IntroductionPrimary hypoparathyroidism is a rare condition caused by parathyroid hormone deficiency and characterized by hypocalcemia. The clinical manifestations of primary hypoparathyroidism include tetany, seizures, paresthesias, dementia, and parkinsonism. Psychiatric manifestations such as mood disorders are unusual and may constitute a major diagnostic challenge, especially if the typical manifestations caused by hypocalcemia are absent.Case presentationThe patient was a 22-year-old Caucasian man with a history of chronic omeprazole use and periodic seizures, who presented to the emergency department of a secondary hospital in Southern Brazil with symptoms of major depression (sadness, anhedonia, loss of appetite, insomnia, and fatigue) associated with paresthesias affecting his toes. The initial electrocardiogram revealed a prolonged QTc interval. A computed tomography scan of his brain revealed bilateral, nonenhancing hyperdense calcifications involving the putamen and caudate nucleus. An electroencephalogram showed generalized bursts of slow spikes. Blood laboratory study results indicated serum hypocalcemia, hypomagnesemia, and hyperphosphatemia associated with a low parathyroid hormone level. His serum levels of albumin, 25-hydroxyvitamin D, thyroid-stimulating hormone, T3 and T4 thyroid hormones, as well as the results of kidney function tests, were normal. The definitive diagnosis was primary hypoparathyroidism with psychiatric manifestations due to chronic hypomagnesemia induced by proton pump inhibitor use.ConclusionsIn some cases, to differentiate between a primary psychiatric disorder and primary hypoparathyroidism with neuropsychiatric symptoms may represent a challenge given that the classical manifestations of hypocalcemia, especially tetany, may be absent in the setting of chronic hypoparathyroidism. Clinicians and psychiatrists should consider primary hypoparathyroidism part of the differential diagnosis during the evaluation of patients with mood symptoms, especially in the context of atypical presentations associated with hypocalcemia.
Objective To evaluate whether the decrease in blood pressure caused by the increase in the positive end-expiratory pressure corresponds to the pulse pressure variation as an indicator of fluid responsiveness. Methods This exploratory study prospectively included 24 patients with septic shock who were mechanically ventilated and subjected to three stages of elevation of the positive end-expiratory pressure: from 5 to 10cmH 2 O (positive end-expiratory pressure level 1), from 10 to 15cmH 2 O (positive end-expiratory pressure level 2), and from 15 to 20cmH 2 O (positive end-expiratory pressure level 3). Changes in systolic blood pressure, mean arterial pressure, and pulse pressure variation were evaluated during the three maneuvers. The patients were classified as responsive (pulse pressure variation ≥ 12%) or unresponsive to volume replacement (pulse pressure variation < 12%). Results The best performance at identifying patients with pulse pressure variation ≥ 12% was observed at the positive end-expiratory pressure level 2: -9% systolic blood pressure variation (area under the curve 0.73; 95%CI: 0.49 - 0.79; p = 0.04), with a sensitivity of 63% and specificity of 80%. Concordance was low between the variable with the best performance (variation in systolic blood pressure) and pulse pressure variation ≥ 12% ( kappa = 0.42; 95%CI: 0.19 - 0.56). The systolic blood pressure was < 90mmHg at positive end-expiratory pressure level 2 in 29.2% of cases and at positive end-expiratory pressure level 3 in 41.63% of cases. Conclusion Variations in blood pressure in response to the increase in positive end-expiratory pressure do not reliably reflect the behavior of the pulse pressure as a measure to identify the fluid responsiveness status.
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