A 49-year-old white woman was brought to our emergency department (ED) after an intentional overdose with 150 mg of amlodipine, 60 mg of escitalopram, and 6 mg of risperidone. Her past medical history included hepatitis C from a blood transfusion in 1993, remote intravenous drug use, diverticulitis, hypertension, mild chronic obstructive pulmonary disease, gastroesophageal reflux disease, anxiety, and depression. She was also seen by the ophthalmology service in 2007 with regards to declining visual acuity, secondary to early optic atrophy. She was seen by family to be normal at 11:00 on the day of admission to our hospital, and was subsequently found by family members to have an altered level of consciousness at 13:50, at which point the emergency services were called. Upon arrival to our ED at 14:00, she was found to be hypotensive with a blood pressure of 84/38 mmHg, tachycardia with a heart rate of 117 beats/minute, and obtunded with a Glasgow Coma Scale (GCS) of 9/15. She was immediately intubated for airway protection, placed on a cardiac monitor, and an arterial and central venous catheter was inserted. The initial resuscitation consisted of a bolus 2 liters of crystalloid administered intravenously, 2 g of calcium gluconate administered intravenously, 5 mg of glucagon administered intravenously, 1 ampule of dextrose 50% in water (D50W) administered intravenously followed by 70 units of bolus short-acting insulin administered intravenously followed by 70 units/hour infusion. She was also given 50 g of activated charcoal via a nasogastric tube for gastric decontamination. The Critical Care team was notified, and she arrived in our Intensive Care Unit at 14:30. Upon arrival, she required 30 mcg/minute of norepinephrine, 30 mcg/minute of epinephrine, and 2.4 units/hour of vasopressin to maintain a mean arterial pressure greater than 65 mmHg. A point-of-care transthoracic echocardiogram was performed at 17:00 to evaluate her profound shock, which demonstrated an under-filled hyperdynamic left ventricle. There was no right ventricle (RV) dilatation, and RV systolic function was intact. This finding was indicative of a severe vasodilatory state causing her shock, as opposed to cardiogenic shock. We began aggressive administration of intravenously administered boluses with crystalloid fluids infused through a Level 1 rapid infuser. Initially, she improved hemodynamically with each 1 L bolus, demonstrating that she was preload-dependent in the setting of her vasoplegia. Her catecholamine requirements decreased significantly, norepinephrine 40 mcg/minute and epinephrine 40 mcg/minute to 25 mcg/minute and 10 mcg/minute, respectively, after a total of 23 liters of intravenously administered crystalloid boluses were given. She was maintained on the vasopressin 2.4 units/hour throughout the resuscitation process. Despite continuous repletion of potassium with intravenously administered potassium chloride and orally administered potassium chloride, she developed refractory hypokalemia with associated changes on the electrocardiogram (ECG; Fig. ). She also required intravenously administered dextrose boluses despite a 10% dextrose infusion. Given the hypokalemia and hypoglycemia that were becoming problematic to treat, the decision was made to abandon hyperinsulinemic-euglycemia therapy in this patient, as she did not appear to have a strong component of insulin resistance. She was mechanically ventilated on assist-control ventilation with a respiratory rate of 18 breaths/minute, pressure control ventilation at 19 cmH2O, positive end-expiratory pressure (PEEP) 5 cmH20, and fraction of inspired oxygen (FiO2) 40% with oxygen saturation of 94%. Following 23 liters of fluid resuscitation, her oxygenation requirements greatly increased due to the volume overload causing significant pulmonary edema. Her mechanical ventilation requirements increased to assist-control ventilation rate of 27 breaths/minute, pressure control 36 cmH2O, PEEP 14 cmH20, and FiO2 100% to maintain oxygen saturation in the mid 80%. A portable chest radiograph confirmed that she had diffuse pulmonary edema and she remained anuric. At 22:15, the nephrology service was consulted to initiate continuous renal replacement therapy (CRRT) for volume overload. At approximately 22:35, we discontinued administration of intravenously administered fluid boluses, minimized all intravenously administered fluid input, and administered a 200 mg bolus of intravenously administered furosemide. She had a good response and her urine output increased to 100 to 225 mL/hour. At 22:50 she continued to deteriorate with low blood pressure, tachycardia, and we proceeded to administer to her 1.5 mL/kg of 20% lipid emulsion therapy, to which she did not initially respond. The cardiovascular surgery service was also consulted to assess the potential need for veno/venous extracorporeal membrane oxygenation (ECMO). At 23:30, the CRRT was started and she responded very well and ultimately did not require ECMO. At 00:30, her oxygenation status began to improve, with oxygenation saturation >90% on 100% FiO2. From 00:30 to 10:30, she had gradual and complete reversal of her shock state. She was slowly weaned off all vasopressors, and continued to make urine after an initial 8 hours of complete anuria postadmission. By 13:00 the following day, she was off CRRT, with a urine output up to 500 ml/hour, thought to be secondary to post-acute tubular necrosis (ATN) diuresis. Her oxygen requirements continued to decrease and by 10:15 she was requiring 60% FiO2 to maintain an oxygen saturation of 96 to 98%. On clinical examination, she continued to recover and demonstrated no persisting organ dysfunction. Three days after admission, she was extubated and liberated from mechanical ventilation. She was alert and oriented, but complained of new onset visual impairment, specifically only seeing red and green colors, but unable to see any objects. Of importance, her visual acuity was relatively intact prior to admission with the exception of the stable optic atrophy. The remaining neurologic examination was otherwise normal. A magnetic resonance imaging (MRI) of her brain showed a few small foci of high signal on the diffusion-weighted image (DWI) sequence in her right frontal and parietal lobes consistent with acute infarcts. These may have been from emboli to the right middle cerebral artery (MCA) territory. Alternatively, these may be deep watershed infarcts between the anterior cerebral artery (ACA) and MCA territories. In addition, both optic nerves were mildly thickened with high signal on DWI and fluid-attenuated inversion recovery (FLAIR), consistent with cytotoxic edema from infarction. A lumbar puncture was performed which showed an elevated opening pressure (18 mmHg), but otherwise normal cerebrospinal fluid, and no evidence of central nervous system (CNS) vasculitis. Subsequent ophthalmologic evaluation revealed she had no light perception bilaterally despite best corrected vision, no light response, and mid-dilated pupils bilaterally. The intraocular pressure of her right and left eyes was 14 mmHg and 16 mmHg, respectively. Examination of the anterior segment was unremarkable bilaterally. Posterior segment examination revealed no evidence of disc edema, hemorrhage, retinitis, or vasculitis bilaterally. Both ophthalmology and neuroradiology concluded that her blindness was probably due to optic nerve injury from the prolonged hypotension during the first 24 hours after the overdose. She was discharged from hospital 8 days postadmission in a stable condition; however, she was still burdened by binocular blindness. She was subsequently seen by ophthalmology as an out-patient; an examination again revealed no light perception in both eyes and complete nonreactivity to both pupils, consistent with complete optic atrophy suggesting severe optic nerve damage.