Case Report

By Dr. Karandeep Rishi , Dr. Meenu Puri
Corresponding Author Dr. Karandeep Rishi
Ophthalmology, Sai Ram Charitable Eye Hospital, Kurukshetra - India 136118
Submitting Author Dr. Karandeep Rishi
Other Authors Dr. Meenu Puri
MMIMSR, Mullana, - India


Posterior ischemic optic neuropathy, Post-partum haemorrhage, Permanent vision loss

Rishi K, Puri M. Posterior Ischaemic Optic Neuropathy Following Vaginal Delivery. WebmedCentral OPHTHALMOLOGY 2012;3(4):WMC003307
doi: 10.9754/journal.wmc.2012.003307

This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Submitted on: 26 Apr 2012 05:46:16 PM GMT
Published on: 27 Apr 2012 05:48:34 PM GMT


Sudden hypotension complicated with anaemia can lead to acute bilateral simultaneous posterior ischaemic optic neuropathy (PION). Such cases have been described in the perioperative period; however PION developing after normal vaginal delivery is a very rare occurrence. We report a case of 32 years old para 3 who presented to us on the second post-partum day after a normal vaginal delivery with bilateral vision loss and had no visual recovery even 8 weeks post-partum.


Ischemic optic neuropathy is a rare complication of massive haemorrhage. Of the reported cases of post haemorrhagic amaurosis, approximately 30% are the result of uterine haemorrhage. The pathogenesis of ischemic optic neuropathy is unclear. Severe anaemia, with or without arterial hypotension that may result in optic nerve hypoxia or ischemia is the proposed mechanism (1) We report a rare case of posterior ischaemic optic neuropathy that occurred on the second post-partum day. She had residual visual loss even after 8 weeks post-partum.

Case Report(s)

A 32 years old para 3 presented to our emergency department with history of sudden, painless loss of vision since 2 days. She had a full term vaginal delivery at a peripheral hospital 4 days back complicated with atonic post-partum haemorrhage managed with uterotonics and 3 blood transfusions. At the time of presentation vision was perception of light in both eyes with inaccurate projection of rays. Her BP was 116/68 mm of Hg and pulse was 90/min. Anterior segment examination was normal. Both pupil were mid-dilated with sluggish reaction to light. Fundus examination revealed no abnormal findings. There was no focal neurological deficit and her higher mental functions were normal. MRI brain and orbit did not reveal any abnormality. Visual evoked potential were carried out in both the eyes which revealed bilateral increased latency. Fundus fluorescence angiography was within normal limits and did not show any area of non-perfusion in the retina. OCT was within normal limits bilaterally. Haemoglobin was 8gm%.

A provisional diagnosis of Posterior ischemic optic neuropathy was made. Patient was given 3 day course of pulse methylprednisolone 1g/day to reverse any neurological injury. On day seven vision improved to 5/200 snellen visual acuity in both eyes and remained the same at 4 week follow up. Fundus examination at 4 week revealed mild disc pallor which increased at 8 week follow up.


The proposed pathogenesis of PION is sudden hypotension leading to ischaemic hypoxia to the posterior optic nerve. Other possible mechanisms include release of circulating vasoconstrictors (i.e., angiotensin, epinephrine, and vasopressin) as a result of activation of the sympathetic nervous system, resulting in vasoconstriction and optic nerve ischemia, Buono et al (2) described the diagnostic criteria for PION which includes (1) an acute decrease in visual acuity, visual field, or both; (2) an ipsilateral relative afferent pupillary defect, unless there is bilateral symmetrical involvement or a pre-existing contralateral optic neuropathy when the pupils are sluggish or nonreactive to light (3) documentation of a normal optic disc at the onset of visual deficit; (4) exclusion of other identifiable causes of visual deficit, including retinal and glaucomatous problems, and other causes of optic neuropathy, such as compression, demyelination, or inflammation with neuroimaging; (5) an abnormal VEP. (6) a normal ERG. (7) development of optic disc pallor within 4 – 8 weeks of onset of visual loss.
Chun and Levin (3) described a similar case of PION that occurred after massive haemorrhage of ruptured ectopic gestation and left the patient with permanent vision loss.
We thus describe an unusual case of PION that occurred after post-partum haemorrhage and led to permanent visual impairment.


1. Hayreh SS. Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. Ophthalmology 1987; 94(11): 1488–1502.
2. Buono LM, Foroozan R, Savino PJ, Danesh-Meyer HV, Stanescu D. Posterior ischemic optic neuropathy after hemodialysis. Ophthalmology 2003; 110(6): 1216–1218.     
3. Chun DM, Levin DK. Ischemic optic neuropathy after hemorrhage from a cornual ectopic gestation. Am J Obstet Gynecol. 1997; 177(6): 1550–1552.

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3 reviews posted so far

Posterior Ischaemic Optic Neuropathy Following Vaginal Delivery
Posted by Anonymous Reviewer on 22 Jun 2012 03:34:00 AM GMT

PION Following Vaginal Delivery
Posted by Dr. Theodore Leng on 28 Apr 2012 03:59:32 AM GMT

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