BibTex RIS Kaynak Göster

The Effects of Perinatal Asphyxia on Hemostasis

Yıl 2012, Cilt: 14 Sayı: 1, 31 - 36, 01.03.2012

Öz

Aim: Perinatal asphyxia is the most important reason that increases morbidity and mortality inthe first week of the life. In this work the tendency of Asphyctic babies on disseminatedintravascular coagulation was investigated.Material and method: Of those who applied to Dr. Behçet Uz Pediatrics Hospital, 30 newbornbabies who had been subjected to different degrees of asphyxia and 20 ones having no problemsas control group were taken. Protein C, protein S, antithrombin III, prothrombin time (PT),partial thromboplastin time (PTT), thrombin time, thrombocyte number, fibrinogen, D-Dimervalues in venous blood were investigated.The patient group was classified in terms of asphyxiadegrees and comparison was made between the groups.Results: In the early period following the birth, antithrombin (AT) III (31,35 12,14), ProteinC(30,45±12,14), Protein C (30,45±15,39) and Protein S (39,76±21,01) levels were found lowin comparison to the control group. PT (21,68±15,49 sec) and PTT (63,40±28,38 sec) inasphyctic group were found high in comparison to the control group. It was seen that as asphyxiadegree grew fibrinogen (200,31±82,14 mg/dl) levels decreased. The rates of the babiesdemonstrating D-dimer (495,26±555,49 ng/ml) height in asphyctic group were high incomparison to the control group. The thrombocyte number (206100±100073) in asphyctic groupwas low and as asphyxia degree grew it decreased more remarkably. In the evaluation doneaccording to the degree of asphyxia within the asphyxia group itself uric acid and SPGT levelswere found high in a directly proportionate way to the degree of asphyxia.Conclusion: Protein C, Protein S, AT III, fibrinojen levels and trombosit numbers are lowoutstandingly in asphyctyc babies. But, PT, PTT, INR and D dimer levels are high

Kaynakça

  • Feldman BF, Madevvell BR, O'Neill S. Disseminated Intravscular Coagulation: Antithrombin Plasminogen, and Coagulation Abnormalities in 41 dogs. J Am Vet Med Assoc. 1981;179:151-4.
  • Inkster M, Sherman LA, Ahmed P, Benton MB, Gaston LW. Preservation of Antithrombin III Activity in Stored Whole Blood. Transfusion. 1984;24:57-9.
  • Neyzi O, Ertuğrul T. Yenidoğan ve Hastalıkları. Pediatri. İstanbul: Nobel Tıp Kitabevi; 1989: 151-292.
  • Finer NN, Robertson CM, Richards RT, Pinnell LE, Peters KL. Hypoxic-Iscemic Encephalopaty in Term Neonates: Perinatal Factors and Outcome. J Pediatr. 1981;98:112-7.
  • Fichera A, Pratico G, Sciacca F. Neonatal Hypoxia and Hemocoagulative Changes.Pediatr Med Chir. 1989;11:643-7.
  • Choudhry VP, Thavaraj V, Saraya AK. Disseminated Intravascular Coagulation: Diagnosis and Current Therapy. Indian Pediatrics. 1990;27:280-8.
  • Beresford CH. Owen MC. Antithrombin III. Int J Biochem. 1990;22:121-8.
  • Blauhut B, Kramar H, Vinazzer H, Bergmann H. Substitution of Antithrombin III in Shock and DIC: A Randomized Study. Thromb Res. 1985;39:81-9.
  • Shirata A, Shirakavva Y. New Approach to the Diagnosis of Disseminated Intravascular Coagulation in Childhood. Nippon Rinsho. 1993;51:61-6.
  • Abad A, Marco Vera P, Mompel A, Garcia Perez A. Levels of Antithrombin III and Proteins C in the Newbom Infant. Sangre (Barc). 1989;34:91-5.
  • Jürgens H, Göbel U, Bokelmann J, von Hoss H, Vahn V. Coagulation Studies on Umbilical Arterial and Venous Blood From Normal Newborn Babies. Aur J Pediatr. 1979;131;199- 204.
  • Ballard RA. Newborn Stabilization and Initial Evaluation. in: Taeusch HW, Ballard RA, Avery' s Diseases of the Nevvborn. Philadelphia: WB Saunders Co; 1998: 319-355.
  • Küçüködük Ş. Yenidoğan ve Hastalıkları (1.baskı). Ankara: Feryal matbaası; 1994: 341-81.
  • Chadd MA, Elwood PC, Gray OP, Muxworthy SM. Coagulation Defects in Hypoxic Full-term Newborn Infants. BMJ. 1971;4:516-8.
  • Schander K, Rehm A, Niesen M. Blood Coagulation Activity and Fibrinolysis in Umbilical Vein Blood of Healthy and Asphyxiated Newborn Infants. Fortschr Med. 1977;95:1477- 81.
  • Suzuki S, Morishita S. Hypercoagulability and DIC in High- Risk Infants. Semin Thromb Hemost. 1998;24:463-6.
  • McDonald TP, Cottrell M, Clift R. Effect of Short-Term Hypoxia on Platelet Counts of Mice. Blood 1978;51:165-175.
  • Mortensen JZ, Jorgensen KA. Antithrombin III. Danish MeDICal Bulletin. 1983;30:100-5.
  • Bick RL, Dukes ML, Wilson WL, Fekete LF. Antithrombin m(AT-III) as a Diagnostic Aid in Disseminated İntravascular Coagulation. Thromb Res. 1977;10:721-9.
  • Bick RL, Bick MD, Fekete LF. Antithrombin III Patterns in Disseminated Intravascular Coagulation. American Society of Clinical Pathologists. 1990;71:577-83.
  • Albert J, Blomquvist H, Gardlund B, et al. Effect of Antithrombin Concentrate on Haemostatic Variables in Critically III Patints. Acta Anaesthesiol Scand. 1992;36:745- 52.
  • Brangenberg R, Bodnesohn M, Bürger U. Antithrombin-III Substitution in Preterm Infants - Effect onIntracranial Hemorrhage and Coagulation Parameters. Biol Neo. 1997;72:76-83.
  • Hanada T, Abe T, Takita H. Antithrombin III Concentrates for Treatment of Disseminated Intravascular Coagulation in Children. Am J Pediatr Hematol Oncol. 1985;7:3-8

Perinatal Asfiksinin Hemostaz Üzerine Etkileri

Yıl 2012, Cilt: 14 Sayı: 1, 31 - 36, 01.03.2012

Öz

Amaç: Perinatal asfiksi, hayatın ilk haftasında morbidite ve mortaliteyi artıran en önemlinedenidir. Bu çalışmada asfiktik bebeklerin dissemine intravasküler koagulasyona eğilimiaraştırıldı.Materyal ve Metod: İzmir Dr. Behçet Uz Çocuk Hastanesi’ne başvuran çeşitli derecelerdeasfiksiye maruz kalmış 30 ve kontrol grubu olarak da herhangi bir problemi olmayan 20yenidoğan bebek alındı. Venöz kanda Protein C, Protein S, Antitrombin III, Protrombin zamanı(PT), Parsiyel tromboplastin zamanı(PTT), Trombin time, Trombosit sayısı, Fibrinojen, D-Dimerdeğerlerine bakıldı. Hasta grubu asfiksi derecelerine göre sınıflandırıldı ve guruplar arasıkarşılaştırma yapıldı.Bulgular: Doğumu izleyen erken dönemde asfiktik bebeklerin Antitrombin(AT) III(31,35±12,14), Protein C (30,45±15,39) ve Protein S (39,76±21,01) düzeyleri kontrol grubunagöre düşük bulundu. PT (21,68±15,49 sn)ve PTT (63,40±28,38 sn) asfiktik grupta kontrolgrubuna göre yüksek bulundu. Asfiksi derecesi arttıkça fibrinojen (200,31±82,14 mg/dl)düzeylerinin düştüğü görüldü. Asfiktik grupta D-dimer (495,26±555,49 ng/ml) yüksekliğigösteren bebeklerin oranı kontrol grubuna göre yüksekti. Trombosit sayısı asfiktik grupta kontrolgrubuna göre düşük idi ve asfiksi derecesi arttıkça daha belirgin bir düşüş gösterdi. Asfiktikgrubun kendi içinde asfiksi derecesine göre yapılan değerlendirmede Ürik asit ve SGPTdüzeylerinin asfiksi derecesi ile doğru orantılı olarak yüksek olduğu bulundu.Sonuç: Asfiktik bebeklerde Protein C, Protein S, AT III, Fibrinojen düzeyleri ve trombositsayıları belirgin olarak düşük, PT, PTT, INR ve D dimer düzeyleri ise yüksektir

Kaynakça

  • Feldman BF, Madevvell BR, O'Neill S. Disseminated Intravscular Coagulation: Antithrombin Plasminogen, and Coagulation Abnormalities in 41 dogs. J Am Vet Med Assoc. 1981;179:151-4.
  • Inkster M, Sherman LA, Ahmed P, Benton MB, Gaston LW. Preservation of Antithrombin III Activity in Stored Whole Blood. Transfusion. 1984;24:57-9.
  • Neyzi O, Ertuğrul T. Yenidoğan ve Hastalıkları. Pediatri. İstanbul: Nobel Tıp Kitabevi; 1989: 151-292.
  • Finer NN, Robertson CM, Richards RT, Pinnell LE, Peters KL. Hypoxic-Iscemic Encephalopaty in Term Neonates: Perinatal Factors and Outcome. J Pediatr. 1981;98:112-7.
  • Fichera A, Pratico G, Sciacca F. Neonatal Hypoxia and Hemocoagulative Changes.Pediatr Med Chir. 1989;11:643-7.
  • Choudhry VP, Thavaraj V, Saraya AK. Disseminated Intravascular Coagulation: Diagnosis and Current Therapy. Indian Pediatrics. 1990;27:280-8.
  • Beresford CH. Owen MC. Antithrombin III. Int J Biochem. 1990;22:121-8.
  • Blauhut B, Kramar H, Vinazzer H, Bergmann H. Substitution of Antithrombin III in Shock and DIC: A Randomized Study. Thromb Res. 1985;39:81-9.
  • Shirata A, Shirakavva Y. New Approach to the Diagnosis of Disseminated Intravascular Coagulation in Childhood. Nippon Rinsho. 1993;51:61-6.
  • Abad A, Marco Vera P, Mompel A, Garcia Perez A. Levels of Antithrombin III and Proteins C in the Newbom Infant. Sangre (Barc). 1989;34:91-5.
  • Jürgens H, Göbel U, Bokelmann J, von Hoss H, Vahn V. Coagulation Studies on Umbilical Arterial and Venous Blood From Normal Newborn Babies. Aur J Pediatr. 1979;131;199- 204.
  • Ballard RA. Newborn Stabilization and Initial Evaluation. in: Taeusch HW, Ballard RA, Avery' s Diseases of the Nevvborn. Philadelphia: WB Saunders Co; 1998: 319-355.
  • Küçüködük Ş. Yenidoğan ve Hastalıkları (1.baskı). Ankara: Feryal matbaası; 1994: 341-81.
  • Chadd MA, Elwood PC, Gray OP, Muxworthy SM. Coagulation Defects in Hypoxic Full-term Newborn Infants. BMJ. 1971;4:516-8.
  • Schander K, Rehm A, Niesen M. Blood Coagulation Activity and Fibrinolysis in Umbilical Vein Blood of Healthy and Asphyxiated Newborn Infants. Fortschr Med. 1977;95:1477- 81.
  • Suzuki S, Morishita S. Hypercoagulability and DIC in High- Risk Infants. Semin Thromb Hemost. 1998;24:463-6.
  • McDonald TP, Cottrell M, Clift R. Effect of Short-Term Hypoxia on Platelet Counts of Mice. Blood 1978;51:165-175.
  • Mortensen JZ, Jorgensen KA. Antithrombin III. Danish MeDICal Bulletin. 1983;30:100-5.
  • Bick RL, Dukes ML, Wilson WL, Fekete LF. Antithrombin m(AT-III) as a Diagnostic Aid in Disseminated İntravascular Coagulation. Thromb Res. 1977;10:721-9.
  • Bick RL, Bick MD, Fekete LF. Antithrombin III Patterns in Disseminated Intravascular Coagulation. American Society of Clinical Pathologists. 1990;71:577-83.
  • Albert J, Blomquvist H, Gardlund B, et al. Effect of Antithrombin Concentrate on Haemostatic Variables in Critically III Patints. Acta Anaesthesiol Scand. 1992;36:745- 52.
  • Brangenberg R, Bodnesohn M, Bürger U. Antithrombin-III Substitution in Preterm Infants - Effect onIntracranial Hemorrhage and Coagulation Parameters. Biol Neo. 1997;72:76-83.
  • Hanada T, Abe T, Takita H. Antithrombin III Concentrates for Treatment of Disseminated Intravascular Coagulation in Children. Am J Pediatr Hematol Oncol. 1985;7:3-8
Toplam 23 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Bölüm Research Article
Yazarlar

Levent Yildirim Yılmaz Bu kişi benim

Abdullah Canbal Bu kişi benim

Yayımlanma Tarihi 1 Mart 2012
Yayımlandığı Sayı Yıl 2012 Cilt: 14 Sayı: 1

Kaynak Göster

APA Yılmaz, L. Y., & Canbal, A. (2012). Perinatal Asfiksinin Hemostaz Üzerine Etkileri. Duzce Medical Journal, 14(1), 31-36.
AMA Yılmaz LY, Canbal A. Perinatal Asfiksinin Hemostaz Üzerine Etkileri. Duzce Med J. Mart 2012;14(1):31-36.
Chicago Yılmaz, Levent Yildirim, ve Abdullah Canbal. “Perinatal Asfiksinin Hemostaz Üzerine Etkileri”. Duzce Medical Journal 14, sy. 1 (Mart 2012): 31-36.
EndNote Yılmaz LY, Canbal A (01 Mart 2012) Perinatal Asfiksinin Hemostaz Üzerine Etkileri. Duzce Medical Journal 14 1 31–36.
IEEE L. Y. Yılmaz ve A. Canbal, “Perinatal Asfiksinin Hemostaz Üzerine Etkileri”, Duzce Med J, c. 14, sy. 1, ss. 31–36, 2012.
ISNAD Yılmaz, Levent Yildirim - Canbal, Abdullah. “Perinatal Asfiksinin Hemostaz Üzerine Etkileri”. Duzce Medical Journal 14/1 (Mart 2012), 31-36.
JAMA Yılmaz LY, Canbal A. Perinatal Asfiksinin Hemostaz Üzerine Etkileri. Duzce Med J. 2012;14:31–36.
MLA Yılmaz, Levent Yildirim ve Abdullah Canbal. “Perinatal Asfiksinin Hemostaz Üzerine Etkileri”. Duzce Medical Journal, c. 14, sy. 1, 2012, ss. 31-36.
Vancouver Yılmaz LY, Canbal A. Perinatal Asfiksinin Hemostaz Üzerine Etkileri. Duzce Med J. 2012;14(1):31-6.
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