Authors |
Avseenko N.D. Doctor of Medicine, Associate Professor, ndavseenko@rambler.ruAlfonsova Y.V. Candidate of Science (Medicine), elena-alfonsova@yandex.ruZabrodina L.A. postgraduate, Department of Medical and Biological bases of Physical Education and Sports, Alfonsova@zabspu.ruStasyuk O.N. graduate student, olga-stasuk4@rambler.ru |
Annotation |
Retrospective analysis of 28 medical patients’ histories from endocrinology department of
the Chita regional clinical hospital from 2009 to 2011 was performed. Acid-base balance and water-
electrolytic balance blood pH parameters, electrolytes and hemostasis volume were estimated. Against the background of progressive metabolic acidosis essential changes of hemostasis were
found out in the form of increase of D-dimers concentration, resolution of platelet number, prolongation
activated partial thromboplastin time (APTT) and international normalized ratio (INR).
There were statistically significant inverse correlations between INR and concentration of standard
bicarbonates (SB), buffer excesses (BE), concentration of hydrogen carbonates (НСО3-), carbon
dioxide СО2. Also there were inverse correlations between prothrombin time and concentration of
hydrogen carbonates (НСО3-), standard bicarbonates (SB), buffer excesses (BE), carbon dioxide
СО2. It testifies to the development of hypercoagulation state. According to the data presented in the
electrocardiography (ECG) sinus tachycardia, ventricular fibrillation, paroxysmal supraventricular
arrhythmia, the increase of creatinine and urea in blood are observed. All patients having metabolic
acidosis have symptoms of development of multiple organ failure on the background of progressing
disseminated intravascular coagulation (DIC).
|
References |
1. Al’fonsov V. V., Al’fonsova E. V. Mehanizmy razvitija morfologicheskogo jekvivalenta DVSsindroma
// Tromboz, gemostaz i reologija. 2010. № 1. S. 44–51.
2. Al’fonsov V. V., Al’fonsova E. V., Bochkarnikova N. V. i dr. Acidoz, gemostaz i morfologija
organov pishhevaritel’noj sistemy. Chita, 2005. 120 s.
3. Bajramov A. A., Bogdanova A. A., Soldatenkov P. A. Metabolicheskaja korrekcija sostojanij
serdechno-sosudistoj sistemy // RMZh. 1999. № 6. S. 53.
4. Barkagan, Z. S., Barkagan A. P Diagnostika i kontroliruemaja terapija narushenij gemostaza. 3-e
izd. M.: N’judiamed, 2008.
5. Butylin V. Ju., Butylin D. Ju. Intensivnaja terapija neotlozhnyh sostojanij. Patofiziologija, klinika,
lechenie. Atlas. Kiev: Novij druk, 2003. 528 s.
6. Gorn M. M., Hejtc U. I., Sveringer P. L. Vodno-jelektrolitnyj balans i kislotno-osnovnoe
ravnovesie. SPb.: Nevskij dialekt, 2000. 325 s.
7. Zags I. O., Lobus T. V., Moroz V. V. Oshhelachivajushhaja terapija pri serdechno-ljogochnoj
reanimacii – sovremennye vozmozhnosti // Reanimatologija i intensivnaja terapija. 1999. № 4. S. 34–42.
8. Strelkov N. S. Postmortal’naja kliniko-farmakologicheskaja ocenka vlijanija vvedjonnyh v
venu rastvorov lekarstvennyh sredstv na process prizhiznennogo razvitija acidoza ili alkaloza // Problemy
jekspertizy v medicine. 2002 № 3. S. 13–16.
9. Tverskoj A. L. Laktat-acidoz // MRZh. Anesteziologija i reanimatologija. 1980. № 3. S. 50–57.
10. Shestakov V. A. Vlijanie N i ON ionov na svjortyvaemost’ krovi v ontogeneze: avtoref. dis. …
kand. med. nauk. M., 1968. 26 s.
11. Shtejnle A. V. Patologicheskaja fiziologija i sovremennye principy lechenija tjazhjolyh
sochetannyh travm // Sibirskij medicinskij zhurnal. 2009. № 3. S. 119–127.
12. Shuteu Ju. Shok. Buharest: Voennoe izd-vo, 1981. 424 s.
13. Behmanesh S., Kempski O. Mechanisms of endothelial cell swelling from lactacidosis studied
in vitro // Am. J. Physiol. Heart Circ. Physiol. 2000. V. 279. № 4. P. 1512–1517.
14. Bleeker-Rovers C. P., Kadir S. W., van Leusen R, Richter C. Hepatic steatosis and lactic acidosis
caused by stavudine in an HIV-infected patient // Neth. J. Med. 2000. V. 57. № 5. P. 190–193.
15. De Backer D. Lactic acidosis // Intensive Care Med. 2003. № 29. R. 699–702
16. Duell T., Mittermuller J., Hiddemann W. Unclear lactate acidosis in a patient with heart failure
under long-term diuretic therapy // Dtsch. Med. Wochenschr. 2000. V. 125. № 41. P. 1232–1234.
17. Dunn R. J. Massive sulfasalazine and paracetamol ingestion causing acidosis, hyperglycemia,
coagulopathy, and methemoglobinemia // J. Toxicol. Clin. Toxicol. 1998. V. 36, N 3. P. 239–242.
18. Hucabee W. E. Laktik – acidosis // Am. I. Med. 1961. V. 30. P. 833 – 839.
19. Janssen J. A. Current role of metformin in treatment of diabetes mellitus type 2 // Ned Tijdschr
Geneeskd. 2000. V. 144, N 40. P. 1900–1902.
20. Lovas K., Fadnes D. J., Dale A. Metformin associated lactic acidosis case reports and literature
review // Tidsskr Nor Laegeforen. 2000. V. 120. № 13. P. 1539–1541.
21. Luft R. (1994). The development of mitochondrial medicine Proc. Natl. Acad. Sci. USA.
P. 8731–8738.
22. Machet G., Coudray J. M. Lactic acidosis and metformin implicated: why better information
about risk factors? // Therapie. 2000. V. 55. № 2. P. 283–294.
23. Otsuka M., Shinozuka K., Hirata G., Kunitomo M. Influences of a shiitake (Lentinus edodes)-
fructo-oligosaccharide mixture (SK-204) on experimental pulmonary thrombosis in rats // Yakugaku
Zasshi. 1996. V. 116. № 2. P. 169–175.
24. Severe self-poisoning with formol / Ferrandiere M., Dequin P. F,, Legras A,, Hazouard E,,
Benchellal Z., Perrotin D. // Ann. Fr. Anesth. Reanim. 1998. V. 17. № 3. P. 254–256. |