Refractory intracranial hypertension in posterior reversible encephalopathy syndrome.

INTRODUCTION: Posterior reversible encephalopathy syndrome (PRES) is a largely reversible disease with long-term favorable outcome. A minority of patients, however, may develop progressive cerebral edema and ischemia resulting in severe disability or death. We report a case of severe intracranial hypertension associated with PRES that was successfully treated according to intracranial pressure (ICP)- and cerebral perfusion pressure (CPP)-driven therapy. METHODS: Case report. RESULTS: A 42-year-old woman underwent bilateral lung transplantation for severe bronchiectasis. Her immunosuppressive regimen consisted of azathioprine, prednisone, and tacrolimus. She acutely developed an aggressive form of PRES that rapidly resulted in severe refractory intracranial hypertension despite discontinuation of potentially causative medications and adequate supportive therapy. Accordingly, second-tier therapies, including barbiturate infusion, were instituted and immunosuppression was switched to anti-thymocyte globulin followed by mycophenolate mofetil. Within 10 h of barbiturate administration, ICP dropped to 20 mmHg. Thiopental was administered for two days and then rapidly tapered because of severe urosepsis. Six months after discharge from the intensive care unit the patient returned to near-normal life, her only complaint being short-term amnesia. CONCLUSIONS: The decision to undertake ICP monitoring in medical conditions in which no clear recommendations exist greatly relies on physicians' judgment. This case suggests that ICP monitoring may be considered in the setting of acute PRES among selected patients, when severe intracranial hypertension is suspected, provided that a multidisciplinary team of neurocritical care specialists is readily available.

Correction to: "Familial venoms": a thallium intoxication cluster.

The original version of this article unfortunately contained a mistake. The presentation of Table 1 was incorrect. The corrected Table 1 is given below.

Beneficial electrophysiological effects of trimetazidine in patients with postischemic chronic heart failure.

The aim of the study was to assess whether trimetazidine (TMZ) could affect dispersion of atrial depolarization and ventricular repolarization. Corrected QT interval (QTc), QTc dispersion (QTc-d), Tpeak-Tend, and Tpeak-Tend dispersion (Tpeak-Tend-d) were measured in 30 patients with chronic heart failure (CHF) before and 6 months after randomization to conventional therapy plus TMZ (17 patients) or conventional therapy alone (13 patients). After 6 months, QTc was significantly reduced in both groups, whereas QT-peak was increased only in control group. Tpeak-Tend-d decreased (from 63.53 +/- 24.73 to 42.35 +/- 21.07 milliseconds, P = .006) only in TMZ group. When subgrouped according to CHF etiology, only ischemic patients on TMZ showed Tpeak-Tend-d reduction (65.00 +/- 27.14 vs 36.67 +/- 11.55 milliseconds, P = .001 in ischemic patients; 60.00 +/- 20.00 vs 56.00 +/- 33.86 milliseconds, P = NS, in nonischemic). These electrophysiological properties indicate an undiscovered mechanism of action of TMZ, which could be useful in conditions at risk of major arrhythmias.