Auricular calcification in a patient with traumatic brain injury and adrenal insufficiency: clinico-radiographic correla
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E N D O CR I N E I M A G I N G
Auricular calcification in a patient with traumatic brain injury and adrenal insufficiency: clinico-radiographic correlation with 3D cinematic rendering Michael T. Caton Jr.
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Fiona Malone1
Received: 19 November 2018 / Accepted: 21 January 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019
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Case description A 47-year-old man with a history of traumatic brain injury (TBI) presented to the hospital with altered mental status. His initial brain injury occurred 3 years before when he was found at the bottom of a staircase and admitted to the hospital with Glasgow Coma Scale score of 6. He was found to have extensive bifrontal brain contusions overlying the anterior cranial fossa. Due to elevated intracranial pressure, he underwent urgent bicoronal craniectomy in addition to tracheostomy and gastrostomy placement. He subsequently developed chronic, refractory hyponatremia requiring daily sodium chloride tablets and new-onset orthostatic hypotension which improved with fludrocortisone. He had no history of documented hypercalcemia, abnormal thyroid function tests, elevated glucose, or hemoglobin A1C levels. Non-contrast head CT was performed to assess confusion and somnolence. Axial CT images revealed bilateral auricular cartilage calcification which had not been recognized on physical examination (Fig. 1a).
Discussion Auricular calcification (AC), sometimes called “petrified auricle”, is a rare clinical entity which was first described in 1866 by the anatomist Bochdalek [1]. The pathogenesis of AC remains elusive. Reported cases have been attributed to trauma, thermal exposure/injury, and systemic inflammatory disorders (polychondritis, dermatomyositis, etc.), invoking bone morphogenetic signaling pathway disruption
* Michael T. Caton [email protected] 1
Brigham and Women’s Hospital, Boston, MA, USA
as a mechanism. Interestingly, AC is also associated with endocrinopathies, including diabetes mellitus, hypothyroidism, hypopituitarism, and adrenal insufficiency [2]. Clinically, most patients are asymptomatic and AC is often detected incidentally. Neuroendocrine dysfunction due to anterior pituitary gland injury is common in TBI and may result in transient or permanent dysfunction [3, 4]. In a study of 50 patients with moderate-to-severe traumatic brain injury, Agha et al. found evidence of ACTH deficiency in 16% [5]. In this case, the patient’s post-traumatic hyponatremia (123–130 mmol/L) was initially suspicious for SIADH; however, serum osmolality levels remained normal (>275 mmol/L). Interestingly, arterial blood gas showed compensated respiratory alkalosis (pH 7.44, PCO2 28 mmHg) with low serum bicarbonate (range 20–21 mmol/L). Decaux et al. showed that this pattern of low total bicarbonate (TCO2) and compensated respiratory alkalosis can differentiate hyponatremia related to ACTH deficiency from SIADH in which TCO2 levels are typically normal [6]. Together, these clinical findings and auxiliary laboratory studies along with the
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