When should nitroglycerine be avoided in hypertensive encephalopathy?

Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1000 words (typed double-spaced) in length and may be subject to editing or abridgment. Intravenous nitroglycerin is a well-recognized treatment of acute hypertension and hypertensive encephalopathy. 1 We are reporting a patient presented with posterior reversible encepha-lopathy syndrome (PRES) secondary to hypertensive crisis who deteriorated when his blood pressure was treated with intravenous nitroglycerin. We, therefore, suggest that nitroglycerine should be discontinued in all patients with hypertensive enceph-alopathy with worsening neurological status or in the presence of typical radiological findings. A 63-year– old man with a history of hypertension and diabetes mellitus presented with a severe headache, associated with nausea and vomiting. He had a history of alcohol abuse complicated by liver cirrhosis but denies drinking for many years. His medications include insulin glargine, atenolol 50 mg, gabapentin, zolpidem, and tamsulosin. His blood pressure was 222/110 mm Hg, and his pulse rate was 68 bpm. Neurological examination revealed mild disorientation but no papilledema or focal neurological deficit. Abnormal laboratory studies on admission included blood glucose 382 mg/dL, alanine transaminase 55 U/L, and aspartate aminotransferase 43 U/L. Toxicology screen was positive for benzodiazepines. Urinalysis revealed proteinuria and glycosuria. A brain computed tomography scan showed hypodensities in the white matter of posterior parietal lobes bilaterally (Figure 1A and 1B). He was started on intravenous labetalol but then became bradycardic, so an intravenous nitroglycerin drip was initiated. His medications stopped temporally because of the nausea and vomiting, and insulin drip was initiated for proper glycemic control. The next day, the blood pressure was 180/100 mm Hg, the heart rate was 90 bpm, and blood sugar was 206 mg/dL, but the conscious level deteriorated, and he started to report visual loss. A follow-up computed tomography scan of the head showed worsening of the initial findings (Figure 2A and 2B). Brain MRI showed abnormal signal on the fluid-attenuated inversion recovery and T2-weighted images involving the occipital lobes with extension to parietal and frontal lobes bilaterally (Figure 3A and 3B). Diffusion-weighted images showed no areas of restriction, excluding infarction, and confirming the diagnosis of PRES. Intravenous nitroglycerin was stopped. We decided to restart the intravenous labetalol drip because his heart rate was 90 bpm. After 12 hours of labetalol infusion, his blood pressure was 145/80 mm Hg, and his conscious level gradually improved. He was fully conscious and coherent the …