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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 29  |  Issue : 2  |  Page : 106-108

Recurrent cerebral/cerebellar infarcts and hemorrhages in a patient with oral anticoagulants for prosthetic valve


1 Department of Cardiology, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
2 Department of Radiology, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
3 Department of Radiology, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh, India
4 Department of Neurosurgery, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India

Date of Web Publication20-Aug-2015

Correspondence Address:
Umamaheswara Reddy Venati
Department of Radiology, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4958.163201

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  Abstract 

Patients on long-term oral anticoagulant therapy (OAT) for prosthetic valves require close monitoring of their international normalized ratio (INR) levels to prevent deleterious effects. We present a case of a 35-year-old male with a known case of rheumatic heart disease who underwent mitral valve replacement and aortic valve replacement. In our patient, there was an undulation of coagulation parameters between low (INR-2.1) and high (INR-6.0) target levels, which eventually lead to ischemic strokes and fatal intracranial hemorrhage (ICH). Repeat INR was 6.0, which was much beyond the therapeutic range. Attempts to correct the coagulation abnormalities did not succeed and the patient succumbed to ICHs. All patients with valve replacement require chronic OAT. Judicious monitoring of the INR levels with dose adjustments can reduce morbidity and mortality from OAT-related complications like hemorrhage and infarction.

Keywords: Anticoagulant, Prosthetic valve, Stroke, Thromboembolic event


How to cite this article:
Reddy CB, Hegde KV, Venati UR, Pentyala S, Agrawal A. Recurrent cerebral/cerebellar infarcts and hemorrhages in a patient with oral anticoagulants for prosthetic valve. J Med Soc 2015;29:106-8

How to cite this URL:
Reddy CB, Hegde KV, Venati UR, Pentyala S, Agrawal A. Recurrent cerebral/cerebellar infarcts and hemorrhages in a patient with oral anticoagulants for prosthetic valve. J Med Soc [serial online] 2015 [cited 2020 Oct 27];29:106-8. Available from: https://www.jmedsoc.org/text.asp?2015/29/2/106/163201


  Introduction Top


All patients with mechanical valve replacement require long-term anticoagulation. [1] Patients on long-term oral anticoagulant therapy (OAT) for prosthetic valves require close monitoring of their international normalized ratio (INR) levels to prevent deleterious effects. The INR levels should always be maintained within the therapeutic range. Recommended therapeutic range depends upon the type and the location of mechanical valves. [1],[2],[3] Depending on the patient's clinical status, anticoagulant treatment must be individualized while taking into consideration risk factors like atrial fibrillation, left ventricular dysfunction, previous thromboembolism, and hypercoagulable condition. [2] Patients with mechanical prosthetic heart valves and on oral anticoagulants with previous thromboembolic episode, and with INR target of 3.0 (range: 2.5-3.5) are recommended additional aspirin therapy. [1],[2] During OAT if the INR levels are below the recommended therapeutic range, the patient can have thromboembolic event, whereas when they are above the therapeutic range, the patient can have intracranial hemorrhage (ICH). [2] In our patient, there was an undulation of coagulation parameters between low (INR of 2.1) and high (INR of 6.0) target levels, which eventually lead to ischemic strokes and fatal ICH.


  Case report Top


A 35-year-old male, with a known case of rheumatic heart disease underwent mitral valve replacement and aortic valve replacement 5 years ago. He was on oral anticoagulants, along with low dose of aspirin since 5 years; he presented to the emergency room with sudden onset altered sensorium. The patient had a past history of cerebrovascular accident 3 years ago from which he recovered completely and had a symptom-free period until the present episode. His vitals were stable on admission. He was febrile (102°F); the Glasgow Coma Scale (GCS) gave the following data: eye opening to pain (E4), verbal response groaning to pain (V2), and motor response localizing to pain (M5). Neurological examination was unremarkable except for extensor plantars. Investigation revealed that the patient had anemia, his prothrombin time (PT) and INR levels were below the recommended therapeutic range, and there was no evidence of atrial fibrillation. Echocardiogram did not show any vegetation or thrombus on the prosthetic valves/left atrium. Three consecutive blood cultures were negative, ruling out infective endocarditis. The magnetic resonance imaging (MRI) performed showed embolic shower of acute infarcts in the thalamus, bilateral parietal cortices, chronic infarcts in the cerebellum and left insular cortex, gliotic area in the left caudate, and lentiform nucleus with hemosiderin rim. MRI also showed punctate microhemorrhages in the midbrain and the bilateral frontotemporal lobes [Figure 1] and [Figure 2]. With symptomatic treatment, the patient recovered well, and his INR was corrected to the therapeutic range before discharge. After 1 month, the patient was presented in coma to the emergency department. He was intubated and emergency computed tomography (CT) was performed, which showed recent onset hemorrhages in the right frontal and temporal lobes, and a large cerebellar hematoma with fluid-fluid levels. Repeat INR was 6.0, which was much beyond the therapeutic range. Attempts to correct the coagulation abnormalities were not successful and the patient succumbed to ICHs.
Figure 1 : Axial T2-weighted (T2W) image showing normal cerebellum (a), Diffusion weighted imaging ( DWI) image at the level of third ventricle showing acute infarct in the right thalamus (b), DWI image at the level of Sylvian fissure showing infarcts (lacunar infarcts) in both parietal lobes (c), Susceptibility-weighted images showing gliotic area with hemosiderin rim

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Figure 2 : Axial NECT showing new onset in right cerebellar hematoma with fluid-fluid levels and no perihematomal edema (a and b) Axial NECT image at the level of third ventricle showing hypodense areas suggestive of gliosis in the head of the caudate, lentiform nucleus, thalamus, and left frontal cortex (c) acute bleeding with minimal perihematomal edema in the right frontal cortex (d)

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  Discussion Top


In developing countries, patients with rheumatic fever who undergo valve replacement therapy early in their lives are put on chronic anticoagulation. In such patients, mechanical prosthetic valves are a prime site for thrombus formation. [3] The risk of thrombotic recurrences, even during anticoagulation, is 1-2%. [2],[3],[4],[5],[6] Maintaining a desired level of anticoagulation is difficult due to many factors including drug absorption, drug interaction with foods, medicines, and variations in liver function. [2] In practice, the patient is maintained within a certain therapeutic range. In our case, the patient, being on indigent INR monitoring, had an ischemic episode followed by OAT-ICH. The erratic fluctuation of his INR levels could be attributed to his pharmacodynamics. It was supported by the indirect evidence that his INR levels were not in the patient recommended therapeutic range of 2.5-3.5. [1],[2] The patient's INR was 2.1 when he had a thromboembolic event and 6.0 when he had ICH. ICH is the most feared and life threatening complication of OAT. [7],[8],[9] Current understanding of OAT-ICH remains limited as compared to spontaneous intracerebral hemorrhage (SICH). The mean age of presentation of OAT-ICH is 70 years. [10] In our patient, OAT-ICH had occurred at a very early age, which was unusual. OAT-ICH is more fatal than SICH, with mortality greater than 50%. [9],[10] In our case, cerebellar hematoma showed classical fluid-fluid levels. [11],[12],[13] Similar findings were described by Jung et al. [11] Consumption of clotting factors with the separation of plasma or serum from the blood cells result in two components, creating a fluid-level. [11],[12] All the hematomas had a decreased amount of perilesional edema, correlated to a study on OAT-induced ICH by Geber et al. [13] We also observed the microhemorrhages in the susceptibility imaging, which were hypothesized to be predictors of anticoagulant induced hematoma. [7] According to the guidelines, for a patient who has an embolic episode while on adequate OAT, the dose of anticoagulant therapy should be increased and low dose aspirin should be initiated. [1],[2] In patients with INR above the therapeutic range, excessive anticoagulation is managed by withholding warfarin and with timely INR determinations. [2],[10] Over- and undercorrection of INR have their own undesirable effects. Excessive anticoagulation (INR >5) highly increases the risk of hemorrhage, whereas a rapid attempt to decrease it can lead to INR falling below the therapeutic level, thereby increasing the risk of thromboembolism. [1],[2],[10] Patients with prosthetic heart valves with an INR between 5 and 10 and who are asymptomatic can be managed by the cessation of warfarin and administration oral vitamin K. [2],[10] Warfarin therapy with dose adjustment can be started to maintain the INR in the therapeutic range, and the INR needs to be determined after 24 h and a serial monitoring is recommended. Fresh frozen plasma may be preferred to high-dose vitamin K1 in emergency situations, as the parenteral vitamin K1 increases the danger of overcorrection with a higher incidence of hypercoagulable states.


  Conclusion Top


Every patient with valve replacement requires chronic OAT. Judicious monitoring of the INR levels with dose adjustments can reduce morbidity and mortality from OAT-related complications. The guidelines for long-term anticoagulation and management of their complications are unclear as there is a lack of evidence from randomized controlled trials. In case of anticoagulant-induced complications, especially oral anticoagulation therapy-induced hemorrhage being an alarming situation, early diagnosis is of utmost importance. Brain CT scan showing fluid-fluid level with least amount of perihematomal edema is moderately specific of oral anticoagulation therapy-induced hemorrhage. Mortality associated with OAT-ICH can only be avoided with rigorous medical management, including reversal of anticoagulation. Newer anticoagulants like dabigatran, currently approved by the Food and Drug Administration (FDA) approved for the treatment of atrial fibrillation, give hope to patients with valve replacement as they do not require monitoring, the absorption is independent of food intake, and they have better safety profile with lesser chances of OAT-induced bleeding.

 
  References Top

1.
Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, et al.; American Heart Association/American Stroke Association Council on Stroke; Council on Cardio vascular Radiology and Intervention; American Academy of Neurology. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: A statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: Co-sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Circulation 2006;113:e409-49.  Back to cited text no. 1
    
2.
Bonow RO, Carabello B, de Leon AC, Edmunds LH Jr, Fedderly BJ, Freed MD, et al. ACC/AHA guidelines for the management of patients with valvular heart disease. Executive summary. A report of the american college of cardiology/american heart association task force on practice guidelines (Committee on Management of Patients with Valvular Heart Disease). J Heart Valve Dis 1998;7:672-707.  Back to cited text no. 2
    
3.
Gohlke-Bärwolf C, Acar J, Oakley C, Butchart E, Burckhart D, Bodnar E, et al. Guidelines for prevention of thromboembolic events in valvular heart disease. Study group of the working group on valvular heart disease of the European Society of Cardiology. Eur Heart J 1995;16:1320-30.   Back to cited text no. 3
    
4.
Vongpatanasin W, Hillis LD, Lange RA. Prosthetic heart valves. N Engl J Med 1996;335:407-416.  Back to cited text no. 4
    
5.
Bloomfield P, Wheatley DJ, Prescott RJ, Miller HC. Twelve-year comparison of a Bjork-Shiley mechanical heart valve with porcine bioprostheses. N Engl J Med 1991;324:573-9.  Back to cited text no. 5
    
6.
Hammermeister K, Sethi GK, Henderson WG, Grover FL, Oprian C, Rahimtoola SH. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: Final report of the Veterans Affairs randomized trial. J Am Coll Cardiol 2000;36:1152-8.  Back to cited text no. 6
    
7.
Hart RG, Boop BS, Anderson DC. Oral anticoagulants and intracranial hemorrhage facts and hypotheses. Stroke 1995;26:1471-7.  Back to cited text no. 7
    
8.
Steiner T, Rosand J, Diringer M. Intracerebral hemorrhage associated with oral anticoagulant therapy: Current practices and unresolved questions. Stroke 2006;37:256-62.  Back to cited text no. 8
    
9.
Goldstein JN, Greenberg SM. Should anticoagulation be resumed after intracerebral hemorrhage? Cleve Clin J Med 2010;77:791-9.  Back to cited text no. 9
    
10.
Aguilar MI, Hart RG, Kase CS, Freeman WD, Hoeben BJ, García RC, et al. Treatment of warfarin-associated intracerebral hemorrhage: Literature review and expert opinion. Mayo Clin Proc 2007;82:82-92.  Back to cited text no. 10
    
11.
Jung YJ, Kim MS, Chang CH, Choi BY. The fluid-blood level in a spontaneous intracerebral hematoma. Kor J Cerebrovascular Surgery 2011;13:80-3.  Back to cited text no. 11
    
12.
Weisberg L. The fluid-blood level in intracranial haematoma due to anticoagulant medication. J Neurol Neurosurg Psychiatry 1987;50:1076.  Back to cited text no. 12
    
13.
Gebel JM, Brott TG, Sila CA, Tomsick TA, Jauch E, Salisbury S, et al. Decreased perihematomal edema in thrombolysis-related intracerebral hemorrhage compared with spontaneous intracerebral hemorrhage. Stroke 2000;31:596-600.  Back to cited text no. 13
    


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