An otherwise healthy 21-yr-old, G3P1 full-term parturient, presented to our labour and delivery unit. She reported a successful labour epidural followed by 6 months of lower back pain, after her previous delivery. Following rapid progress of her current labour, the patient requested neuraxial analgesia after initial refusal, reporting unbearable contraction pain. Before neuraxial analgesia had been established, however, and after a period of hyperventilation, the patient was found lying supine with both arms and legs extended, and both wrists in extreme flexion (carpopedal spasm), looking upwards and breathing vigorously (6080 bpm). The patient had experienced sudden spastic paresis involving both upper and lower extremities 5 min earlier, with loss of passive ability to straighten her upper extremities, and a high muscle tone. She also complained of dizziness, blurred vision, and numbness in her lower extremities during the event, and a 5 min prodromal episode of paraesthesia in her nose and toes leading up to it. Management of the patient included re-breathing of carbon dioxide by placing a non-rebreathing reservoir face mask, with the oxygen supply turned off over her face, and i.v. sedation (fentanyl 50 µg), leading to resolution of the symptoms over 10 min. The patient delivered a vigorous healthy boy, 25 min later. Neurological and laboratory investigations revealed only a low total blood calcium (8.6 mg dl1) and a high alkaline phosphatase (207 U litre1), which is normal during pregnancy because of increased placental production. Both patient and baby were discharged home after a normal neurological examination.
The most likely cause of this event, we feel, is transient hypocalcaemia induced by hyperventilation-induced respiratory alkalosis.2 Raised maternal progesterone increases minute ventilation during pregnancy, but does not change arterial pH.3 Acute hyperventilation in excess of this will, however, increase arterial pH, the effect of which may not be favourable to the fetus. In vitro work has shown that changing serum pH by 0.5 pH units can alter ionized calcium from between 0.20.4 mM.4 This occurs because of increased calcium binding to serum albumin, reducing ionized serum calcium. While bovine parturient paresis is common when taking a low calcium diet,5 other hypocalcaemic disorders do not appear to cause significant neuromuscular problems in pregnancy.
It is possible that this patient was experiencing a seizure or pseudo-seizure.6 However, we feel this is unlikely as the patient had no previous history of seizures. There was no history of pre-eclampsia or hypertension, and the transient nature and quality of this single episode with no loss of consciousness, would not suggest such an aetiology. Conditions such as periodic paralysis occur because of changes in serum potassium and lead to hypotonic or flaccid paralysis.7 No change in serum potassium was found in this patient. There is a report of tetany induced by hyperventilation in a dental patient,8 showing that it can be caused by acute hyperventilation in normal patients, and cases of tetany have been reported in normocalcaemic patients.9 Our patient had a dramatic 15 min sustained spastic quadraparetic episode, after a prolonged period of hyperventilation during labor. The most likely cause of this event is transient hypocalcaemia from hyperventilation-induced respiratory alkalosis. Both awareness of this differential diagnosis and prevention of extreme hyperventilation is important in the management of obstetric patients, especially those without prenatal education (e.g. instruction in the Lamaze breathing pattern or similar preparatory training).10 11 This is important before establishing neuraxial and/or other means of analgesia.
Durham, NC, USA
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