Treatment Of Traumatic Optic Neuropathy Research Articles

Analysis of the Effect of Bedside Nursing Mode in Treatment of Traumatic Optic Neuropathy with Optic Nerve Decompression

Objective: To explore the effect of bedside work-based nursing mode on psychological stress response and quality of life of patients undergoing nasal endoscopic optic nerve decompression for traumatic optic neuropathy. Methods: Thirty patients with traumatic optic neuropathy were selected from our hospital from March 2016 to October 2019. All patients underwent nasal endoscopic optic nerve decompression and were grouped according to the order of admission. The control group received routine nursing intervention and the observation group had 15 Cases were given bedside nursing intervention based on the control group. The depression (SDS), anxiety (SAS), postoperative quality of life (SF-36) scores, and postoperative clinical effects were compared between the two groups at admission and discharge. Results: The SDS and SAS scores of the observation group at the time of discharge were lower than those of the control group, and the differences were statistically significant (P < 0.05). The clinical effect of the observation group was better than the control group, and the total effective rate of the observation group was 93.33% (14/15) which was higher than the 80.00% (12/15) of the control group, the difference was statistically significant (P < 0.05). SF-36 scores of physiological function, physical function, emotional function, social function, etc. in the observation group were higher than those in the control group, and the difference was statistically significant. (P < 0.05). Conclusion: Treatment of traumatic optic neuropathy with bedside work-based nursing mode by nasal endoscopic optic nerve decompression has significant effects, which can improve their psychological stress response and quality of life with high safety.

Controversial issues in the treatment of traumatic optic neuropathy: a journey through historical course

Controversial issues in the treatment of traumatic optic neuropathy: a journey through historical course

Acteoside inhibits autophagic apoptosis of retinal ganglion cells to rescue glaucoma-induced optic atrophy.

BackgroundGlaucoma is the world's second biggest cause of blindness, and patients progressively lose their eyesight. The current clinical treatment for glaucoma involves controlling intraocular pressure with drugs or surgery; however, some patients still progressively lose their eyesight. This treatment is also similar to the treatment of traumatic optic neuropathy. Thus, saving retinal ganglion cells (RGCs) from apoptosis is essential.MethodsThe role of Acteoside on autophagy modulation in the 661 W cell line.ResultsIn this study, we first find that Acteoside inhibits autophagy, Rapamycin alleviates this inhibition and the PI3K inhibitor, 3‐MA or LY294002, synergistically promotes it. In a mechanistic study, we find that Optineurin (OPTN) mediates Acteoside regulation of autophagy. OPTN overexpression or knockdown activates or inhibits autophagy, respectively. OPTN is inhibited by autophagy inhibitors, such as Acteoside and 3‐MA and is promoted by the autophagy activator, Rapamycin. Meanwhile, PI3K and AKT are elevated by Acteoside and 3‐MA and inhibited by Rapamycin. Finally, we find that Acteoside inhibits apoptosis in parallel to autophagy and that this inhibition is also mediated by OPTN.ConclusionIn summary, we conclude that Acteoside inhibits autophagy‐induced apoptosis in RGCs through the OPTN and PI3K/AKT/mTOR pathway, and glaucoma patients may benefit from Acteoside treatment alone or in combination with other autophagy inhibitors.

Clinical treatment of traumatic optic neuropathy in children: Summary of 29 cases.

Clinical features and treatments for traumatic optic neuropathy (TON) in children are reported. Twenty-nine children were enrolled in the Affiliated Hospital of Qingdao University from April 1999 to May 2015 for retrospective analysis. Of these 29 patients, 5 received drug therapy, and 24 received drug therapy combined with surgical therapy. Among the patients who received surgical therapy, 23 received nasal endoscopic optic decompression under general anaesthesia, and 1 received nasal endoscopic orbital decompression under general anaesthesia. All the patients were followed up for at least 6 months. In 29 cases, 48.28% (14/29) had visual improvement. Of the 5 patients who received drug therapy, 3 showed improvement (60%). Of the 24 cases who received drug and surgical therapy, 11 showed improvement (45.83%). Of the 22 patients who lost visual sensitivity, 10 showed improvement (45.45%). Of the 7 cases with visual acuity above basic light sensitivity, 4 showed improvement (57.14%). In conclusion, TON in children can lead to poor diagnosis and prognosis because of the difficulty of examining children and their limited language expression ability. Early ophthalmologic examination is therefore essential for children with craniofacial injuries, and proper treatment should be undertaken as soon as possible.

The sedative efficacy of nasal dexmedetomidine used for premedication in ocular trauma children undergoing emergency surgery

Objective To evaluate the efficacy of optic canal decompression for traumatic optic neuropathy, and analyse the effect of flash visual evoked potential (F-VEP) on early diagnosis and evaluation of surgical efficacy in traumatic optic neuropathy. Methods The data of 40 eyes of 40 patients with traumatic optic neuropathy from Jun. 2010 to May 2017 were retrospectively analysed. They were randomly divided into 2 groups. The observation group, 17 cases were treated with optical canal decompression through transsphenoidal approach under neuroendoscopye. The control group, 23 cases were treated with craniooptic canal decompression. The visual acuity and P2 wave latency changes of F-VEP were examined before surgery, 10 days and 3 months after surgery. The follow-up time was 3 months after surgery. Results The difference of the age, gender, Glasgow Coma Scale, visual acuity, duration trauma to surgery and P2 wave latency than the healthy eye before surgery were not statistically significant between the two groups (P>0.05). The effective rate in observation group at 10 days after surgery was 82.35%, and 69.56% of the control group. The total effective rate of the observation group at 3 months after surgery was 82.35%, and 78.26% of the control group. The difference was not significant between the two groups (P>0.05). Visual acuity was significantly correlated with the prolongation of P2 wave latency in the corresponding F-VEP at 10 days and 3 months after operation. Conclusion It is a significant correlation between P2 wave latency in F-VEP and visual acuity. Endoscopic transnasal optic canal decompression is an effective method for the treatment of traumatic optic neuropathy. Key words: Neuropathy, optic, traumatic; Decompression, canal, optic; Evoked potential, visual, flash

Surgical Treatment for Traumatic Optic Neuropathy.

Traumatic optic neuropathy (TON) is an important cause of severe visual loss after blunt or penetrating head and facial trauma. High-dose steroids and surgical interventions have been applied in the indirect TON. However, there is no convincing evidence that results of the treatment have any strong benefits in terms of improvement of visual acuity. Nevertheless, surgical decompression should be considered in the case of a direct bony compression to the optic nerve and a progressive visual loss in indirect TON. Neurosurgeon should be aware the surgical indication, optimal timing and relevant technique for the optic canal (OC) decompression. In this review article, we will focus on the surgical approaches to the OC and how to decompress it.

A 212 cases analysis of treatment for traumatic optic neuropathy by nasal endoscopic opticnerve decompression

Objective:To explore the clinical features and therapeutic efficacy of nasal endoscopic optic nerve decompression for traumatic optic neuropathy (TON)treatment.Method:Two hundred and twelve cases (217 eyes) with TON were retrospectively analyzed in our study, who were treated with nasal endoscopic optic nerve decompression in our institution from 1999 to 2016. χ ² -test was used to explore the potential prognostic factors on visual acuity.Result:All patients were followed up from 6 months to 2 years postoperatively, and the effective rate was 54.38%(118/217).In the 166 eyes with no light perception (NLP), the effective rate was 46.39% (77/166), while in the 51 eyes with light perception (LP), the effective rate was 80.39% (41/51).The therapeutic efficacy of patients with LP or above LP was better than that of NLP, and the difference was statistically significant(χ ²=18.186, P< 0.01).Moreover, the therapeutic efficacy of patients without an optic canal fracture was better than that with an optic canal fracture，and the difference had statistical significance (χ ²=10.096, P<0.01).Conclusion:The efficacy of nasal endoscopic optic nerve decompression on TON was positive, and even for the patients with NLP or a long history also should have a try.

The Efficacy of Progesterone in Treatment of Traumatic Optic Neuropathy (Proton Study)

To evaluate the visual function improvement for treatment of indirect traumatic optic neuropathy Study design was comparative historical controlled trial. Seven patients newly diagnosed with indirect traumatic optic neuropathy Study design was comparative historical controlled trial. Seven newly diagnosed with indirect traumatic optic neuropathy (TON) were enrolled for progesterone group. Nineteen indirect Ton patients were reviewed medical records for steroid group (N= 12) and observation group (N= 7). Patients in progesterone group were given Depot medroxyprogesterone acetate (DMPA) 1 mg/kg. intramuscular injection every 12 hrs. for 5 days and observed for side effects. All patients were examined and reviewed for visual acuity by ETDRS chart, color vision test by Ishihara test, visual field testing by Humphrey automated perimetry, fundus and optic disc examination at baseline, follow-up 1 week, 1 month and 3 months. Demographic and clinical characteristic of patients in 3 groups were not different in terms of age, sex, underlying disease, side of eye, type of injury, baseline visual acuity, associated orbital fracture, history of amnesia, time to visit hospital and time to start treatment. Improvement in best-corrected visual acuity (BCVA) compared at 3 months from baseline showed no difference between 3 groups (p= 0.891). Analysis within steroid group showed statistically significant improvement of BCVA at 1 and 3 months (p= 0.015, 0.028 respectively). No improvement was shown in color vision and visual field in progesterone group. Only better baseline BCVA was the protective factor for better visual outcome (p= 0.027, Odds ratio = 0.004, 95%CI = 0.000 - 0.537). No side effects of progesterone were found in this study. Progesterone is a safe and promising neuroprotective agent that could be adjunctive or alternative to steroid in case of contraindication to corticosteroid treatment. This study showed no difference among choices of treatment therefor study in larger population is required. Steroid remains an effective option contrast with recent studies.

Comparison of the effect of treatment with or without glucocorticoid for traumatic optic neuropathy

Objective To compare the therapeutic effect between glucocorticoid and non-glucocorticoid treatment for traumatic optic neuropathy(TON). Methods Total of 316 eyes of 316 cases with TON who were treated in Beijing Tongren Hospital from May 2013 to August 2016, were divided into clinical trial group (group A, 187 cases) and control group (group B, 129 cases) randomly. Group A received methylprednisolone treatment and group B without glucocorticoid treatment. The therapeutic effect was observed and compared. Results The total effective rate in group A was 34.8%, in group B was 33.3%, the difference was not statistically significant between the two groups(χ2=0.069, P=0.793). The efficacy between the two groups was compared under different conditions: the difference in optic canal fracture(χ2=0.077, P=0.782), no light perception(χ2=0.073, P=0.787), optic canal fracture with no light perception(χ2=0.030, P=0.863), all were not statistically significant between the two groups. Conclusion Methylprednisolone and non-glucocorticoid treatment in the treatment of traumatic optic neuropathy under different conditions there is no statistically significant difference. Key words: Optic neuropathy, traumatic; Methylprednisolone; No light perception; Optic canal fracture

Protective effect of rapamycin on hypoxia-injuried retinal ganglion cells and its mechanism

Background Studies showed that rapamycin (Rapa) plays a protective effect on central nervous system by improving the aging of human brain tissue and ameliorating rat cerebral metabolism after ischemia.Optical nerve and retinal ganglion cells (RGCs) are central nerve, however, whether Rapa can protect hypoxia-injuried RGCs is still unclear. Objective This study was to explore the protective role of Rapa on hypoxia RGC-5, a rat RGC line, and its underlying mechanism in order to provide a new strategy for the treatment of traumatic optic neuropathy. Methods Rat RGC-5 cells were cultured using DMEM with 10% fetal bovine serum, and the cells were observed under the inverted phase contrast microscope.The cells were treated by 50, 100, 200, 400 and 600 μmol/L CoCl2 for 24 hours and 48 hours, respectively, and Clone Select Imager was employed to assess the survival rate.The CoCl2-induced hypoxia cell models were established by adding 200 μmol/L CoCl2 in the medium for 24 hours, and then the 0.1, 0.4, 1.6, 6.4 μmol/L Rapa was used to treat the models for 24 hours in the Rapa intervention group, respectively.The cells cultured by DMEM with 10% fetal bovine serum served as the normal control group.The survival rate of the cells was evaluated by Clone Select Imager; the apoptotic rate of the cells was assayed by AnnexinV-FITC/PI double-staining flow cytometry; JC-1 probe was used to detect the mitochondrial trans-membrane potential, and the expression of bax mRNA in the cells was detected by real-time fluorescence quantitative PCR. Results The survival rate of the cells was (70.51±5.00)% in the 200 μmol/L CoCl2-treated group, which was significantly lower than (100.00±3.29)% in the normal control group (P<0.01). The survival rate of the cells was significantly different among the normal control group and 0.1, 0.4, 1.6, 6.4 μmol/L Rapa intervention groups (F=167.904, P=0.000), and the survival rate was evidently higher in the 0.1 μmol/L Rapa intervention group than that in the model control group (P<0.05). The apoptotic rate was 25.4%, 37.7% and 25.3%, while mitochondrial trans-membrane potential reduced by 0.4%, 6.3% and 1.4% in the normal control group, model control group and 0.1 μmol/L Rapa intervention group, respectively.The relative expression of bax mRNA in the cells was 1.01±0.21, 3.52±0.30 and 1.66±0.20 in the normal control group, model control group and 0.1 μmol/L Rapa intervention group, showing a significant difference among the groups (F=88.034, P=0.000), and the relative expression of bax mRNA in the model control group was considerably elavated in comparison with the normal control group and 0.1 μmol/L Rapa intervention group (both at P<0.05). Conclusions Rapa protects the RGC-5 cells against CoCl2-induced hypoxic damage primarily by down-regulating the expression of bax in the cells and improving the survival rate of RGC-5 cells in vitro. Key words: Rapamycin; Retinal ganglion cells; Mammalian target of rapamycin; Apoptosis

Is there treatment for traumatic optic neuropathy?

The purpose of this study is to discuss current controversies surrounding the proposed treatments for traumatic optic neuropathy (TON) and review recent evidence from the literature relating to these therapeutic options. No recent randomized controlled trials investigating surgical or medical interventions for TON exist. The current literature regarding treatment of TON consists mainly of small, mostly retrospective, observational studies. Treatment of TON with corticosteroids, surgical decompression of the optic canal or combinations of surgery and corticosteroids does not appear to offer improved visual outcomes compared with observation alone. Recent evidence suggests that there may be diminished functional reserve of the optic nerve following trauma. Novel neuroprotective therapies, such as erythropoietin, are currently under investigation in the treatment of TON. TON may lead to profound visual disability. Because of the absence of Class I evidence relating to treatment of TON, a lack of consensus exists among clinicians regarding the appropriate treatment for TON. Our review of the recent literature finds that there is still no reliable evidence that treatment of TON with corticosteroids, surgical optic canal decompression or both confers any benefit over observation alone, and yet these interventions incur an additional risk that may not warrant their routine use.

Current Treatment of Traumatic Optic Neuropathy

Current Treatment of Traumatic Optic Neuropathy

Traumatic Optic Neuropathy and Second Optic Nerve Injuries

Current controversy about the primary treatment of traumatic optic neuropathy (TON) has anchored on final vision following injury, but, to our knowledge, no study has examined the effect of different treatments on regaining and protecting optic nerve reserve or on the outcome of second optic nerve injuries. To assess vision improvement in patients treated by various methods who have a second incidence of TON. Retrospective medical record review of 12 patients with a second TON seen in an 18-year period (mean follow-up, 11.3 months) at a single tertiary care oculoplastic practice. Observation, high-dose corticosteroids, optic nerve decompression, or high-dose corticosteroids plus optic nerve decompression. Change in vision on the Snellen eye chart. RESULTS All second TON events involved the same-side optic nerve as initially injured, and with observation alone, corticosteroids, or corticosteroids and partial optic canal decompression, all patients had vision improvement after their initial injury (P = .004). However, following the second optic nerve injury, most patients' vision fell to the pretreatment level of the first injury, and subsequent management of the second injury with corticosteroids and/or optic canal decompression provided little or no vision return (P = .05). In contrast, optic canal decompressions performed for 91 primary TON injuries resulted in 82.4% having some degree of vision improvement. Patients with TON may have a second optic nerve insult, and vision recovery from the second event may be limited regardless of primary treatment choice.

A modified surgical procedure for endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy.

Background:Although the endoscopic anterior-to-posterior technique offers many advantages, the long-term effects of the iatrogenic trauma (removal of the uncinate process and anterior ethmoidal sinus) resulting from the complete ethmoidectomy procedure used to gain full access to the optic nerve canal is unknown, and sequelae such as nasal synechia and sinusitis should not be ignored.Aims:The aim of our study is to develop a less invasive procedure for endoscopic optic nerve decompression.Materials and Methods:We proposed a modified trans-sphenoidal surgical procedure for endoscopic optic nerve decompression in five patients with traumatic optic neuropathy (TON), all with high sphenoidal pneumatisation and without Onodi cellulae.Results:After performing a direct sphenoidotomy through the natural ostium of the sphenoid sinus rather than a complete ethmo-sphnoidectomy, we found that the modified approach provided adequate access to the optic nerve canal and the apex using a 45° angled endoscope. Successful decompression of the canal optic nerve was performed trans-sphenoidally in all five TON patients using an angled endoscope. No surgical complications occurred, and none of the patients suffered from anterior ethmoidal sinus or skull base damage.Conclusions:The modified trans-sphenoidal approach is a feasible, safe, effective, and minimally invasive approach for TON patients with high sphenoidal pneumatisation and without supersphenoid-ethmoid cellulae.

Exploiting mTOR Signaling: A Novel Translatable Treatment Strategy for Traumatic Optic Neuropathy?

Retinal ganglion cell (RGC) death and a failure of axon regeneration contribute to the profound visual loss experienced by patients after traumatic optic neuropathy (TON), for which there are no effective treatments. Experimental manipulations of cellular signaling pathways in animal models have demonstrated that neuronal survival and axon regeneration in the mature central nervous system (CNS) are possible, and increased understanding of the molecular basis of prosurvival and regenerative signals has led to the identification of candidate targets for novel therapeutic strategies. The axogenic pathway is activated sequentially, after growth factor/receptor binding, through phosphoinositide-3-kinase (PI3K) and the downstream serine/threonine kinase Akt. Akt is a nodal point for the regulation of growth cone dynamics by glycogen synthase kinase (GSK3β) and axon protein synthesis/RGC survival by the mammalian target of rapamycin (mTOR). The mTOR signaling pathway has a pivotal role in numerous cellular processes. It is active during development, but downregulated in the mature CNS and further suppressed by axonal injury, and experimental upregulation of mTOR signaling promotes RGC survival and axon regeneration after optic nerve crush injury. However, several translational challenges remain, including understanding the regulatory mechanisms of axotomy-induced mTOR and GSK3β signaling, and the disparity between the RGC survival and axon regenerative effects. In this review, we explore the molecular basis of RGC regenerative failure and assess the potential for manipulations of mTOR signaling as a novel translatable treatment for TON.

Diagnosis and treatment of traumatic optic neuropathy with carotid artery cavernous segment pseudoaneurysm

To summarize our experience in diagnosis of carotid cavernous segment pseudoaneurysm in patients with traumatic optic neuropathy, and to make recommendations for treatment. Retrospective study. Clinical data of 133 cases with traumatic optic neuropathy (TON) were reviewed. The diagnosis and treatment of four cases with carotid cavernous segment pseudoaneurysm (PSA) were analyzed. The incidence of traumatic optic neuropathy with pseudoaneurysm for this group of patients was 3.01% (4/133). Preliminary screening was performed with vascular-enhanced computed tomography (CT) scan, and was further confirmed by digital subtraction angiography (DSA). Among the four cases with pseudoaneurysm, three cases were successfully treated with vascular embolization. In one of the three cases, coil embolization was employed; and in the other two cases stent embolization was performed. The pseudoaneurysm disappeared after embolization, and nosebleeds subsided without significant complications. All four patients did not undergo nasal endoscopic optic nerve decompression. There was no recurrence of nose bleeding after embolization in the following 1 to 12 months, and in one case the patient's vision improved from no light perception to perceiving hand movement. There is a possibility of fatal epistaxis for traumatic optic neuropathy with carotid artery cavernous segment pseudoaneurysm. Endoscopic optic nerve decompression treatment (EOND) is not suitable for these cases; instead, it is recommended that patients with traumatic optic neuropathy go through vascular-enhanced computed tomography screening. Suspected cases should be diagnosed by digital subtraction angiography and be treated by embolization in a timely manner, with stent vascular interventional embolization being the ideal choice.

The therapeutic efficacy of endoscopic optic nerve decompression and its effects on the prognoses of 96 cases of traumatic optic neuropathy

Traumatic optic neuropathy (TON) is an important cause of severe loss of vision due to blunt or penetrating head trauma. The pathogenesis of TON remains unclear, and there are several potential causes for the observed loss in vision. Endoscopic optic nerve decompression (EOND) has been reported to improve the visual prognosis in TON cases, but its efficacy remains controversial. It is important to investigate the therapeutic efficacy of EOND in the treatment of TON and to evaluate the relevant prognostic factors. A retrospective study was conducted to analyze the clinical characteristics and prognoses of 96 TON cases. The χ(2) test and multiple logistic regression analyses were used to evaluate potential prognostic factors. : The overall rate of EOND effectiveness was 40.6% (39 of 96). A significantly higher effective rate (83.3%) was observed for patients with light perception compared with those without light perception (26.4%, p < 0.05). Univariate and multiple logistic regression analyses identified three variables (no light perception, undergoing EOND 3 days after trauma, and hemorrhage within the ethmoid and/or sphenoid sinus) that were significantly associated with unrecovered visual acuity. Age, loss of consciousness, optic canal fracture, preoperative steroid megadose treatment, and optic nerve sheath incision were all factors that showed no significant correlation with therapeutic efficacy. However, patients with fractures in a single medial wall of the optic canal appeared to have better prognoses than patients with multiple fractures or those with a single fracture in a lateral wall. The overall therapeutic efficacy of EOND for the treatment of TON is far from satisfactory, especially for patients without light perception. The factors that impact TON prognoses are complex and may be interrelated. The indication for EOND must be individualized. III, epidemiological study.

VEP clinical application in the treatment of traumatic optic neuropathy

Objective To observe the effect of treating traumatic optic neuropathy(TON)through the visual evoked potential(VEP).Methods 35cases of traumatic optic neuropathy were devided into three groups randomly,treated with routine management,routine management plus methyl-prednisone and hyperbaric oxygen(HBO)combined with methyl-prednisone,observed the difference of the latent period and amplitudes of VEP after treatment.Results The amplitudes of VEP was significant differently in methyl-prednisone and HBO combined with methyl-prednisone treatment groups compared with the routine management group(P ＜ 0.05).Conclusion The VEP determination has certain clinical value in the injury of the optive nerve.The VEP results show that the treatment with the basic management plus methyl-prednisone and HBO early can improve the function of the optic nerve. Key words: Visual evoked potential; Traumatic optic neuropathy; Hyperbaric oxygen

Traumatic Optic Neuropathy - to Treat or to Observe?

We present a case of acute traumatic optic neuropathy in 54 year old male patient. The patient presented with acute loss of vision in the right eye due to a blunt trauma to the eye. Lid haematoma and subconjunctival hemorrhage were present. Fluorescein staining was negative, anterior chamber and lens was clear. Intraocular pressure was normal. Retina and optic nerve head appeared normal on fundoscopy. The vision was “counting fingers at 1 meter” in the right eye. Color test indicated color perception dysfunction of the right eye. Relative afferent pupillary defect (RAPD) was positive. Ocular ultrasound, orbital X ray and CT scan was normal, but visual evoked potentials test was pathologic. The consideration was made whether to treat a patient or not since there are no consensus on the treatment of traumatic optic neuropathy. We decided to treat the patient immediately with the megadoses of steroids following the protocol suggested by Cerovski. The patient responded well to the treatment and recovered vision to normal.

Mechanisms and management of vision loss following orbital and facial trauma

To examine the proposed mechanisms of vision-threatening injuries occurring secondary to orbital and facial trauma: traumatic optic neuropathy (TON), retrobulbar haemorrhage (RBH) and penetrating eye injury. To evaluate the evidence supporting different management options for traumatic vision-threatening injury. Despite considerable debate over the roles of surgical decompression and systemic steroid therapy for TON, these interventions have not been proved to be more effective than conservative management and there is limited evidence that the use of steroids may be associated with an adverse outcome. Lateral canthotomy and inferior cantholysis have been proven to be effective treatments for RBH. Orbital exploration and surgical evacuation of haematoma remains a second line intervention. Open globe injuries require immediate primary surgical exploration and repair. Irretrievable devastating globe injuries require either enucleation or evisceration. There is no consensus as to which is the best treatment with recent surveys indicating that enucleation is preferred in the USA and evisceration in the United Kingdom. Conservative management is the first line treatment for TON. The evidence strongly supports lateral canthotomy and inferior cantholysis as best treatment for RBH. There is no consensus as to whether enucleation or evisceration is the best treatment for irretrievable devastating globe injury. The choice of management is currently determined by surgeon preference.