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   <subfield code="a">Acute hypoxemia in a parturient with primary ciliary dyskinesia following the administration of intravenous oxytocin: a case report</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Amar Nandhakumar, Gregory Silverman]</subfield>
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   <subfield code="a">Hypoxémie aiguë chez une parturiente ayant une dyskinésie ciliaire primitive après l'administration intraveineuse d'ocytocine: une étude de cas</subfield>
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   <subfield code="a">Purpose: We present the case of a parturient diagnosed with primary ciliary dyskinesia with secondary bronchiectasis who developed significant hypoxemia following administration of intravenous oxytocin during Cesarean delivery under spinal anesthesia. This case suggests that oxytocin can affect pulmonary vascular tone and interfere with the protective effects of hypoxic vasoconstriction. Clinical features: A 35-yr-old primigravida at 37 weeks gestation presented for a scheduled Cesarean delivery due to breech positioning and fetal abnormalities. The patient had a diagnosis of primary ciliary dyskinesia and had undergone a right middle lobectomy seven years earlier for resultant bronchiectasis. Pulmonary function testing in the month prior to delivery showed a 4% decline in her baseline FEV1 to 1.06 L (32% of predicted value) but she was functionally well. The patient initially had an uneventful spinal anesthetic and maintained an oxygen saturation of 97% on room air in the supine position until delivery of her baby. An intravenous infusion of oxytocin for uterine contraction was started following removal of the placenta. The patient then became acutely hypoxemic with a drop in room air saturation to 84% but with no other accompanying hemodynamic instability. Maternal oxygen saturation did not improve with the addition of supplemental oxygen, and the patient had a significant arterial-alveolar oxygen gradient suggesting an intrapulmonary shunt. No supporting clinical, radiologic, or laboratory evidence of a thrombotic, air, or amniotic fluid embolism or mucous plug was detected. The patient remained hypoxemic during the postoperative period with gradual improvement back to baseline saturation in approximately 48hr. Conclusion: The vasodilatory effects of intravenous oxytocin on the pulmonary vasculature may worsen shunting and interfere with hypoxic pulmonary vasoconstriction, producing clinically significant hypoxemia in patients with comorbid lung disease. Oxytocin should be used with caution in patients with compromised lung function.</subfield>
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   <subfield code="a">Canadian Anesthesiologists' Society, 2013</subfield>
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   <subfield code="a">Nandhakumar</subfield>
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   <subfield code="t">Canadian Journal of Anesthesia/Journal canadien d'anesthésie</subfield>
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