Lorazepam/magnesium-valproate overdose

  • PDF / 171,751 Bytes
  • 1 Pages / 595.245 x 841.846 pts (A4) Page_size
  • 9 Downloads / 183 Views

DOWNLOAD

REPORT


1 OS

Toxic optic neuropathy: case report A 19-year-old woman developed toxic optic neuropathy following overdose of magnesium valproate and lorazepam in a suicide attempt. The woman presented with bilateral diminution of visual acuity and a contracted visual field for 5 months in July 2019. Her medical history was significant for depression. In February 2019, she had attempted suicide by ingesting 19mg lorazepam [Lora; Atlantic Laboratories Corporation Ltd.] and 60g of magnesium valproate sustained-release tablets [Shentai, Xiangzhong Pharmaceutical Co. Ltd.] with a 330mL alcohol ≥3.1% by volume (i.e., acute alcohol intoxication), simultaneously. She had a combined overdose of two drugs i.e., lorazepam and magnesium valproate. She was then taken to the local emergency room, where she was comatose with unstable vital signs. Ocular symptoms included chemosis and miosis. A cranial CT scan demonstrated unclear bilateral cerebral and cerebellar sulcus and gyrus. Subsequently, she received intubation, fluid infusion, blood transfusion and unspecified antibiotics in the ICU. One month later, she recovered and left the ICU with neurological sequelae in her eyes only. During this stage, she received further treatment with mecobalamin and hyperbaric oxygen therapy. The first recorded visual acuity test revealed no light perception (NLP) in the right eye (OD) and hand motion in less than one foot in the left eye (OS). She was then continued on mecobalamin. In June 2019, the visual acuity test of OS improved to 20/100 with a –2.50 diopter sphere, +1.25 diopter cylinder and 85° in the axis. At presentation, the visual acuity test was NLP OD and 20/125 OS (pinhole 20/100). The intraocular pressure (IOP) was 16.3mm Hg OS and 15.3mm Hg OD. The slit lamp test demonstrated a clear cornea and lens. Both pupils were dilated (5mm) with a relative afferent pupillary defect OD. Her eye movement was normal with intermittent exotropia. The fundus examinations showed a bilateral pale optic nerve head (ONH) typically on the temporal side. An eye examination showed that the visual field remained in the inferior-nasal area in her left eye, and the regions between the disc and macula were affected. Cranial MRI showed no signs of cerebral or cerebellar oedema. Based on above-mentioned results, she was eventually diagnosed with toxic optic neuropathy (TON) [time to reaction onset not stated]. The woman was prescribed mecobalamin to prevent further damage to her visual field. During the 5-month follow-up in November 2019, her visual field was almost stable but tended to decline. The mean ocular deviation was 24.9dB, 24.0dB and 25.5dB, in July, September and November, respectively. During the last visit, optical coherence tomography revealed the significant thinning of the retinal nerve fiber layer thickness in the ONH and ganglion cell complex in the macula. During the follow-up period, visual field defects were significant. Flash visual evoked potential demonstrated a severe delay in P2 wave peak latency in the right eye and a medium decrease in