Nephrol Dial Transplant (2000) 15: 107-109
© 2000 European Renal Association-European Dialysis and Transplant Association
Case Reports
Treatment of subdural and intracerebral haematomas in a haemodialysis patient with tranexamic acid
o 
abovi
21 Department of Nephrology and Dialysis, Slovenj Gradec General Hospital and 2 University Medical Centre, Trnovo Hospital of Internal Medicine, Ljubljana, Slovenia
Correspondence and offprint requests to:
Mio abovi MD, PhD, University Medical Centre, Trnovo Hospital of Internal Medicine, Riharjeva 24, 1000 Ljubljana, Slovenia. E-mail: miso.sabovic{at}trnovo.kclj.si.
Keywords: haemodialysis; intracerebral haematoma; subdural haematoma; tranexamic acid
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Introduction |
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Intracranial bleeding in a haemodialysis patient is a serious, life threatening condition. Haemodialysis patients have a higher rate of spontaneous and traumatic subdural and/or intracerebral haematoma than the general population. This is, at least partially, attributed to impaired haemostasis, which is associated with end-stage renal disease and haemodialysis. The estimated incidence of subdural haematoma in chronic haemodialysis patients was 3.3%, with a high mortality rate reaching 85% [1]. There are no recent data available on the incidence of subdural and/or intracerebral haematoma in the haemodialysis population at large. The incidence is probably lower than 3.3% due to changing anticoagulation techniques involving the use of low-dose heparin rather than systemic heparinization, and the infrequency of the need for oral anticoagulation to maintain modern angioaccess patency [2]. However, a high mortality rate is still characteristic of haemodialysis patients suffering intracranial haemorrhage [3,4]. The recommended treatment of subdural/intracerebral haematoma is a combination of surgical drainage, if possible, and conservative supportive measures such as heparin-free dialysis, strict bed rest and anti-oedema treatment. However, the correction of impaired haemostasis is not a focus of current treatment. In this report, we describe an apparently successful management of intracranial bleeding in a haemodialysis patient using the antifibrinolytic agent tranexamic acid.
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Case |
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A 65-year-old haemodialysis patient was admitted to the hospital in July 1997 with a severe headache, fatigue, nausea and vomiting. Two weeks before admission he was already complaining of headaches which resolved within 5 days. Upon admission, his somatic and neurological status was otherwise unremarkable. The patient had a 10-year history of untreated arterial hypertension and slowly progressive uraemia, which led to the start of intermittent haemodialysis treatment in December 1995. Unenhanced computed tomography (CT) showed hypodense/hyperdense subdural fluid collection in both fronto-temporal regions (Figure 1A
). He denied having had a recent fall or being assaulted. Prothrombin time, partial thromboplastin time, thrombin time, platelets and fibrinogen were in the normal range. The patient was treated conservatively with bed rest. Heparin-free haemodialysis was performed afterwards. On the 12th day the patient became somnolent, and therefore he was treated with a single burr hole evacuation of both haematomas and aggressive subdural irrigation with normal saline. However, the subdural blood collection was entirely reconstituted within a few days. Overall, three evacuations of blood from both subdural spaces were performed. On the 25th day the patient suddenly deteriorated to a comatose state with left-side haemiplegia (Glasgow Coma Scale 7). CT showed a large intracerebral (spontaneous) parieto-occipital haemorrhage (30x25x30 mm), in addition to fronto-parietal subdural haematomas (Figure 1B). Since we previously treated successfully recurrent bleeding from colonic angiodysplasias in a haemodialysis patient, we started to treat the patient with the antifibrinolytic agent tranexamic acid (Cyklokapron, Pharmacia & Upjohn AB, Stockholm, Sweden) at the dosage of 20 mg/kg/48 h intravenously [5]. After 4 days of treatment he surprisingly was completely alert, with only mild left-sided haemiparesis. Continuous bleeding into the subdural space, which had lasted for almost 1 month, was stopped, as was intracerebral bleeding. A rapid resolution of both subdural and intracerebral haematomas took place, as shown by a repeat CT scan (Figure 1C). After 4 weeks the dosage of tranexamic acid was reduced to 10 mg/kg/48 h orally for an additional 4 weeks. The neurological deficit was no longer found. During treatment with tranexamic acid no complications in terms of arterial or venous thrombosis were observed. After 1 year of follow-up his neurological status is normal, and no further episode of subdural haematoma has occurred.
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Discussion |
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Haemodialysis patients and patients with other types of bleeding tendency are prone to spontaneous and traumatic subdural and intracerebral haematoma. Moreover, the surgical evacuation of blood from the subdural space is often followed by reforming of haematomas [1,6]. This appears to be associated with the well-known impaired haemostasis in haemodialysis patients. In addition, the (locally) deficient haemostasis plays a role in the recurrence of subdural haematoma after surgical evacuation in patients without an apparent bleeding tendency [7]. Accordingly, a pharmacological treatment which would improve the haemostatic function of blood might improve the outcome of haemodialysis patients with subdural and/or intracerebral haematoma. Tranexamic acid is a potent antifibrinolytic agent which shifts the delicate balance between coagulation and fibrinolysis in the direction of the former, thereby improving haemostatic capabilities of blood. Tranexamic acid has been successfully used in several bleeding conditions [8,9]. We found tranexamic acid very effective in the treatment of acute and recurrent bleeding from colonic angiodysplasias in a haemodialysis patient [5]. On the basis of that case we decided to administer tranexamic acid to the present haemodialysis patient. He had suffered spontaneous, recurrent subdural haematomas. Despite three sequential surgical evacuations, heparin-free dialysis and strict bed rest his clinical status progressively worsened over a time period of 3 weeks. After each surgical evacuation blood reformed in the subdural space. Finally, a spontaneous intracerebral haematoma occurred. A poor outcome was expected. We then started a treatment with tranexamic acid. Surprisingly, a rapid and complete clinical recovery was observed which was accompanied by CT proven resolution of haematomas. Such spontaneous remission is extremely unusual, in particular in patients with an evident bleeding tendency [1,6,10]. Therefore, it seems likely that tranexamic acid, by improving impaired haemostasis, stopped the intracranial bleeding, prevented further extension of the haematomas, and favoured fast resorption.
In conclusion, we suggest that tranexamic acid might be useful in haemodialysis patients with subdural and/or intracerebral haematoma. Although clearly one cannot extrapolate from a single case to all similar situations a therapeutic attempt with tranexamic acid is advisable based on the generally unfavourable course of this condition and the safety of tranexamic acid. In addition, tranexamic acid might also be of benefit in patients without a previous bleeding tendency who experience recurrent bleeding after surgical drainage of a subdural haematoma. Obviously, the suggested efficacy of tranexamic acid (in conjunction with surgical treatment and supportive measures) in haemodialysis patients suffering intracranial haemorrhage requires further study.
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References |
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- Said G. Neurological aspects of dialysis patients. In: Jacobs C, Kjellstrand CM, Koch KM, Winchester JF eds. Replacement of renal function by dialysis. Dordrecht/Boston/London, Kluwer Academic Publishers; 1996; 1243–1259
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Accepted in revised form: 8. 9.99
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