Merrison and and Samden1 describe an interesting and rare case of postpartum Horner's syndrome in a young lady presenting two weeks after delivery. The authors describe prolonged labour with forceps assisted delivery of a healthy 10 lb baby. The authors have postulated straining during labour with unusual neck movements and high spinal anaesthesia as possible mechanisms for this rare phenomenon that possibly resulted in dissection and acute thrombosis of the extracranial internal carotid artery.
We were surprised to read the mode of assisted delivery and were at loss to know what could possibly be the indication for ‘high’ forceps application, which is rarely practised in modern obstetrics. Horner's syndrome is now a well-recognised complication of spinal anaesthesia or analgesia during labour.2 However, it is usually an immediate occurrence. Two-week latency in this case makes it difficult to associate the spinal anaesthesia with such a delayed onset of Horner's syndrome, especially in the absence of any associated delayed neurological deficits. The authors have also discussed possibility of neck movements during the delivery as another possible mechanism of the Horner's. Considering that a significant proportion of women do assume unusual neck posture at some stage during the second stage of labour, one would have expected Horner's syndrome to occur much more commonly if it was mainly related to intrapartum neck movements. Even in patients with severe cervical spine injuries, Horner's syndrome is rare in the absence of spinal cord involvement. From the history provided, the patient in the case described was young and was not susceptible to carotid dissection in any way and should not have normally developed any neurological deficit with voluntary neck movements during labour. Although both the mechanisms postulated by the authors are valid, they do not convincingly establish a cause and effect relationship in this case.
On the contrary, it is possible that she may have developed thrombosis of her internal carotid artery spontaneously. Although intracranial venous system is more prone to thrombosis in puerperium—mainly due to its slow blood flow and low pressure, the arterial system is by no means completely exempt from such a phenomenon. Difficult delivery, prolonged labour with possible dehydration, spinal anaesthesia with further hypotension and slowing of the blood flow in combination with the natural hypercoagulability of the blood normally seen in puerperium may have resulted in spontaneous internal carotid thrombosis, obliteration of vasa nervosa and subsequent Horner's syndrome. Complete resolution of symptoms with anticoagulation within three months supports this theory that there was no anatomical disruption of the sympathetic fibres, which would have been the case if it was due to trauma caused by neck movements.