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during times of stress might play a role in the development of hemorrhage as well.13
Anticoagulation, especially the use of heparin, which binds antithrombin III, has been shown to be a risk factor in patients found to have adrenal hemorrhage. Apixaban and rivaroxaban are both factor Xa inhibitors. Since the development of these NOACs, there have been very few reports of patients developing adrenal detailed reports using apixaban. The Aristotle trial documented one case of adrenal hematoma in a patient taking apixaban, however, no further details are available regarding the history of the patient or characteristics of the bleed.14 We performed multiple Pubmed and Google searches, but were unable to identify any other reports of adrenal bleeding in patients on apixaban. This leads the authors to reported cases of adrenal hemorrhage in a patient taking apixaban.
Regarding other reports of hemorrhage in patients taking
other NOACs, one case illustrates a 63-year old woman taking rivaroxaban who presented with abdominal pain and was found to have bilateral adrenal hemorrhage and the possible presence
of anticardiolipin antibodies. The author declared, at the time of case of an adrenal gland hemorrhage under treatment with a non-vitamin-k oral anticoagulant alone.15 The author concedes, however, that another case of adrenal hemorrhage was reported in 2013; a patient was notably treated with prophylactic dabigatran etexilate following hip replacement surgery.16
It should be noted that a Google Scholar search revealed a similar case abstract presented in March 2015, which was then thought to A 75-year old man who had undergone total knee replacement
and was placed on rivaroxaban 10mg daily for venous thrombosis prophylaxis, found to have bilateral adrenal hematomas, low serum cortisol levels, and severe shock responsive to hydrocortisone, to adrenal hemorrhage.17
As there were multiple risk factors present in the previously
as the sole cause of adrenal hemorrhage. The same idea holds true for this case, similarly. Aside from the presence of the patient’s underlying hypercoagulable disease, it is important to remember that the possibility of drug interactions enhancing anticoagulant effects can negatively affect outcomes as well, regardless of the type of anticoagulant used. Our patient was treated for erysipelas apixaban. There are no documented adverse reactions between
shown to increase serum concentration of apixaban. Though the
adversely affecting anticoagulant properties of apixaban in this case is minimal, considering the chronology of treatment and half-life of the antifungal. Given known previous risks factors
for hemorrhage, and the possibility of drug interactions, further research needs to be completed regarding hemorrhage rates of the NOACs compared to heparin. Furthermore, additional reports on management of concurrent bleeding and thrombosis in this setting also require development.
A retrospective cohort study performed in 2002 examined 66 patients with antiphospholipid antibody syndrome treated with warfarin to
a target INR of 3.5. The results were notable for one patient who suffered an intracranial bleeding complication as a result of an uncontrolled INR. Subsequently, she developed venous thrombosis when deprived of thromboprophylaxis postoperatively.18 Another case report illustrates a 35-year-old woman with antiphospholipid antibody syndrome on warfarin who took norethisterone for
15 days to postpone menstruation, and subsequently developed thrombocytopenia, inferior vena cava thromboses, bilateral common iliac thromboses, and severe anemia secondary to menorrhagia. She was transfused pack erythrocytes and restarted on anticoagulation on the second day of her hospitalization.19
It is certainly interesting that our patient’s initial testing for Cardiolipin IgG antibody was found to be positive. Since our patient had a long history of recurrent venous thromboses despite anticoagulation, a workup for hypercoagulable state prior to this episode of major hemorrhage might not have altered management acutely. The stable patient with multiple past thromboses would need lifelong anticoagulation in the presence of acute thrombosis regardless of the presence of primary antiphospholipid antibody syndrome. In the setting of adrenal hemorrhage and concurrent venous thrombosis, however, the knowledge of likely presence
of procoagulant state might warrant changes in the course of management: given the clinical situation and knowledge of past patients with concurrent bleeds and thrombi, it might be prudent to consider restarting anticoagulation as soon as possible. Furthermore, it should also be mentioned that secondary antiphospholipid antibody syndrome, in which systemic lupus erythromatosus or autoimmune connective tissue disease is present, might necessitate initiation of immunosuppressive medication, depending on clinical course.
As the real possibility of concurrent bleeding and thrombus exists, there are no evidence-based reports to help guide management. One particular decision, in this case, was to initiate low molecular weight heparin at a dose of 30 mg every 12 hours as prophylaxis against any further manifestations of thrombosis or progression of clotting, as the patient was hemodynamically stable and there was no obvious drop
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Del Med J | February 2018 | Vol. 90 | No. 2
