How to Cite
Abstract
Background: To determine levels of Anti thrombin III and its prognostic value in predicting neonatal sepsis.
Methods: In this descriptive study full term neonates (n=70)were recruited. For the diagnosis of neonatal sepsis 2 or more of the physical signs and laboratory criteria were taken into account for (temperature instability< 35 or > 38.5C;tachypnea > 60/min; tachycardia > 200/min;capillary refill > 3 sec; C-reactive protein level > 1 ng/ml). Neonates in which factors which affect the prognosis irrespective of disease severity of neonatal sepsis and neonates who presented with complications of sepsis such as, multiple congenital anomalies, birth weight < 2 kg, birth asphyxia, neonates who received prior treatment or presenting with complications were excluded. Patients with Anti-thrombin III levels less than 35 UIU/dl were considered as bad prognostic group and those with Anti-thrombin III level between 50 – 75 IU/ dl were considered as good prognostic group .The neonates were followed for 2 weeks. Outcomes were assessed in terms of total duration of hospital stay, complications developed, discharge or death of the neonate. p- value less than or equal to 0.05 was considered significant.
Results: The mean Anti-thrombin III level in the good prognosis group was 53.098.8 whereas in the bad prognosis group was 41.6610.58 IU/dl(p <0.05). Anti-thrombin III level below 50 IU/dl had a sensitivity of 62.8%, specificity of 77.1%, positive predictive value of 73.3% and a negative predictive value of 67.5% for predicting poor prognosis and
death.
Conclusion: Anti-thrombin III levels can be a potential indicator of prognosis in neonatal sepsis.
Key Words: Sepsis, Newborn, Anti-thrombin III
References
Zaidi AK, Huskins WC, Thaver D. Hospital-acquired neonatal infections in developing countries. Lancet. 2005;365:1175–88.
Darmstadt GL, Batra M, Zaidi AKM. Parenteral antibiotics for the treatment of serious neonatal bacterial infections in developing country settings. Pediatr Infect Dis J 2009;28:37–42
Martines J, Paul VK, Bhutta ZA. Neonatal survival: a call for action. Lancet. 2005;365:1189 –97.
Thor AW, Courtney AG, Sara H, Viju S, Janna CP .Emerging biomarkers for the diagnosis of severe neonatal infections applicable to low-resource settings. Journal of Global Health 2011; 2: 210-23
Hagag AA, Elmahdy HS, Ezzat AA.Prognostic value of plasma pro-adrenomedullin and antithrombin levels in neonatal sepsis. Indian Pediatr. 2011 ;48(6):471-73.
Fourrier F, Chopin C, Goudemand J, Hendrycx S, Caron C, Rime A, et al. Septic shock, multiple organ failure, and disseminated intravascular coagulation.Compared patterns of antithrombin III, protein C,and protein S deficiencies. Chest 1992;101;816-23.
Vinazzer H. Therapeutic use of antithrombin III in shock and disseminated intra-vascular coagulation. Semin Thromb Hemost 1989; 15:347-52
Tanaka H, Kobayashi N, Maekawa T. Studies on production of antithrombin III with special reference to endotoxininduced DIC in dogs. Thromb Haemost 1986;56:137-43.
Seitz R, Wolf M, Egbring R, Radtke KP, Liesenfeld A, Pittner P. Participation and interactions of neutrophil elastase in haemostatic disorders of patients with severe infections. Eur J Haematol. 1987; 35:231-40.
Pizzo SV. Serpin receptor 1: a hepatic receptor that mediates the clearance of antithrombin III-proteinase complexes. In: Rosenberg ED, ed. Role of antithrombin III in coagulation disorders: state of the art review. Am J Med 1989; 87:l-14.
Hesselvik JC, Malm J, Dahlback B, Blomb M. Protein C. Protein S and C4b-binding protein in severe infection and septic shock. Thromb Hemost 1991; 65:126-31.
Phillipe J, Offner F, Declerck PJ, Leroux-Roels C, Vogelaers D. Fibnnolysis and coagulation in patients with infectious disease and sepsis. Thromb Haemost 1991; 65:291-95. Lorente A, García-Frade L, Landín L, de Pablo R, Torrado C, Renes E, et al. Time course of hemostatic abnormalities in sepsis and its relation to outcome. Chest 1993;103;1536-42.
Lorente A, García-Frade L, Landín L, de Pablo R, Torrado C, Renes E, et al. Time course of hemostatic abnormalities in sepsis and its relation to outcome. Chest 1993;103;1536-42.
Fourrier F, Jourdain M, Tournoys A. Clinical trial results with antithrombin III in sepsis. Critical Care Medicine 2000;28: 38–43.
El Beshlawy A, Alaraby I, Abou Hussein H, Abou-Elew HH.Study of protein C, protein S, and antithrombin III in newborns with sepsis. Pediatr Crit Care Med. 2010 ;11(1):52-59.
Ostermann H. Antithrombin III in Sepsis. New evidences and open questions. Minerva Anestesiologica 2002:68: 445-48.
Lauterbach R, Pawlik D, Radziszewska R, Woźniak J Rytlewski K. Antithrombin III and protein C levels in early recognition of late-onset sepsis in newborns. European J Pediatr 2006;165:585-89.
Kountchev J, Bijuklic K, Bellmann R, Wiedermann CJ, Joannidis M. Reduction of D-dimer levels after therapeutic administration of antithrombin in acquired antithrombin deficiency of severe sepsis. Crit Care 2005;9:596–600.
Gary T, Yan SB, Basson B, Comp P, Russell JA, Cariou A. Universal changes in biomarkers of coagulation and inflammation occur in patients with severe sepsis, regardless of causative micro-organism. Crit Care 2004;8:82–90.
Gando S, Nanzaki S, Sasaki S, Kenichiro A. Activation of the extrinsic coagulation pathway in patients with severe sepsis and septic shock. Crit Care Med 1998;26:2005–09
Martinez MA, Pena JM, Fernandez A, Jimenez M, Juarez S, Madero R, Vazquez JJ. Time course and prognostic significance of hemostatic changes in sepsis: relation to tumor necrosis factor-α. Crit Care Med 1999;27:1303– 08.
Hesselvik JF, Blomback M, Brodin B, Maller R. Coagulation, fibrinolysis, and kallikrein systems in sepsis: relation to outcome. Crit Care Med 1989;17:724–33.
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
Copyright (c) 2016 Journal of Rawalpindi Medical College