Incidence estimates for perioperative vision loss (POVL) after nonocular surgery range from 0.013% for all surgeries up to 0.2% following spine surgery. The most common neuro-ophthalmologic causes of POVL are the ischemic optic neuropathies (ION), either anterior (AION) or posterior (PION). We identified 111 case reports of AION following nonocular surgery in the literature, with most occurring after cardiac surgery, and 165 case reports of PION following nonocular surgery, with most occurring after spine surgery or radical neck dissection. There were an additional 526 cases of ION that did not specify if the diagnosis was AION or PION. We also identified 933 case reports of central retinal artery occlusion (CRAO), 33 cases of pituitary apoplexy, and 245 cases of cortical blindness following nonocular surgery. The incidence of POVL following ocular surgery appears to be much lower than that seen following nonocular surgery. We identified five cases in the literature of direct optic nerve trauma, 47 cases of AION, and five cases of PION following ocular surgery. The specific pathogenesis and risk factors underlying these neuro-ophthalmic complications remain unknown, and physicians should be alert to the potential for loss of vision in the postoperative period.
perioperative; postoperative; vision loss; ocular surgery; nonocular surgery
Perioperative visual loss (POVL) is a devastating injury that has been reported infrequently after nonocular surgery. The most common cause of POVL is ischemic optic neuropathy (ION). Increasing numbers of cases of ION are being reported after spine surgery, but the etiology of postoperative ION remains poorly understood. After a MEDLINE search of the literature, we reviewed published case reports of ION, specifically those reported after spine surgery performed with the patient in the prone position. Most of the cases involved posterior ION (PION, n = 17), and the remainder anterior (AION, n = 5). Most patients had no or few preoperative vascular disease risk factors. All except one PION and 2 of 5 AION cases reported symptom onset within the first 24 hours after surgery. Visual loss was frequently bilateral (40% of AION, 47% of PION cases). Mean operative time exceeded 450 minutes. The lowest average intraoperative mean arterial blood pressure was 64 mm Hg and the mean lowest intraoperative hematocrit was 27%. The average blood loss was 1.7 L for AION and 5 L for PION patients. PION patients received an average of 8 L of crystalloid solution and 2.2 L of colloid intraoperatively. This compilation of case reports suggests that a combination of prolonged surgery in the prone position, decreased ocular perfusion pressure, blood loss and anemia/hemodilution, and infusion of large quantities of intravenous fluids are some of the potential factors involved in the etiology of postoperative ION. However, levels of blood pressure and anemia intraoperatively were frequently at levels considered acceptable in anesthesia practice. The etiology of postoperative ION remains incompletely understood. Potential strategies to avoid this complication are discussed.
ischemic optic neuropathy; optic nerve; spine surgery; visual loss
Postoperative vision loss (POVL) after major non-ocular surgery is a very rare but devastating complication since it has the potential to cause bilateral, severe and permanent loss of vision. The common major procedures resulting in POVL are cardiac and spinal procedures. We are reporting two patients who presented with features of bilateral anterior ischaemic optic neuropathy after coronary artery bypass grafting.
Coronary artery bypass grafting; postoperative visual loss; ischemic optic neuropathy
Postoperative visual loss is a devastating perioperative complication. The commonest aetiologies are anterior ischaemic optic neuropathy (AION), posterior ischaemic optic neuropathy (PION), and central retinal artery occlusion (CRAO). These appear to be related to certain types of operation, most commonly spinal and cardiac bypass procedures; with the rest divided between: major trauma causing excessive blood loss; head/neck and nasal or sinus surgery; major vascular procedures (aortic aneurysm repair, aorto-bifemoral bypass); general surgery; urology; gynaecology; liposuction; liver transplantation and duration of surgery. The non-surgical risk factors are multifactorial: advanced age, prolonged postoperative anaemia, positioning (supine v prone), alteration of venous drainage of the retina, hypertension, smoking, atherosclerosis, hyperlipidaemia, diabetes, hypercoagulability, hypotension, blood loss and large volume resuscitation. Other important cardiac causes are septic emboli from bacterial endocarditis and emboli caused by atrial myxomata. The majority of AION cases occur during CPB followed by head/neck surgery and prone spine surgery. CPB is used to allow coronary artery bypass grafting on a motionless heart. It has many side-effects and complications associated with its use and we report here a case of bilateral retinal infarction during routine coronary artery bypass grafting in a young male patient with multiple risk factors for developing this complication despite steps to minimise its occurrence.
Post-operative visual loss (POVL) following spinal surgery is a rare but devastating complication. Although a number of intra-operative and post-operative factors have been implicated, the exact etiology may still remain unclear.
To report a unique case of transient bilateral POVL in a patient who had undergone lumbar surgery in the prone position.
This patient was followed up prospectively for 1 year.
Prospective follow-up of a single patient following spinal surgery, who developed transient bilateral POVL.
This patient’s visual loss improved within 48 h.
This is the only documented case of POVL to have resolved completely within 48 h.
Post-operative; Visual loss; Spinal surgery
Postoperative vision loss (POVL) associated with spine surgery is a well known, albeit very rare complication. POVL incidence after spinal surgery ranges from 0.028 to 0.2%; however, due to the increase in number and duration of annual complex spinal operations, the incidence may increase. Origin and pathogenesis of POVL remain frequently unknown. A 73-year-old patient presented with lumbar disc herniation with associated neurological deficits after conservative pre-treatment at a peripheral hospital. Known comorbidities included arterial hypertension, moderate arterial sclerosis, diabetes mellitus type 2, mildly elevated blood lipids and treated prostate gland cancer. During lumbar spine surgery in modified prone position the patient presented with an acute episode of severe hypotension, which required treatment with catecholamines and Trendelenburg positioning. Three hours postoperatively, a visual loss in the right eye occurred, resulting in a complete amaurosis. Antihypertensive medication, arteriosclerosis and intraoperative hypotension are possible causes for the POVL. Intraoperative administration of catecholamines and Trendelenburg positioning for treatment of systemic hypotension might further compromise ocular perfusion. In patients with comorbidities compromising arterial blood pressure, blood circulation and microcirculation, POVL must be considered as a severe postoperative complication. It is recommended to inform patients about such complications and obtain preoperative informed consent regarding POVL. Any recent modification of antihypertensive medication must be reported and analysed for potential intraoperative hemodynamic consequences, prior to spine surgery in prone position.
Amaurosis; Blood pressure; Spinal surgery; Prone position; Postoperative vision loss (POVL)
Postoperative vision loss, a rare but devastating complication, has been reported after spine, cardiac, and head–neck surgeries. Its incidence following spine surgeries exceeds that after cardiothoracic surgeries. Various causes attributed to postoperative blindness include ischemic optic neuropathy, central or branch retinal artery occlusion, cortical blindness, and rarely external ocular injury. Other contributory factors described are microvascular diseases and intraoperative hemodynamic compromise. However, the exact association of these factors with postoperative blindness has not yet been confirmed. In this review, we describe causes, presentation, and treatment of postoperative blindness and also recommend practical guidelines to avoid this complication. The search strategies for this review included both search of electronic databases as well as manual search of relevant articles.
Postoperative blindness; spine surgery; vision loss
OBJECTIVE: To determine patients' opinions regarding the person, method, and timing for disclosure of postoperative visual loss (POVL) associated with high-risk surgery.
PATIENTS AND METHODS: On the basis of findings of a pilot study involving 219 patients at Mayo Clinic in Florida, we hypothesized that at least 80% of patients would prefer disclosure of POVL by the surgeon, during a face-to-face discussion, before the day of scheduled surgery. To test the hypothesis, we sent a questionnaire to 437 patients who underwent prolonged prone spinal surgical procedures at Mayo Clinic in Rochester, MN, or Mayo Clinic in Arizona from December 1, 2008, to December 31, 2009.
RESULTS: Among the 184 respondents, 158 patients gave responses supporting the hypothesis vs 26 with at least 1 response not supporting it, for an observed incidence of 86%. The 2-sided 95% confidence interval is 80% to 91%.
CONCLUSION: At least 80% of patients prefer full disclosure of the risk of POVL, by the surgeon, during a face-to-face discussion before the day of scheduled surgery. This finding supports development of a national patient-driven guideline for disclosing the risk of POVL before prone spinal surgery.
Perioperative optic neuropathy is a disease which can lead to serious, irreversible damage of vision. This complication could be the result of non-ocular surgery, for example, cardiac or spinal procedures.
We present a case of anterior ischemic neuropathy (AION) which occurred following a conventional coronary artery bypass graft procedure.
A 57-year-old man, 4 days after Conventional Coronary Artery Bypass Graft surgery as result of multi-vessel stabile coronary artery disease and history of anterolateral wall myocardial infarction, was admitted to the Eye Clinic due to significant loss of vision in his right eye. The patient had hypertension and was a heavy smoker. On admission, the slit lamp examination revealed a relative afferent pupillary defect in the right eye. The fundus examination showed optic disc edema with the presence of flame hemorrhages. Best corrected visual acuity (BCVA) was 0.02. The results of eye examination and fluorescein angiography confirmed the diagnosis of AION. Anti-aggregation and antithrombotic treatment was continued with steroids and vasodilators. After 7 days of this treatment we noticed the improvement of BCVA to 0.2. At 6-month follow-up, the vision was stable, and fundus examination revealed optic disc atrophy.
After cardiac surgical operations, such as coronary artery bypass graft procedures, anterior ischemic optic neuropathy may occur. In those cases, close cooperation between the various specialists is necessary.
coronary artery bypass graft; off-pump coronary artery bypass; perioperative ischemic neuropathy; anterior ischemic optic neuropathy
Incidence of perioperative visual loss ranges from 0.06% to 0.2% with the most common cause as ischemic optic neuropathy. We report one-year follow up of a 50-years-old hypertensive housewife who underwent lumbar decompression and fusion for degenerative scoliosis, but woke up with painless unilateral visual loss. Fundus examination was normal. Her visual acuity improved from initial finger counting close to face to finger counting at 3 m at 1 year. Identification of high risk patients may help in appropriate preoperative counselling, prevention and early recognition of this devastating complication.
Spine surgery; degenerative scoliosis; vision loss
Visual loss following head trauma is common, and the diagnosis can be challenging for the neurologist called to perform an emergency room assessment. The approach to the patient with post-traumatic visual loss is complicated by a wide range of potential ocular and brain injuries with varying pathophysiology. In addition to direct injuries of the eye and orbit, traumatic optic neuropathies, carotid cavernous fistulas, and damage to the intracranial visual pathways are classic causes of visual loss after head trauma. This review provides an update on the diagnosis and management of these conditions.
Carotid cavernous fistula; Traumatic brain injury; Traumatic optic neuropathy; Visual field defect; Visual loss
To report a patient who developed an unusual combination of central retinal artery occlusion with ophthalmoplegia following spinal surgery in the prone position.
A 60-year-old man underwent a cervical spinal surgery in the prone position. Soon after recovery he could not open his right eye and had ocular pain due to the general anesthesia. Upon examination, we determined that he had a central retinal artery occlusion with total ophthalmoplegia.
Despite medical treatment, optic atrophy was still present at the following examination. Ptosis and the afferent pupillary defect disappeared and ocular motility was recovered, but visual loss persisted until the last follow-up.
A prolonged prone position during spinal surgery can cause external compression of the eye, causing serious and irreversible injury to the orbital structures. Therefore, if the patient shows postoperative signs of orbital swelling after spinal surgery the condition should be immediately evaluated and treated.
Central retinal artery occlusion; Ophthalmoplegia; Prone position; Spinal surgery
We report a case of non-arteritic anterior ischaemic optic neuropathy (NAION) associated with neovascular glaucoma (NVG). A 63-year-old man who had undergone cataract surgery 3 months previously presented with sudden visual loss in his right eye. Ocular examination revealed a relative afferent pupillary defect, intraocular pressure (IOP) of 27 mm Hg, and 360° neovascularisation. Fundus examination revealed a pale and swollen optic disc with diabetic retinopathy. NAION associated with NVG was diagnosed. NVG, leading to reduced optic nerve perfusion pressure, concurrent with ischaemic processes of diabetic retinopathy, resulted in NAION.
AIM—Ocular involvement in giant cell arteritis (GCA) is an ophthalmic emergency which, if untreated, can progress to permanent blindness. There is little evidence in the literature to support current protocols for the acute treatment of GCA with steroids. The authors sought to review the effects of intravenous and oral steroids in GCA.
METHODS—This retrospective study reviewed the records of 100 consecutive patients with biopsy proved giant cell arteritis. 73 patients with visual loss who were treated at the Royal Victorian Eye and Ear Hospital (RVEEH) and St Vincent's Hospital were included in the final series. The authors studied the management of the patients in the first week after presentation, analysing types of treatment, dose, effect on visual acuity, and complications.
RESULTS—All the patients except one had visual loss due to anterior ischaemic optic neuropathy (AION). 17 patients (23%) had bilateral eye involvement. Visual acuity improved in 21 of 73 patients (29%) by a mean of two Snellen chart lines after commencement of steroids. There was an increased likelihood of improved vision in the group who had intravenous steroids (40%) compared with those who received oral steroids (13%). In all except four patients (95%) vision remained stable at 1 month review.
CONCLUSIONS—Prompt treatment of GCA with steroids leads to improvement of visual acuity in a significant number of cases. Intravenous steroids may offer a greater prospect of improvement compared with oral steroids. A prospective trial comparing intravenous with oral steroids is needed to validate these findings and would not expose elderly patients to unacceptable risks.
Primary open angle glaucoma (OAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and associated visual field loss. OAG is an emerging disease with increasing costs and negative outcomes, yet its fundamental pathophysiology remains largely undetermined. A major treatable risk factor for glaucoma is elevated intraocular pressure (IOP). Despite the medical lowering of IOP, however, some glaucoma patients continue to experience disease progression and subsequent irreversible vision loss. The scientific community continues to accrue evidence suggesting that alterations in ocular blood flow play a prominent role in OAG disease processes. This article develops the thesis that dysfunctional regulation of ocular blood flow may contribute to glaucomatous optic neuropathy. Evidence suggests that impaired vascular autoregulation renders the optic nerve head susceptible to decreases in ocular perfusion pressure, increases in IOP, and/or increased local metabolic demands. Ischemic damage, which likely contributes to further impairment in autoregulation, results in changes to the optic nerve head consistent with glaucoma. Included in this review are discussions of conditions thought to contribute to vascular regulatory dysfunction in OAG, including atherosclerosis, vasospasm, and endothelial dysfunction.
glaucoma; autoregulation; blood flow; atherosclerosis; vasospasm; endothelial dysfunction
We present a case as a rare sign of traumatic optic neuropathy and central retinal artery occlusion following blunt ocular trauma. A 10-year-old child suffered complete loss of the vision of one eye following a blunt ocular injury. He sustained an occlusion of the central retinal artery and traumatic optic neurupathy of the affected eye. Isolated cases of central retinal vessel occlusions and traumatic optic neurapathy following ocular blunt trauma are rare conditions. Clinicians to be aware of the potential for blunt ocular trauma to cause optic nerve damage and retinal vessel occlusions.
Blunt ocular trauma; Retinal artery occlusion; Traumatic optic neuropathy
Background. Giant cell arteritis (GCA) is a systemic granulomatous vasculitis that affects large- and medium-sized arteries of the head and neck. Ocular manifestations of GCA usually are anterior ischaemic optic neuropathy (AION) or retinal vessel occlusion. Case Report. We report an interesting case of a 70-year-old man who presented with sudden vision loss and choroidal infarction in his left eye. Thorough clinical and paraclinical evaluation revealed an underlying GCA, the treatment of which prevented further vision loss and systemic complications. Conclusion. This is an unusual presentation of choroidal infarction associated with CGA and emphasizes the need of thorough systemic evaluation in patients with choroidal infarction.
Postoperative vision loss following routine nasal surgery is an extremely rare and devastating complication. We report a case of unilateral blindness due to central retinal artery occlusion associated with third cranial nerve following septoplasty.
We report a patient who developed an unusual central retinal artery occlusion with unilateral blindness following nasal surgery under general anesthesia. A 45-year-old man underwent a nasal septal surgery for severe epistaxis. Soon after recovery, the patient noticed loss of vision in his right eye and was unable to lift his upper eyelid. Upon ophthalmic examinations, we determined that he had right-sided third cranial nerve palsy with central retinal artery obstruction and ptosis of right upper eyelid, restriction of ocular movements, and no perception of light in the right eye. Postoperative computerized tomography scan revealed multiple fractures of the left medial orbital wall, including one near the optic canal. Ptosis and ocular defects were recovered partially, but visual loss persisted until the last follow-up.
This paper highlights one case of complete unilateral blindness from direct central retinal artery occlusion associated with third cranial nerve palsy following an apparently uneventful septorhinoplasty. Ophthalmologists and otolaryngologists should therefore be aware of the possible occurrence of such complications.
Central retinal artery occlusion; Third nerve palsy; Septoplasty; Nasal polypectomy; Visual loss
Recognition of myocardial injury after non-cardiac surgery is difficult, since strong analgesics (e.g. opioids) can mask anginal symptoms, and ECG abnormalities are subtle or transient. Thorough knowledge of the pathophysiological mechanisms is therefore essential. These mechanisms can be subdivided into four groups: type I myocardial infraction (MI), type II MI, non-ischaemic cardiac pathology, and non-cardiac pathology. The incidence of type I MI in patients with a clinical suspicion of perioperative acute coronary syndrome (ACS) is 45–57 %. This percentage is higher in patients with a high likelihood of MI such as patients with ST-elevation ACS. Of note, the generalisability of this statement is limited due to significant study limitations. Non-ischaemic cardiac pathology and non-cardiac pathology should not be overlooked as a cause of perioperative myocardial injury (PMI). Especially pulmonary embolism and dysrhythmias are a common phenomenon, and may convey important prognostic value. Implementation of routine postoperative troponin assessment and accessible use of minimally invasive imaging should be considered to provide adequate individualised therapy. Also, addition of preoperative imaging may improve the stratification of high-risk patients who may benefit from preoperative or perioperative interventions.
Perioperative myocardial injury; Non-cardiac surgery; Perioperative myocardial infarction; Etiology
Postoperative visual loss associated with spine surgery is a rare complication with no established definitive etiology. Multiple case reports have been published in the literature, and an overview of the case reports of the various visual disturbances following spine surgery is presented. Our objective was to review the current literature and determine if there were any risk factors that suggest what kind of patients have a higher likelihood of developing postoperative visual loss. Furthermore, analysis of factors common to the cases may offer a better understanding of possible etiologies leading to prevention strategies of postoperative visual loss. We used PubMed to perform a search of literature with spine surgery cases that are associated with visual disturbances. A total of 7 studies representing 102 cases were reviewed and evaluated in regard to age, sex, comorbidities, diagnosis, operative time, blood loss, systolic blood pressure, lowest hematocrit, and visual deficits and improvement. Ischemic optic neuropathy, especially posterior ischemic optic neuropathy, was the most common diagnosis found in the studies. The average age of the patients ranged from 46.5 years to 53.3 years with the majority having at least one comorbidity. Operative time ranged on average from 385 min to 410 min with a median in one case series of 480 min, average blood loss ranged from 3.5 l to 4.3 l and no visual improvement was seen in the majority of the cases. The etiology of postoperative visual loss is probably multifactorial, however, patients with a large amount of blood loss producing hypotension and anemia along with prolonged operative times may be causing a greater risk in developing visual disturbances. An acute anemic state may have an additive or synergistic effect with other factors (medical comorbidities) leading to visual disturbances. Although our study failed to provide definitive causative factors of postoperative visual loss, suggestions are made that warrant further studies.
Spine surgery; Blindness; Visual loss/disturbance; Ischemic optic neuropathy
Ten patients (14 eyes) with chronic simple glaucoma are described, each with features atypical for this disease and more suggestive that each had suffered an acute ischaemic optic neuropathy. Diagnosis of an acute ischaemic optic neuropathy in these cases is important, as treatment of ocular hypertension in the contralateral 'normal' eye may prevent a similar attack. Optic nerve disease and visual loss in chronic simple glaucoma probably occur as a result of several different mechanisms. Sudden field loss following an acute ischaemic optic neuropathy may be only one of them.
The practice of ophthalmology and psychiatry meet over in several aspects of patient diagnosis, management & therapy. The ophthalmologists should be able to recognise signs and symptoms of psychiatric disorder. Non organic disorders could have ophthalmologic manifestations related both the afferent system and motor system related symptoms. Ophthalmologist should be aware of conditions like functional vision loss and visual field loss, voluntary nystagmus, spasm of near reflex, non-organic disturbances of eyelid function, ocular and facial sensation and psychosomatic diseases of eye.
Many of the drugs used in psychiatry may cause ophthalmological side effects. These drugs can affect retina, optic nerve, higher visual centre, cornea, lens, ocular motor system and intra ocular pressure. Thalidomide used in 1950s was known to cause congenital ocular defects. Psychological reaction and psychiatric complications are well known after cataract surgery.
Other then these problems there are psychiatric disorders which can present ophthalmologic signs and symptoms.
Ophthalmologic manifestations; functional disorders; functional vision loss; Visual field loss; black patch psychosis; flash backs
Demyelinating optic neuritis (ON) is the most common cause of optic neuropathy
typically presenting with a subacute painful visual loss. In 20% of patients
with multiple sclerosis (MS), ON is the presenting symptom and half of the
patients with isolated ON develop MS within 15 years. The diagnosis of ON plays
an important role in neurological practice. A correct and early diagnosis is
necessary to ensure optimal further investigations and treatment. Other causes
of optic neuropathies such as connective tissue disorders, infectious diseases,
tumours or ischaemic neuropathies are less frequent but clinical and therapeutic
management can differ dramatically. We present five patients admitted to our
hospital with suspected demyelinating ON, but the clinical work up revealed
different causes of optic neuropathy. We discuss the differential diagnosis of
ON and clinical red flags that require careful diagnostic assessment of other
diseases. A workflow for the diagnosis of optic neuropathies is presented.
differential diagnosis; multiple sclerosis; optic neuritis
Interferon (INF)-associated retinopathy occurs in 15–64% of INF-treated patients, transforming this complication into a significant risk for visual impairment. This retinopathy has been described as an ocular complication with a variable clinical course, usually benign and asymptomatic. The most common findings are hemorrhages and cotton wool spots. Atypical ocular side effects include branch or central retinal artery occlusion, central retinal vein occlusion, anterior ischemic optic neuropathy, optic disc edema, neovascular glaucoma and vitreous hemorrhage. Some case series suggest that in most cases the clinical course of the disease is benign, asymptomatic and without long-term consequences and therefore do not recommend any specific treatment; they only recommend the discontinuation of INF in patients with severe manifestations or risk factors such as hypertension or diabetes mellitus. The case reported here presents an atypical manifestation of INF-associated retinopathy consisting of a mixed retinal vascular occlusion (arterial and venous), associated with severe occlusive inflammatory microangiopathy with extensive retinal damage by ischemia and a torpid clinical course despite suspension of treatment. These varieties of occlusive vascular events have not yet been found simultaneously in the literature and neither with an unfavorable clinical course. Although the clinical course of INF-associated retinopathy in most cases is asymptomatic, there may be complications with risk to vision, which is less common. The magnitude and severity of the consequences associated with INF therapy are to be determined in prospective further studies.
Mixed vascular occlusion; Hepatitis C virus; Interferon-associated retinopathy
To evaluate the efficacy of surgical treatment of vitrectomy combined with silicone oil tamponade in the treatment of severely traumatized eyes with the visual acuity of no light perception (NLP).
This was a retrospective uncontrolled interventional case-series of 19 patients of severely traumatized eyes with NLP who underwent vitrectomy surgery at the Affiliated Hospital of Medical College, Qingdao University (Qingdao, China) during a 3-year period. We recorded perioperative factors with the potential to influence functional outcome including duration from the injury to intervention; causes for ocular trauma; open globe or closed globe injury; grade of vitreous hemorrhage; grade of endophthalmitis; grade of retinal detachment; size and location of intraocular foreign body (IOFB); extent and position of retinal defect; grade of proliferative vitreoretinopathy (PVR); type of surgery; perioperative complications and tamponade agent. The follow-up time was from 3 to 18 months, and the mean time was 12 months.
After a mean follow-up period of 12 months (3-18 months) 10.53% (2/19) of eyes had visual acuity of between 20/60 and 20/400, 52.63% (10/19) had visual acuity less than 20/400 but more than NLP, and 36.84% (7/19) remained NLP. Visual acuity was improved from NLP to light perception (LP) or better in 63.16% (12/19) of eyes and the rate of complete retinal reattachment was 73.68% (14/19). Good visual acuity all resulted from those patients of blunt trauma with intact eyewall (closed globe injury). The perioperative factors of poor visual acuity prognosis included delayed intervention; open globe injury; endophthalmitis; severe retinal detachment; large IOFB; macular defect; a wide range of retinal defects and severe PVR.
The main reasons of NLP after ocular trauma are severe vitreous hemorrhage opacity; refractive media opacity; retinal detachment; retinal and uveal damages and defects, especially defects of the macula; PVR and endophthalmitis. NLP after ocular trauma in some cases does not mean permanent vision loss. Early intervention of vitrectomy combined with silicone oil tamponade and achieving retinal reattachment of the remaining retina, may make the severely traumatized eyes regain the VA of LP or better.
vitrectomy; silicone oil tamponade; severely traumatized eyes; no light perception