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| CASE REPORTS |
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| Year : 1992 | Volume
: 38
| Issue : 4 | Page : 199-200 |
Use of aminocaproic acid (ACA) in extra-amniotic MTP in patients on anti-coagulant therapy.
PP Kale, MA Shah, AV Pathare
Dr JC Patel Haematology Department, Seth G S Medical College, Parel, Bombay, Maharashtra.
Correspondence Address:
P P Kale
Dr JC Patel Haematology Department, Seth G S Medical College, Parel, Bombay, Maharashtra.
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 0001307594 
A case of rheumatic heart disease (RHD) with prosthetic mitral valve endocarditis receiving anticoagulation with heparin, underwent medical termination of pregnancy in a second trimester. The following report entails the use of aminocaproic acid (ACA) in preventing excessive bleeding during and after the procedure, while the patient continued to receive anticoagulant therapy.
Keywords: Abortion, Therapeutic, methods,Adult, Aminocaproic Acids, administration &dosage,therapeutic use,Case Report, Cerebrovascular Disorders, drug therapy,etiology,Endocarditis, drug therapy,etiology,Female, Heart Valve Prosthesis, Heparin, adverse effects,Human, Mitral Valve Insufficiency, complications,drug therapy,surgery,Pregnancy, Pregnancy Complications, Cardiovascular, drug therapy,Rheumatic Heart Disease, complications,drug therapy,surgery,
How to cite this article:
Kale P P, Shah M A, Pathare A V. Use of aminocaproic acid (ACA) in extra-amniotic MTP in patients on anti-coagulant therapy. J Postgrad Med 1992;38:199-200 |
How to cite this URL:
Kale P P, Shah M A, Pathare A V. Use of aminocaproic acid (ACA) in extra-amniotic MTP in patients on anti-coagulant therapy. J Postgrad Med [serial online] 1992 [cited 2023 Jun 2];38:199-200. Available from: https://www.jpgmonline.com/text.asp?1992/38/4/199/671 |
Aminocaproic acid (ACA) is a synthetic anti-fibrinolytic agent used in a variety of clinical setting[1],[2]. Anti-fibrinolytic agents have also been used in certain obstetric and gynaecological conditions to prevent excessive bleeding[1],[2],[3],[4]. However, medical termination of pregnancy (MTP) in a patient on anti-coagulants has the added risk of excessive bleeding. We report here, the use of ACA in a patient, who required continuous anti-coagulant therapy to protect against the risk of choking the mitral prosthetic valve and precipitating an embolic episode.
MDP, a 21-year-old unmarried patient, a known case of RHD with mitral valve replacement done 7 years ago, presented to us with history of frontal headache, right sided weakness with facial asymmetry, along with low grade pyrexia of recent onset. Investigations revealed that she had developed a left embolic cardiovascular accident resulting in the right sided weakness, associated with infective endocarditis. 2-D echo and colour doppler studies showed vegetations at the junction of the mitral and aortic valves, although blood cultures were sterile. Patient was thus put on oral warfarin therapy in addition to antibiotics and other supportive measures. Anti-coagulant therapy was monitored using standard techniques[5].
She was also found to be pregnant with five months amenorrhea and being unmarried, a decision of MTP was taken, with her informed consent. The patient was thus switched from oral warfarin therapy to intravenous continuous heparin administration 10 units/kg/clay. MTP was done by instillation of ethacridine lactate extraamniotically with the help of a Foley's catheter. Twenty mi of 25% ACA was also instilled along with it. Heparin therapy was not omitted during the procedure. Patient aborted the abortus and placenta 36 hours later. No active bleeding was observed per vaginum. Abdominal examination showed the uterus to be well contracted. Abdominal ultrasonography done later showed some retained products of conception, which were removed uneventfully. Importantly, the patient did not require to be transfused with any blood or blood products during the entire period.
The uterus is an organ rich in plasminogen activators[2]. With placental separation, there is a loss of inhibitors of fibrinolysis, resulting in a high fibrinolytic activity at the ulcerated surface which accounts for the bleeding observed[2],[4]. Obviously therefore, patients on anti-coagulant therapy are likely to bleed profusely, necessitating withdrawal. However, for patients in whom continuous anticoagulation is a must, the use of anti-fibrinolytic therapy is of great value, although extensive clinical experience is not available.
The mode of action of ACA involves the suppression of the activation of plasminogen to plasmin by physical bondage to the enzyme activation "kringle" region of the plasminogen molecule[2]. Therefore, the mechanism by which it can act or exert signif icant beneficial effect at 36 hours after instillation is rather unclear. It is likely that its presence locally may be helpful in either inhibiting or neutralizing the plasminogen activators and/or stabilizing the fibrin clot formed as a result of the separation of the membrances due to the instillation of ethacridine lactate. Thus excessive bleeding may be prevented in spite of the ongoing anti-coagulant therapy.
We wish to thank the Dean, Seth GS Medical College and King Edward Memorial Hospital and Dr GH Tilve, Prof and Head of the Department of Hematology, for permission to publish this manuscript. We also thank Dr Vinita Salvi, Assoc Professor, Department of Obstetrics and Gynaecology for having managed the patient.
| :: References | |  |
| 1. |
Nilsson W, Andersson L, Bjorkman SE. Epsilon-aminocaproic acid (E-ACA) as a therapeutic agent based on 5 year's clinical experience. Acta Med Scand 1966; 180:1-46.  |
| 2. | Verstraete M. Clinical applications of inhibitors of fibrinolysis. Drugs 1985; 29:236-261. |
| 3. | Astedt B. Significance of placenta in depression of fibrinolytic activity during pregnancy. J Obstet Commonwealth Gynaecol (Br) 1972; 79:205-209. |
| 4. | Svanberg L, Astedt B, Niisson IM. Abruptio placentae - treatment with the fibrinolytic inhibitor, tranexamic acid. Acta Obstet Gynecol Scand 1980; 59:127-130. |
| 5. | Hirsh J. Heparin. N Engl J Med 1991; 324:1565-1574.
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