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Haemarthrosis following thrombolytic therapy for acute myocardial infarction
Copyright ELSEVIER
Injury Vol. 28, No. 2, pp. 146147, 1997 0 1997 Elsevier Science Ltd. All rights reserved Printed in Great Britain ooze-1383/97 $17.00 + 0.00
PII: SOO20-1383(96)00168-4
Haemarthrosis following thrombolytic acute myocardial infarction J. Finlayson’ ‘Department UK
therapy
for
and R. A. Dunsmui? of Medicine
and ?Department
of Orthopaedic
Injury, Vol. 28, No. 2, 146-147, 1997
Introduction Tissue plasminogen activator (t-PA) is widely used in the acute treatment of myocardial infarction. Despite the widespread use of thrombolytic therapy regimens, spontaneous haemarthrosis remains a rare complication of such treatment. We describe a patient who developed a haemarthrosis of his right ankle following thrombolytic therapy for acute myocardial infarction.
Case report A 41-year-old man was admitted with a 1 h history of central chest pain. He gave a history of a minor inversion injury to his right ankle 4 days earlier. He was not taking regular medication. Electrocardiogram was diagnostic of acute anteroseptal myocardial infarction (later confirmed by cardiac enzymes). Initial laboratory investigations showed normal platelet level at 349 x 10y/l. Haemoglobin was normal at 16.4 g/d1 with a raised white cell count of 16.7 x lo’/1 consistent with an acute stress response. In keeping with the results of the GUSTO study group as relating to anterior infarction in young patients, thrombolysis was initiated using a regimen of accelerated tissue plasminogen activator (t-PA) in combination with intravenous heparin’. The activated partial thromboplastin time (aPPT) was checked at 6 h after initiation and found to be within the therapeutic range at 62 s (control 29 s). Two and a half hours after commencing treatment the patient complained of increasingly severe pain in his right ankle joint. On examination the joint was swollen and warm with signs of a tense effusion. The patient was apyrexial and WCC = 20.8 x 10y/l. Radiographs of the joint showed no bony abnormality. Seven millilitres of blood were aspirated from the joint under aseptic conditions. The ankle was splinted in a plaster of Paris backslab producing symptomatic relief. Splintage was removed at 36 h to allow mobilization.
Surgery, Crosshouse Hospital,
Kilmarnock,
Scotland,
Discussion Spontaneous haemarthrosis with subsequent joint damage is a well-known complication of oral anticoagulant therapy2. Similar complications have been reported rarely for heparin therapy3*“. During the ISIS-2 trial no reports of spontaneous haemarthrosis were made5. Only three previous reports of five patients have highlighted this problem”R. All these patients suffered knee haemarthroses. No previous cases involving the ankle or specifically implicating recent injury have been reported. Four of the five reported cases had pre-existing joint disease. Three patients received streptokinase and two tissue plasminogen activator. Four of these cases received heparin intravenously as our patient did. It has been suggested that heparin may have a potentiating effects. If this proves to be true, we may expect an increase in similar complications as the findings of the GUSTO study group become more widely accepted and the use of t-PA in combination with intravenous heparin increases. Haemarthrosis after thrombolytic therapy is rare. It requires prompt identification and treatment to minimize the risk of articular damage. Although minor joint injuries will not exclude such patients from thrombolytic therapy, their presence should be carefully sought to raise awareness of this potential complication of thrombolytic therapy.
Acknowledgements We would like to thank Dr D. O’Neill, Consultant Physician, Crosshouse Hospital for allowing us to report this case.
References 1 GUSTO. Global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries. N Engl J Med 1993; 329: 673.
147
Case reports 2 Andes WA and Edmunds JO. Hemarthrosis and Warfarin: joint destruction with anticoagulation. Thromb Haemost 1983; 49: 187. 3 Basu D, Gallus A, Hirsh J and Cade J. A prospective study of the value of monitoring heparin treatment with the activated partial thromboplastin time. N En@ J Med 1972; 287: 324. 4 Salzman EW, Deykin D, Shapiro RM and Rosenberg R. Management of heparin therapy: controlled prospective trial. N Engl ] Med 1975; 292: 1046. 5 ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; ii: 349. 6 Oldroyd KG, Hornung RS, Jones AM, Andrews NP, Dawes PT and Carson PHM. Spontaneous haemarthrosis
following thrombolytic therapy for myocardial infarction. Postgrad Med J 1990; 66: 387. 7 Sanders PA. Haemarthrosis associated with thrombolytic therapy. Br J Rheumatol 1991; 30: 236. 8 Birnbaum Y, Stahl B and Rechavia E. Spontaneous hemarthrosis following thrombolytic therapy for acute myocardial infarction. Int J Cardiology. 1993; 40: 289.
Paper
accepted
14 October
1996.
Requests for reprints should be addressed to: Mr R. A. Dunsmuir, Victoria Royal Infirmary NHS Trust, Langside Road, Glasgow G42 9TY, Scotland, UK.
Injury Vol. 28, No. 2, pp. 146147, 1997 0 1997 Elsevier Science Ltd. All rights reserved Printed in Great Britain ooze-1383/97 $17.00 + 0.00
PII: SOO20-1383(96)00168-4
Haemarthrosis following thrombolytic acute myocardial infarction J. Finlayson’ ‘Department UK
therapy
for
and R. A. Dunsmui? of Medicine
and ?Department
of Orthopaedic
Injury, Vol. 28, No. 2, 146-147, 1997
Introduction Tissue plasminogen activator (t-PA) is widely used in the acute treatment of myocardial infarction. Despite the widespread use of thrombolytic therapy regimens, spontaneous haemarthrosis remains a rare complication of such treatment. We describe a patient who developed a haemarthrosis of his right ankle following thrombolytic therapy for acute myocardial infarction.
Case report A 41-year-old man was admitted with a 1 h history of central chest pain. He gave a history of a minor inversion injury to his right ankle 4 days earlier. He was not taking regular medication. Electrocardiogram was diagnostic of acute anteroseptal myocardial infarction (later confirmed by cardiac enzymes). Initial laboratory investigations showed normal platelet level at 349 x 10y/l. Haemoglobin was normal at 16.4 g/d1 with a raised white cell count of 16.7 x lo’/1 consistent with an acute stress response. In keeping with the results of the GUSTO study group as relating to anterior infarction in young patients, thrombolysis was initiated using a regimen of accelerated tissue plasminogen activator (t-PA) in combination with intravenous heparin’. The activated partial thromboplastin time (aPPT) was checked at 6 h after initiation and found to be within the therapeutic range at 62 s (control 29 s). Two and a half hours after commencing treatment the patient complained of increasingly severe pain in his right ankle joint. On examination the joint was swollen and warm with signs of a tense effusion. The patient was apyrexial and WCC = 20.8 x 10y/l. Radiographs of the joint showed no bony abnormality. Seven millilitres of blood were aspirated from the joint under aseptic conditions. The ankle was splinted in a plaster of Paris backslab producing symptomatic relief. Splintage was removed at 36 h to allow mobilization.
Surgery, Crosshouse Hospital,
Kilmarnock,
Scotland,
Discussion Spontaneous haemarthrosis with subsequent joint damage is a well-known complication of oral anticoagulant therapy2. Similar complications have been reported rarely for heparin therapy3*“. During the ISIS-2 trial no reports of spontaneous haemarthrosis were made5. Only three previous reports of five patients have highlighted this problem”R. All these patients suffered knee haemarthroses. No previous cases involving the ankle or specifically implicating recent injury have been reported. Four of the five reported cases had pre-existing joint disease. Three patients received streptokinase and two tissue plasminogen activator. Four of these cases received heparin intravenously as our patient did. It has been suggested that heparin may have a potentiating effects. If this proves to be true, we may expect an increase in similar complications as the findings of the GUSTO study group become more widely accepted and the use of t-PA in combination with intravenous heparin increases. Haemarthrosis after thrombolytic therapy is rare. It requires prompt identification and treatment to minimize the risk of articular damage. Although minor joint injuries will not exclude such patients from thrombolytic therapy, their presence should be carefully sought to raise awareness of this potential complication of thrombolytic therapy.
Acknowledgements We would like to thank Dr D. O’Neill, Consultant Physician, Crosshouse Hospital for allowing us to report this case.
References 1 GUSTO. Global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries. N Engl J Med 1993; 329: 673.
147
Case reports 2 Andes WA and Edmunds JO. Hemarthrosis and Warfarin: joint destruction with anticoagulation. Thromb Haemost 1983; 49: 187. 3 Basu D, Gallus A, Hirsh J and Cade J. A prospective study of the value of monitoring heparin treatment with the activated partial thromboplastin time. N En@ J Med 1972; 287: 324. 4 Salzman EW, Deykin D, Shapiro RM and Rosenberg R. Management of heparin therapy: controlled prospective trial. N Engl ] Med 1975; 292: 1046. 5 ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; ii: 349. 6 Oldroyd KG, Hornung RS, Jones AM, Andrews NP, Dawes PT and Carson PHM. Spontaneous haemarthrosis
following thrombolytic therapy for myocardial infarction. Postgrad Med J 1990; 66: 387. 7 Sanders PA. Haemarthrosis associated with thrombolytic therapy. Br J Rheumatol 1991; 30: 236. 8 Birnbaum Y, Stahl B and Rechavia E. Spontaneous hemarthrosis following thrombolytic therapy for acute myocardial infarction. Int J Cardiology. 1993; 40: 289.
Paper
accepted
14 October
1996.
Requests for reprints should be addressed to: Mr R. A. Dunsmuir, Victoria Royal Infirmary NHS Trust, Langside Road, Glasgow G42 9TY, Scotland, UK.