Non-hemorrhagic adrenal infarction

2021 ◽  
Author(s):  
H. Scott Beasley, MD, FACR
Keyword(s):  
Author(s):  
Iza F R Machado ◽  
Isabel Q Menezes ◽  
Sabrina R Figueiredo ◽  
Fernando Morbeck Almeida Coelho ◽  
Debora R B Terrabuio ◽  
...  

Abstract Context Coronavirus disease 2019 (COVID-19) is a proinflammatory and prothrombotic condition, but its impact on adrenal function has not been adequately evaluated. Case report A 46-year-old woman presented with abdominal pain, hypotension, skin hyperpigmentation after COVID-19 infection. The patient had hyponatremia, serum cortisol <1.0 ug/dL, ACTH of 807 pg/mL and aldosterone <3 ng/dL. Computed tomography (CT) findings of adrenal enlargement with no parenchymal and minimal peripheral capsular enhancement after contrast were consistent with bilateral adrenal infarction. The patient had autoimmune hepatitis and positive antiphospholipid antibodies, but no previous thrombotic events. The patient was treated with intravenous hydrocortisone, followed by oral hydrocortisone and fludrocortisone. Discussion Among 115 articles, we identified nine articles, including case reports, of new-onset adrenal insufficiency and/or adrenal hemorrhage/infarction on CT in COVID-19. Adrenal insufficiency was hormonally diagnosed in five cases, but ACTH levels were measured in only three cases (high in one case and normal/low in other two cases). Bilateral adrenal non- or hemorrhagic infarction was identified in five reports (two had adrenal insufficiency, two had normal cortisol levels and one case had no data). Interestingly, the only case with well-characterized new-onset acute primary adrenal insufficiency after COVID-19 had a previous diagnosis of antiphospholipid syndrome. In our case, antiphospholipid syndrome diagnosis was established only after the adrenal infarction triggered by COVID-19. Conclusions Our findings support the association between bilateral adrenal infarction and antiphospholipid syndrome triggered by COVID-19. Therefore, patients with positive antiphospholipid antibodies should be closely monitored for symptoms or signs of acute adrenal insufficiency during COVID-19.


Rheumatology ◽  
1992 ◽  
Vol 31 (2) ◽  
pp. 117-120 ◽  
Author(s):  
D. E. AMES ◽  
R. A. ASHERSON ◽  
B. AYRES ◽  
J. CASSAR ◽  
G. R. V. HUGHES

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A107-A108
Author(s):  
Firas Warda ◽  
Gunjan Yogendra Gandhi

Abstract Background: The differential diagnosis for pregnant patient presenting with abdominal pain is broad. Adrenal infarction is a rare cause of such presentation. Clinical Case: A 24-year-old woman, 30 weeks pregnant, presented to the emergency room with severe, sharp, left upper quadrant abdominal pain that radiated to the back and was associated with nausea and vomiting. Abdominal exam showed tenderness to light palpation in the left upper area with voluntary guarding. Genitourinary exam revealed a closed cervical os. Abdominal MRI noted a T2 hypointense left adrenal gland with loss of normal diffusion restriction. Edematous changes were identified within the left perinephric and anterior pararenal spaces. Left adrenal gland non-hemorrhagic infarction with necrosis was diagnosed, and patient was started on enoxaparin. Patient was admitted for hydration and pain control. A morning serum cortisol was equivocal at 10.3 µg/dL with a mid-normal ACTH of 38.9 pg/mL. ACTH stimulation noted a suboptimal cortisol response with a serum cortisol at baseline of 9.1 µg/dL, at 30 minutes 10.7 µg/dL, and at 60 minutes 11.0 µg/dL. Patient was started on stress dose intravenous hydrocortisone. Evaluation for thrombophilia was undertaken and patient initiated on therapeutic weight-based enoxaparin. Investigations for etiology included normal factor V leiden, proteins C and S activity, antithrombin III antigen, antiphospholipid screening, C3 and C4 complement, anti-double stranded DNA antibody, anti-neutrophil cytoplasmic antibody, cryoglobulin, homocysteine, and factor II mutation. Factor VIII activity was increased >200%, which is within expected range during pregnancy. Patient was heterozygous for MTHFR C677T and A1298C mutations. Hydrocortisone was tapered and patient discharged on a physiologic dose, in addition to enoxaparin. Conclusion: Unilateral adrenal infarction is an uncommon entity in general, and even more uncommon during pregnancy (1). Thrombophilia evaluation is warranted as antiphospholipid syndrome and MTHFR gene mutations have been associated with this condition. Given the rarity of this disease, it may not be included in the differential diagnosis of pregnant patients who present with acute abdominal pain. MRI is superior to other imaging modalities due to its sensitivity in detecting adrenal infarct and even hemorrhage, if present. Unfortunately, there are no guideline on managing such patients, but the focus is usually placed on anticoagulation to prevent the infarction of the contralateral adrenal gland, with cautious monitoring as hemorrhagic conversion is possible. Screening patient for adrenal insufficiency for prompt supplementation of corticosteroids if needed is necessary, while attempting to find the underlying cause. Reference: (1) Green P., et al. Unilateral adrenal infarction in pregnancy. BMJ Case reports. 2013; bcr2013009997


2021 ◽  
pp. FSO718
Author(s):  
Myriam Jerbaka ◽  
Tracy Slaiby ◽  
Zahraa Farhat ◽  
Yara Diab ◽  
Nawal Toufayli ◽  
...  

Abdominal pain is the most presenting complaint during pregnancy with multiple etiologies. The diagnosis could be unpredictable. We present a case of 36-year-old pregnant woman gravida 10 para 7 abortus 2 at 36 + 5 weeks of gestation presenting twice for an increasing left abdominal pain, not relieved despite analgesics. She was delivered for severe oligohydramnios. After delivery, she was found to have a left adrenal infarction on computed tomography scan. She was found to have two mutations of the gene  MTHFR 677CC. Our presented case should remind physicians to consider the presence of thromboembolic state during pregnancy. The diagnosis of adrenal infarction should be among the differentials of an ambiguous flank pain that is resilient to medical therapy. Diagnosis in a pregnant patient can be easily confirmed with MRI, after which anticoagulation should be started and the workup for hypercoagulable state investigated.


2019 ◽  
Vol 35 (11) ◽  
pp. 941-944 ◽  
Author(s):  
F. Chasseloup ◽  
N. Bourcigaux ◽  
S. Christin-Maitre

2019 ◽  
Vol 5 (6) ◽  
pp. e334-e339 ◽  
Author(s):  
Jee Young You ◽  
Norman Fleischer ◽  
Smita B. Abraham

Objective: To describe a case of sequential bilateral adrenal infarction and hemorrhage resulting in an unusual pattern of adrenal function over time. Methods: A 50-year-old male with autoimmune antiphospholipid syndrome (APS) presented to the emergency room with severe abdominal pain. Diagnostic studies performed included contrast-enhanced computerized tomographic (IV-CT) imaging of abdomen and pelvis, and laboratory assessment of the hypothalamic-pituitary-adrenal axis. Results: IV-CT of abdomen and pelvis on day 1 showed acute left adrenal gland infarction; cortisol level was 19.9 μg/dL and serum sodium was 133 mEq/L. The patient subsequently developed hyponatremia and hypotension. Repeat IV-CT of abdomen and pelvis on day 3 showed hemorrhagic conversion of the left infarcted adrenal gland and a new right adrenal gland infarction. Cosyntropin stimulation test (CST) confirmed primary glucocorticoid insufficiency. Plasma renin activity and the serum aldosterone level were within normal limits with normokalemia. At 7-month follow-up, CST demonstrated cortisol and aldosterone deficiency. Conclusion: Adrenal infarction is a rare complication of APS but is the most common endocrine complication. Evidence of bilateral adrenal infarction on imaging does not predict the type of adrenal dysfunction that might ensue, as demonstrated in this case. Thorough evaluation of glucocorticoid, mineralocorticoid, and androgen deficiency should be conducted both at the time of the event and in follow-up.


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