LAUSR

267 A 22‐year‐old man was brought to the hospital with a history of alleged consumption of about 100 ml of herbicide two hours prior to admission. He was drowsy and cyanotic with an oxygen saturation of 70%. However arterial blood gas (ABG) analysis showed normal partial pressure of oxygen (PaO2). Methemoglobin level in the ABG analyzer was greater than 40%. The content of the herbicide was found to be nitrobenzene which causes methemoglobinemia. Gastric lavage was done and patient was treated with intravenous methylene blue. He was asymptomatic for five days after which he developed mult iple organ dysfunction syndrome (MODS)— hepatitis, pancreatitis, rhabdomyolysis, and acute kidney injury—due to probable delayed nitrobenzene release from storage organs. The patient required mechanical ventilation and was given supportive treatment. He was noticed to have titubation with bilateral horizontal nystagmus, and rigidity of the limbs over the next two to three days. Magnetic resonance imaging (MRI) of the brain was done on day 9, which showed a characteristic pattern of symmetrical fluid‐attenuated inversion recovery (FLAIR) hyperintensities in the splenium of the corpus callosum and bilateral dentate nuclei. Patchy FLAIR hyperintensities were seen in the substantia nigra bilaterally [Figure 1]. Diffusion‐weighted imaging (DWI) showed hyperintensities in the corpus callosum and dentate nuclei with high apparent diffusion coefficient (ADC) values suggesting a T2 shine‐through effect [Figure 2]. There was no enhancement in post‐contrast T1‐weighted images (T1WI) or blooming in the gradient sequences [Figure 3]. A diagnosis of toxic encephalopathy due to nitrobenzene poisoning was made and he was given supportive treatment. Patient gradually recovered from MODS and was weaned off the ventilator. However, he had persisting bradykinesia with tremors of the head, dysarthria and truncal ataxia. Over the next few months, the patient made partial recovery and was able to ambulate without support.