Ophthalmic Surgery, Lasers and Imaging Retina

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Brief Report 

Terson’s Syndrome Managed with 25-Gauge Vitrectomy

Brian C. Joondeph, MD, FACS; Hoang Nguyen, CRA, OCT-C; Thomas Politzer, OD, FCOVD, FAAO; Alan Weintraub, MD

Abstract

Terson’s Syndrome represents vitreous hemorrhage due to intracranial hemorrhage. A series of 18 adult eyes with Terson’s Syndrome, due to either traumatic brain injury or ruptured aneurysm, successfully managed with 25-gauge vitrectomy was reported. All patients had improved vision, although some had limitation due to effects of surgery or the underlying pathology.

Abstract

Terson’s Syndrome represents vitreous hemorrhage due to intracranial hemorrhage. A series of 18 adult eyes with Terson’s Syndrome, due to either traumatic brain injury or ruptured aneurysm, successfully managed with 25-gauge vitrectomy was reported. All patients had improved vision, although some had limitation due to effects of surgery or the underlying pathology.

From Colorado Retina Associates, PC, Denver, Colorado.

Presented in part as poster at the American Society of Retinal Specialists meeting, December 5, 2007, Palm Springs, California.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Brian C Joondeph, MD, Colorado Retina Associates, PC, 8101 E Lowry Blvd, Suite 210, Denver, CO 80230.

Accepted: November 11, 2009
Posted Online: March 09, 2010

Introduction

Terson’s Syndrome refers to vitreous and intracranial hemorrhage.1–3 It usually results from subarachnoid hemorrhage and is frequently bilateral. A current theory of pathogenesis suggests that the acute rise in intracranial pressure from the injury and brain hemorrhage leads to intraorbital venous stasis. This in turn causes a rapid rise in intraocular venous pressure, causing rupture of peripapillary and retinal vessels. We describe a series of 18 eyes of 13 patients with Terson’s Syndrome successfully managed with 25-gauge pars plana vitrectomy.

Design and Methods

We retrospectively reviewed 18 eyes of 13 consecutive patients with Terson’s Syndrome managed by 25-gauge vitrectomy. Patient information including demographics is listed in Table 1.

Patient Demographics and Treatment Results

Table 1: Patient Demographics and Treatment Results

Results

The etiology of Terson’s Syndrome was traumatic brain injury in 10 eyes and ruptured cerebral aneurysm in 8 eyes (Table 1). There were 2 women and 11 men. Presenting visual acuities were 20/200 or worse in all but one case, which had 20/60 visual acuity in the affected eye.

All patients had non-clearing vitreous and preretinal hemorrhage for which surgery was recommended and performed. Six patients had unilateral hemorrhage and seven had bilateral hemorrhage. The mean duration of observation from hemorrhage to surgery was 3.4 months (1 to 9 months). When the retina could not be visualized, B-scan ultrasound was performed to rule out retinal detachment. No eyes had preoperative retinal detachment.

The surgery consisted of a 25-gauge pars plana vitrectomy with removal of hemorrhage and removal of a detached internal limiting membrane (ILM) over the macula when indicated. 14 of the 18 eyes had a detached ILM with sub-ILM hemorrhage. If there was no ILM detachment, no effort was made to peel ILM. No additional surgical maneuvers were required other than an air bubble, which was placed in all eyes to prevent hypotony. No sclerotomy sutures were required and no patients experienced hypotony postoperatively.

Patients received standard postoperative care. With a variable range of follow-up, ranging from 1 to 24 months, most patients had a significant improvement in vision as listed in Table 1. Reasons for limited postoperative vision included cortical vision loss in both eyes of two patients, a postoperative retinal detachment in another patient, which was successfully repaired but with vision loss, and cataract in both eyes of a third patient. The retinal detachment occurred 4 months after vitrectomy, was superior, macula-off, and was due to a small superior break not adjacent to any of the sclerotomies. The patient was phakic and contraction of the remaining peripheral vitreous was the likely cause of the break. In spite of successful repair, the vision never improved beyond 20/400.

Two patients with bilateral Terson’s syndrome declined surgery on their fellow eye following significant vision improvement in the first eye (patients 7 and 13). One of these patients had dense amblyopia in the fellow eye such that the hemorrhage was visually insignificant and another declined second eye surgery due to cost and insurance issues.

Discussion

The results of this small series of patients suggest that vitreous hemorrhage due to Terson’s Syndrome can be successfully managed with 25-guage vitrectomy.

Most patients had sub-ILM hemorrhage requiring ILM removal (14 of 18 eyes). The white ridge noted at the edge of the hemorrhage preoperatively (Fig. 1) represents the edge of the detached ILM. At the time of surgery, blood was found beneath a detached ILM. The ILM could be removed to the limits of where it inserts at the edges of the macula. After surgery, a white ridge is visible at the limits of the ILM detachment (Fig. 2). This finding has been noted previously and described as a pigmented macular ring.4

The White Ridge (arrows) Noted at the Edge of the Hemorrhage Preoperatively Represents the Edge of the Detached ILM.

Figure 1. The White Ridge (arrows) Noted at the Edge of the Hemorrhage Preoperatively Represents the Edge of the Detached ILM.

A White Ridge (arrows) is Visible at the Limits of the ILM Detachment Postoperatively.

Figure 2. A White Ridge (arrows) is Visible at the Limits of the ILM Detachment Postoperatively.

Initial treatment includes observation since the hemorrhage sometimes clears spontaneously with improvement of vision. In this group of patients, the hemorrhage was dense and yellow in color. These hemorrhages can persist indefinitely without clearing. Likewise, sub ILM hemorrhage usually was not clear as it is loculated and cannot disperse. These patients all had neurologic injury and were inpatients in a rehabilitation hospital. From a global rehabilitation perspective, early intervention was beneficial by restoring other visual senses such as binocular vision, stereopsis and peripheral vision, hastening their rehabilitation progress. These factors apply to unilateral hemorrhage cases as well, with removal of hemorrhage providing expansion of the binocular vs. monocular visual field. Case 13 had 20/60 vision preoperatively, but the fellow eye had dense amblyopia, hence the recommendation for surgery. While unilateral cases could be observed indefinitely with the possibility of eventual clearing of the hemorrhage, restoration of binocular vision was beneficial from the perspective of global rehabilitation. Lastly, many of these patients lived in adjacent states without access to retinal follow-up care or surgery. If possible, surgery was performed prior to discharge from the rehabilitation hospital so their visual and global rehabilitation could be near complete by the time of hospital discharge.

While there are risks to surgical intervention, including cataract, retinal detachment, and endophthalmitis, these risks are outweighed by the benefits of faster rehabilitation as discussed above. There are also potential risks to observation including hemosiderosis secondary to sub-ILM hemorrhage, epiretinal membrane, retinal detachment, and hemolytic glaucoma.

The timing of surgery was also based on their being stable for surgery from a medical and neurological perspective. Depending on the extent of initial injury and surgery, patients may be stable enough for retinal surgery within 1 to 2 months. While local anesthesia is preferable in medically unstable patients, general anesthesia was used in most of these cases. Because of the brain injuries in these patients, many were restless and could not reliably remain immobile, which would be necessary for either local or topical anesthesia.

The final visual outcome depends on concurrent ocular or central nervous system damage from the initial injury. Some patients have been mistakenly diagnosed as “cortically blind”, when they actually have bilateral Terson’s syndrome. Patients need to be informed of the possibility of partial or even no improvement in vision after vitrectomy surgery because of cortical vision loss, which cannot be ascertained prior to surgery. This limited the final vision in both eyes of two patients.

In summary, 25-guage pars plana vitrectomy is an effective management option for adult eyes with non-clearing vitreous hemorrhage from Terson’s Syndrome.

References

  1. Kuhn F, Morris R, Witherspoon CD, et al. Terson syndrome: results of vitrectomy and the significance of vitreous hemorrhage in patients with subarachnoid hemorrhage. Ophthalmol. 1998;105:472–477. doi:10.1016/S0161-6420(98)93030-5 [CrossRef]
  2. Schultz PN, Sobol WM, Weingeist TA. Long-term visual outcome in Terson syndrome. Ophthalmol. 1991;98:1814–1819.
  3. Clarkson JG, Flynn HW, Daily MJ. Vitrectomy in Terson’s syndrome. Am J Ophthalmol. 1980; 90: 549–552.
  4. Sadeh AD, Lazar M, Loewenstein A. Macular ring in a patient with Terson’s syndrome. Acta Ophthalmol Scand. 1999;77:599–600. doi:10.1034/j.1600-0420.1999.770526.x [CrossRef]

Patient Demographics and Treatment Results

CaseAge/SexLateralEtiologyInitial VaDuration Observe (mo)Final VaFollow-up (mo)ILM Detach?Comment
155/MUniTBI20/200420/3010Yes
219/MUniTBI20/400920/401Yes
355/FBilAneurLP4CF24YesCortical Va loss
455/FBilAneurLP5HM24YesCortical Va loss
521/MUniAneurCF320/201No
618/MUniTBI20/400220/302Yes
753/MBilAneurCF220/203No
819/MBilTBICF320/2024Yes
919/MBilTBICF320/40024YesRD
1049/MBilTBIHM620/6014NoCataract
1149/MBilTBICF620/609NoCataract
1249/MUniAneurCF320/308Yes
1356/MBilAneur20/60420/3010Yes
1454/MUniTBI20/200220/308Yes
1531/MBilTBIHM220/252Yes
1631/MBilTBICF220/402Yes
1730/FBilAneur20/400120/4001YesCortical Va loss
1830/FBilAneur20/400120/4001YesCortical Va loss
Authors

From Colorado Retina Associates, PC, Denver, Colorado.

Presented in part as poster at the American Society of Retinal Specialists meeting, December 5, 2007, Palm Springs, California.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Brian C Joondeph, MD, Colorado Retina Associates, PC, 8101 E Lowry Blvd, Suite 210, Denver, CO 80230.

10.3928/15428877-20100215-85

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