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Case Report

Bull Emerg Trauma 2018;6(2):178-180.

An Unforeseeable Complication; Posterior Ischemic Optic Neuropathy after Penetrating Injury to the Heart

Joseph J. Eid1*, Brian C. Cronin2, Susan Seman3

1Providence-Providence Park Hospital, Michigan State University College of Human Medicine, Southfield, Michigan, USA
2St. John Macomb-Oakland Hospital, Warren, Michigan, USA
3Sinai-Grace Hospital – Detroit Medical Center, Detroit, Michigan, USA


*Corresponding Author: Joseph J. Eid
Address: Providence-Providence Park Hospital, Michigan State University College of Human Medicine, Southfield, Michigan, USA.
e-mail: eidjose1@msu.edu

Received: November 10, 2017
Revised: February 26, 2018
Accepted: March 2, 2018


Please cite this paper as:
Eid JJ, Cronin BC, SemanS. An Unforeseeable Complication; Posterior Ischemic Optic Neuropathy after Penetrating Injury to the Heart. Bull Emerg Trauma. 2018;6(2):178-180. doi: 10.29252/beat-060214 .


Trauma surgeons are currently encountering unusual adverse events after traumatic injuries. Ischemic optic neuropathy is a rare complication that may occur in trauma and burn patients that present in extremis and require massive resuscitation. A 29-year-old male patient sustains a penetrating injury to the heart that required primary repair. He remained hemodynamically stable and required a limited amount of resuscitative fluids and products. Postoperatively, the patient develops acute painless bilateral loss of vision. These findings were consistent with posterior ischemic optic neuropathy. Ischemic optic neuropathy are uncommon entities that arise in trauma patients who require massive resuscitation. Given the limited treatment options, early diagnosis is key in limiting the hemodynamic insult to the optic nerve.

Keywords:  Ischemic optic neuropathy; Posterior ischemic optic neuropathy penetrating wound; Postoperative complication.


After improvements in the management of life threatening traumatic injuries and surgical critical care, trauma surgeons are currently encountering rare complications not commonly seen in clinical practice. Ischemic optic neuropathy (ION) is one of the many rare complications arising in trauma and burn patients that require large volumes of resuscitative fluid and blood products [1-4]. Persistent hypotension is the main inciting event and clinical presentation is characterized by acute painless loss of vision [1,2]. In this case report, we present a case of posterior ION that occurred in a hemodynamically stable trauma patient with limited fluid resuscitation.

Case Report
We present a case of a 29-year-old male patient who was brought in to our emergency department triage unit after sustaining a penetrating injury to chest. The patient’s past medical history was significant for untreated neurosyphilis and Human Immunodeficiency Virus (HIV) infection. The timing of presentation in relation to the initial insult was unknown.
The patient was immediately transferred to the trauma bay where initial vital signs showed a blood pressure of 76/49 mmHg and a pulse rate of 117 beats per minute. These initial findings were concerning for hemorrhagic shock. Primary and secondary surveys were conducted per the Advance Trauma Life Support protocol. During the primary survey the patient was found to have to a Glasgow Coma Scale Score of 7 for which an endotracheal tube was placed for airway protection. The stab wound entry site was at the right parasternal region along the 3rd intercostal space. Decreased breath sounds were noted over the right hemi-thorax, which required placement of a right thoracostomy tube that yielded 200 milliliters (ml) of sanguineous output. Intravenous crystalloid boluses were given, and the massive transfusion protocol was initiated which improved the patient’s hemodynamic status with a blood pressure of 98/54 mmHg.  A Focused Assessment with Sonography for Trauma (FAST) exam was performed at bedside, with the sub-xiphoid window revealing a significant amount of pericardial fluid. Given the patient’s presenting hemodynamic lability, a pericardiocentesis was performed and 60 ml of fresh blood was aspirated. A concern for penetrating injury to the heart prompted an emergent transfer to the operating theater for a median sternotomy and exploration. At the conclusion of the primary and secondary survey the patient had received a total of 2 liters (L) of crystalloids, 2 units (u) of packed red blood cells, 2u of fresh frozen plasma, and 1u of platelets. This totals to 1400ml of blood products.
In the operating theater a median sternotomy was performed, and a significant amount of clotted blood was encountered upon entry into the pericardium. Examination of the heart revealed a single 1-centimeter laceration to the right ventricle that was repaired with a single pledgeted U-stitch polyprolene suture. The patient remained hemodynamically stable throughout the entirety of the procedure and did not require any additional blood products. This prompted discontinuation of the massive transfusion protocol. The patient was successfully extubated in the post-anesthesia care unit after 102 minutes of operative time. The patient required a total of 2 liters of intraoperative crystalloids and estimated blood loss was 300 ml.
Immediately after extubation, the patient complained of acute painless bilateral loss of vision. On ophthalmological examination, the patient was found to have lack light perception, normal intraocular pressures, 3-millimeter pupils with significantly delayed reaction times, and an unremarkable anterior exam. On posterior chamber examination the optic nerve was flat and pink optic with a cup:disc ration 0.3, normal vessels and flat peripheral retina. A CT scan of the head and neck did not visualize any intracranial bleeding, signs of cerebral ischemia, or vascular dissection of the branches of the internal carotid artery. Therein the patient was diagnosed with posterior ischemic optic neuropathy. The patient received supportive care and an alpha-2-adrenergic agonist eye drops (brimonidine). The patient had gradual regain of vision and light perception starting 48 hours after surgery. On postoperative day 3, the patient had full regain of visual acuity.  

Perioperative vision loss after non-ocular traumatic injury is a rare entity that arises due to relative ischemia to the optic nerve [1,2]. Ischemic insults to the visual tract and the visual cortex may present similarly. Painless postoperative vision loss has been previously described in trauma [2,3] and burn [4] patients requiring massive transfusion and resuscitation. It has also been reported in patients undergoing elective abdominal, orthopedic, spinal, and cardiac surgery [5-7].
Anatomically, the optic nerve consists of 4 portions: (1) intra-ocular (anterior), (2) intra-orbital (posterior), (3) intra-canalicular, and (4) intra-cranial. Ischemic optic neuropathies classically affect the intra-ocular and intra-orbital portions of the optic nerve: therefore, described as anterior (AION) or posterior ischemic optic neuropathy (PION). The watershed area in the anterior portion and pial plexus along the posterior portion of the optic nerve predisposes it to significant ischemic insult in the face of hemodynamic instability [8,9]. Clinically patients report acute, unilateral or bilateral, partial or complete vision loss. On examination, patients with ION have afferent pupillary reflex deficit, visual field defects. While PION has no obvious findings on funduscopic examination, AION presents with pale disc edema.
In our case report, the patient reported painless loss of vision immediately after extubation. Fundoscopic examination was normal. A brain CT was performed which did not reveal any acute intra-cranial bleeding, dissection of the internal carotid artery, occlusion of the ophthalmic artery, or ischemia in the visual cortex. An echocardiogram with a bubble study essentially eliminated the possibility of an air embolus that may have migrate to the arterial circulation via a congenital patent foramen ovale or an acquired defect in the ventricular septum secondary to the penetrating injury. All these findings were consistent with PION. The patient did not have any previous visual deficits, however his history of neurosyphilis may have predisposed him to this ischemic insult.
AION occurs at a rate of 2.6% in trauma patients which may be secondary to prone position and massive resuscitation [2]. Previous reports of post-traumatic ION have been associated with severe prolonged hypotension, need large volume resuscitation, and prolonged ventilator days [1-4]. Kudo et al., [3] described two cases of blunt trauma requiring where one patient required 38.4 liters of crystalloid and 6 liters of blood product during the perioperative period. The second reported patient required even large volumes of resuscitative fluid up to 50 L and 10 L of blood products [3]. Similar findings are seen in patients with large burns requiring large volume of crystalloid resuscitation. In a case series by Medina et al., [4] patients with OIN had burn surface areas ranging 57-68%, requiring 20-47.6 L of crystalloids within the first 24 hours after the initial insult.  However, in our patient the total volume of resuscitative fluid was 5.4 L which is merely a fraction of what is reported in the literature.
The best of our knowledge, this is the first report to describe PION in the setting of transient perioperative hypotension, relative hemodynamic stability, and limited resuscitative fluid intake. Given the limited treatment options, trauma surgeons should remain vigilant of this entity to avoid ongoing hemodynamic insult to the optic nerve.

Ethics approval and consent to participate: Institutional Review Board approval was not required for this case report.
Consent for publication: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Conflict of Interest: The authors declare that they have no competing interests.



  1. Foroozan R, Buono LM, Savino PJ. Optic disc structure and shock-induced anterior ischemic optic neuropathy. Ophthalmology. 2003;110(2):327-31. 
  2. Cullinane DC, Jenkins JM, Reddy S, VanNatta T, Eddy VA, Bass JG, et al. Anterior ischemic optic neuropathy: a complication after systemic inflammatory response syndrome. J Trauma. 2000;48(3):381-6; discussion 6-7. 
  3. Kudo D, Yamamura H, Nishiuchi T, Ishikawa K, Mizushima Y, Matsuoka T, et al. Anterior and posterior ischemic optic neuropathy related to massive fluid resuscitation after blunt trauma. J Trauma. 2010;68(3):E67-70.
  4. Medina MA, 3rd, Moore DA, Cairns BA. A case series: bilateral ischemic optic neuropathy secondary to large volume fluid resuscitation in critically ill burn patients. Burns. 2015;41(3):e19-23. 
  5. Roth S, Thisted RA, Erickson JP, Black S, Schreider BD. Eye injuries after nonocular surgery. A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology. 1996;85(5):1020-7.
  6. Nuttall GA, Garrity JA, Dearani JA, Abel MD, Schroeder DR, Mullany CJ. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg. 2001;93(6):1410-6, table of contents.
  7. Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: the Johns Hopkins Hospital Experience. Spine (Phila Pa 1976). 2005;30(11):1299-302
  8. Hayreh SS. Anterior ischaemic optic neuropathy. I. Terminology and pathogenesis. Br J Ophthalmol. 1974;58(12):955-63.
  9. Boghen DR, Glaser JS. Ischaemic optic neuropathy. The clinical profile and history. Brain. 1975;98(4):689-708.


Journal compilation © 2018 Trauma Research Center, Shiraz University of Medical Sciences