Bilateral adrenal infarction in pregnancy is a rare but potentially life-threatening condition that can lead to acute adrenal insufficiency and is often misdiagnosed due to nonspecific symptoms. We report a 25-year-old primigravida at 34 weeks presenting with abdominal and lumbar pain, fever, and vomiting, initially treated as acute pyelonephritis. Clinical deterioration with tachypnea and metabolic acidosis prompted further investigations. Computed tomography pulmonary angiography ruled out pulmonary embolism, while contrast-enhanced abdominal computed tomography revealed bilateral non-enhancing adrenal enlargement. Serum cortisol was inappropriately low (128.2 nmol/L), supporting acute adrenal insufficiency. Immediate intravenous hydrocortisone and therapeutic anticoagulation led to rapid improvement. The patient delivered vaginally at 38 weeks under epidural analgesia with stress-dose corticosteroids. This case highlights the importance of early imaging and prompt corticosteroid therapy in pregnant patients with unexplained persistent abdominal pain.

A 22-year-old man with untreated congenital adrenal hyperplasia (CAH) developed an acute adrenal crisis following bilateral orchiectomy for testicular adrenal rest tumors. The patient survived into adulthood without treatment until progressive testicular masses led to surgery due to misinterpretation of malignancy. Eighteen days postoperatively, he presented with severe asthenia, hyponatremia, and hyperkalemia. Diagnostic evaluation revealed markedly elevated 17-hydroxyprogesterone, androstenedione, and adrenocorticotropic hormone levels, with bilateral adrenal hyperplasia on imaging. Genetic testing identified a homozygous pathogenic variant in the CYP21A2 gene. Following glucocorticoid and mineralocorticoid replacement, the patient achieved clinical stability. This case illustrates that surgical removal of testicular adrenal rest tumors in untreated individuals can precipitate severe acute adrenal insufficiency, highlighting these tumors as a critical sentinel finding for late-diagnosis congenital adrenal hyperplasia.

Adrenal crisis is a life-threatening condition which is caused by an insufficient level of glucocorticoids in the body. Most patients have preexisting adrenal insufficiency, and physical or emotional stress triggers the adrenal crisis. This includes acute illness and surgery. It is important that patients receive a life-saving emergency injection of 100 mg hydrocortisone immediately and a continuous supplementation afterwards. This article focuses on the pathophysiology, trigger factors, prevention and emergency treatment of adrenal crisis in adult patients. By adjusting the regular dosage of glucocorticoids in stressful situations, adrenal crisis can be prevented. Patients at risk for adrenal crisis should keep an emergency injection kit and a standardised European emergency card and receive life-saving doses of glucocorticoids in emergency situations as quickly as possible.

Hemorrhagic adrenal infarction is a rare and potentially under-recognized cause of acute flank pain. We report the case of a 29-year-old woman presenting with acute left flank pain of two days' duration. Initial contrast-enhanced abdominal CT, including unenhanced and portal venous phases, was interpreted as normal. Retrospective review demonstrated subtle enlargement of the left adrenal gland with mildly reduced enhancement compared with the contralateral gland. Following clinical deterioration with fever, a repeat CT performed five days later showed marked enlargement of the left adrenal gland with absent enhancement and surrounding periadrenal fat stranding, consistent with hemorrhagic adrenal infarction. MRI confirmed heterogeneous signal intensity, diffusion restriction, and lack of post-contrast enhancement, supporting the diagnosis. Laboratory evaluation revealed severe primary hypothyroidism consistent with autoimmune thyroiditis and heterozygous hemoglobin S (sickle cell trait). Endocrine assessment showed preserved adrenal function without evidence of adrenal insufficiency. Initial thrombophilia testing demonstrated abnormalities in coagulation factors interpreted in the context of an acute inflammatory state, and was considered non-contributory on hematology review. The patient was managed conservatively following multidisciplinary discussion, without anticoagulation, and showed favorable clinical and radiological evolution. This case highlights an important imaging pitfall: early unilateral adrenal infarction may present with subtle CT findings and can be missed on initial interpretation. Careful adrenal evaluation and short-interval follow-up imaging are essential in patients with persistent or worsening acute flank pain despite an initially negative CT.

100 years ago in the U.S., tuberculosis was the most common cause of primary adrenal insufficiency (AI) (Addison's disease). Autoimmune adrenalitis is now responsible for 80-90% of AI in this country and Europe; nevertheless today, in the U.S. and certainly abroad, diverse infections can involve the adrenals in both the immunocompetent and immunocompromised and potentially produce AI. Such infections range widely: bacterial (e.g., Mycobacterium tuberculosis, in particular), fungal (e.g., histoplasmosis), viral and even protozoal (e.g., severe Plasmodium falciparum malaria). Suspecting AI, especially if chronic, is not straightforward, delays in AI diagnosis may reach > 6 months in 50%, and 50-75% of patients initially present in overt adrenal crisis. Diagnosing adrenal involvement by an infection may be drawn out, typically requires careful imaging, a thorough infectious disease evaluation, and may require adrenal biopsy.

Pituitary apoplexy is a rare but potentially life-threatening complication of pituitary macroadenomas that classically presents with acute headache, visual field deficits, and signs of optic chiasm compression. However, atypical neuro-ophthalmologic presentations without chiasmal involvement may delay recognition and treatment. This report highlights an unusual presentation of pituitary apoplexy associated with radiographic oculomotor nerve compression secondary to cavernous sinus extension in a patient with prolactinoma. We report the case of a 29-year-old Hispanic woman who presented to the emergency department (ED) with acute right-sided headache, dizziness, and transient blurry vision after the reinitiation of cabergoline therapy for a previously diagnosed prolactinoma. The patient had a prolonged history of migraine-like headaches, amenorrhea, intermittent galactorrhea, and inconsistent adherence to dopamine agonist therapy due to medication intolerance. Magnetic resonance imaging (MRI) revealed a 1.5 cm right sellar macroadenoma with intralesional hemorrhage consistent with pituitary apoplexy. Imaging demonstrated extension into the right cavernous sinus with compression and lateral displacement of the oculomotor nerve, without contact or compression of the optic chiasm or optic nerves. Endocrine evaluation demonstrated hyperprolactinemia and secondary adrenal insufficiency. The patient underwent endoscopic transsphenoidal resection with subsequent clinical stabilization and normalization of prolactin levels. Pathology confirmed a lactotroph pituitary adenoma. This case highlights an atypical presentation of pituitary apoplexy without classic chiasmal syndrome and emphasizes the importance of recognizing cavernous sinus cranial neuropathy as a potential presenting feature. Clinicians should maintain suspicion for pituitary apoplexy in patients with prolactinoma presenting with acute headache and cranial nerve (CN) abnormalities, even in the absence of visual field defects or optic pathway compression.

The utilization of immunotherapy and targeted therapies in advanced malignancies is rapidly increasing due to advancing technologies. While highly effective, the unintended toxicities and immune-related adverse events (irAEs) associated with these treatments require vigilant monitoring. Autoimmune hypophysitis and subsequent pituitary dysfunction represent critical complications of immune checkpoint inhibitors (ICIs), particularly pembrolizumab. Hypopituitarism can manifest as panhypopituitarism leading to a life-threatening secondary adrenal crisis or as selective anterior pituitary hormone deficiencies, such as isolated adrenocorticotropic hormone (ACTH) or gonadotropin deficiency. We report the case of a 73-year-old man with recurrent melanoma who presented with pituitary dysfunction secondary to pembrolizumab therapy. This case highlights the necessity of investigating, screening, and promptly treating new constitutional symptoms in patients undergoing ICI therapy, as these endocrine complications can be fatal if left unrecognized.

Background: COVID-19 causes adrenal injury that may amplify etomidate-induced adrenal suppression. We compared 30-day mortality between etomidate and ketamine for emergency intubation. Methods: We conducted a TriNetX-based propensity-matched cohort study of adult COVID-19 patients undergoing emergency intubation with etomidate or ketamine (January 2020-June 2025). The primary outcome was 30-day mortality. Three independent propensity-matched cohorts were created using different vasopressor inclusion criteria: primary (no vasopressor on day -1), hemodynamically stable (no vasopressor on day -1 or day 0), and critically ill (vasopressor on both day -1 and day 0). Sensitivity and negative control analyses addressed confounding. Results: Among 9462 primary-cohort pairs, etomidate was associated with higher 30-day mortality (34.43% vs. 31.57%; HR 1.11, 95% CI 1.06-1.17, p < 0.001; NNH 35). The association persisted in stable patients (HR 1.16, p = 0.013) and in critically ill patients (HR 1.15, p < 0.001). Mortality hazard ratios rose progressively with longer follow-up (day 0-7: HR 1.05; day 0-30: HR 1.11), indicating a delayed effect. In stable patients, etomidate was associated with higher vasopressor initiation (HR 1.15, p = 0.005); the between-group difference appeared early (4.41% by day 1) and narrowed thereafter, while the mortality difference emerged later and widened through day 30. Conclusions: Etomidate was consistently associated with higher 30-day mortality in COVID-19 patients (HR 1.11-1.16), unlike the results seen in general critical illness. The temporal pattern of early vasopressor divergence and late mortality divergence, together with consistency across hemodynamic strata, supports disease-specific adrenal vulnerability rather than acute peri-intubation harm. Ketamine may be the preferred induction agent in COVID-19 patients without contraindications.

Autoimmune Polyglandular Syndrome Type 2 (APS-2), also called Schmidt's syndrome, is a rare endocrine disorder characterized by primary adrenal insufficiency with autoimmune thyroid disease or type 1 diabetes mellitus. We report a case of a 40-year-old female patient with a history of primary hypothyroidism who presented to the emergency department with abdominal pain, vomiting, hypotension, hypoglycemia, and progressive hyperpigmentation. Laboratory studies confirmed an acute Addisonian crisis and revealed profound hyponatremia, hypocalcemia, hypomagnesemia, low serum cortisol, high adrenocorticotropic hormone (ACTH), and an elevated thyroid-stimulating hormone (TSH). The physiologic stress of an incidental hormonally inactive left ovarian serous cystadenoma likely precipitated this acute life-threatening event and also contributed to the unmasking of the patient's underlying adrenal deficiency. She was successfully resuscitated with intravenous fluids, vasopressors, and corticosteroid replacement and was discharged on a long-term regimen of oral steroids and thyroxine. This case highlights the significance of a high clinical suspicion for concomitant endocrine failures in patients with known autoimmune endocrinopathies presenting with acute systemic deterioration, as an early multidisciplinary intervention is key to improving prognosis and avoiding death.