CC BY
39
Study of immunoglobulin concentrations depending on duration of the disease revealed that IgA and IgG levels were significantly reduced compared to the control group. And it was established that the long duration of the inflammatory process leads to significant decline in the local humoral immunity. This may indicate marked in-
In study oflocal immunity, depending on the localization of inflammation of urogenital organs showed not authentic increase level of IgA and IgG in patients with anterior urethritis with more pronounced rise of IgA. Indicators of IgG were significantly higher than the control numbers ofpatients with complicated forms of urogenital chlamydiosis, respectively, the ratio of IgG/IgA increased. This may indicate that the strain oflocal humoral immunity and the ability ofmicroorganism has to fight with the existing infectious process.
Thus, the results justifies that the state ofthe local humoral immunity in men with inflammatory diseases of the genitourinary sys-
hibition of the ability of immune cells lining the urethra to the local synthesis of immunoglobulins and absence of an adequate level of compensatory immunodiffusion degree of peripheral blood flow associated with the development of the state of secondary immunodeficiency due to the long-term persistent infection.
tem caused by urogenital chlamydiosis and reproductive disorders are accompanied by changes in the concentration of immunoglobulins in different directions, the degree of impairment depends on the duration of the disease and the prevalence of inflammation in the urogenital tract. According to indicators of the local immune response, one can judge about the state of the general immune response, as there is a close relationship between them.
These data must be considered in the development of immunotherapy which is aimed to the activation of humoral immunity and leucocytes that they have phagocytic activity.
Table 4. - Comparative characteristics of local humoral immunity, depending on localization of process
Index Control group Anterior urethritis Total urethritis
Ig A, mg/% 87 ± 9,4 119 ± 4,4 74 ± 9,7
IgMmg/% 53 ± 6,2 55 ± 5,6 38 ± 7,9
Ig G, mg/% 1021±82 1105 ±91 1322±78
References:
1. Adaskevich V. P. Sexual transmitted Infections. Manual for doctors. - M.: Med. Book, - 2002. - P. 416 c.
2. Glazkova L. K., Alimov O. E. Practical aspects of persistant chlamydiosis infection.//STI. - 1999. -№ 4. - P. 29-34.
3. Zalyalieva M. V. The estimation methods of subpopulation of lymphocytes of peripheral blood in man. Method. recommendations. -Tashkent, -2004. - P. 15.
4. Ismailova G. A., Saidkulov A. M., Babaeva M. The index of interferon status in patients with herpetic infection in the process of therapy of antiviral and with preparation and immunomodulators.//Theoretical and clinical medicine. -2003. - № 1. - P. 76-79.
5. Pozdnyak A. L., Lobzin Yu. V., Sidorchuk S. N. and others. Chlamydiosis affects of respiratory tract//Epidemiology and infectious disease. -2002. -№ 5. - P. 46-53.
6. Mastibekov N., Talipov F. M., Shukurov I. I. Biological statistics: Textbook for undergraduates ofmedical institutes. - Tashkent, - 1998. - P. 52.
7. Porsokhonova D. F., Yuldashev K. A. The analysis of some factors, promoting the increase of growth of STI, the results of anonymous survey.//The news of dermatology and venereology - 2002. - № 2. - P. 145-146.
8. Soliyev S. T., Porsokhonova D. F., Kurbanov D. D., Alimov B. D. The importance of chlamydiosis and ureamycoplasmosis infection in the development of reproductive and visceral disorders.//Med. journal of Uzbekistan. - 2004. - № 3. - P. 117-119.
9. Sulakadze Z. M. Development of the new methods of treatment in patients with chronic diseases of urogenital tract with chlamydial and ureaplasmic etiology with considering ofmicrobiocenosis ofintestine. Abstract. dissert.... cand. med. sciences, - Tashkent, - 2005. - P. 18.
Khadjibaev Abdukhakim Muminovich, Phd, ScD, Professor Republic Research Center of Emergency Medicine, Tashkent,
Uzbekistan, Director General E-mail: uzbek_ems@uzsci.net Alidjanov Fotih Bakievich, PhD, ScD, Professor 2-Tashkent Institute for Post-graduate Education of Doctors, Uzbekistan
Rizaev Kamal Saidakbarovich, PhD Republic Research Center of Emergency Medicine, Tashkent, Uzbekistan, Deputy Director General E-mail: rizaev@rambler.ru Makhamadaminov A. G., PhD 2-Tashkent Institute for Post-graduate Education of Doctors, Uzbekistan
Pulmonary ventilation disturbances in patients with pancreatogenic toxemia (literary review)
Abstract: Steady increasing of acute pancreatitis (AP), especially its destructive forms, significant difficulties at its recognition and a big percentage of diagnostic mistakes, disputability in treatment tactics issues, high mortality determine the necessity
of further study some etiopathogenetic aspects of this illness. The main reasons of lethality at acute destructive pancreatitis (ADP) are uncorrected endotoxicosis and multiple failure.
As die result of penetration into blood and lymph pancreatic ferments, toxic polypeptides, biogenic amines and the other products of ferment autoagression and also due to activation kallikrein- kinin, plasmin and thrombin blood system a severe level of toxemia is developed, significant disorders of blood and lymph micro-circulation, morpho-functional changes of organs of different anatomico-physiological systems.
According to some authors view broncho-pulmonary complications (BPC) are determined in y 15-55% patients with AP clinics. At ADP complicated by spread peritonitis pancreatogenic acute pulmonary failure is formed due to influence of pancreatic enzymes on pulmonary capillaries and breathing disorder is observed in each second patient, sometimes being a reason of the death. So, further deep study of respiratory apparatus functional condition in different periods of pancreatogenic toxemia in patients with ADP is an actual task of emergency pancreatology. It will allow to determine some pathogenic mechanisms ofviolation of respiratory apparatus functions, to work out on their base effective treatment-preventing procedures for reducing the frequency of BPC in total and to improve the prognosis of performing surgical treatment of patients with acute destructive pancreatitis.
Acute pancreatitis (AP) is destructive lesion ofpancreas parenchyma, surrounding tissues and organs, different by etiology and particularly autolytic by nature initially. These lesions can progress with or without the necrosis development joining infection, to recur within one pathologic condition [43; 44; 50; 59].
AP morbidity increases year by year. According to A. S. Er-molov, V. S. Saveliev and Yu. L. Shevchenko data — AP makes up 10-12% from all emergency cases in surgery and has the third place in the structure of acute morbidities of the abdominal cavity after acute appendicitis and cholecystitis [29; 31]. Meanwhile pu-rulent-necrotic forms of destructive pancreatitis (infectious necrosis of pancreas, septic phlegmona of retroperitoneal fat, secondary purulent pancreatogenic peritonitis, abscess of different locations) followed by high mortality occur in up to 30-40% observations [2; 17; 20; 31; 49]. Steady rise ofAP morbidity, significant difficulties at its recognition and the high percentage of diagnostic mistakes, disputes in treatment tactics, high mortality determine the further study of some etio-pathogenetic aspects of this disease [2; 28; 38].
The main reasons of mortality at the acute destructive pancreatitis are uncorrectable endotoxicosis and multiple organ failure [2; 19; 20; 33; 35; 45; 59; 61]. Endotoxicosis at the beginning of the morbidity is determined by the development of early post-necrotic aseptic complications and is followed by aseptic system inflammatory reaction of the organ, due to alteration of the tissues of noninfectious nature and the development of early endogenic intoxication (EI), the base of which is enzymatic and aseptic resorbtive- tissue toxemia. In the second period infectious- inflammatory alteration and septic reaction of tissues, the development of early or late El the base ofwhich is infectious-resorptive tissue or bacterial toxemia [2; 5; 6; 7; 8; 10; 11; 32; 49; 60].
It is necessary to point that pancreatogenic toxemia, first, is followed by the deep disorders of the central and peripheral hemodynamics [3; 20; 25; 35; 37]. Meanwhile lysis of venule's walls occurs and it leads to extensive hemorrhage and the rapid spread of hemor-rhagic exudation with the further developing peritonitis. There is an enhancement of the local disorders of micro- circulation, increasing of edema and forming of disseminated micro-thrombosis in the micro-circulatory and lymphatic course [2; 19; 39; 40; 41; 49; 59]. Due to penetration of pancreatic ferments, toxic polypeptides, biogenic amines and other products of ferment auto aggression into blood and lymph and also due to activating kallikrein-kinin, plasma and throm-botic blood systems a severe level of toxemia is developed, disorders of blood and lymph micro-circulation [2* 9; 10; 20; 23; 37; 42; 49; 61].
That is why the clinics of acute destructive pancreatitis besides of known symptomatology of this morbidity is fulfilled by the pre-
sentations of different pathologies conditioned by pancreatogenic endotoxicosis [2; 20; 23; 44]. They can be like abdominal, hepato-pancreas, pancreato-renal, pancreato-suprarenal, pancreato-cardio-vascular and pancreato-cerebral syndromes followed by functional failure of appropriate organs [1; 19; 27; 44; 60].
The influence of pancreatogenic toxemia on the functional conditions of the respiratory system and lung ventilation indications presents a big interest. Due to some authors' data, bronchopulmonary complications (BPC) are determined in 15-55%pa-tients with AP clinics. At ADP complicated by extensive peritonitis pancreatogenic acute pulmonary failure is formed due to effect of pancreatic enzymes on the lung capillaries [13; 14; 24; 52; 61] and respiratory impairment is observed in every second patient and it is often a reason of the death [46, 50, 53, 54]. It is clinically evident by dyspnea, acrocyanosis, and changes of acid-alkaline balance, often to the side of decompensated respiratory acidosis, decrease by pul-sometric data of oxygen partial pressure in the arterial blood [19; 37; 43; 55; 57].
Occurrence of the acute respiratory failure (ARF) determined mainly by the pathologic influence ofregulatory (nervous-reflectory, humoral) or toxic effects outgoing from pancreas and also the effects of thrombotic and purulent- septic complications of acute pancreatitis [16, 28, 35, 38, 50, 60, 61].In clinical conditions ARF is often provoked by the combination of factors disordering ventilation, perfusion or diffusion in the pulmonary parenchyma. By the final functional results of interactions of these factors to the gas exchange, there are two main types of ARF: parenchymatic (pulmonary) and ventilating [43; 44; 49; 61].
Parenchymatous ARF occurs as the result of:
— direct toxic injury of the pulmonary parenchyma by ЭИ factors especially coming into the blood by the lymphatic way (pancreatic enzymes, kinins, products of ПОЛ and others);
— partial disorders of the airway conductance and atelectasis due to the injury of natural sanation mechanisms of the bronchial tree under the effect of intoxication, vomiting, patient static position in bed [43; 44; 50; 61];
— pulmonary blood circulation disorders at the embolism of pulmonary circulation vessels due to pathologic hyper coagulation and thrombophilia, and also due to pulmonary circulation disorders [3; 18; 25];
— lung's collapse by air or pleural exudation, its basal compression at diaphragm's high position on the background of intestinal paresis with the formation of so called syndrome of abdominal compartment determining translocation of bacteria and their toxins into the portal and system blood circulation changing oxygenation pro-
cesses but not influencing on excretion of carbon dioxide [22; 26; 48, 55; 58];
— induration of the pulmonary parenchyma at the development of inflammatory processes in the lungs' respiratory zone as presentations of hospital (nosocomial) pneumonia with the activation of the autogenic microflora on the background of the secondary metabolic immunodeficiency [15; 17; 36; 54; 55].
Ventilating ARF in patients with ADP is more often determined by acute appearance of the massive lung's collapse at pancretogenic pleuritic, spontaneous or iatrogenic pneumothorax and also extensive reduction of the functionally stable pulmonary parenchyma due to the total atelectasis or massive pulmonary embolism (PE), pulmonary edema [36; 44; 57].
It is necessary to point an importance of pancreatogenic pleural exudation (PE) which are characterized by the liquid accumulation into pleural cavity and being in the direct relation with the evidence of EI and tissue destruction of pancreas. The frequency of the last ones due to the latest data of some authors at ADP reaches up to 38% [38; 43; 44]. In the forming of pancreatogenic lesions, an important thing is to involve diaphragm into inflammatory process and transmission of the purulent inflammation from pancreas and retroperitoneal fat into pleura with the blocking of resorption ways of the pleural liquid. Sometimes ventilating ARF is the final stage of the developing parenchymatous failure or arise directly due to progressing lungs' induration as a manifestation of the toxic injury of this organ on the background of enzymatic-productive ЭH. Such parenchyma's injury leads to the development of syndrome of respiratory emaciation of adults [43; 44; 57; 58].
Syndrome of respiratory emaciation (SRE) as clinical phenomenon has a special place in the pulmonary pathology at AP and its complications as it leads to extreme levels of respiratory
disorders and inefficiency. According to decision of conciliation commission of pulmonologists since 1992, this phenomenon has been named as syndrome of acute pulmonary injury (SAPI). SAPI is as often as not observed on EI stages and at pus-inflammatory complications due to corrosion bleeding, spread peritonitis or septic shock. In its developed form, SAPI occurs in about 15% patients with destructive acute pancreatitis with the mortality up to 50-70% [37; 43; 44; 46].
Thus, on the base of the given literary review analysis, it can be concluded that pulmonary ventilation disturbances are one of the frequent and severe complications ofpancreatogenic toxemia in patients with ARF.
Increasing of the frequency of those complications is directly response with the evidence and severity of manifestations of pancreatogenic toxemia. Essential situation is aggravated by the fact that general condition of such patients is always severe due to the deep disorders of essential functions and forming pancreatogenic ARF.
However, there are rather many unsolved issues in this problem. In particular, pathogenic mechanisms of forming respiratory failure subject to the stage of pancreatogenic toxemia are not studied enough. The issues of balance condition between pathogenic microbe aggression and protection mechanisms of the respiratory ways at ADP are not detected. Therefore, the further deep study of functional condition of respiratory apparatus in the different periods of pancreatogenic toxemia in patients with ADP is an actual task of emergency pancreatology. It will allow detecting some pathogenic mechanisms of the respiratory disorders and on their base to work out effective treatment-preventive procedures for reducing the frequency of BPC in general and to improve the prognosis of performed surgical treatment of patients with acute destructive pancreatitis.
References:
1. Atanov Yu. P., Clinical evaluation of some syndromes of pancreonecrosis. I I Khirurgia. - 1993. - #10. - P. 64-70.
2. Alperovich В. I., Kazantsev N. I., Merzlikin N. V. The reasons of mortality at acute pancreatitis and the ways of its decreasing//Sov. Meditsina. -1991. - #8. - P. 61-63.
3. Aeksandrova N. P., Petukhov E. B., Ryabova S. Blood reology and microcirculation in dynamics of acute pancreatitis in experiment//Bull. Experiment. Biol, and med. - #1. - T.105. - 1988. - P. 106-108.
4. Bagnenko S. F. and others. Diagnostics and treatment protocols of acute pancreatitis. S-Peterburg, 2004.
5. Basinskiy V. A., GJuk I.,//Acute and chronic pancreatitis. - Grodno, 1990. - P. 24-27.
6. Boyko Yu. G., Prokopchik N. I., Basinskiy V. A., and others//Zdravoochranenie Belorussii. - 1989. - № 6, - P. 13-16.
7. Boyko Yu. G.//Acute and chronic pancreatitis. - Grodno, 1990. - P. 8-11.
8. Boyko Yu. G., Prokopchik N. L., Basinskiy V. A., and others. Бойко Ю. r.//Tam je. - P. 12-20.
9. Boyko Yu. G., Prokopchik N. I., Postoperative pancreatitis. - Minsk, 1992. P. 128.
10. Boyko Yu. G. Actual issues of treatment tactics at acute destructive pancreatitis from the position of clinical pathologists: Official speech. - Grodno, 1997.
11. Boyko Yu. G., Prokopchik N. L., Silaeva N. F., and others.//Clin.med. - 1993. - № 1. - P. 28-29.
12. Bagnenko S. F., Rukhlyada N. V., Tolstoy A. D. and others. Treatment of acute pancreatitis at early stage.- Sankt-Peterburg, 2002. - P. 24.
13. Borisov A. E. and others. Using of small-invasive surgery in treatment of patients with cholelithiasis complicated by choledocholithiasis//Cholecystitis and its complications: Tez.dokl.Resp.nauch-prac. s mejd.uchastiem.Bukhara., 1997. P. 45-46.
14. Briskin B. S. and others. Anhepatic bile ducts injury at cholecystectomy.//Annali khirurgicheskoy gepatologii stran SNG: Tez.dokl.VIII mejd.nauch.konf, khirurgov gepatologov stran SNG. Tashkent, 2000. T. 5. № 2. P. 99-100.
15. Beburishvili A. G., Pugacheva L. L. and others. Immune disorders, their correction at acute pancreatitis and purulent peritonitis. -Khirurgia.. - 1992. - № 7-8. - P. 114-118.
16. Voevodina T. V., Nifantiev O. E., Methods of detection ofbiologic environments toxicity at eczo- and endotoxicosis. Krasnoyarsk: IBF, 1990. P. 35: graf. (Prepr./AN SSSR, Sib.otdelenie, Insitut biofiziki; № 128B).
17. Gelfand B. R., Gologorskiy Z. A., Gelfand E. B. and others. Strategy and tactics of anti-bacterial therapy of abdominal sespsis. Anesteziologia i reanomatologia. 1998 - № 4. - P. 16-19.
18. Guhnan M. I., Vinnik Yu. S.and others. Investigation of organ blood flow of pancreas at experimental pancreonecrosis.//Use of laser-Dooppler flowmeter in medical practice. Mater.Perv.Vseros.Sipm. - M., 1996. - P. 27.
19. Gulman M. I., Vinnik Yu. S. and others. Acute pancreatitis: issues of pathogenesis, clonics, treatment. - Krasnoyarsk; Zelenogorsk, 1997.
20. Gostishev V. K., Glushko V. A. "Pancreonecrosis and its complications, main principles of surgical tactics". Khirurgia 3, 2003.
21. Gostishev V. K., Fedorovskiy N. M., Glushko V. A., Destructive pancreatitis (Main principles of complex therapy)//Annali khirurgii, 1997; 4: 60-65.
22. Hospital pneumonia in adults: diagnostics, estimation of illness severity, primary antimicrobe treatment and prevention strategy. American thoracic society Medical department of pulmonology association. Conformal statement. 1995.
23. Danilov M. V., Fedorov V. D. Surgery ofpancreas. - M., 1995.
24. Dederer Yu. M., Diagnostics and treatment tactics of different forms of acute cholecystitis.//Klin.vestnik. - 1997. - № 3. - P. 10-11.
25. Kalmishova Yu. A., Bubneva V. L., Svechnikova L. V., Chemogubova E. A., Shepelev A. P. Membranes of erythrocytes and antioxidant provision at experimental acute pancreatitis//Patfiziologia, 1992; 3: 27-29.
26. Krivoruchko I. A., Gusak I. V., Smagilo R. M., and others. The role of intestine in pathogenesis of acute pancreatitis: oxygen extraction and translocation of bacteria in rats. Klinichna khirurgia. 1999. - № 12. - P. 40-42.
27. Levit A. L., Prudkov M. P., Korkin O. V., and others. Estimation scale of poliorgan disfunction in surgical patients. Anesteziologiya i reanimatologia - 2000. - № 3. - P. 26-28.
28. Malinovskiy N. N., Agafonov N. P., Reshetnikov E. A., Treatment of acute destructive alimentary pancreatitis. Khirurgia. 2000. № 1. P. 4-7.
29. Materials of the seminar of SRI of emergency medicine named after N. V. Sklifosovskiy, Moscow, 2001.
30. Molitvoslovov A. B., Kadoshuk Yu. T., Gass M. V., Modem principles of acute pancreatitis treatment//Khirurgia. - 1994. - #6. - P. 38-41.
31. Mamakeev M. M., Sopuev A. A., Imanov B. M., Surgical treatment of extensive pancreanecrosis//Khirurgia, 1998; 7: 31-33.
32. Pugaev A. V., Bogomolova N. S., Bagdasarov V. V., Sirojitdinov K. B. To pathogenesis of purulent complications of acute pancreatitis. -Vestn.khir. - M., 1995.
33. Pugaev A. V., Treatment tactics of acute pancreatitis: Avtoref.diss... doct.med.nauk. - M., 1988. - P. 25.
34. Pathogenesis and principles of surgical treatment of the spread forms of pancreanecrosis./S. A. Shalimov, M. E. Nechitaylo, AJ. Pankov and others.//Klin.khirurgia. - 1992. - #11. - P. 63-67.
35. Pantsirev Yu. M., Milnikov E. D., Fedorov P. L., Acute biliary pancreatitisipossibilities of diagnostics and treatment. Rossiyskiy jumal gastroenterologii, gepatologii, koloproctologii. 1999. № 2. P. 73-80.
36. Rodionov V. V., Mamilyaev R. M., Broncho-pulmonary complications after operations on abdominal cavity organs., 1991.
37. Saveliev V. S., Buyanov V. M., Ognev Yu. V., Acute pancreatitis. - M.: Meditsina, 1983. - P. 240.
38. Saveliev V. S., Kubishkin V. A., Pancreanecrosis. Condition and perspective. Khirurgia. 1993. № 6. P. 22-28.
39. Saripbekova S.Sh., Change of hemomicrocirculatoty course of pancreas at experimental acute pancreatitis//Patologia sosudov serdtsa. -Alma-Ata 1988. - P. 36-39.
40. Sigal Z. M., Valter V. O., Diagnostics and treatment of organ hemodynamic disorders at acute pancreatitis ft Khirurgia. - 1988. - #1. - p. 53-58.
41. Sirbu I. F., Kapshitar A. V., Mogilniy V. A., Diagnostics and treatment of acute pancreatitis//Khirurgia. - 1993. - #1. - P. 47-51.
42. Titova G., Permyakov N. K.//Novosti khir. - 1995. - № 1. - P. 61.
43. Filin V. I., Kostyuchenko A. L. Emergency pancreatology. - SPb.: Piter, 1994. - P. 416.
44. Filimonov M. I., Gelfand B. R., Bumevich S. Z., Orlov B. B., Tsidenjapov E.Ts. Acute pancreatitis. Moscow, 2002.
45. Shalimov S. A., Radzikhovskiy A. P., Nechitaylo M. E. Acute pancreatitis and its complications.- Kiev: Nauk.dumka, 1990. - P. 272.
46. Zaytsev V. T., Goloborodko N. K., Krivoruchko I. A., and others. Prevention and treatment pulmonary complications after emergency operations of abdominal cavity organs in patients elder than 60 years old.//Vestnik khirurgii 1992 148 № 2 216-220.
47. Zaytsev V. T., Krivoruchko I. A., Boyko V. V., and others. Syndrome of multiple disftmction at acute pancreatitis: scientific conception of biological mechanisms of developing destructive processes. If Проблема вшськово!' охорони здоров'я. 36. Наук. Праць Укр.. вШськ. мед.академп. К.,2000. - С. 392-398.
48. Sharafutdinova G.Kh., and others. Hospital pneumonias in surgical practice. Uzbekistan khirurgiyasi,% 84-86, 2005.
49. Schulz H., Schulz E., Akute pankreatitis - atiologie, pathologische anatomie und pathogenese. - Zschr. Inn. Med. - V. 117. - № 8. -1990. - P. 467-475.
50. Sashi M., Ercke A., Klassifikationen der Acuten Pankreatitis aus Chirurgieher Sicht, Art Chir. 1993r-28, 3, 95.
51. Hospital-acquired Pneumonia in Adults: Diagnosis, Assessment of Severity, Initial Antimicrobial Therapy, and Preventative Strategies. A Consensus Statement. Official Statement of the American Thoracic Society was Adopted by the ATS Board of Directors, November 1995.
52. Kirtland SH. et al. The Diagnosis of Ventilator-Associated Pneumonia. II Chest - 1997; 112: 445-57.
53. Guidelines for prevention of nosocomial pneumonia. Centers for Disease Control and Prevention.//MMWR.-1997.-46 (Rl). - P. l-79.
54. Montravers P., Veber B., Auboyer C., et al. Diagnostic and therapeutic management of nosocomial pneumonia in surgical patients: results of the Eole Study.//Crit Care Med. - 2002; 30: 368-375.
55. Veber B., Montravers P., Auboyer C., et al. Diagnostic and therapeutic management of nosocomial pneumonia in surgical patients: results of the Eole Study.//Crit Care Med. - 2002; 30: 368-375.
56. Fabergas N., Torres A., Strategies in the Diagnosis of Pneumonia. Refresher course lectures.//10th ESA Anniversary Meeting and 24th EAA Annual Meeting. Euroanaesthesia 2002.
57. Guide A., to Infection Control in the Hospital. An official publication of the International Society of Infection Diseases. 2nd Edition. Editors: R. Wenzel, T. Brewer, J.-P. Butzler. BC Decker Inc. Hamilton, London, 2002.
58. Montravers P, Veber B, Auboyer C, et al. Diagnostic and therapeutic management of nosocomial pneumonia in surgical patients: results of the Eole Study.//Crit Care Med. - 2002; 30: 368-375.
Ultra sound diagnostics of brachiocephal arteries in multifocal atherosclerotic damage
59. Hollender L., Lehnert P., Wanke M., Akute Pankreatitis. - Munchen, 1993.
60. Donahue P. E. Vasoactive drugs in acute pancreatitis//Arch. Surg. - 1994. - V.119, N.4. - P. 477-480.
61. Schulz H., et all. Akute pankreatitis - atiologie, pathologische anatomie und pathogenese//Zschr. Inn. Med. - V.107, N.6. - 1993. -S. 437-443.
Khaidarov Nodir Kadirovich, Neuropathologist of the 3rd clinic, Tashkent Medical Academy
E-mail: mbshakur@mail.ru
Ultra sound diagnostics of brachiocephal arteries in multifocal atherosclerotic damage
Abstract: It was determined that ultra sound assessment of the degree of arteries damage possessing high descriptiveness, no invasion and absence of radiation load, in combination with aortal arteriography, provides optimal tactics of stages of surgical or endovascular re-vasvularization performance.
Keywords: multifocal atherosclerosis, damage of brachiocephal arteries, ultra sound diagnostics.
Topicality. Cardiac-vascular diseases take a leading place in the structure of mortality rate of the population in the world. In the mortality structure of cardiac vascular diseases 85-90% is the part of insult and myocardial infarction. In the structure of cerebral vascular diseases the leading place is taken by the disorders of cerebral blood circulation of ischemic character (up to 80%) conditioned by atherosclerosis. Surgical therapy of stenose (including asymptomic) damages of aortal arch branches provide significant diminishing ofthe possibility of insult development, and improvement ofthe quality life ofmultiple contingent of the patients, which conditions not only medical, but also social-economic significance of the problem [1; 2; 11].
For a long time a special attention in clinical practice was paid to local manifestations of atherosclerotic process [3; 10]. Though atherosclerotic damage of vessels of one arterial lumen is rather an exclusion, than a rule. At the modern time according to many authors combined damage of several arterial lumens compose up to 50-60% [4; 5]. Often patients with asymptomic stenoses of aortal arch branches apply for medical aid because of the damage of other vascular lumens: coronary, renal, arteries oflower limbs, aortal aneurism. That's why in modern conditions it is rational to perform active diagnostic tests for detection of the lesion of carotid arteries if there are clinical manifestations of atherosclerosis of any location [6].
The most informative methods of the modern diagnostics today are ultra sound doplerography with duplex scanning, roentgenologic angiography, magnetic-resonance angiography [9]. According to the report of some researchers the most reliable information about the degree of stenosis and the structure of atherosclerotic plaque can be received with duplex scanning, and, respectively, on the basis of these data perform surgical treatment [7; 8].
The objective is to study peculiarities of ultra sound values of brachiocephal arteries in multifocal atherosclerosis
Materials and methods. The work was based on the study of the results of checking of 40 patients with atherosclerotic stenosis ofbrachiocephal arteries in multifocal atherosclerosis, among them 30 men 30 (75%) and 10 women (25%). Hyper cholesterolemia was observed in all examined patients.
In the analysis of the values of ultra sound diagnostics it was determined that among these 40 patients seven had combination of atherosclerotic damage with renal artery, 22 with coronary artery, and eleven with arteries of the lower limbs.
Simultaneous damage of several vascular lumens by atherosclerosis promotes development of clinical picture from clear manifesta-
tion to asymptomic latent progress. Among these 40 patients with atherosclerotic stenoses of brachiocephal arteries we registered asymptomic progression in fourteen (35.0%), and that corresponded to the results of other authors. Bilateral hem dynamically significant stenoses (60% and more) of carotid arteries in combination with stenoses ofvertebral arteries were diagnosed in 21 (52.4%) of 40 patients, interim stenoses (50%) in 12 (30.0%) patients. Bifurcation stenoses were detected in 29 (72.5%) patients.
Hem dynamic significance of stenosis-occlusive damage is determined by its potential danger to be a source ofblood supply deficit in distal part. With stenosis more than 60% along the diameter (and occlusion) and absence of compensatory mechanisms distal deficit of blood supply develops.
Unilateral stenosis of brachiocephal arteries was diagnosed in 8 (20.0%) patients. The more expressed were the stenoses of brachiocephal arteries, the more hem dynamically significant stenoses (70% and more) of CA were detected with the help of coronary angiography.
Ataxy, weakness of legs, headaches, dizziness was noted in 23 (57.5%) out of 40 patients.
In 16 (80%) patients with diabetes mellitus there was visualization ofheterogenic atherosclerotic plaques with prevailing of hyper echogenic component and inclusions of calcinates.
In 17 (42.5%) patients with hypo echogenic and heterogenic atherosclerotic plaques with prevailing hypo echogenic component on computer tomography we revealed post ischemic cysts of brain with various location.
Ultra sound technologies provided definition of stenosis degree, morphology of atherosclerotic damage ofbrachiocephal arteries in 40 patients, and that was confirmed in aortal arteriography.
Performed comparative analysis of the results of complex USD and digital angiography in the definition of stenosis degree in arteries further undergoing stenting confirmed the fact that USD data provide reliable definition of artery stenosis.
Different from the data of digital angiography, ultra sound research methods more accurately defined duration and structure of atherosclerotic plaque in superficially located arteries, and that was important for the choice of stent length. The choice of the optimal length of the stent is important factor for prevention of the development of dangerous dissection and re-stenosis.
Thus, the results of non-invasive sonographic researches are informative, reliable, available, safe in the definition of artery stenosis
