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Thrombolysis for postoperative pulmonary embolism SIR,-Your July 4 editorial mentions the understandable reluctance of physicians to treat postoperatively patients with pulmonary embolism with thrombolysis because of the risks of bleeding. As in many areas of medicine the physician must weigh the risks and benefits of such treatment when making a clinical decision. In massive pulmonary embolism mortality is high and may justify a high-risk strategy. We describe two cases of massive pulmonary embolism complicating surgery which we have treated with thrombolysis. Patient 1-An 82-year-old man had a large pleomorphic sarcoma removed from his right thigh. 13 days after operation he suddenly collapsed, his blood pressure fell to 80/50 mm Hg, and he had a narrow complex tachycardia of 150 beats/min. Jugular venous pressure was raised at 4 cm above the sternal angle and he subsequently had haemoptysis. Tachycardia responded to intravenous amiodarone but he remained hypotensive (blood pressure 90/60 mm Hg) and tachycardic (heart rate 100 beats/min). Arterial blood gases showed pH 72, POz 49 kPa, PCOz 2-9 kPa, saturation 76%, and ventilation/perfusion scan confirmed multiple pulmonary emboli. He was treated with an intravenous bolus of 250 000 units of streptokinase followed by 100 000 units per hour by constant infusion for 24 hours during which the oxygen saturation increased from 93% to 98% on 6 litres oxygen per min. The next day he developed a left hemiparesis and computed tomography of the brain showed a cerebral infarct. He was treated with intravenous heparin 25 000 units until he was adequately anticoagulated with oral warfarin. He made a complete neurological and physical recovery and never bled from the operation site. He was discharged well on day 30. Patient 2-An 83-year-old woman had an open reduction and internal fixation for a fractured wrist. On the first postoperative day she complained of dizziness and pleuritic chest pain. Blood pressure was 80/60 mm Hg with an irregular pulse of 80 beats/min. The electrocardiogram showed right bundle branch block and left axis deviation (having preoperatively shown left bundle branch block). Several hours later she collapsed and lost consciousness briefly. Blood pressure was 60/30 mm Hg, heart rate 90 beats/min, and jugular venous pressure was raised; pulmonary embolism was diagnosed and she was treated with the same regimen of streptokinase as patient 1. She recovered promptly with a blood pressure of 155/70 mm Hg and pulse rate of 106 beats/min. Heparin was continued at a dose of 25 000 units by intravenous infusion over 24 hours. Over the next 48 hours she bled profusely from the surgical wound which was opened to relieve swelling. Haemoglobin dropped at one point to 5 .1 g/dl. Heparin was discontinued and she was transfused with 8 units of packed cells. After delayed primary wound closure and skin grafting she was discharged clinically well on day 24. These two cases illustrate that streptokinase can be used in the postoperative period for massive pulmonary embolism with good results. In the first patient bleeding did not occur probably because the surgical wound was 13 days old. In the second, bleeding did occur from the wound, but with supportive care, with transfusion and surgical toilet, it was arrested. We believe that without thrombolysis both these patients would probably have died. Department of Cardiology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK
A. T. WILSON P. A. WOODMANSEY K. S. CHANNER
SIR,-Your July 4 editorial on thrombolysis for pulmonary embolism raises the question of the efficacy of the large bolus dose of streptokinase in the treatment of this condition. We report a patient with an excellent result from the use of such a regimen. A 25-year-old previously healthy woman had a sudden collapse and dyspnoea. She was recovering from chicken pox and had largely remained in bed for the previous 10 days. She took oral contraceptives but did not smoke. On admission, she was cyanotic and in shock: systolic blood pressure was 60 mm Hg, heart rate was 100/min, and the peripheral circulation was shut down. Blood gas analysis revealed pronounced hypoxaemia despite hyperventilation:
was 7-4 kPa (normal 11.3-13-3) and PACO, was 44 kPa (4.6-6.0). Only the right middle lobe was normally perfused in a pulmonary perfusion scan, suggesting massive pulmonary embolism. Ultrasonography revealed right ventricular enlargement. The interventricular septal movement was paradoxical and the left ventricle was slightly compressed. The peak systolic gradient in tricuspid regurgitation was 27 mm Hg corresponding to a somewhat high estimated pulmonary artery systolic blood pressure of 38-40 mm Hg.
PaOz
Streptokinase 1 ’5 million U was infused within 1 hour into a peripheral vein. At the beginning of the infusion blood pressure was not measurable despite fluid infusion (3500 ml per 2 hour) and maximum dopamine and dobutamine administration. Shortly before the infusion finished the circulation improved with peripheral opening. Blood pressure rose to 110/75 mm Hg and respiratory rate fell from 28 to 20/min. Oxygen saturation increased from 95 % to 99%. A few hours later she had minor bleeding from the nose but otherwise made a rapid recovery and was symptomfree after the first day. Treatment continued with intravenous heparin for 6 days, with warfarin. A second echocardiogram on day 3 was normal with no tricuspid regurgitation. A control perfusion scan on day 7 showed only minor defects in the upper lobes of both
lungs. The
patient recovered well from the circulatory collapse after with a large bolus of streptokinase for 1 hour instead of the traditional infusion over 24-48 hours. The regimen was the same as that used in myocardial infarction. It has several advantages: it is cheap, easy to use, and fast, which is of utmost importance in massive pulmonary embolism. Nor are invasive procedures necessary; these are not always feasible, delay treatment, and increase severe complications.1 Moreover, the good result in this woman compares favourably with those of the more complex therapies.z treatment
First Department of Medicine, Helsinki University Central Hosptial, 00290 Helsinki, Finland 1.
Meyer G, Sors H, Charbonnier B,
SINIKKA POHJOLA-SINTONEN
JUHANI PARTANEN et
al. Effects of
intravenous
urokinase
versus
alteplase on total pulmonary resistance in acute massive pulmonary embolism a European multicenter double-blind trial. J Am Coll Cardiol 1992; 19: 239-45 2. Essop MR, Middlemost S, Skoularigis J, Sareli P. Simultaneous mechanical clot fragmentation and pharmcologic thrombolysis in acute massive pulmonary embolism. Am J Cardiol 1992; 69: 427-30.
megakaryocyte migration after thrombolytic therapy and benefit of aspirin with streptokinase Excessive
SIR,- The Second International Study of Infarct Survival showed enhanced survival by adding aspirin to streptokinase. It has been suggested that platelets are produced by circulating megakaryocytes.We describe a patient in whom generated plasmin might have induced excessive megakaryocyte migration leading to increased platelet formation. A 61-year-old man was admitted for acute myocardial infarction and received streptokinase. This therapy was stopped after 15 min because systolic blood pressure was under 50 mm Hg. He was treated with dopamine, dobutamine, intravenous diamorphine, and aspirin 80 mg daily. He developed increasingly severe forward and backward failure, necessitating intubation 60 h after admission. Because of suspicion of pulmonary embolism he was again treated with intravenous streptokinase. A systemic lytic state was achieved and no further adverse reactions were reported. Further analyses indicated that pulmonary embolism was highly unlikely and streptokinase was stopped. 2 h later and 3 days after intubation, while the patient was still on ventilatory assistance and with the same vasoactive medication, blood was collected from the pulmonary artery. In the first sample we found 200 intact megakaryocytes and in the second only 2 megakaryocytes per ml. Previously we did not find such a high megakaryocyte count in patients with septicaemia, adult respiratory distress syndrome, or on vasoactive medication; the number of megakaryocytes recovered from central venous blood of patients in stable condition undergoing cardiac catheterisation was 4’5/ml (range 0-24).’ Megakaryocytes obtained 2 h after streptokinase stained 100°o
Thrombolysis for postoperative pulmonary embolism SIR,-Your July 4 editorial mentions the understandable reluctance of physicians to treat postoperatively patients with pulmonary embolism with thrombolysis because of the risks of bleeding. As in many areas of medicine the physician must weigh the risks and benefits of such treatment when making a clinical decision. In massive pulmonary embolism mortality is high and may justify a high-risk strategy. We describe two cases of massive pulmonary embolism complicating surgery which we have treated with thrombolysis. Patient 1-An 82-year-old man had a large pleomorphic sarcoma removed from his right thigh. 13 days after operation he suddenly collapsed, his blood pressure fell to 80/50 mm Hg, and he had a narrow complex tachycardia of 150 beats/min. Jugular venous pressure was raised at 4 cm above the sternal angle and he subsequently had haemoptysis. Tachycardia responded to intravenous amiodarone but he remained hypotensive (blood pressure 90/60 mm Hg) and tachycardic (heart rate 100 beats/min). Arterial blood gases showed pH 72, POz 49 kPa, PCOz 2-9 kPa, saturation 76%, and ventilation/perfusion scan confirmed multiple pulmonary emboli. He was treated with an intravenous bolus of 250 000 units of streptokinase followed by 100 000 units per hour by constant infusion for 24 hours during which the oxygen saturation increased from 93% to 98% on 6 litres oxygen per min. The next day he developed a left hemiparesis and computed tomography of the brain showed a cerebral infarct. He was treated with intravenous heparin 25 000 units until he was adequately anticoagulated with oral warfarin. He made a complete neurological and physical recovery and never bled from the operation site. He was discharged well on day 30. Patient 2-An 83-year-old woman had an open reduction and internal fixation for a fractured wrist. On the first postoperative day she complained of dizziness and pleuritic chest pain. Blood pressure was 80/60 mm Hg with an irregular pulse of 80 beats/min. The electrocardiogram showed right bundle branch block and left axis deviation (having preoperatively shown left bundle branch block). Several hours later she collapsed and lost consciousness briefly. Blood pressure was 60/30 mm Hg, heart rate 90 beats/min, and jugular venous pressure was raised; pulmonary embolism was diagnosed and she was treated with the same regimen of streptokinase as patient 1. She recovered promptly with a blood pressure of 155/70 mm Hg and pulse rate of 106 beats/min. Heparin was continued at a dose of 25 000 units by intravenous infusion over 24 hours. Over the next 48 hours she bled profusely from the surgical wound which was opened to relieve swelling. Haemoglobin dropped at one point to 5 .1 g/dl. Heparin was discontinued and she was transfused with 8 units of packed cells. After delayed primary wound closure and skin grafting she was discharged clinically well on day 24. These two cases illustrate that streptokinase can be used in the postoperative period for massive pulmonary embolism with good results. In the first patient bleeding did not occur probably because the surgical wound was 13 days old. In the second, bleeding did occur from the wound, but with supportive care, with transfusion and surgical toilet, it was arrested. We believe that without thrombolysis both these patients would probably have died. Department of Cardiology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK
A. T. WILSON P. A. WOODMANSEY K. S. CHANNER
SIR,-Your July 4 editorial on thrombolysis for pulmonary embolism raises the question of the efficacy of the large bolus dose of streptokinase in the treatment of this condition. We report a patient with an excellent result from the use of such a regimen. A 25-year-old previously healthy woman had a sudden collapse and dyspnoea. She was recovering from chicken pox and had largely remained in bed for the previous 10 days. She took oral contraceptives but did not smoke. On admission, she was cyanotic and in shock: systolic blood pressure was 60 mm Hg, heart rate was 100/min, and the peripheral circulation was shut down. Blood gas analysis revealed pronounced hypoxaemia despite hyperventilation:
was 7-4 kPa (normal 11.3-13-3) and PACO, was 44 kPa (4.6-6.0). Only the right middle lobe was normally perfused in a pulmonary perfusion scan, suggesting massive pulmonary embolism. Ultrasonography revealed right ventricular enlargement. The interventricular septal movement was paradoxical and the left ventricle was slightly compressed. The peak systolic gradient in tricuspid regurgitation was 27 mm Hg corresponding to a somewhat high estimated pulmonary artery systolic blood pressure of 38-40 mm Hg.
PaOz
Streptokinase 1 ’5 million U was infused within 1 hour into a peripheral vein. At the beginning of the infusion blood pressure was not measurable despite fluid infusion (3500 ml per 2 hour) and maximum dopamine and dobutamine administration. Shortly before the infusion finished the circulation improved with peripheral opening. Blood pressure rose to 110/75 mm Hg and respiratory rate fell from 28 to 20/min. Oxygen saturation increased from 95 % to 99%. A few hours later she had minor bleeding from the nose but otherwise made a rapid recovery and was symptomfree after the first day. Treatment continued with intravenous heparin for 6 days, with warfarin. A second echocardiogram on day 3 was normal with no tricuspid regurgitation. A control perfusion scan on day 7 showed only minor defects in the upper lobes of both
lungs. The
patient recovered well from the circulatory collapse after with a large bolus of streptokinase for 1 hour instead of the traditional infusion over 24-48 hours. The regimen was the same as that used in myocardial infarction. It has several advantages: it is cheap, easy to use, and fast, which is of utmost importance in massive pulmonary embolism. Nor are invasive procedures necessary; these are not always feasible, delay treatment, and increase severe complications.1 Moreover, the good result in this woman compares favourably with those of the more complex therapies.z treatment
First Department of Medicine, Helsinki University Central Hosptial, 00290 Helsinki, Finland 1.
Meyer G, Sors H, Charbonnier B,
SINIKKA POHJOLA-SINTONEN
JUHANI PARTANEN et
al. Effects of
intravenous
urokinase
versus
alteplase on total pulmonary resistance in acute massive pulmonary embolism a European multicenter double-blind trial. J Am Coll Cardiol 1992; 19: 239-45 2. Essop MR, Middlemost S, Skoularigis J, Sareli P. Simultaneous mechanical clot fragmentation and pharmcologic thrombolysis in acute massive pulmonary embolism. Am J Cardiol 1992; 69: 427-30.
megakaryocyte migration after thrombolytic therapy and benefit of aspirin with streptokinase Excessive
SIR,- The Second International Study of Infarct Survival showed enhanced survival by adding aspirin to streptokinase. It has been suggested that platelets are produced by circulating megakaryocytes.We describe a patient in whom generated plasmin might have induced excessive megakaryocyte migration leading to increased platelet formation. A 61-year-old man was admitted for acute myocardial infarction and received streptokinase. This therapy was stopped after 15 min because systolic blood pressure was under 50 mm Hg. He was treated with dopamine, dobutamine, intravenous diamorphine, and aspirin 80 mg daily. He developed increasingly severe forward and backward failure, necessitating intubation 60 h after admission. Because of suspicion of pulmonary embolism he was again treated with intravenous streptokinase. A systemic lytic state was achieved and no further adverse reactions were reported. Further analyses indicated that pulmonary embolism was highly unlikely and streptokinase was stopped. 2 h later and 3 days after intubation, while the patient was still on ventilatory assistance and with the same vasoactive medication, blood was collected from the pulmonary artery. In the first sample we found 200 intact megakaryocytes and in the second only 2 megakaryocytes per ml. Previously we did not find such a high megakaryocyte count in patients with septicaemia, adult respiratory distress syndrome, or on vasoactive medication; the number of megakaryocytes recovered from central venous blood of patients in stable condition undergoing cardiac catheterisation was 4’5/ml (range 0-24).’ Megakaryocytes obtained 2 h after streptokinase stained 100°o
