Rotation of a toric intraocular lens from neodymium:YAG laser posterior capsulotomy.

A 77-year-old man had cataract surgery in the left eye in March 2017. A toric intraocular lens (IOL) was implanted because of astigmatism. The postoperative meridian of the IOL was located nearly exactly in the planned meridian, which was controlled 1 week later with ray-tracing aberrometry (iTrace) and the smartphone application Axis Assistant. The referring ophthalmologist proceeded directly with a neodymium:YAG (Nd:YAG) laser posterior capsulotomy in his own office, after which the meridian of the implanted toric IOL was rotated more than 115 degrees. The rotation of the IOL was likely the result of a very early Nd:YAG treatment. Therefore, when a toric IOL is implanted it is important to wait at least 3 months after cataract surgery before proceeding with Nd:YAG to ensure complete rotational stability of the IOL.

Dynamics of inflammation parameters prior to tachyarrhythmias in critically ill patients.

BACKGROUND: The aim of this study was to assess the dynamics of inflammation parameters prior to a tachyarrhythmic event in critically ill patients. We evaluated the course of inflammation parameters over 48 hours before the occurrence of tachyarrhythmias. METHODS: Prospective observational study conducted at a cardiologic medical-postoperative tertiary intensive care unit at the Vienna university hospital. Between November 1996 and July 1999 all consecutive patients (n = 756) were screened for the occurrence of arrhythmias. Patients with sustained tachyarrhythmias (n = 119) form the basis of the report. The tachyarrhythmia episodes were related to the evolution of C-reactive protein, leukocytes and fibrinogen during the 48 hours before the arrhythmic event. RESULTS: A total of 278 tachyarrhythmia episodes was identified (wide QRS complex tachycardia, n = 168; narrow QRS complex tachycardia, n = 108; ventricular fibrillation, n = 2). The body temperature on the day of arrhythmia was 37.4 +/- 1 degrees C. Overall, there was no statistically significant change in any inflammation parameter within 48 hours prior to tachyarrhythmias (C-reactive protein: 17.4 +/- 12 [-48 h], 16.2 +/- 11 [-24 h], 15.2 +/- 12 [0 h] mg/dl, p = 0.2). When stratifying for different levels of C-reactive protein on the day of arrhythmia, the trend was inhomogenous. For lower strata, values were significantly decreasing towards arrhythmias; for higher strata, an increase in C-reactive protein was observed (stratum A: 8.5 +/- 7.2 [-48 h], 6.6 +/- 4.9 [-24 h], 4.8 +/- 2.9 mg/dl [0 h], p = 0.0001; stratum B: 16.0 +/- 7.1 [-48 h], 13.8 +/- 6.0 [-24 h], 14.4 +/- 2.6 mg/dl [0 h], p = 0.09; stratum C: 21.2 +/- 7.4 [-48 h], 21.5 +/- 7.5 [-24 h], 24.9 +/- 3.0 mg/dl [0 h], p = 0.008; stratum D: 34.3 +/- 13.4 [-48 h], 35.7 +/- 9.0 [-24 h], 39.7 +/- 5.5 mg/dl [0 h], p = 0.13). CONCLUSION: In this group of critically ill patients inflammation parameters did not change significantly during the 48 hours prior to the arrhythmic event. For different levels of C-reactive protein at the time of arrhythmia, no clear dynamics of inflammatory signs were observed.

Circadian variation in ventricular tachycardia and atrial fibrillation in a medical-cardiological ICU.

OBJECTIVE: To assess the diurnal distribution of ventricular tachycardia (VT) and atrial fibrillation (AF) in critically ill patients. DESIGN AND SETTING: Prospective observational study (episode-based design) in an eight-bed medical/cardiological ICU at a university hospital that also admits postoperative patients. PATIENTS: 98 consecutive patients with AF ( n=55) or ventricular tachycardia ( n=43). MEASUREMENTS AND RESULTS: There were a total of 218 arrhythmia episodes (83 AF, 136 VT). The time of arrhythmia onset was not evenly distributed. Circadian variation in VT but not AF onset was well represented by a sine wave function. Both VT and AF fibrillation showed a trough during the night. The distribution of VT and AF episodes did not differ significantly with or without analgosedation. CONCLUSIONS: In critically ill patients the onset of VT and AF over 24-h is nonuniformly distributed. In VT this circadian pattern of occurrence is well modeled by a sine wave function peaking between noon and 2 p.m. The circadian pattern is less clear for AF. The circadian variation is seen irrespective of the presence of absence of analgosedation for both arrhythmias.