower extremities of atherosclerotic origin]. Grodno, RB: GrGMU; 2007. 315 p.
  20. Bilenko MV. Ishemicheskie i reperfuzionnye povrezhdeniia organov (molekuliarnye mekhanizmy, puti preduprezhdeniia i lecheniia) [Ischemic and reperfusion injury of organs (molecular mechanisms, ways of prevention and treatment]. Moscow, RF: Meditsina; 1989. 368 p.
  21. Makeeva AV, Popova TN, Sukhoveeva OV, Panchenko LF. Vliianie guanidinovykh proizvodnykh na aktivnost’ superoksiddismutazy i katalazy pri postishemicheskoi reperfuzii golovnogo mozga u krys [The effect of guanidine derivatives on the activity of superoxide dismutase and catalase in postischemic brain reperfusion in rats]. Neirokhimiia. 2010;(3):245-50.
  22. Barsukov AE, Makhnov NA. Disfunktsiia endoteliia: printsipy diagnostiki i klinicheskaia znachimost’ pri obliteriruiushchem ateroskleroze perifericheskikh arterii [Endothelial dysfunction: the principles of diagnosis and clinical significance for obliterating atherosclerosis of peripheral arteries]. Vestn Khirurgii im II Grekova. 2005;164(1):102-104.
  23. Kashibadze KN, Napashidze IM. Oksidantno-antioksidantnye protsessy v tkaniakh pri ishemicheskom i reperfuzionnom povrezhdeniiakh tonkogo kishechnika [Oxidant-antioxidant processes in tissues in ischemic and reperfusion injuries of the small intestine]. Patol Fiziologiia i Eksperim Terapiia. 2009;(2):19-21.
  24. Manukhina EB, Terekhina OL, Belkina LM, Abramochkin DV, Budanova OP, Mashina SI, i dr. Vazoprotektornyi effekt adaptatsii pri ishemicheskom i reperfuzionnom povrezhdenii serdtsa [Vasoprotective adaptative effect in ischemic and reperfusion injury of the heart]. Patol Fiziologiia i Eksperim Terapiia. 2013;(4):26-31.
  25. Kalinin RE, Suchkov IA, Pshennikov AS. Endotelial’naia disfunktsiia i sposoby ee korrektsii pri obliteriruiushchem ateroskleroze [Endothelial dysfunction and ways of its correction with obliterating atherosclerosis]. Moscow, RF: GEOTAR-Media; 2014. 152 p.
  26. Sergienko VI, Petrosian EA, Onopriev VI, Laipanov KhIKhM. Morfologicheskie izmeneniia legkikh pri modelirovanii i lechenii ishemicheskikh i reperfuzionnykh povrezhdenii konechnosti [Morphological changes in the lungs in the modeling and treatment of ischemic and reperfusion injury of the limb]. Obshch Reanimatologiia. 2006;2(5-6):129-32.
  27. Shcherbak NS, Galagudza MM, Iutkina GIu, Barantsevich ER, Tomson VV, Shliakhto EV. Morfofunktsional’nye izmeneniia piramidnykh neironov razlichnykh polei gippokampa pri ishemicheskom postkonditsionirovanii [Morphofunctional changes of pyramidal neurons of various fields of the hippocampus in ischemic post-conditioning]. Morfologiia. 2013;(3):7-13.
  28. Ioannou A, Dalle Lucca J, Tsokos GC. Immunopatogenesis of ischemia/reperfusion-associated tissue damage. Clin Immunol. 2011 Okt;141(1):3-14.
  29. Ioskevich NN, Zinchuk VV. Prooxidant-antioxidant balance in blood during the surgical treatment of obliterating arterial atherosclerosis in the lower extremities. Rocz Acad Med Bialst. 2004;49:222-26.
  30. Gladwin MT, Kato GJ, Weiner D, Onyekwere OC, Dampier C, Hsu L, et al. Nitric oxide for inhalation in the acute treatment of sickle cell pain crisis: a randomized controlled trial. JAMA. 2011;305(9):893-902.
  31. Rodrigues SF, Granger DN. Role of blood cells in ischemia-reperfusion-induced endothelial barrier failure. Cardiovasc Res. 2010 Jul 15;87(2):291-99.
  32. Gourdin MJ, Bree B, De Kock M. The impact of ischemia-reperfusion on the blood vessel. Eur J Anaesthesiol. 2009 Jul;26(7):537-547.
  33. Proebstl D, Voisin MB, Woodfin A, Whiteford J, D Añquisto F, Jones GE, et al. Pericytes support neutrophil subendothelial cell crawling and breaching of venular walls in vivo. J Exp Med. 2012 Jun 4;209(6):1219-34.
  34. Depre C, Park JY, Shen YT, Zhao X, Qiu H, Yan L, et al. Molecular mechanisms mediating preconditioning following chronic ischemia differ from those in classical second window. Am J Physiol Heart Circ Physiol. 2010 Sep;299(3):H752-62.
  35. Savel’ev VS, Kirienko AI, red. Klinicheskaia khirurgiia [Clinical Surgery ]: nats ruk: v 3 t. Moscow, RF: GEOTAR-Media; 2010;III. 1008 p.
  36. Suchkov IA, Pshennikov AS, Gerasimov AA, Agapov AB, Kamaev AA. Profilaktika restenozov v rekonstruktivnoi khirurgii magistral’nykh arterii [Prevention of restenosis in reconstructive surgery of the main arteries]. Nauka Molodykh - Eruditio Juvenium. 2013;(2):12-19.
  37. Suchkov IA, Kalini RE. Endoteliotropnaia terapiia kak sposob profilaktiki restenoza zony rekonstruktsii i korrektsii disfunktsii endoteliia u patsientov s obliteriruiushchim aterosklerozom arterii nizhnikh konechnostei [Endotheliotropic therapy as a way to prevent restenosis of the zone of reconstruction and correction of endothelial dysfunction in patients with obliterating atherosclerosis of the arteries of the lower extremities]. Kardiologiia i Serdech-Sosud Khirurgiia. 2013;6(5):54-57.
  38. Rautou PE, Vion AC, Amabile N, Chironi G, Simon A, Tedgui A, et al. Microparticles, vascular function and atherothrombosis. Circ Res. 2011 Aug 19;109(5):593-606.
  39. Iakusheva EN, Chernykh IV, Shul’kin AV, Gatsanoga MV. Ishemiia i ishemiia-reperfuziia kak moduliator funktsionirovaniia belka-transportera glikoproteina-R [Ischemia and ischemia-reperfusion as a modulator of the glycoprotein-P protein transporter]. Farmatsiia i Farmakologiia.2015;(5s):124-25
  40. Khiabani HZ, Anvar MD, Kroese AJ, Stranden E. Transcapillary forces and the development of oedema in the lower limb of patients with chronic critical ischemia (CLI). Eur J Vasc Endovasc Surg. 2000;19(6):598-604.
  41. Kozlov IA, Romanov AA, Dzybinskaia EV, Balandiuk AE. Ingaliatsionnyi oksid azota dlia profilaktiki narusheniia arterial’noi oksigenatsii pri revaskuliarizatsii miokarda s iskusstvennym krovoobrashcheniem [Inhalation nitric oxide for the prevention of arterial oxygenation disorders in myocardial revascularization with artificial circulation]. Obshch Reanimatologiia. 2011;7(1):31-35.
  42. Savel’ev VS, Koshkin VM, Kunizhev AS. Kriticheskaia ishemiia, kak sledstvie neadekvatnogo lecheniia bol’nykh khronicheskimi obliteriruiushchimi zabolevaniiami arterii nizhnikh konechnostei na ambulatornom etape [Critical ischemia, as a result of inadequate treatment of patients with chronic obliterating diseases of the arteries of the lower extremities at the outpatient stage]. Angiologiia i Sosudistaia Khirurgiia. 2004;10(1):7-11.
  43. Harkin DW, Barros DSaAA, McCallion K, Hoper M, Halliday MI, Campbell FC. Bactericidal/permeability-increasing protein attenuates systemic inflammation and acute lung injury in porcine lower limb ischemia-reperfusion injury. Ann Surg. 2001 Aug; 234(2):233-44.
  44. Inchina VI, Smirnov LD, Romanov MD, Kokoreva EV, Morozov MIu. Angioprotektivnaia aktivnost’ meksikora pri obliteriruiushchem ateroskleroze arterii nizhnikh konechnostei [Angioprotective activity of mexicore with obliterating atherosclerosis of arteries of lower extremities]. Angiologiia i Sosud. Khirurgiia. 2007;13(3):17-20.
Address for correspondence:
224027, Republic of Belarus,
Brest, Meditsinskaya str., 7,
ME "Brest Regional Hospital",
Vascular Surgery Unit,
Tel.office: +375 162 27-23-64,
E-mail: zasimovich.v@gmail.com,
Vladimir N. Zasimovich
Information about the authors:
Zasimovich V.N., Head of the Vascular Surgery Unit of ME “Brest Regional Hospital”.
Ioskevich N.N., MD, Professor of the Department of Surgical Diseases ¹1 of EE “Grodno State Medical University”.

R.E. KALININ, I.A. SUCHKOV, N.D. MZHAVANADZE, E.A. KLIMENTOVA, S.A. ISAKOV, A.N. RYABKOV, R.M. VORONIN

IMPACT OF INTRINSIC COAGULATION PATHWAY FACTORS ACTIVITY AND HEMOSTATIC MARKERS OF ENDOTHELIAL DYSFUNCTION ON THROMBOTIC COMPLICATIONS IN PATIENTS WITH ATHEROSCLEROTIC PERIPHERAL ARTERIAL DISEASE

FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”, Ryazan
The Russian Federation

Modern vascular surgery has various options for performing open and percutaneous endovascular interventions aimed to treat patients with peripheral arterial disease. One of the most common complications of surgical interventions is thrombosis. According to different authors’ data, postoperative thrombosis develops in 60-90% of cases, especially when performing distal reconstructions. The coagulating blood system plays the main role in the development of thrombotic complications. The effect of the extrinsic pathway of the coagulation cascade on the process of thrombus formation in patients with peripheral atherosclerosis is widely covered and investigated, which facilitated the introduction of a variety of antithrombotic drugs. The intrinsic pathway has always been considered less important. Nowadays, the internal pathway is of considerable interest from the point of view of the development of thromboses and the pathogenesis of inflammatory processes. With a high level of XI, IX factors, the risk of thrombotic complications increases, their newest inhibitors have been developed. XII and VIII factors are not well understood. No less important role in the development of thrombosis belongs to haemostatic markers of endothelial dysfunction, such as von Willebrand factor (WF), plasminogenactivator inhibitor-1 (PAI-1), protein C (PRC) and its endothelial receptor. Changes in hemostatic markers of the endothelial dysfunction in the postoperative period, such as an increased PV and PAI-1 and deficiency of PRC, play a significant role in the development of thrombotic complications and may determine the patency of vascular reconstructions. Further study in this direction permits to establish the predictors of thrombotic complications and to develop algorithms for optimal antithrombotic therapy.

Keywords: atherosclerosis, intrinsic coagulation pathway, hemostatic markers of endothelial dysfunction, thrombotic complications, antithrombotic therapy
p. 643-654 of the original issue
References
  1. Dua A, Lee CJ. Epidemiology of Peripheral Arterial Disease and Critical Limb Ischemia. Tech Vasc Interv Radiol. 2016 Jun;19(2):91-95. doi: 10.1053/j.tvir.2016.04.001.
  2. Sigvant B, Lundin F, Wahlberg E. The Risk of Disease Progression in Peripheral Arterial Disease is Higher than Expected: A Meta-Analysis of Mortality and Disease Progression in Peripheral Arterial Disease. Eur J Vasc Endovasc Surg. 2016 Mar;51(3):395-403. doi: 10.1016/j.ejvs.2015.10.022.
  3. Ye W, Liu CW, Ricco JB, Mani K, Zeng R, Jiang J. Early and late outcomes of percutaneous treatment of TransAtlantic Inter-Society Consensus class C and D aorto-iliac lesions. J Vasc Surg. 2011 Jun;53(6):1728-37. doi: 10.1016/j.jvs.2011.02.005.
  4. Kalinin RE, Suchkov IA, Pshennikov AS, Slepnev AA. Effektivnost’ L-arginina v lechenii ateroskleroza arterii nizhnikh konechnostei i profilaktike restenoza zony rekonstruktsii [Efficiency of L-arginine in the treatment of atherosclerosis of the arteries of the lower extremities and the prevention of restenosis of the reconstruction zone]. Vestn Ivan Med Akad. 2013;18(2):18-21.
  5. Asher E, Pokrovskii AV, red. Sosudistaia khirurgiia po Khaimovichu [Vascular surgery in the manner of Haimovich]: v 2 t. T. 1 = Haimovici’s Vascular Surgery. 2-e izd. (el.). Moscow, RF: BINOM. Laboratoriia znanii; 2012. 646 p.
  6. Pokrovskii AV. Klinicheskaia angiologiia [Clinical Angiology]: ruk v 2 t. Moscow, RF: Meditsina; 2004;2. 203 p.
  7. Suchkov IA, Pshennikov AS, Gerasimov AA, Agapov AB, Kamaev AA. Profilaktika restenoza v rekonstruktivnoi khirurgii magistral’nykh arterii [Prevention of restenosis in reconstructive surgery of the main arteries]. Nauka Molodykh - Eruditio Juvenium. 2013;(2):12-19.
  8. Kuijpers MJ, van der Meijden PE, Feijge MA, Mattheij NJ, May F, Govers-Riemslag J, et al. Factor XII regulates the pathological process of thrombus formation on ruptured plaques. Arterioscler Thromb Vasc Biol. 2014 Aug;34(8):1674-80. doi: 10.1161/ATVBAHA.114.303315.
  9. Dahlbäck B. Blood coagulation. Lancet. 2000 6 May;355(9215):1627-32. doi: 10.1016/S0140-6736(00)02225-X.
  10. Cushman M, O’Meara ES, Folsom AR, Heckbert SR. Coagulation factors IX through XIII and the risk of future venous thrombosis: the Longitudinal Investigation of Thromboembolism Etiology. Blood. 2009 Oct 1;114(14):2878-83. doi: 10.1182/blood-2009-05-219915.
  11. Delvaeye M, Conway EM. Coagulation and innate immune responses: can we view them separately? Blood. 2009 Sep 17;114(12):2367-74. doi: 10.1182/blood-2009-05-199208.
  12. Kuhli C, Scharrer I, Koch F, Ohrloff C, Hattenbach LO. Factor XII deficiency: a thrombophilic risk factor for retinal vein occlusion. Am J Ophthalmol. 2004 Mar;137(3):459-64.
  13. Girolami A, Randi ML, Gavasso S, Lombardi AM, Spiezia F. The occasional venous thromboses seen in patients with severe (homozygous) FXII deficiency are probably due to associated risk factors: a study of prevalence in 21 patients and review of the literature. J Thromb Thrombolysis. 2004 Apr;17(2):139-43.
  14. Zeerleder S, Schloesser M, Redondo M, Wuillemin WA, Engel W, Furlan M, et al. Reevaluation of the incidence of thromboembolic complications in congenital factor XII deficiency–a study on 73 subjects from 14 Swiss families. Thromb Haemost. 1999 Oct;82(4):1240-46.
  15. Yazdani-Biuki B, Krippl P, Brickmann K, Fuerst F, Langsenlehner U, Paulweber B, et al. The functional promoter polymorphism of the coagulation factor XII gene is not associated with peripheral arterial disease. Angiology. 2010 Feb;61(2):211-15. doi: 10.1177/0003319709337305.
  16. Kleinschnitz C, Stoll G, Bendszus M, Schuh K, Pauer HU, Burfeind P, et al. Targeting coagulation factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis. J Exp Med. 2006 Mar 20;203(3):513-18. doi: 10.1084/jem.20052458.
  17. Von dem Borne PA, Cox LM, Bouma BN. Factor XI enhances fibrin generation and inhibits fibrinolysis in a coagulation model initiated by surface-coated tissue factor. Blood Coagul Fibrinolysis. 2006 Jun;17(4):251-57.
  18. Chan JCY, Ganopolsky JG, Cornelissen I, Suckow MA, Sandoval-Cooper MJ, Brown EC, et al. The characterization of mice with a targeted combined deficiency of protein C and factor XI. Am J Pathol. 2001 Feb;158(2):469-79. doi: 10.1016/S0002-9440(10)63989-2.
  19. Minnema MC, Peters RJ, de Winter R, Lubbers YP, Barzegar S, Bauer KA, et al. Activation of clotting factors XI and IX in patients with acute myocardial infarction. Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2489-93.
  20. Yang DT, Flanders MM, Kim H, Rodgers GM. Elevated factor XI activity levels are associated with an increased odds ratio for cerebrovascular events. Am J Clin Pathol. 2006 Sep;126(3):411-15.
  21. Smith LM 2nd, Orwat MJ, Hu Z, Han W, Wang C, Rossi KA, et al. Novel phenylalanine derived diamides as Factor XIa inhibitors. Bioorg Med Chem Lett. 2016 Jan 15;26(2):472-78. doi: 10.1016/j.bmcl.2015.11.089.
  22. Spanier TB, Oz MC, Madigan JD, Rose EA, Stern DM, Nowygrod R, et al. Selective anticoagulation with active site blocked factor IXa in synthetic patch vascular repair results in decreased blood loss and operative time. ASAIO J. 1997 Sep-Oct;43(5):M526-30.
  23. Rosendaal FR, Briët E, Stibbe J, van Herpen G, Leuven JA, Hofman A, et al. Haemophilia protects against ischaemic heart disease: a study of risk factors. Br J Haematol. 1990 Aug;75(4):525-30.
  24. Heikal NM, Murphy KK, Crist RA, Wilson AR, Rodgers GM, Smock KJ. Elevated factor IX activity is associated with an increased odds ratio for both arterial and venous thrombotic events. Am J Clin Pathol. 2013 Nov;140(5):680-85. doi: 10.1309/AJCPAGOR4Q2IIKUG.
  25. Howard EL, Becker KC, Rusconi CP, Becker RC. Factor IXa inhibitors as novel anticoagulants. Arterioscler Thromb Vasc Biol. 2007 Apr;27(4):722-27.
  26. Zanolini D, Merlin S, Feola M, Ranaldo G, Amoruso A, Gaidano G, et al. Extrahepatic sources of factor VIII potentially contribute to the coagulation cascade correcting the bleeding phenotype of mice with hemophilia A. Haematologica. 2015 Jul;100(7):881-92. doi: 10.3324/haematol.2014.123117.
  27. Lijfering WM, Veeger NJ, Brouwer JL, van der Meer J. The risk of venous and arterial thrombosis in hyperhomocysteinemic subjects may be a result of elevated factor VIII levels. Haematologica. 2007 Dec;92(12):1703-6.
  28. Jacquemin M, Stassen JM, Saint-Remy JM, Verhamme P, Lavend’homme R, VanderElst L, et al. A human monoclonal antibody inhibiting partially factor VIII activity reduces thrombus growth in baboons. J Thromb Haemost. 2009 Mar;7(3):429-37. doi: 10.1111/j.1538-7836.2008.03271.x.
  29. Jenkins PV, Rawley O, Smith OP, O’Donnell JS. Elevated factor VIII levels and risk of venous thrombosis. Br J Haematol. 2012 Jun;157(6):653-63. doi: 10.1111/j.1365-2141.2012.09134.x.
  30. Cortellaro M, Boschetti C, Cofrancesco E, Zanussi C, Catalano M, de Gaetano G, et al. The PLAT Study: hemostatic function in relation to atherothrombotic ischemic events in vascular disease patients. Arterioscler Thromb. 1992; 12(9):1063-70.
  31. Sartori M, Conti E, Favaretto E, Frascaro M, Legnani C, Palareti G. Thrombotic risk factors and cardiovascular events after endovascular intervention for peripheral arterial disease. Thrombotic risk factors and cardiovascular events after endovascular intervention for peripheral arterial disease. Eur J Vasc Endovasc Surg. 2011 Dec;42(6):817-23. doi: 10.1016/j.ejvs.2011.08.016.
  32. Babichev AV. Rol’ endoteliia v mekhanizmakh gemostaza [The role of the endothelium in the mechanisms of hemostasis]. Pediatr. 2013; 4(1):122-27.
  33. Yau JW, Teoh H, Verma S. Endothelial cell control of thrombosis. BMC Cardiovasc Disord. 2015 Oct 19;15:130. doi: 10.1186/s12872-015-0124-z.
  34. Likhacheva EA, Polyanskaya TYu., Zorenko VYu. Mezhdunarodnyi opyt diagnostiki bolezni Villebranda [The diagnosis and treatment of von Willebrand’s disease: International experience]. Gematologiia i Tranfuziologiia. 2013; 58(4):45-49.
  35. Sanders YV, Eikenboom J, de Wee EM, van der Bom JG, Cnossen MH, Degenaar-Dujardin ME, et al. Reduced prevalence of arterial thrombosis in von Willebrand disease. J Thromb Haemost. 2013 May;11(5):845-54. doi: 10.1111/jth.
  36. Du Y, Wang F, Qi H, Ding H, Hou L, Gao Q, et al. Effects of percutaneous lower-extremity arterial interventions on endothelial function and inflammation response in patients with both type 2 diabetes and lower-extremity peripheral arterial disease. Int J Clin Exp Pathol. 2015;8(7):8115-21.
  37. Woodburn KR, Rumley A, Lowe GD, Pollock JG. Fibrinogen and markers of fibrinolysis and endothelial damage following resolution of critical limb ischaemia. Eur J Vasc Endovasc Surg. 1995 Oct;10(3):272-78. doi: 10.1016/S1078-5884(05)80042-5.
  38. Yang H, Xu JX, Kong XZ, Ren ZG, Xia ZY, Qu HQ, et al. Relations between plasma von Willebrand factor or endothelin-1 and restenosis following carotid artery stenting. Med Princ Pract. 2012;21:538-42. doi. 10.1159/000337940.
  39. De Meyer SF, Stoll G, Wagner DD, Kleinschnitz C. von Willebrand factor: an emerging target in stroke therapy. Stroke. 2012 Feb;43(2):599-606. doi: 10.1161/STROKEAHA.111.628867.
  40. Yildiz SY, Kuru P, Oner ET, Agirbasli M. Functional stability of plasminogen activator inhibitor-1. Sci World J. 2014;2014:858293. doi: 10.1155/2014/858293.
  41. Nikolopoulos GK, Bagos PG, Tsangaris I, Tsiara CG, Kopterides P, Vaiopoulos A, et al. The association between plasminogen activator inhibitor type 1 (PAI-1) levels, PAI-1 4G/5G polymorphism, and myocardial infarction: a Mendelian randomization meta-analysis. Clin Chem Lab Med. 2014 Jul;52(7):937-50. doi: 10.1515/cclm-2013-1124.
  42. Mota AP, de Castro Santos ME, Lima e Silva Fd, de Carvalho Schachnik NC, de Oliveira Sousa M, das Gracas Carvalho M. Hypercoagulability markers in patients with peripheral arterial disease: association to ankle-brachial index. Angiology. 2009 Oct-Nov;60(5):529-35. doi: 10.1177/0003319708325444.
  43. Björck M, Lepkowska Eriksson M, Bylockd A, Steuer J, Wanhainen A, Carlsson BCL, et al. Plasminogen activator inhibitor-1 levels and activity decrease after intervention in patients with critical limb ischaemia. Eur J Vasc Endovasc Surg. 2013 Aug;46(2):214-22.
  44. Rayt HS, Merker L, Davies RS. Coagulation, fibrinolysis, and platelet activation following open surgical or percutaneous angioplasty revascularization for symptomatic lower limb chronic ischemia. Vasc Endovasc Surg. 2016 Apr;50(3):193-201. doi: 10.1177/1538574416638759.
  45. Kotschy D, Kotschy M, Socha P, Masłowski L, Kwapisz J, Żuk N, et al. Selected endothelial hemostatic markers in patients with peripheral arterial disease after endovascular revascularization and restenosis formation. Postepy Hig Med Dosw (Online). 2015 Aug 11;69:905-12. [Article in Polish]
  46. Makatsariia AD, Abramian RA, Khizroeva DKh, Abramian GR, Abramian RR. Sistema proteina C i patologicheskie sostoianiia organizma, v chastnosti v akusherskoi praktike [Protein C system and pathological conditions of the body, in particular in obstetrical practice]. Med Nauka Armenii NAN RA. 2013;LIII(4):8-20.
  47. Mahmoodi BK, Brouwer JL, Veeger NJ, van der Meer J. Hereditary deficiency of protein C or protein S confers increased risk of arterial thromboembolic events at a young age: results from a large family cohort study. Circulation. 2008 Oct 14;118(16):1659-67. doi: 10.1161/CIRCULATIONAHA.108.780759.
  48. Komai H, Juri M. Impact of reduced endogenous anti-coagulation protein activity on vascular events of peripheral arterial disease. Int Angiol. 2009 Apr;28(2):138-43.
  49. Komai H, Shindo S, Sato M, Ogino H. Reduced protein c activity might be associated with progression of peripheral arterial disease. Angiology. 2015 Jul;66(6):584-87. doi: 10.1177/0003319714544946.
  50. Curi MA, Skelly CL, Baldwin ZK, Woo DH, Baron JM, Desai TR, et al. Long-term outcome of infrainguinal bypass grafting in patients with serologically proven hypercoagulability. J Vasc Surg. 2003 Feb;37(2):301-6.
Address for correspondence:
390026, Russian Federation,
Ryazan, Vyisokovoltnaya str., 9,
FSBEE HE “Ryazan State Medical University
named after Academician I.P. Pavlov”
Department of Cardiovascular,
X-ray Endovascular, Operative Surgery
and Topographic Anatomy,
tel.: +7 4912 46-08-03,
e-mail: Suchkov_med@mail.ru
Igor A. Suchkov
Information about the authors:
Kalinin R.E., MD, Professor, Rector, Head of the Department of Cardiovascular, X-ray Endovascular, Operative Surgery and Topographic Anatomy of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Suchkov I.A., MD, Associate Professor, Vice-rector for research and innovative development, Professor of the Department of Cardiovascular, X-ray Endovascular, Operative Surgery and Topographic Anatomy of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Mzhavanadze N.D., PhD, Assistant of the Department of Cardiovascular, X-ray Endovascular, Operative Surgery and Topographic Anatomy of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Klimentova E.A., Post-Graduate of the Department of Cardiovascular, X-ray Endovascular, Operative Surgery and Topographic Anatomy of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Isakov S.A., MD, Professor of the Department of Dermato-Venerology of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Ryabkov A.N., MD, Associate Professor of the Department of Pharmacology with the Course of Pharmacy of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.
Voronin R.M., MD, Professor of the Department of Mobilization Training of Public Health and Disaster Medicine of FSBEE HE “Ryazan State Medical University named after Academician I.P. Pavlov”.

CASE REPORTS

V. SIHOTSKÝ 1,2, P. BEREK 1,2, I. KOPOLOVETS 1,4, M. KUBÍKOVÁ 1,2, M. TOMEČKO 1, M. STANČÁKOVÁ 2,3, I. DRAHOVSKÁ 2,3, M. FRANKOVIČOVÁ 1,2

AORTOBIFEMORAL GRAFT INFECTION: POSSIBILITIES OF TREATMENT

Clinic of Vascular Surgery VÚSCH a.s. 1,
Faculty of Medicine PJ Šafárik 2,
University Hospital of L. Pasteur 3, Košice,
Slovakia
DSME “Uzhgorod National University” 4, Uzhgorod,
Ukraine

Authors describe two case reports of patients with infected aortobifemoral graft. Both were treated by total graft excision. In the first case they decided for extra anatomical revascularization of lower extremities after total graft excision, because of virulent infection (Staphylococcus aureus and G+ bacteries) and graft enteral fistula. They performed axilobifemoral bypass grafting. In the second case, where infection was not so virulent (Staphylococcus epidermidis) they decided for in situ reconstruction with desobliterated native aorta, iliac arteries and femoral vein. Both patients are now without signs of infection and they can walk without claudication pain. Graft infection is one of the most serious complications of aortobifemoral bypass surgery therefore the prevention of infection is very important. It is important to keep all rules of asepsis and antisepsis during surgery. Treatment of graft infection is based on intravenously administered antibiotics and excision of infected graft. Limb revascularization after graft removal can be provided by extra anatomical bypass or in situ arterial reconstruction.

Keywords: infection, aortobifemoralgraft, revascularization, extra anatomical bypass
p. 655-661 of the original issue
References
  1. Back Martin R. Chapter 42: Local Complications: Graft Infection. In: Cronenwett JL, Johnston KW. Rutherford’s Vascular Surgery. 8-th ed. Philadelphia, PA: Saunders/Elsevier; 2014. ð. 654-72.e2.
  2. O’Hara PJ, Hertzer NR, Beven EG, Krajewski LP. Surgical management of infected abdominal aortic grafts: review of a 25-year experience. J Vasc Surg. 1986 May;3(5):725-31.
  3. Campbell WB, Tambeur LJ, Geens VR. Local complications after arterial bypass grafting. Ann R Coll Surg Engl. 1994 Mar;76(2):127-31.
  4. Campbell WB, Tambeur LJ, Geens VR. Local complications after arterial bypass grafting. Ann R Coll Surg Engl. 1994 Mar;76(2):127-31.
  5. Maltezou HC, Giamarellou H. Community-acquired methicillin-resistant Staphylococcus aureus infections. Int J Antimicrob Agents. 2006 Feb;27(2):87-96.
  6. Bergamini TM, Bandyk DF, Govostis D, Vetsch R, Towne JB. Identification of Staphylococcus epidermidis vascular graft infections: a comparison of culture techniques. J Vasc Surg. 1989 May;9(5):665-70.
  7. Bandyk DF, Novotney ML, Back MR, Johnson BL, Schmacht DC. Expanded application of in situ replacement for prosthetic graft infection. J Vasc Surg. 2001 Sep;34(3):411-19; discussion 419-20.
  8. Clagett GP, Bowers BL, Lopez-Viego MA, Rossi MB, Valentine RJ, Myers SI, et al. Creation of a neo-aortoiliac system from lower extremity deep and superficial veins. Ann Surg. 1993 Sep;218(3):239-48; discussion 248-49.
  9. Kieffer E, Gomes D, Chiche L, Fléron MH, Koskas F, Bahnini A. Allograft replacement for infrarenal aortic graft infection: early and late results in 179 patients. J Vasc Surg. 2004 May;39(5):1009-17.
  10. Bisdas T, Bredt M, Pichlmaier M, Aper T, Wilhelmi M, Bisdas S, et al. Eight-year experience with cryopreserved arterial homografts for the in situ reconstruction of abdominal aortic infections. J Vasc Surg. 2010 Aug;52(2):323-30. doi: 10.1016/j.jvs.2010.02.277.
  11. Oderich GS, Bower TC, Hofer J, Kalra M, Duncan AA, Wilson JW, et al. In situ rifampin-soaked grafts with omental coverage and antibiotic suppression are durable with low reinfection rates in patients with aortic graft enteric erosion or fistula. J Vasc Surg. 2011 Jan;53(1):99-106, 107.e1-7; discussion 106-7. doi: 10.1016/j.jvs.2010.08.018.
Address for correspondence:
88000, Ukraine, Uzhgorod,
Universitetskaya st., 10,
Uzhgorod National University
Tel.: +380 50 558 82 11
E-mail: i.kopolovets@gmail.com
Ivan I. Kopolovets
Information about the authors:
Sihotský V., PhD, Vascular Surgeon, Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute and P.J. Šafýrik´s University, Košice, Slovakia. Deputy of the Head of the Department for Pedagogics.
Berek P., PhD, Vascular Surgeon, Deputy of the Head of the Department for Treatment Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute and P.J. Šafýrik´s University, Košice, Slovakia.
Kopolovets I., PhD, Researcher of DSME "Uzhgorod National University", Uzhgorod, Ukraine. Vascular surgeon, Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute, Košice, Slovakia.
Kubikový M., PhD, Vascular Surgeon, Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute and P.J. Šafýrik´s University, Košice, Slovakia.
Tomečko M., PhD, Vascular Surgeon, Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute and P.J. Šafýrik´s University, Košice, Slovakia.
Stančýkový M., General Surgeon, I. Surgical Clinic, University Hospital of J. Pasteur and P.J. Šafýrik´s University, Košice, Slovakia.
Drahovský I., PhD, Head of the Department, I. Clinic of Radiodiagnosics and Imagine Techniques, University Hospital of J. Pasteur and P.J. Šafýrik´s University, Košice, Slovakia
Frankovičový Ì., PhD, Professor, Head of the Department, Clinic of Vascular Surgery, East Slovakian Cardiovascular Institute and P.J. Šafýrik´s University, Košice, Slovakia.

EXCHANGE OF EXPERIENCE

O.I. OKHOTNIKOV, M.V. YAKOVLEVA, S.N. GRIGORIEV

PERCUTANEOUS TRANSHEPATIC EXTRACTION OF ENDOBILIARY FOREIGN BODIES

BME “Kursk Regional Clinical Hospital” 1,
FSBEE HE “Kursk State Medical University” 2, Kursk
The Russian Federation

Objective. To present the own experience of removing foreign bodies from the biliary tree while performing mini-invasive antegrade endobiliary interventions.
Methods. We observed 11 patients with endobiliary foreign bodies (fragments of a 0.035 «metal conductor, 5 Fr manipulation catheter, 10 Fr endobiliary drainage, 9 mm self-expanding stent, incorrectly installed self-expanding 10 mm stent, blocked uncoated self-expanding stent 8 mm), that were caught in the bile ducts during the antegrade transhepatic mini-invasive X-ray surgical interventions. Foreign bodies entered the biliary ducts directly during transhepatic cholangiostomy, as well as during manipulations performed after the initial drainage (drainage replacement, endobiliary stenting).
Foreign bodies were removed by antegrade access. Manipulations were carried out through the lumen of the vascular introducer 6-10Fr, established instead of the cholangiostomical drainage. Percutaneous transhepatic access with a diameter of 28 Fr was used to extract self-expanding stents; in one case a retrograde endoscopic access was used.
Results. Antegrade transhepatic access successfully removed 10 of 11 foreign bodies. Fragments of conductors and manipulative catheters were extracted with endoscopic forceps and an endoscopic basket through the lumen of the commensurate introducer. The drainage fragment was removed by antegrade asses by endoscopic forceps after fixing it to the end face of the introducer 10 Fr. An incorrectly installed self-expanding stent, as well as 2 irreversibly blocked stents, were removed by antegrade transhepatic access under visual control after telescopic dilatation of the puncture canal into the gall-tree to 28 Fr. One fragmented, self-expanding, covered stent was removed endoscopically. There were no complications related to the creation of access for the extraction of foreign bodies, as well as to the technique of their extraction.
Conclusions. Minimally invasive percutaneous transhepatic access seems to be an alternative to open surgical access to the gall-tree in case of extracting of large foreign bodies, in particular - irreversibly blocked endobiliary stents.

Keywords: biliary tract, foreign bodies, antegradecholangiostomy, endobiliary stent, endobiliary interventions
p. 662-668 of the original issue
References
  1. Woodhouse JB, Uberoi R. Techniques for intravascular foreign body retrieval. Cardiovasc Intervent Radiol. 2013 Aug;36(4):888-97. doi: 10.1007/s00270-012-0488-8.
  2. Floridi C, Nocchi-Cardim L, De Chiara M, Ierardi AM, Carrafiello G. Intravascular foreign bodies: what the radiologist needs to know. Semin Ultrasound CT MR. 2015 Feb;36(1):73-79. doi: 10.1053/j.sult.2014.11.001.
  3. Laroia ST, Morales SA, Rowberry T. A Novel Technique for the Retrieval of a “Vanished” Nephrostomy Tube. Cardiovasc Intervent Radiol. 2015 Oct;38(5):1373-75. doi: 10.1007/s00270-014-1048-1.
  4. Cazzato RL, Garnon J, Ramamurthy N, Tsoumakidou G, Caudrelier J, Thénint MA, et al. Percutaneous management of accidentally retained foreign bodies during image-guided non-vascular procedures: novel technique using a large-bore biopsy system. Cardiovasc Intervent Radiol. 2016 Jul;39(7):1050-56. doi: 10.1007/s00270-016-1302-9.
  5. Ray S, Bhattacharya SP. Endoclip migration into the common bile duct with stone formation: a rare complication after laparoscopic cholecystectomy. JSLS. 2013 Apr-Jun;17(2):330-32. doi: 10.4293/108680813X13654754534350.
  6. Van Steenbergen W, Lecluyse K, Maleux G, Pirenne J. Successful percutaneous cholangioscopic extraction of vascular coils that had eroded into the bile duct after liver transplantation. Endoscopy. 2007 Feb;39(Suppl 1):E210-11. doi: 10.1055/s-2007-966314.
  7. Ghalim F, Alatawi A, Leblanc S, Vienne A, Gaudric M, Chaussade S, et al. Endoscopic retrograde cholangioscopic removal of migrated vascular coils from the common bile duct. Clin Res Hepatol Gastroenterol. 2014 Apr;38(2):e31-32. doi: 10.1016/j.clinre.2013.08.007.
  8. Liatsos C, Kyriakos N, Anthopoulos G, Galanopoulos M, Kalafatis E, Mavrogiannis C. An alternative method of endoscopic retrieval of a proximally migrated biliary plastic stent using a “sphincterotome hooking the stent” technique. Endoscopy. 2015;47(Suppl 1) UCTN:E64-65. doi: 10.1055/s-0034-1391242.
  9. Sejpal DV, Vamadevan AS, Trindade AJ. Removal of an embedded, migrated plastic biliary stent with the use of cholangioscopy. Gastrointest Endosc. 2015;81(6):1482-83. doi: 10.1016/j.gie.2014.12.015.
  10. Ikeura T, Shimatani M, Takaoka M, Masuda M, Hayashi K, Okazaki K. Reintervention for an occluded metal stent under the guidance of peroral direct cholangioscopy by using an ultra-slim enteroscope. Gastrointest Endosc. 2015 Jan;81(1):226-27. doi: 10.1016/j.gie.2014.04.037.
  11. Franzini TA, Moura RN, de Moura EG. Advances in Therapeutic Cholangioscopy. Gastroenterol Res Pract. 2016;2016:5249152. doi: 10.1155/2016/5249152.
  12. Singh MK, Kinder KZ, Braverman SE. Transhepatic Management of a Migrated Intraductal Surgical Clip after Cholecystectomy and Gastrectomy. J Vasc Interv Radiol. 2015 Dec;26(12):1866. doi: 10.1016/j.jvir.2015.08.025.
  13. Zurera LJ, Canis M, Espejo JJ, García-Revillo J, Delgado F, Benito A. Practical aspects in the percutaneous extraction of foreign bodies using a Goose-Neck Snar. Radiologia. 2007 Jul-Aug;49(4):247-54. [Article in Spanish]
  14. Okhotnikov OI, Grigor’ev SN, Iakovleva MV. Opyt 100 uspeshnykh antegradnykh transpechenochnykh kontaktnykh kholedokholitotripsii v lechenii endoskopicheski trudnogo kholedokholitiaza [Experience of 100 successful antegrade transhepatic contact choledocholithotripsies in the treatment of endoscopically difficult choledocholithiasis]. Diagnost i Intervents Radiologiia. 2011;5(1):67-72.
Address for correspondence:
305007, Russian Federation,
Kursk, Sumskaya str., 45-a,
BME “Kursk Regional Clinical Hospital”,
Unit of X-ray Surgical Methods
of Diagnosis and Treatment ¹2,
tel.: +7 4712 35-93-30
e-mail: oleg_okhotnikov@ mail.ru,
Oleg I. Okhotnikov
Information about the authors:
Okhotnikov O.I., MD, Professor, Head of the Unit of X-ray Surgical Methods of Diagnosis and Treatment ¹2 of BME “Kursk Regional Clinical Hospital”, Professor of the Department of Radiation Diagnostics and Therapy of FSBEE HE “Kursk State Medical University».
Yakovleva M.V., PhD, Associate Professor of the Department of Surgical Diseases of FSBEE HE “Kursk State Medical University», Physician of the Unit of X-ray Surgical Methods of Diagnosis and Treatment ¹2 of BME “Kursk Regional Clinical Hospital”.
Grigoriev S.N., PhD, Head of the Unit of Purulent Surgery, Physician of the Unit of X-ray Surgical Methods of Diagnosis and Treatment ¹2 of BME “Kursk Regional Clinical Hospital”.
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