Lingual and Sublingual Haematoma in a Patient Following Streptokinase Administration in Acute Myocardial Infarction- A Case Report

2017 ◽  
Vol 10 (1) ◽  
pp. 97-100
Author(s):  
Shoaeb Imtiaz Alam ◽  
Abu Bakar Md Jamil ◽  
Tanjima Parvin ◽  
SM Ear E Mahbub ◽  
Md Abu Siddique

The value of thrombolysis by Streptokinase administration in the treatment of acute myocardial infarction is well established. Haemorrhage is a common complication of fibrinolytic therapy. Here, we report an unusual case of spontaneous lingual and sublingual haematoma following streptokinase therapy after acute myocardial infarction. A 57-year-old man with a diagnosis of acute ST elevated myocardial infarction treated with streptokinase developed a large lingual and sublingual haematoma. Though his airway was not compromised, he had difficulty in swallowing. A conservative approach was made by starting parenteral nutrition, preventing rethrombosis by not reversing the action of streptokinase as his coagulation profile was within normal limits and maintaining optimum blood pressure, blood glucose level and urine output. His tongue swelling subsided after four days and oral medication and feeding was started. No complication occurred during this period. Though there is no adequate information regarding the management of the patient, a vigilant monitoring of the patency of the airway with a conservative approach by not reversing the effect of streptokinase and preventing coronary rethrombosis may produce a better outcome in such cases.Cardiovasc. j. 2017; 10(1): 97-100

Heart ◽  
1985 ◽  
Vol 54 (5) ◽  
pp. 455-459 ◽  
Author(s):  
F W Verheugt ◽  
M J van Eenige ◽  
J C Res ◽  
M L Simoons ◽  
P W Serruys ◽  
...  

2003 ◽  
Vol 145 (3) ◽  
pp. 508-514 ◽  
Author(s):  
John K. French ◽  
Krishnan Ramanathan ◽  
James T. Stewart ◽  
Wanzhen Gao ◽  
Pierre Théroux ◽  
...  

1991 ◽  
Vol 37 (6) ◽  
pp. 845-852 ◽  
Author(s):  
Johannes Mair ◽  
Erika Artner-Dworzak ◽  
Peter Lechleitner ◽  
Jörn Smidt ◽  
Ina Wagner ◽  
...  

Abstract Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.


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