Preventative effect of deferoxamine on degenerative changes in the optic nerve in experimental retrobulbar haematoma

Pelit, Aysel; Haciyakupoğlu, Gülhanım; Zorludemir, Suzan; Mete, Ufuk; Dağlıoğlu, Kenan; Kaya, Mehmet

doi:10.1046/j.1442-9071.2003.00603.x

Cited by 9 publications

(4 citation statements)

References 36 publications

(37 reference statements)

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“…13 In rat models of ICH, intraperitoneal administration of deferoxamine ameliorates ICH-induced changes in markers of oxidative DNA damage, increases levels of APE/Ref-1, which is involved in DNA repair, significantly attenuates the brain edema induced by stereotactic infusion of hemoglobin and its breakdown products into the brain, and improves neurological and functional recovery with to vehicle-treated controls. 14 …”

Section: In Vivo Studiesmentioning

confidence: 98%

Deferoxamine Mesylate

Selim

2009

Stroke

115

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Abstract-Iron resulting from hemoglobin degradation is linked to delayed neuronal injury after intracerebral hemorrhage. Extensive preclinical investigations indicate that the iron chelator, deferoxamine mesylate, is effective in limiting hemoglobin-and iron-mediated neurotoxicity. However, clinical studies evaluating the use of deferoxamine in intracerebral hemorrhage are shortcoming. This article reviews the potential role of deferoxamine as a promising neuroprotective agent to target the secondary effects of intracerebral hemorrhage to limit brain injury and improve outcome, and ongoing efforts to translate the preclinical findings into clinical investigations. Key Words: deferoxamine Ⅲ ICH Ⅲ edema Ⅲ neuroprotection A t present, there is no specific treatment for spontaneous intracerebral hemorrhage (ICH) beyond supportive medical care. Therapeutic attempts to target hematoma and its expansion might provide some benefit in carefully selected patients. However, this strategy alone is likely to be of limited usefulness because hematoma expansion often occurs within the first hours after onset. Furthermore, neuronal injury in ICH is not only related to hematoma expansion. Other secondary processes, including apoptosis, necrosis, autophagy, inflammation, and edema formation, have been implicated. 1,2 A potential adjunctive approach to the treatment of ICH might be to target hemoglobin-and iron-mediated neurotoxicity. Iron-Mediated NeurotoxicityHemoglobin degradation products resulting from hemolysis after ICH include the iron-containing heme. Iron plays a role in neuronal injury by catalyzing a sequence of reactions "Haber-Weiss reaction" that yield highly reactive toxic hydroxyl radicals leading to oxidative stress and cell death, activating lipid peroxidation, and exacerbating excitotoxicity. 3,4 The time course for hemoglobin hemolysis and toxicity after ICH is 2 to 3 days. 5,6 This delayed time window can have important therapeutic advantages. Deferoxamine MesylateDeferoxamine has been used in clinical practice for more than 30 years in iron-overloaded patients with acute iron intoxication or overload due to transfusion-dependent anemia. It is a hydrophilic chelator, which chelates Fe ϩϩϩ and hemosiderin forming a stable complex that prevents iron from entering into Haber-Weiss reaction. The drug is relatively well tolerated. Serious adverse effects are uncommon. Hypotension and shock occur in 2% of patients, mostly with rapid intravenous administration at high doses. The infusion rate should not exceed 15 mg/kg per hour, and the total amount administered should not exceed 6000 mg in 24 hours. PharmacokineticsDeferoxamine is rapidly absorbed. Plasma concentrations between 80 and 130 mol/L are recorded 3 minutes after intravenous injections. The drug's serum protein-binding rate is Ͻ10%. It is distributed throughout all body fluids and has a volume of distribution of 0.8 to 1.35 L/kg. The drug is mostly metabolized by oxidative deamination, yielding metabolite B. The drug, its iron chelate complex (ferrioxamin...

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Section: In Vivo Studiesmentioning

confidence: 98%

Deferoxamine Mesylate

Selim

2009

Stroke

115

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“…Occlusion of the short posterior ciliary artery may result in optic nerve infarction. 16 However, ophthalmoscopic examination performed immediately after our injections failed to reveal any retinal or vascular complication in any of the cases. Therefore, we speculate that any difference in optic nerve head topography most likely resulted from the effects of the anaesthetic agent on intraorbital volume.…”

Section: Discussionmentioning

confidence: 70%

“…Following retrobulbar haematoma, visual loss can be detected even in cases with intact retinal circulation. 16 In these cases, visual loss can be explained from optic nerve ischaemia. Occlusion of the short posterior ciliary artery may result in optic nerve infarction.…”

Section: Discussionmentioning

confidence: 99%

Acute orbital effects of retrobulbar injection on optic nerve head topography

Akar

Apaydin²,

Ozel³

2004

British Journal of Ophthalmology

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Aim: To assess the effects of acute orbital volume changes after retrobulbar injection on optic nerve head topography. Methods: The study population consisted of 95 patients with type 2 diabetes mellitus with clinically significant macular oedema who required focal pattern laser photocoagulation therapy in one eye. Before each laser treatment, 49 patients required a retrobulbar injection (approximately 7 ml of a mix of lidocaine 2% with epinephrine and bupivacaine 0.75% in equal volumes) to provide ocular akinesia. Both eyes of all patients underwent optic nerve head topographic analysis once before laser treatment (within 30 minutes), and repeated within 1 hour, 1 day, 1 week, 2 weeks, and 4 weeks after treatment, respectively. Topographic analyses were performed using a confocal scanning laser ophthalmoscope, HRT-II. The disc area, topography standard deviation, and a total of 12 topographic parameters were calculated by HRT-II. Results: The mean age of the patients was 37.9 (SD 3.2) years. The mean disc area of the subjects was 2.12 (0.44) mm 2 . Fellow eyes which were not treated with laser, and those treated eyes which did not receive retrobulbar injection before therapy were found not to reveal significant changes in disc topography in any of the examinations (all p values .0.05). In the topographic examinations in the first hour, first day, and first week, laser treated eyes which underwent retrobulbar injection demonstrated significant increase in the disc area, rim area, rim volume, rim area/disc area, and cup shape measure parameters while optic cup parameters significantly decreased (all p values ,0.05). In the second week examinations, they did not show significant difference in disc area measurements (p.0.05). By the fourth week, all of the optic nerve head topographic variables were not significantly different from the preinjection values (all p values .0.05). Colour stereoscopic photographs did not reveal any differences in optic disc appearance. Conclusion: Acute orbital volume change following retrobulbar injection may cause significant topographic evidence of optic disc oedema lasting approximately 1 week. Significant changes in optic rim and cup area may last for 2 weeks after injection, with all topographic changes returning to baseline by 1 month after injection. The present findings could be a model to reflect the pathological processes that occur in cases of acute orbital volume changes such as retrobulbar haemorrhage.

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“…Since this experience, I have used a combined use of a scalp vein set and a vacuumed blood sampling bottle for the purpose of the prevention from the postoperative intraorbital hematoma in all of orbital surgeries. Up to now there are some studies about the retrobulbar hematoma in the orbital surgery [3,4]. But I can not find a study about methodological intraoperative prevention from the intraorbital hematoma after the orbital surgery.…”

Section: Discussionmentioning

confidence: 99%

Idea on Prevention from Postoperative Intraorbital Hematoma in Orbital Surgery

Lee

2012

Indian J Otolaryngol Head Neck Surg

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The retrobulbar hematoma is a rare complication after orbital surgery. Despite of its rareness, the retrobulbar hematoma may be disastrous to the patient's vision (Chen et al. in J Craniofac Surg 20:963-967, 2009). Since 2007, I have applied the combined use of a scalp vein set and a vacuumed blood sampling bottle in all of the orbital surgeries. In my study, I achieved a good result, and I will introduce this simple method as one of alternatives for the prevention from the postoperative intraorbital hematoma including the retrobulbar hematoma.

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Preventative effect of deferoxamine on degenerative changes in the optic nerve in experimental retrobulbar haematoma

Abstract: Systemic deferoxamine treatment is effective in preventing degenerative changes in retrobulbar haema-toma.

Cited by 9 publications

References 36 publications

Deferoxamine Mesylate

Deferoxamine Mesylate

Acute orbital effects of retrobulbar injection on optic nerve head topography

Idea on Prevention from Postoperative Intraorbital Hematoma in Orbital Surgery

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