Hostname: page-component-586b7cd67f-r5fsc Total loading time: 0 Render date: 2024-11-25T06:14:30.107Z Has data issue: false hasContentIssue false

Fatal Streptokinase-Induced Intracerebral Haemorrhage in Cerebral Amyloid Angiopathy

Published online by Cambridge University Press:  18 September 2015

D.A. Ramsay
Affiliation:
Department of Pathology, Queen's University and Kingston General Hospital, Kingston
J.L. Penswick
Affiliation:
Department of Pathology, Queen's University and Kingston General Hospital, Kingston
D.M. Robertson*
Affiliation:
Department of Pathology, Queen's University and Kingston General Hospital, Kingston
*
Department of Pathology, Richardson Laboratory, Queen's University, Kingston, Ontario, Canada K7L 3N6
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

A fatal intracerebral haemorrhage (ICH) associated with streptokinase (SK) treatment of an acute myocardial infarction is described. Autopsy examination showed a lobar ICH and severe cerebral amyloid angiopathy (CAA). The close temporal relationship between SK administration and intracranial haemorrhage, the absence of pretreatment risk factors for ICH, and the presence of CAA suggests that these are related phenomena. Accordingly: 1. There may be a synergistic relationship between CAA and intracranial haemorrhage induced by fibrinolytic agents; 2. Thrombolytic agents may induce more frequent than expected intracranial haemorrhage in conditions associated with a high incidence of CAA, notably old age and Alzheimer's disease; 3. A regional defect in haemostasis other than vessel fragility may contribute to the intracranial haemorrhagic predisposition of CAA; 4. Autopsy examination of cases of ICH is an essential part of the audit of clinical trials of fibrinolytic agents.

Résumé:

RÉSUMÉ:

Les auteurs décrivent un cas d'hémorragie intracérébrale (HIC) fatale associée au traitement par la streptokinase (SK) d'un infarctus aigu du myocarde. À l'autopsie, on a constaté une HIC lobaire et une angiopathie amyloïde cérébrale sévère (AAC). La relation temporale étroite entre l'administration de SK et l'hémorragie intracrânienne, l'absence de facteurs de risque pour l'HIC en prétraitement et la présence d'AAC suggèrent que ces phénomènes sont reliés. Par conséquent: 1. Il peut y avoir une relation synergique entre l'AAC et l'hémorragie intracrânienne induite par les agents fibrinolytiques; 2. Les agents thrombolytiques peuvent induire plus fréquemment que prévu une hémorragie intracrânienne dans les affections associées à une incidence élevée d'AAC, particulièrement chez les vieillards et les patients atteints de la maladie d'Alzheimer; 3. Un défaut régional de l'hémostase autre que la fragilité vasculaire peut contribuer à la prédisposition à l'hémorragie intracrânienne de l'AAC; 4. L'autopsie des cas d'HIC est un élément essentiel de la révision des essais cliniques avec des agents fibrinolytiques.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1990

References

REFERENCES

1. European working party. Streptokinase in recent myocardial infarction: a controlled multicentre trial. Br Med J 1971; 3: 325331.CrossRefGoogle Scholar
2. Fletcher, AP, Alkjaersig, N, Lewis, M. A pilot study of urokinase therapy in cerebral infarction. Stroke 1976; 7: 135142.Google Scholar
3. Fletcher, AP, Sherry, S, Alkjaersig, N, et al. The maintenance of a sustained thrombolytic state in man. II. Clinical observations on patients with myocardial infarction and other thromboembolic disorders. J Clin Invest 1959; 38: 11111119.CrossRefGoogle Scholar
4. Marder, VJ, Sherry, S. Thrombolytic therapy: current status (second of two parts). New Engl J Med 1988; 318: 15851595.CrossRefGoogle Scholar
5. Meissner, AJ, Misiak, A, Ziemski, JM, et al. Hazards of thrombolytic therapy in deep vein thrombosis. J Surg 1987; 74: 991993.Google Scholar
6. Meyer, JS, Gilroy, J, Barnhard, M. Therapeutic thrombolysis in cerebral thromboembolism: randomized evaluation of intravenous streptokinase. In: Millikan, CH, Siekert, RG, Whisnant, JP, eds. Cerebral vascular diseases New York, Grune and Stratton 1965; 200211.Google Scholar
7. Meyer, JS, Gilroy, J, Barnhart, MI, et al. Anticoagulants plus streptokinase therapy in progressive stroke. JAMA 1964; 189: 373 CrossRefGoogle ScholarPubMed
8. Gruppo Italiano per Lo Studio della Streptochinasi nell’Infarcto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1: 397401.Google Scholar
9. ISIS–2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 1988; 2: 349360.Google Scholar
10. Kennedy, JW, Martin, GV, David, KB, et al. The western Washington intravenous streptokinase in acute myocardial infarction randomized trial. Circulation 1988; 77: 345352.Google Scholar
11. The Thrombolysis in Myocardial Infarction (T1MI) Phase II Pilot Study. Tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1987; 10: 51B-64B.Google Scholar
12. Topol, EJ, Morris, DC, Smalling, RW. A multicenter, randomized, placebo-controlled trial of a new form of intravenous recombinant tissue-type plasminogen activator (Activase) in acute myocardial infarction. J Am Coll Cardiol 1987; 9: 12051213.Google Scholar
13. Sherry, S. Appraisal of various thrombolytic agents in the treatment of acute myocardial infarction. Am J Med 1987; 83 (Suppl 2A): 3145.Google Scholar
14. Marder, VJ, Sherry, S. Thrombolytic therapy: current status (first of two parts). New Engl J Med 1988; 318: 15121520.CrossRefGoogle Scholar
15. Hanaway, J, Torack, R. Fletcher, AP, et al. Intracranial bleeding associated with urokinase therapy for acute ischemic hemispheric stroke. Stroke 1976; 7: 143146.Google Scholar
16. Gorelick, PB, Parikh, M, Mcdonald, L. Intracoronary streptokinase and fatal cerebellar hemorrhage. Ill Med J 1987; 171: 2830.Google Scholar
17. Ozaki, H, Reagan, TJ, Campbell, JR. Clinicopathologic studies of primary cerebral amyloid angiopathy. Mayo Clin Proc 1979; 54: 2231.Google Scholar
18. Case records of the Massachusetts General Hospital. Case 49–1982. New Engl J Med 1982; 15071514.Google Scholar
19. Gilbert, JJ, Vinters, HV. Cerebral amyloid angiopathy: incidence and complications in the aging brain. I. Cerebral hemorrhage. Stroke 1983; 14: 915923.CrossRefGoogle ScholarPubMed
20. Kalyan-Raman, UP, Kalyan-Raman, K. Cerebral amyloid angiopathy causing intracranial hemorrhage. Ann Neurol 1984; 16: 321329.CrossRefGoogle ScholarPubMed
21. Mandybur, TI. Cerebral amyloid angiopathy: the vascular pathology and complications. J Neuropathol Exp Neurol 1986; 7990.CrossRefGoogle ScholarPubMed
22. Case reports of the Massachusetts General Hospital. Case 10–1988. New Engl J Med 1988; 318: 623631.Google Scholar
23. Vinters, HV. Cerebral amyloid angiopathy: a critical review. Stroke 1987; 18: 311324.Google Scholar
24. Weisberg, LA. Significance of the fluid-blood interface in intracranial hematomas in anticoagulated patients. Comput Radiol 1987; 4: 175179.Google Scholar
25. Vinters, HV, Gilbert, JJ. Cerebral amyloid angiopathy: incidence and complications in the aging brain. II.The distribution of amyloid vascular changes. Stroke 1983; 14: 924928.Google Scholar
26. Aldrich, MS, Sherman, SA, Greenberg, HS. Cerebrovascular complications of streptokinase infusion. JAMA 1985; 253: 17771779.CrossRefGoogle ScholarPubMed
27. Vanley, CT, Aguilar, MJ, Kleinhenz, RJ, et al. Cerebral amyloid angiopathy. Hum Pathol 1981; 12: 609616.CrossRefGoogle ScholarPubMed
28. Carlson, SE, Aldrich, MS, Greenberg, HS, et al. Intracerebral hemorrhage complicating intravenous tissue plasminogen activator treatment. Arch Neurol 1988; 45: 10701073.Google Scholar
29. Bergeron, C, Ranalli, RJ, Miceli, PN. Amyloid angiopathy in Alzheimer’s disease. Can J Neurol Sci 1987; 14: 564569.Google Scholar
30. Lew, AS, Hod, H, Cercek, B, et al. Mortality and morbidity rates of patients older and younger than 75 years with acute myocardial infarction treated with intravenous streptokinase. Am J Cardiol 1987; 59: 15.CrossRefGoogle ScholarPubMed
31. Torack, RM. Congophilic angiopathy complicated by surgery and massive hemorrhage: a light and electron microscopic study. Am J Pathol 1975; 81: 349366.Google Scholar
32. Yood, RA, Skinner, M, Rubinow, A, et al. Bleeding manifestations in 100 patients with amyloidosis. JAMA 1983; 249: 13221324.CrossRefGoogle ScholarPubMed
33. Cole, FM, Yates, P. Intracerebral microaneurysms and small cerebrovascular lesions. Brain 1967; 90: 759767.Google Scholar
34. Powers, JM, Schlaepfer, WW, Willingham, MC, et al. An immunoperoxidase study of senile cerebral amyloidosis with pathogenetic considerations. J Neuropathol Exp Neurol 1981; 40: 592612.Google Scholar
35. Liebman, H, Chinowsky, M, Valdin, J, et al. Increased fibrinolysis and amyloidosis. Arch Intern Med 1983; 143: 678682.Google Scholar
36. Takahashi, H, Koike, T, Yoshida, N, et al. Excessive fibrinolysis in suspected amyloidosis: demonstration of plasmin-oii-plasmin inhibitor complex and von Willebrand factor fragment in plasma. Am J Hematol 1986; 23: 153166.Google Scholar
37. Furie, B, Voo, L, Mcadam, K, et al. Mechanism of factor X deficiency in systemic amyloidosis. New Engl Med J 1981; 304: 827830.CrossRefGoogle ScholarPubMed
38. Griepp, PR, Kyle, RA, Bowie, EJW. Factor X deficiency in amyloidosis: a critical review. Am J Hematol 1981; 11: 443450.CrossRefGoogle Scholar
39. Sixma, JJ. Role of blood platelets, plasma proteins and the vessel wall in haemostasis In: Bloom, AL, Thomas, DP, eds. “Haemostasis and Thrombosis”. New York, Churchill Livingstone 1987; 283311.Google Scholar