Page 25 - Delaware Medical Journal - February 2018
P. 25
CASE REPORT
on this set of imaging, and extended subtly down to the posterior
consistent with bilateral adrenal hemorrhages, with the right side
by magnetic resonance imaging.
The patient was transferred to the intensive care unit, where his
cortisol level was drawn around 1300 on the day of admission, revealing a level of 4.6 g/dL (normal range 6.7 to 22.6 g/dL). The patient was started on 100mg of hydrocortisone every eight hours, which was tapered during his hospital stay. The patient’s vital signs proved to be stable after a 24-hour stay without signs of bleeding, so he was shortly transferred from the intensive care unit.
His coagulation studies were repeated on hospital day four, as it was thought that his initially high PTT was an apixaban effect. He had been transfused one unit of fresh frozen plasma and 5mg of intravenous vitamin K during his hospital course. With treatment, his INR corrected to 1.4, his repeat PT had fallen to 15.9 seconds, while his PTT dropped to 63.8 seconds. Given the persistently elevated value, a mixing study was performed revealing a PTT that did not correct after patient’s serum was mixed with controlled pool serum. Furthermore, Cardiolipin IgG antibody was strongly positive at a level of 84 G phospholipids (negative value less
than 15 G phospholipids). The rest of his hypercoagulable state workup, including proteins C and S activities, prothrombin gene mutation, factor V Leiden mutation, Cardiolipin IgA antibody
and Cardiolipin IgM antibody, was unremarkable. Anti-nuclear antibody was found to be negative.
The need for anticoagulation was addressed in the setting of adrenal hemorrhage and concurrent acute deep vein thrombosis. considered too high-risk for complications from the device. It was eventually decided to start the patient on a prophylactic dose of low-molecular weight heparin 30mg subcutaneously every 12 hours four days after admission. He was monitored for any evidence
of bleeding and overall, his hemodynamic status remained
stable throughout the rest of his hospital stay. A repeat computed tomography scan was performed one week after admission, revealing slightly smaller hemorrhages. He was discharged
home after the imaging on low-molecular weight heparin 30mg subcutaneously every 12 hours, with intent to continue for four weeks. Future plans include transition to full dose anticoagulation given the absence of any further bleeding. Additionally, his Cardiolipin IgG antibody.
At the time of preparation of this manuscript, his outpatient follow- up has showed stability in his symptoms, with no obvious signs of
further bleeding. A repeat hemoglobin and hematocrit has shown
measurement of Cardiolipin IgG antibody was found to be positive, this time at a level of 90 G phospholipids, verifying the diagnosis of antiphospholipid antibody syndrome.
DISCUSSION
This case illustrates the development of rare and potentially life- threatening condition in a patient taking long-term anticoagulation. As the patient’s initial presenting symptoms were somewhat vague and the early differential diagnoses are quite large, it is fortunate that the diagnosis was arrived at expeditiously, and the outcome was favorable, given previously documented historical outcomes.
In 1965, Amador, working from Peter Bent Brigham Hospital in Boston, retrospectively examined the autopsy reports of ten deceased patients on anticoagulant therapy at the time of death that were found to have adrenal hemorrhage postmortem, of the 4325 autopsies performed since 1949 when anticoagulant therapy was adopted. The two types used at the time were heparin and dicoumarol. Interestingly, adrenal hemorrhage was not detected during life in any of these ten patients, but he found that adrenal crisis was the main cause of death in three of ten patients or a main contributory cause in six of ten patients. In this retrospective review, adrenal hemorrhage was clinically apparent in six of ten and might have been suspected in another two of ten patients.2 As computed tomography scanning can quickly verify the source of bleeding, the decision to order such imaging requires a strong index of suspicion and knowledge of possible risk factors.
The proposed risk factors of adrenal hemorrhage include the use of anticoagulant medications, thromboembolic disease, the antiphospholipid antibody syndrome, and settings of increased stress such as trauma, severe sepsis, bacteremia, burns, pregnancy, and the post-operative state.3, 4, 5, 6 Other reports have demonstrated adrenal hemorrhage in the setting of adrenal tumors and heparin-induced thrombocytopenia.7, 8 Kovacs, in 2001, found in a case-controlled study that thrombocytopenia, heparin exposure of any route or type for more than three days, and sepsis were most strongly and independently associated with development of bilateral massive adrenal hemorrhage.9 Furthermore, the characteristics of the vascular supply and drainage of the glands likely contribute to their vulnerability in these settings. A study of about 400 autopsies showed that there may be as many as 50 arteries supplying each individual gland, with vascular drainage limited to only one adrenal vein.10 This abrupt transition to venous drainage, especially in settings of and subsequent hemorrhage.11, 12 Increased adrenal blood
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