Key result
Severe hypothyroidism with acute metabolic acidosis linked to central neurogenic hyperventilation post-aortoaortic bypass.
Why the study?
Central neurogenic hyperventilation is a rare syndrome requiring exclusion of other causes, with limited data on its occurrence secondary to severe hypothyroidism in critically ill patients after vascular surgery.
Case Report (n=1)
Highlights a rare case of central neurogenic hyperventilation following aortoaortic bypass, emphasizing severe hypothyroidism and metabolic acidosis as potential secondary causes.
Answers are grounded in this paper and cite their sources.
Alerts clinicians to hypothyroidism in unexplained post-vascular hyperventilation; leaves open causal confirmation in larger cohorts.
Central neurogenic hyperventilation (CNH) is a rare condition and defined as a syndrome comprising normal or elevated arterial oxygen tension, decreased arterial carbon dioxide tension, respiratory alkalosis with hyperventilation even during sleep, and the absence of a peripheral respiratory stimulus. The diagnosis of CNH requires the exclusion of pulmonary, cardiac, metabolic-immunological disorders and some medicines that can result in hyperventilation. We detailed the case of CNH in the 4th day after vascular surgery probably secondary to acute metabolic acidosis with hyperlactatemia, due to severe hypothyroidism in the context of critically ill patient.
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Ana Belén Méndez Fernández (2017) conducted a case report in Central neurogenic hyperventilation (n=1). Severe hypothyroidism and acute metabolic acidosis was evaluated. Severe hypothyroidism with acute metabolic acidosis likely caused central neurogenic hyperventilation in a critically ill patient on the 4th day after aortoaortic bypass surgery.
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