Toxic optic neuropathy in the setting of docetaxel chemotherapy: a case report

Background: To describe the first reported case of toxic optic neuropathy secondary to docetaxel (Taxotere®) chemotherapy. Case presentation. A 53-year-old female presented with predominantly unilateral visual loss, but extensive bilateral visual field defects and bilateral optic nerve head swelling 2 weeks after first dose of docetaxel (Taxotere®) and trastuzumab (Herceptin®) chemotherapy for a left sided node-positive, HER2 positive breast cancer. Extensive investigation ruled out other causes of optic neuropathy. She was treated with high dose corticosteroids intravenously for 1 week then a tapering oral dose over 8 weeks. Visual field defects gradually resolved and visual acuity improved. Docetaxel chemotherapy was discontinued but targeted therapy with trastuzumab continued without further complication. Conclusion: Docetaxel can cause a toxic optic neuropathy possibly due to an ischemic or neurotoxic mechanism at the optic nerve head. With cessation of docetaxel therapy and treatment with systemic corticosteroids, visual recovery can occur without significant residual visual deficit

Toxic optic neuropathy in the setting of docetaxel chemotherapy: a case report

BACKGROUND: To describe the first reported case of toxic optic neuropathy secondary to docetaxel (Taxotere®) chemotherapy. CASE PRESENTATION: A 53-year-old female presented with predominantly unilateral visual loss, but extensive bilateral visual field defects and bilateral optic nerve head swelling 2 weeks after first dose of docetaxel (Taxotere®) and trastuzumab (Herceptin®) chemotherapy for a left sided node-positive, HER2 positive breast cancer. Extensive investigation ruled out other causes of optic neuropathy. She was treated with high dose corticosteroids intravenously for 1 week then a tapering oral dose over 8 weeks. Visual field defects gradually resolved and visual acuity improved. Docetaxel chemotherapy was discontinued but targeted therapy with trastuzumab continued without further complication. CONCLUSION: Docetaxel can cause a toxic optic neuropathy possibly due to an ischemic or neurotoxic mechanism at the optic nerve head. With cessation of docetaxel therapy and treatment with systemic corticosteroids, visual recovery can occur without significant residual visual deficit

Indigenous Australians have a greater prevalence of heart, stroke, and vascular disease, are younger at death, with higher hospitalisation and more aeromedical retrievals from remote regions

Background: We aimed to determine whether heart, stroke, and vascular disease (HSVD) prevalence and emergency primary evacuation (EPE), hospitalisation, and mortality differ by patient characteristics. Methods: An Australian-wide incidence population based study, with prospective data collected form the 1 July 2019 to the 30 October 2020. Findings: Indigenous Australians reported significantly higher prevalence of HSVD at 229.0 per-1000 as compared to 152.0 per-1000 non-Indigenous Australians: risk ratio 1.5 (95% CI 1.2-1.8). 583 remote patients received an EPE for HSVD, consisting of 388 (66.6%; 95% CI: 62.6-70.4) males and 195 (33.0%; 95% CI: 29.6-37.4) females. There were 289 (49.6%; 95% CI 45.4- 53.7) patients who identified as Indigenous, and 294 (50.4%; 95% CI 46.3- 54.6) as non-Indigenous. The mean Indigenous age during EPE was 48.0 (95% CI 45.9-50.1) years old, significantly lower than the non-Indigenous mean age of 55.6 (95% CI 53.8-57.4). Indigenous patients hospitalised for HSVD were younger, the majority younger than 65 years (n=21175; 73.7% 95% CI 73.2-74.2) as compared to non-Indigenous patients (n= 357654; 33.1% 95% CI 33.0-33.15). When adjusted for HSVD prevalence, remote Indigenous patients had a higher hospitalisation rate as compared to non-remote Indigenous patients (rate ratio: 1.6; 95% CI 1.3-2.0) and remote non-Indigenous patients (rate ratio: 1.2; 95% CI 1.0-1.5). More Indigenous patients died of HSVD before the age of 65 years (n=1875; 56.5% 95% CI 54.8-58.2) as compared to non-Indigenous patients (n= 16161; 10.6% 95% CI 10.45-10.8). Interpretation: Indigenous Australians have a higher prevalence, and younger age during EPE, and hospitalisation for HSVD than non-Indigenous Australians. Funding: This is a self/internally-funded study, with the lead organisation being the Royal Flying Doctor Service (RFDS) of Australia. For the duration of the study period, the RFDS provided in-kind support including one full-time equivalent (FTE) and resources (office space, computer, research software, and office equipment). There was no external funding source that had a role in study design or data analysis or interpretation.</p