Active ankylosing spondylitis increases blood loss during total hip arthroplasty for a stiff hip joint.
Ankylosing spondylitis
Blood loss
Disease activity
Total hip arthroplasty
Journal
BMC musculoskeletal disorders
ISSN: 1471-2474
Titre abrégé: BMC Musculoskelet Disord
Pays: England
ID NLM: 100968565
Informations de publication
Date de publication:
15 Apr 2020
15 Apr 2020
Historique:
received:
07
08
2019
accepted:
07
04
2020
entrez:
16
4
2020
pubmed:
16
4
2020
medline:
8
1
2021
Statut:
epublish
Résumé
Total hip arthroplasty (THA) has been highlighted as the best treatment option for ankylosing spondylitis (AS) patients with advanced hip involvement. The huge blood loss associated with THA is a common concern of postoperative complications. Disease activity is a specific reflection of systematic inflammation of AS. The purpose of this study was to determine the effect of disease activity on blood loss during THA in patients with AS. Forty-nine patients with AS who underwent unilateral THAs were retrospectively studied. Ankylosing Spondylitis Disease Activity Score (ASDAS) was employed to evaluate the disease activity. Orthopedic Surgery Transfusion Hemoglobin European Overview (OSTHEO) formula was used to assess the surgical blood loss. The patients were divided into active group (ASDAS≥1.3; n = 32) and stable groups (ASDAS< 1.3; n = 17) based on the ASDAS. Peri-operative laboratory values, plain radiographs, intra-operative data, transfusion volume, and use of hemostatic agents were recorded and statistically analyzed. The ASDAS, pre-operative C-reactive protein level, erythrocyte sedimentation rate, and fibrinogen concentration in the active group were higher than the stable group (all P < 0.05); however, the pre-operative hemoglobin concentration and albumin level were higher in the stable group (both P < 0.05). The total blood loss during THA in stable patients was 1415.31 mL and 2035.04 mL in active patients (P = 0.006). The difference between the two groups was shown to be consistent after excluding the gender difference (P = 0.030). A high transfusion rate existed in both groups (stable group, 76.47% with an average of 1.53 units; active group, 84.37% with an average of 2.31 units), but there was no significant difference between the two groups (both P > 0.05). Compensated blood loss, corresponding to transfusion, was noted significantly more in the active group compared to the stable group (P = 0.027). There was no significant difference with regard to functional recovery (P > 0.05). Active AS patients are at high risk for increased blood loss during THA compared to stable patients. The underlying mechanism includes disorders of the coagulation and fibrinolytic systems, poor nutrition status, osteoporosis, imbalance of oxidative-antioxidative status and local inflammatory reaction. It is strongly recommended to perform THA in AS patients with stable disease.
Sections du résumé
BACKGROUND
BACKGROUND
Total hip arthroplasty (THA) has been highlighted as the best treatment option for ankylosing spondylitis (AS) patients with advanced hip involvement. The huge blood loss associated with THA is a common concern of postoperative complications. Disease activity is a specific reflection of systematic inflammation of AS. The purpose of this study was to determine the effect of disease activity on blood loss during THA in patients with AS.
METHODS
METHODS
Forty-nine patients with AS who underwent unilateral THAs were retrospectively studied. Ankylosing Spondylitis Disease Activity Score (ASDAS) was employed to evaluate the disease activity. Orthopedic Surgery Transfusion Hemoglobin European Overview (OSTHEO) formula was used to assess the surgical blood loss. The patients were divided into active group (ASDAS≥1.3; n = 32) and stable groups (ASDAS< 1.3; n = 17) based on the ASDAS. Peri-operative laboratory values, plain radiographs, intra-operative data, transfusion volume, and use of hemostatic agents were recorded and statistically analyzed.
RESULTS
RESULTS
The ASDAS, pre-operative C-reactive protein level, erythrocyte sedimentation rate, and fibrinogen concentration in the active group were higher than the stable group (all P < 0.05); however, the pre-operative hemoglobin concentration and albumin level were higher in the stable group (both P < 0.05). The total blood loss during THA in stable patients was 1415.31 mL and 2035.04 mL in active patients (P = 0.006). The difference between the two groups was shown to be consistent after excluding the gender difference (P = 0.030). A high transfusion rate existed in both groups (stable group, 76.47% with an average of 1.53 units; active group, 84.37% with an average of 2.31 units), but there was no significant difference between the two groups (both P > 0.05). Compensated blood loss, corresponding to transfusion, was noted significantly more in the active group compared to the stable group (P = 0.027). There was no significant difference with regard to functional recovery (P > 0.05).
CONCLUSION
CONCLUSIONS
Active AS patients are at high risk for increased blood loss during THA compared to stable patients. The underlying mechanism includes disorders of the coagulation and fibrinolytic systems, poor nutrition status, osteoporosis, imbalance of oxidative-antioxidative status and local inflammatory reaction. It is strongly recommended to perform THA in AS patients with stable disease.
Identifiants
pubmed: 32293393
doi: 10.1186/s12891-020-03278-2
pii: 10.1186/s12891-020-03278-2
pmc: PMC7158031
doi:
Substances chimiques
Hemostatics
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
243Références
Osteoporos Int. 2001;12(7):605-9
pubmed: 11527060
J Arthroplasty. 2017 May;32(5):1516-1519
pubmed: 28089468
Rheumatol Int. 2007 Oct;27(12):1131-4
pubmed: 17443328
Lancet. 2007 Apr 21;369(9570):1379-1390
pubmed: 17448825
Rheumatol Int. 2013 Jul;33(7):1779-83
pubmed: 23297014
Arthritis Care Res (Hoboken). 2017 Dec;69(12):1845-1854
pubmed: 28129484
Ann Rheum Dis. 2009 Mar;68(3):362-6
pubmed: 18390569
Semin Arthritis Rheum. 2014 Dec;44(3):345-52
pubmed: 25077842
Br J Anaesth. 2005 Jul;95(1):33-42
pubmed: 15486006
J Bone Joint Surg Am. 2017 Mar 1;99(5):373-378
pubmed: 28244907
Cochrane Database Syst Rev. 2015 Apr 18;(4):CD005468
pubmed: 25887212
Arthritis Rheumatol. 2016 Feb;68(2):282-98
pubmed: 26401991
Clin Rheumatol. 2013 Aug;32(8):1115-20
pubmed: 23624589
J Rheumatol. 1999 Oct;26(10):2205-9
pubmed: 10529141
Br J Anaesth. 2007 Dec;99(6):794-800
pubmed: 17928302
Semin Arthritis Rheum. 2004 Dec;34(3):585-92
pubmed: 15609262
Curr Opin Rheumatol. 2002 Jul;14(4):354-60
pubmed: 12118167
Ann Rheum Dis. 2011 Nov;70(11):1921-5
pubmed: 21784726
Biomed Res Int. 2014;2014:742393
pubmed: 24959587
Arthritis Rheum. 2009 Aug 15;61(8):1032-6
pubmed: 19644896
Curr Opin Rheumatol. 2007 Jul;19(4):335-9
pubmed: 17551362
Bone Joint J. 2017 Jun;99-B(6):732-740
pubmed: 28566391
J Arthroplasty. 2016 Jul;31(7):1504-9
pubmed: 27006146
Rheumatology (Oxford). 2010 Jan;49(1):73-81
pubmed: 19605374
Clin Exp Immunol. 2003 Apr;132(1):158-62
pubmed: 12653851
Clin Rheumatol. 2012 Nov;31(11):1529-35
pubmed: 22706444
Rheumatology (Oxford). 2019 Jun 1;58(6):1040-1046
pubmed: 30624693
J Rheumatol. 2018 Aug;45(9):1334-1336
pubmed: 30173183
Clin Exp Rheumatol. 2015 Jul-Aug;33(4):465-70
pubmed: 25962324
J Bone Joint Surg Am. 1970 Apr;52(3):457-67
pubmed: 5425640
Yonsei Med J. 2003 Jun 30;44(3):379-84
pubmed: 12833574
J Back Musculoskelet Rehabil. 2018;31(3):499-505
pubmed: 29504521
J Thromb Haemost. 2003 Dec;1(12):2510-5
pubmed: 14675085
Curr Opin Rheumatol. 2014 May;26(3):259-68
pubmed: 24625371
J Rheumatol. 2006 Aug;33(8):1516-22
pubmed: 16881108
Clin Rheumatol. 2011 Apr;30(4):511-4
pubmed: 20714763
Rheumatol Int. 2012 Sep;32(9):2801-8
pubmed: 21858541
Br J Haematol. 2001 Apr;113(1):24-31
pubmed: 11328275
Ann Rheum Dis. 2009 Dec;68(12):1811-8
pubmed: 19060001
Transfusion. 2003 Apr;43(4):459-69
pubmed: 12662278
Clin Rheumatol. 2007 Feb;26(2):211-5
pubmed: 16583185
Anesthesiology. 2010 Aug;113(2):482-95
pubmed: 20613475
Z Rheumatol. 1993 Nov-Dec;52(6):383-9
pubmed: 8147132
Arthritis Res Ther. 2012 May 08;14(3):R108
pubmed: 22569245
Rheumatology (Oxford). 2006 Oct;45(10):1288-93
pubmed: 16595514
Rheumatol Int. 2012 Jul;32(7):2117-24
pubmed: 21516494