[Extracorporeal membrane oxygenation for acute respiratory distress syndrome in patients with COVID-19]. / Ekstrakorporal membranoksygenering ved akutt lungesviktsyndrom hos covid-19-pasienter.

BACKGROUND: COVID-19 can lead to acute respiratory distress syndrome (ARDS). In some patients for whom conventional mechanical ventilation is insufficient, venovenous (VV) extracorporeal membrane oxygenation (ECMO) can be life-saving. MATERIAL AND METHOD: Retrospective analysis of data from patients with ARDS triggered by COVID-19 who received ECMO therapy between March 2020 and February 2022. Premorbid health condition, course of respiratory distress and respiratory support before, during and after ECMO therapy were registered. RESULTS: Thirty patients received ECMO therapy. Median age was 57 years, median body mass index 28 kg/m2, and 23 patients were men. Median duration of lung protective mechanical ventilation with tidal volume 5.8 mL/kg predicted body weight before initiation of ECMO therapy was 8 days. Treatment indication was primarily severe hypoxaemia, frequently combined with hypercapnia. Twenty-three patients developed at least one severe complication while receiving ECMO therapy. Sixteen patients died, 13 during ongoing ECMO therapy. Fourteen were discharged from hospital. Median duration of ECMO and mechanical ventilation was 27 and 37 days, respectively. INTERPRETATION: ECMO therapy for patients with ARDS triggered by COVID-19 can be life-saving, but the treatment is accompanied by severe complications and a high mortality rate.

Adenosine-assisted clipping of intracranial aneurysms.

Temporary parent vessel clip occlusion in aneurysm surgery is not always practical or feasible. Adenosine-induced transient cardiac arrest may serve as an alternative. We retrospectively reviewed our clinical database between September 2011 and July 2014. All patients who underwent microsurgical clipping of intracranial aneurysms under adenosine-induced asystole were included. A total of 18 craniotomies were performed, and 18 aneurysms were clipped under adenosine-induced asystole (7 basilar arteries, 8 internal carotid arteries, 1 middle cerebral artery, and 1 anterior communicating artery) in 16 patients (10 females, 6 males). Nine cases were elective and seven after subarachnoid hemorrhage. Mean age was 54 years (range 39-70). The indications for adenosine use were proximal control in narrow surgical corridors in 13 cases and "aneurysm softening" in 4 cases. A single dose was used in 14 patients; 3 patients had multiple boluses. The median (range) total dose was 30 (18-135) mg. Adenosine induced a bradycardia with concomitant arterial hypotension in all patients, and the majority also had asystole for 5-15 sec. Transient cardiac arrhythmias were noted in one patient (AFib in need of electroconversion after two boluses). Nine clinical scenarios where adenosine-induced temporary cardiac arrest and deep hypotension was an effective adjunct to temporary clipping during microsurgical clipping of intracranial aneurysms were identified.

The effect of tracheotomy on drug consumption in patients with acute aneurysmal subarachnoid hemorrhage: an observational study.

BACKGROUND: Patients with aneurysmal subarachnoid hemorrhage (aSAH) are common in intensive care units (ICU). In patients with aSAH, sedation is used as a neuroprotective measure in order to secure adequate cerebral perfusion pressure (CPP). Compared with the use of an endotracheal tube, a tracheotomy has the advantage of securing the airway at a much lower level of distress, and aSAH patients can often be awakened more rapidly. Little is known about the impact of tracheotomy on the consumption of sedative/analgesic and vasoactive drugs and the maintenance of CPP within defined limits in aSAH patients. METHODS: We conducted an observational study of aSAH patients who underwent percutaneous tracheotomy. A prospective registry of patient data was supplemented with retrospective retrievals from medical records. Sedative, analgesic and vasoactive drug doses were registered for 3 days prior to and after percutaneous tracheotomy, respectively. Blood pressure, CPP, and the mode of mechanical ventilation were registered 24 h prior to and after tracheotomy. RESULTS: Between January 2001 and June 2009, 902 aSAH patients were admitted to our hospital; 74 (8%) were deeply comatose/dying upon arrival. The ruptured aneurysm was repaired in 828 patients (surgical repair 50%) and percutaneous tracheotomy was performed 182 times in 178 patients (59 men and 119 women). This subpopulation (178 of 828 patients) was significantly older (56 vs. 53 years) and presented with a more severe Hunt & Hess grade (p < 0.001). Percutaneous tracheotomy caused a marked decline in mean daily consumption of the analgesics/sedatives fentanyl, midazolam, and propofol, as well as the vasoactive drugs noradrenaline and dopamine. These declines were statistically and clinically significant. The mean CPP was 76 mmHg (SD 8.6) the day before and 79 mmHg (SD 9.6) 24 h after percutaneous tracheotomy. After percutaneous tracheotomy, mechanical ventilatory support could be reduced to a patient-controlled ventilatory support mode in a significant number of patients (p < 0.001). CONCLUSIONS: Percutaneous tracheotomy in aSAH patients is a swift procedure with low risk that is associated with a significant decline in the consumption of sedative/analgesic and vasoactive drugs while clinical surveillance parameters remain stable or improve.

Methylprednisolone reduces pain, emesis, and fatigue after breast augmentation surgery: a single-dose, randomized, parallel-group study with methylprednisolone 125 mg, parecoxib 40 mg, and placebo.

We compared methylprednisolone 125 mg IV (n = 68) and parecoxib 40 mg IV (n = 68) with placebo (n = 68) given before breast augmentation surgery in a randomized, double-blind parallel group study. Surgery was performed under local anesthesia combined with propofol/fentanyl sedation. Methylprednisolone and parecoxib decreased pain at rest and dynamic pain intensity from 1 to 6 h after surgery compared with placebo (mean summed pain intensity(1-6 h): methylprednisolone [17.25; 95% confidence interval [CI], 14.85-19.65] versus placebo [21.7; 95% CI, 19.3-24.1]; P < 0.03; parecoxib [15.25; 95% CI, 13.25-17.25] versus placebo; P < 0.001; mean summed dynamic pain intensity(1-6 h): methylprednisolone [22.7; 95% CI, 20.1-23.3] versus placebo [28.4; 95% CI, 26.0-30.8]; P < 0.01; parecoxib [20.9; 95% CI, 18.6-23.2] versus placebo; P < 0.001). Both rescue drug consumption and actual pain (all observations before and after rescue) during the first 6 h were similar in the two active drug groups and significantly reduced compared with placebo. Using a composite score of actual pain intensity and rescue analgesic use, the active drugs were significantly superior to placebo (P < 0.001 for both active drugs). Postoperative nausea and vomiting was reduced after methylprednisolone administration (incidence, 30%), but not after parecoxib (incidence, 37%), during the first 24 h compared with placebo (incidence, 60%; P < 0.001). Fatigue was reduced by methylprednisolone (incidence, 44%), but not by parecoxib (incidence, 59%), compared with placebo (incidence, 66%; P < 0.05). In conclusion, methylprednisolone 125 mg IV given before breast augmentation surgery had analgesic and rescue analgesic-sparing effects comparable with those of parecoxib 40 mg IV. Methylprednisolone, but not parecoxib, reduced nausea, vomiting, and fatigue.