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LYSIS OF BASILAR ARTERY OCCLUSION WITH TISSUE PLASMINOGEN ACTIVATOR
1391
Letters
to
the Editor
LYSIS OF BASILAR ARTERY OCCLUSION WITH TISSUE PLASMINOGEN ACTIVATOR
SIR,--Occlusion of the basilar artery has a very poor prognosis. Depending on site and extent of the thrombus, case fatality rates of up to 90% have been reported, especially in patients with coma at the onset of symptoms.1 Recanalisation within 3 or 4 hours of the stroke may prevent severe neurological damage, so the diagnostic procedure must be rapid and simple. Local injection of a fibrinolytic agent via an arterial catheter proximal to the thrombus2 is often difficult and time-consuming. Systemic administration would be preferable, provided haemorrhagic complications can be avoided. Tissue plasminogen activator (tPA) shows greater clot selectivity than streptokinase or urokinase, and myocardial infarction studies show that it does not induce systemic fibrinolysis. We describe here the emergency treatment of a patient with thrombosis of the basilar artery, using tPA (predominantly single chain tPA, Genentech; supplied by Thomae, Biberach, West Germany).
A 64-year-old woman with a history of myocardial infarction suddenly became comatose at home and was admitted to our emergency ward 50 min later. She was breathing spontaneously via a nasotracheal tube and showed left hemiparesis with a bilateral positive Babinski’s sign. During the neurological examination decerebrate rigidity developed. A cranial computed tomographic scan was normal except for some small calcifications surrounding the fourth ventricle. Arterial digital subtraction angiography via the right femoral artery 130 min after the onset of symptoms (7F
’Sidewinder’ catheter) revealed basilar artery occlusion. With the informed consent of the patient’s relatives we immediately administered a bolus injection of 15 mg tPA, followed by an infusion of 50 mg tPA over 30 min via the catheter placed in the proximal part of the left vertebral artery and then 35 mg tPA over the following 60 min (total dose 15 mg/kg body weight). Digital subtraction studies 90 min and 20 h after the start of fibrinolysis revealed recanalisation of the whole basilar artery (figure). Cranial computerised tomographic scans 1 h and 20 h after fibrinolysis did not reveal any haemorrhagic complications. Further therapy consisted of heparin and antihypertensive medication. Her fibrinogen level dropped from 370 mg/dl pre-treatment to 105 mg/dl and then rose to 220 mg/dl in the ensuing 24 hours. The patient regained consciousness in 6 days and was extubated on day 8. 4 weeks after the event she showed only periodic disorientation, mild paresis of horizontal gaze, and slightly ataxic
walking. Occlusion of the basilar artery is a neurological emergency requiring rapid fibrinolysis of the thrombus. Arterial digital subtraction arteriography is a safe and rapid procedure. The clot-selective activity of tPA permits systemic application. In the rabbit carotid artery model tPA achieved a significant reduction in neurological damage, suggesting that this thrombolytic agent might be of great value for the emergency treatment of embolic stroke.4-<’> In our patient, tPA given 2hours after vessel occlusion resolved the clot immediately without haemorrhagic complications. Departments of Neurology, Cardiology and Radiology, University Hospital, 3400 Gottingen, West Germany
TH. HENZE A. BOEER U. TEBBE J. ROMATOWSKI
1. Archer CR, Horenstein S. Basilar artery occlusion. Stroke 1977; 8: 383-90. 2. Zeumer H, Hacke W, Ringelstein EB. Intra-arterial thrombolysis in vertebrobasilar thromboembolic disease. A J Neuroradiol 1983; 4: 401-04. 3. Verstraete M, Bernard R, Bory M, et al. Randomised trial of intravenous recombinant tissue-type plasminogen activator versus intravenous streptokinase in acute myocardial infarction. Lancet 1985; i: 842-47. 4. Zivin JA, Fisher M, De Girolami U, Hemenway CC, Stashak JA. Tissue plasminogen activator reduces neurological damage after cerebral embolism. Science 1985; 230: 1289-92. 5. Zivin JA, Hemenway CC, DeGirolami U. Delayed therapy of embolic stroke with tissue plasminogen activator. Ann Neurol 1986; 20: 154. 6. Kissel P, Chehrazi B, Seibert JA, Wagner FC. Digital angiographic quantification of blood flow dynamics in embolic stroke treated with tissue-type plasminogen activator.
Stroke 1987; 18: 293.
REMISSION OF CROHN’S DISEASE WITH ANTIMYCOBACTERIAL CHEMOTHERAPY
SIR,—The patient is a 52-year-old man with Crohndisease. His
began in 1983 with a rectal fissure, and biopsy revealed granulomatous infiltrations. Over the next 2 years he experienced insidious development of intermittent mid-lower abdominal pain, rectal bleeding, weakness, and malaise. 2 years before his latest hospital admission, while travelling overseas, he experienced an acute episode of vomiting, fever, chills, toxaemia, and bloody, mucoid stools (May, 1985). Colonoscopy revealed extensive inflammation of the descending colon with linear ulcerations and pseudopolyps, along with rectal sparing-fmdings characteristic of illness
Digital subtraction angiograms. Upper: total occlusion of basilar artery before tPA. Lower: 20 hours after fibrinolysis with tPA, showing recanalisation of basilar artery.
Crohn’s colitis. Amelioration of his symptoms was achieved with intravenous and oral corticosteroids and fluids. During the next two years maintenance therapy with oral metronidazole or oral sulfasalazine was unsuccessful. Treatment with 5-aminosalicylic acid (’Rowasa’, 4 g) by daily rectal enema for 21 days was also unsuccessful. The patient was incapacitated with cramps and passage of bloody mucus four to six times a day, and by prolonged, painful passage of formed stool followed by fever and
Letters
to
the Editor
LYSIS OF BASILAR ARTERY OCCLUSION WITH TISSUE PLASMINOGEN ACTIVATOR
SIR,--Occlusion of the basilar artery has a very poor prognosis. Depending on site and extent of the thrombus, case fatality rates of up to 90% have been reported, especially in patients with coma at the onset of symptoms.1 Recanalisation within 3 or 4 hours of the stroke may prevent severe neurological damage, so the diagnostic procedure must be rapid and simple. Local injection of a fibrinolytic agent via an arterial catheter proximal to the thrombus2 is often difficult and time-consuming. Systemic administration would be preferable, provided haemorrhagic complications can be avoided. Tissue plasminogen activator (tPA) shows greater clot selectivity than streptokinase or urokinase, and myocardial infarction studies show that it does not induce systemic fibrinolysis. We describe here the emergency treatment of a patient with thrombosis of the basilar artery, using tPA (predominantly single chain tPA, Genentech; supplied by Thomae, Biberach, West Germany).
A 64-year-old woman with a history of myocardial infarction suddenly became comatose at home and was admitted to our emergency ward 50 min later. She was breathing spontaneously via a nasotracheal tube and showed left hemiparesis with a bilateral positive Babinski’s sign. During the neurological examination decerebrate rigidity developed. A cranial computed tomographic scan was normal except for some small calcifications surrounding the fourth ventricle. Arterial digital subtraction angiography via the right femoral artery 130 min after the onset of symptoms (7F
’Sidewinder’ catheter) revealed basilar artery occlusion. With the informed consent of the patient’s relatives we immediately administered a bolus injection of 15 mg tPA, followed by an infusion of 50 mg tPA over 30 min via the catheter placed in the proximal part of the left vertebral artery and then 35 mg tPA over the following 60 min (total dose 15 mg/kg body weight). Digital subtraction studies 90 min and 20 h after the start of fibrinolysis revealed recanalisation of the whole basilar artery (figure). Cranial computerised tomographic scans 1 h and 20 h after fibrinolysis did not reveal any haemorrhagic complications. Further therapy consisted of heparin and antihypertensive medication. Her fibrinogen level dropped from 370 mg/dl pre-treatment to 105 mg/dl and then rose to 220 mg/dl in the ensuing 24 hours. The patient regained consciousness in 6 days and was extubated on day 8. 4 weeks after the event she showed only periodic disorientation, mild paresis of horizontal gaze, and slightly ataxic
walking. Occlusion of the basilar artery is a neurological emergency requiring rapid fibrinolysis of the thrombus. Arterial digital subtraction arteriography is a safe and rapid procedure. The clot-selective activity of tPA permits systemic application. In the rabbit carotid artery model tPA achieved a significant reduction in neurological damage, suggesting that this thrombolytic agent might be of great value for the emergency treatment of embolic stroke.4-<’> In our patient, tPA given 2hours after vessel occlusion resolved the clot immediately without haemorrhagic complications. Departments of Neurology, Cardiology and Radiology, University Hospital, 3400 Gottingen, West Germany
TH. HENZE A. BOEER U. TEBBE J. ROMATOWSKI
1. Archer CR, Horenstein S. Basilar artery occlusion. Stroke 1977; 8: 383-90. 2. Zeumer H, Hacke W, Ringelstein EB. Intra-arterial thrombolysis in vertebrobasilar thromboembolic disease. A J Neuroradiol 1983; 4: 401-04. 3. Verstraete M, Bernard R, Bory M, et al. Randomised trial of intravenous recombinant tissue-type plasminogen activator versus intravenous streptokinase in acute myocardial infarction. Lancet 1985; i: 842-47. 4. Zivin JA, Fisher M, De Girolami U, Hemenway CC, Stashak JA. Tissue plasminogen activator reduces neurological damage after cerebral embolism. Science 1985; 230: 1289-92. 5. Zivin JA, Hemenway CC, DeGirolami U. Delayed therapy of embolic stroke with tissue plasminogen activator. Ann Neurol 1986; 20: 154. 6. Kissel P, Chehrazi B, Seibert JA, Wagner FC. Digital angiographic quantification of blood flow dynamics in embolic stroke treated with tissue-type plasminogen activator.
Stroke 1987; 18: 293.
REMISSION OF CROHN’S DISEASE WITH ANTIMYCOBACTERIAL CHEMOTHERAPY
SIR,—The patient is a 52-year-old man with Crohndisease. His
began in 1983 with a rectal fissure, and biopsy revealed granulomatous infiltrations. Over the next 2 years he experienced insidious development of intermittent mid-lower abdominal pain, rectal bleeding, weakness, and malaise. 2 years before his latest hospital admission, while travelling overseas, he experienced an acute episode of vomiting, fever, chills, toxaemia, and bloody, mucoid stools (May, 1985). Colonoscopy revealed extensive inflammation of the descending colon with linear ulcerations and pseudopolyps, along with rectal sparing-fmdings characteristic of illness
Digital subtraction angiograms. Upper: total occlusion of basilar artery before tPA. Lower: 20 hours after fibrinolysis with tPA, showing recanalisation of basilar artery.
Crohn’s colitis. Amelioration of his symptoms was achieved with intravenous and oral corticosteroids and fluids. During the next two years maintenance therapy with oral metronidazole or oral sulfasalazine was unsuccessful. Treatment with 5-aminosalicylic acid (’Rowasa’, 4 g) by daily rectal enema for 21 days was also unsuccessful. The patient was incapacitated with cramps and passage of bloody mucus four to six times a day, and by prolonged, painful passage of formed stool followed by fever and