SummaryBackground and objectives A simple anticoagulation protocol was developed for sustained low-efficiency dialysis (SLED) in patients with AKI, based on the use of anticoagulant citrate dextrose solution formulation A (ACD-A) and standard dialysis equipment. Patients' blood recalcification was obtained from calcium backtransport from dialysis fluid.Design, setting, participants, & measurements All patients treated with SLED (8-to 12-hour sessions) for AKI in four intensive care units of a university hospital were studied over a 30-month period, from May 1, 2008 to September 30, 2010. SLED interruptions and their causes, hemorrhagic complications, as well as coagulation parameters, ionized calcium, and blood citrate levels were recorded.Results This study examined 807 SLED sessions in 116 patients (mean age of 69.7 years [SD 12.1]; mean Acute Physiology and Chronic Health Evaluation II score of 23.8 [4.6]). Major bleeding was observed in six patients (5.2% or 0.4 episodes/100 person-days follow-up while patients were on SLED treatment). Citrate accumulation never occurred, even in patients with liver dysfunction. Intravenous calcium for ionized hypocalcemia (, 3.6 mg/dl or , 0.9 mmol/L) was needed in 28 sessions (3.4%); in 8 of these 28 sessions (28.6%), low ionized calcium was already present before SLED start. In 92.6% of treatments, SLED was completed within the scheduled time (median 8 hours). Interruptions of SLED by impending/irreversible clotting were recorded in 19 sessions (2.4%). Blood return was complete in 98% of the cases. In-hospital mortality was 45 of 116 patients (38.8%).Conclusions This study protocol affords efficacious and safe anticoagulation of the SLED circuit, avoiding citrate accumulation and, in most patients, systematic calcium supplementation; it can be implemented with commercial citrate solutions, standard dialysis equipment, on-line produced dialysis fluid, and minimal laboratory monitoring.

The purpose of our study was to identify general factors and distinctive clinical features differentiating patients with chronic cluster headache (CH) evolved from episodic CH and patients with episodic CH. Our study sample included 28 patients suffering from chronic CH evolved from episodic CH and 258 patients with episodic CH; all were referred to the Headache Center of Parma between December 1975 and June 1998. Patients with episodic CH were selected from all episodic CH referrals (n = 485) and selection was based on the duration of the disorder, which was to exceed the average period needed for an episodic form to turn into a chronic form (4.5 years for females and 7.0 years for males). At CH onset, the mean age for patients with chronic CH evolved from episodic CH was older than for those with episodic CH. Among patients with chronic CH, more were smokers or heavy drinkers, and had suffered a head injury. Clinically, episodic CH evolving into chronic CH was characterized by a high frequency of cluster periods, a larger proportion of patients with attacks not occurring strictly within cluster periods, and remission periods lasting less than 6 months. Possible predictive factors in the development of chronic CH appear to be CH onset from the third decade of life onward, the occurrence of more than one cluster period a year, and the short-lived duration of remission periods. The role played by head injury and cigarette smoking in the evolution of the disorder still cannot be established with certainty.

We applied the International Headache Society (IHS) classification coding parameters to a study population of 652 cluster headache (CH) patients, in order to determine how many patients did not fulfil the diagnostic criteria for group 3.1 and to find out any diagnostic elements that could be changed in the upcoming revision of the classification to make it more relevant to current clinical practice. Ninety-nine patients were found to have cluster-like disorder (3.3), including 74 (74.7%) who did not fulfil the diagnostic criteria for CH, because either pain was not associated with any of the accompanying autonomic phenomena listed in the classification or it was not located orbitally, supraorbitally and/or temporally. A review of our total sample showed that 72.0% of patients reported frontal and occipital pain location; in 61.8%, 33.4% and 39.1% of cases, attacks were also accompanied by restlessness/agitation, nausea and photophobia, respectively. In a coding system that took into account the diagnostic elements that we considered in our study, group 3.1 of the existing IHS classification would actually include 51 of the 99 patients currently coded as 3.3.

Our data suggest that AKI patients may be more vulnerable than ESRD patients to cerebral hypoperfusion during IHD. Our findings do not support a clear-cut role of rapid changes in blood osmolarity, rheological properties or vasoreactivity of the cerebral circulation to O(2) supply in modulating CBF during hemodialysis.

The International Headache Society (IHS) classification divides chronic cluster headache (CH) into two subtypes: chronic CH unremitting from onset (CCHU) and chronic CH evolved from episodic (CCHE). The purpose of our study was to point out any similarities and differences between the two chronic CH subtypes and to determine whether or not they can be considered as two separate clinical entities. We reviewed data about 31 CCHE patients and 38 CCHU patients referred to the Parma Headache Centre between 1975 and 1999. Clinically, CCHE patients exhibited statistically significant differences from CCHU patients, i.e. earlier CH onset and duration of attacks varying more frequently between 120 and 180 min. From the point of view of lifestyle, heavy alcohol and coffee drinkers prevailed among CCHU patients, while CCHE patients were more frequently heavy smokers. Based on clinical features, it seems reasonable to suppose that chronic CH may occur as two distinct entities.