Background:
Initiation of veno-arterial (VA) Extracorporeal Membrane Oxygenator (ECMO) is associated with severe complications. It is unknown whether these adverse consequences occur more often after ...initiations during out of hours service compared to working hours.
Methods:
All patients receiving VA-ECMO for cardiogenic shock between 2009 and 2020 were categorized into a working hours group (between 8 am and 5 pm on weekdays) and an out of hours service group (between 5 pm and 8 am, or between Friday 5 pm and Monday 8 am). Primary outcome was all-cause mortality at 30 days. Secondary outcomes included vascular complications (including limb ischemia and/or bleeding), bloodstream infections and length of ICU stay. Propensity scores were used to adjust for potential confounding effects.
Results:
Among 250 patients (median (IQR) age 56 (42–64) years) receiving VA-ECMO (median duration 3.5 (1.0–9.0) days), 160 (64%) runs were initiated between 5 pm and 8 am whereas the remainder (36%) started during working hours. Characteristic did not differ between the working hours- and out of hours-group. By day 30, 37 (41.1%), and 68 (42.5%) patients in either group had died, respectively (p = 0.831). VA-ECMO support duration and length of stay on the ICU did not differ significantly in both crude and adjusted analyses. More complications occurred during out of hours service (p = 0.039).
Conclusions:
Out of hours- versus working hours-initiation of VA-ECMO for cardiogenic shock was not associated with higher mortality, longer VA-ECMO support duration, or longer length of stay on the intensive care. Vascular complications were more common in the out of hours group.
The aim of the present cross-over study was to compare the β-cell response to gliclazide and glibenclamide administered orally during and following a hyperglycaemic clamp in sulphonylurea treated ...Type 2 diabetes. Nine patients (6 males), aged 61.4 (S.D. 6.9) years with a body mass index of 27.5 (3.1) kg m
−2 and HbA
1c at baseline of 7.2 (0.9)% were included. Eight healthy control subjects underwent the same tests. Patients received 80–240 mg gliclazide or 5–15 mg glibenclamide for 6 weeks. Thirty minutes after administration of 160 mg of gliclazide or 10 mg of glibenclamide a 1-h hyperglycaemic clamp (11.0 mmol l
−1) was begun, and followed by a 3.5-h observation period. Nadir blood glucose levels were 4.2 (1.0), 4.3 (1.2) and 3.4 (1.0) mmol l
−1 for glibenclamide gliclazide and controls, respectively (both
P=0.07 vs. controls). Glucose levels decreased slowly and linearly in people with diabetes and reached nadirs after 204 (8) and 198 (18) min, respectively, after cessation of glucose infusion, while in controls, glucose levels declined steeply to a nadir at 98 (47) min (
P<0.003 vs. both drugs). No first phase insulin secretion peak was observed in people with diabetes. Insulin levels remained elevated during the 3-h observation period in SU treated patients but, in control subjects decreased to baseline values within 2 h of the clamp. The proinsulin to C-peptide ratio increased during the observation period. In conclusion, the effects of glibenclamide and gliclazide on insulin secretion are very similar in patients with Type 2 diabetes who are in moderate glycaemic control, with a slow rise to lower amplitude, poor responsiveness to falling glucose levels, and raised proinsulin to C-peptide ratio.
The synthetic hexapeptide growth hormone-releasing peptide (GHRP)-2 specifically stimulates GH release in man. To determine the effects of prolonged treatment and whether response attenuation occurs ...in man, we administered to nine healthy subjects a daily s.c. injection of 100 microg GHRP-2 over 5 days. Every day blood samples were taken to determine GH, IGF-I, IGF-binding protein (IGFBP)-3 and osteocalcin levels. On days 1,3 and 5, GH was measured at -20,0,20,40,60,90,120 and 180 min using an immunometric and an immunofunctional assay. Mean-/+S.D). peak GH concentrations were 83+/-31, 59+/-22 and 51+/-13 microg/l on days 1, 3 and 5 respectively. Mean+/-S.D. areas under the curve for days 1, 3 and 5 were 6366+/-2514, 3987 +/- 1418 and 3392+/-1215 mU/l per min. Despite the maintained GH release, analysis of variance revealed that significant response attenuation occurred (P < 0.01). Mean serum IGF-I concentration did not increase after a 5 day treatment with GHRP-2. Mean basal levels were 22, 25,23,25,23,24 nmol/l measured on days 1 to 6. However, osteocalcin, another serum marker of GH activity in tissue, increased significantly from 3.2+/-1.0 to 4.2+/-0.4 microg/l (mean+S.D.) (P< 0.01).
