Septic shock is a major burden to healthcare with mortality rates remaining high. Blood purification techniques aim to reduce cytokine levels and resultant organ failure. Regarding septic shock, hemoadsorption via CytoSorb seems promising, but the main effects on organ failure and mortality remain unclear. In this retrospective single-center study, septic shock patients receiving CytoSorb in addition to renal replacement therapy (n = 42) were analyzed and compared to matched controls (n = 42). A generalized propensity-score and Mahalanobis distance matching method (‘genetic’ matching) was applied. Baseline comparability was high. Differences were merely present in higher initial Sequential Organ Failure Assessment (SOFA) scores (median and interquartile range: 13.0 (12.0–14.75) vs. 12.0 (9.0–14.0)) and requirements of norepinephrine equivalents (0.54 (0.25–0.81) vs. 0.25 (0.05–0.54) µg/kg/min) in the CytoSorb group. While remaining fairly constant in the controls, the catecholamines decreased to 0.26 (0.11–0.40) µg/kg/min within 24 h after initiation of CytoSorb therapy. In-hospital mortality was significantly lower in the CytoSorb group (35.7% vs. 61.9%; p = 0.015). Risk factors for mortality within the CytoSorb group were high lactate levels and low thrombocyte counts prior to initiation. Hereby, a cut-off value of 7.5 mmol/L lactate predicted mortality with high specificity (88.9%). Thus, high lactate levels may indicate absent benefits when confronted with septic shock patients considered eligible for CytoSorb therapy.

Hemodynamic instability due to dysregulated host response is a life-threatening condition requiring vasopressors and vital organ support. Hemoadsorption with Cytosorb has proven to be effective in reducing cytokines and possibly in attenuating the devastating effects of the cytokine storm originating from the immune over-response to the initial insult. We reviewed the PubMed database to assess evidence of the impact of Cytosorb on norepinephrine needs in the critically ill. We further analyzed those studies including data on control cohorts in a comparative pooled analysis, defining a treatment effect as the standardized mean differences in relative reductions in vasopressor dosage at 24 h. The literature search returned 33 eligible studies. We found evidence of a significant reduction in norepinephrine requirement after treatment: median before, 0.55 (IQR: 0.39–0.90); after, 0.09 (0.00–0.25) μg/kg/min, p < 0.001. The pooled effect size at 24 h was large, though characterized by high heterogeneity. In light of the importance of a quick resolution of hemodynamic instability in the critically ill, further research is encouraged to enrich knowledge on the potentials of the therapy.

Developing hypernatremia while on intensive care unit (ICU) is a common problem with various undesirable effects. A link to persistent inflammation, immunosuppression and catabolism syndrome (PICS) can be established in two ways. On the one hand, hypernatremia can lead to inflammation and catabolism via hyperosmolar cell stress, and on the other, profound catabolism can lead to hypernatremia via urea-induced osmotic diuresis. In this retrospective single-center study, we examined 115 patients with prolonged ICU stays (≥14 days) and sufficient renal function. Depending on their serum sodium concentrations between ICU day 7 and 21, allocation to a hypernatremic (high) and a nonhypernatremic group (low) took place. Distinct signs of PICS were detectable within the complete cohort. Thirty-three of them (28.7%) suffered from ICU-acquired hypernatremia, which was associated with explicitly higher signs of inflammation and ongoing catabolism as well as a prolonged ICU length of stay. Catabolism was discriminated better by the urea generation rate and the urea-to-creatinine ratio than by serum albumin concentration. An assignable cause for hypernatremia was the urea-induced osmotic diuresis. When dealing with ICU patients requiring prolonged treatment, hypernatremia should at least trigger thoughts on PICS as a contributing factor. In this regard, the urea-to-creatinine ratio is an easily accessible biomarker for catabolism.

To elucidate patterns of and risk factors for acute traumatic injuries in climbers in need of professional rescue, a retrospective evaluation was performed of the Austrian National Registry of Mountain Accidents regarding rock climbing incidents over a 13-year timeframe from 2005 to 2018. From 2992 recorded incidents, 1469 were uninjured but in need of recovery, mainly when alpine climbing. Acute traumatic injuries (n = 1217) were often classified as severe (UIAA ≥ 3; n = 709), and commonly involved fractures (n = 566). Main injury causes were falls (n = 894) frequently preceded by rockfall (n = 229), a stumble (n = 146), a grip or foothold break-out (n = 143), or a belaying error (n = 138). In fatal cases (n = 140), multiple trauma (n = 105) or head injuries (n = 56) were most common, whereas lower extremity injuries (n = 357) were most common in severely injured patients. The risk for severe or fatal injuries increased with age and fall height when ascending or bouldering, during the morning hours, and when climbing without a helmet or rope. The case fatality rate was 4.7%, and the estimated total mortality rate was 0.003–0.007 per 1000 h of rock climbing. Acute traumatic injuries requiring professional rescue when rock climbing are often severe or fatal. Consequent use of a helmet when sport climbing, consistent use of a rope (particularly when ascending), proper spotting when bouldering, and proper training, as well as high vigilance when belaying are likely to help prevent such injuries.

Fibrinogen supplementation is recommended for treatment of severe trauma hemorrhage. However, required dosages and aimed for post-treatment fibrinogen levels remain a matter of discussion. Within the published RETIC study, adult patients suffering trauma-induced coagulopathy were randomly assigned to receive fibrinogen concentrate (FC) as first-line (n = 50) or crossover rescue (n = 20) therapy. Depending on bodyweight, a single dose of 3, 4, 5, or 6 g FC was administered and repeated if necessary (FibA10 < 9 mm). The dose-dependent response (changes in plasma fibrinogen and FibA10) was analyzed. Receiver operating characteristics (ROC) analysis regarding the need for massive transfusion and correlation analyses regarding fibrinogen concentrations and polymerization were performed. Median FC single doses amounted to 62.5 (57 to 66.66) mg.kg⁻¹. One FC single-dose sufficiently corrected fibrinogen and FibA10 (median fibrinogen 213 mg.dL⁻¹, median FibA10 11 mm) only in patients with baseline fibrinogen above 100 mg.dL⁻¹ and FibA10 above 5 mm, repeated dosing was required in patients with lower baseline fibrinogen/FibA10. Fibrinogen increased by 83 or 107 mg.dL⁻¹ and FibA10 by 4 or 4.5 mm after single or double dose of FC, respectively. ROC curve analysis revealed post-treatment fibrinogen levels under 204.5 mg.dL⁻¹ to predict the need for massive transfusion (AUC 0.652; specificity: 0.667; sensitivity: 0.688). Baseline fibrinogen/FibA10 levels should be considered for FC dosing as only sufficiently corrected post-treatment levels limit transfusion requirements.

Canyoning has become a popular recreational sport. Nevertheless, little is known about injuries or diseases associated with canyoning. The aim of this study was to examine accident causes, injury patterns, out-of-hospital and in-hospital treatment and outcomes. For this purpose, national out-of-hospital data from the Austrian Alpine Safety Board and regional in-hospital data from Innsbruck Medical University Hospital were analysed for the period from November 1, 2005 to October 31, 2018. Nationally, 471 persons were involved in such accidents; 162 (34.4%) were severely injured, nine of whom died. Jumping (n = 110, 23.4%), rappelling (n = 51, 10.8%), sliding (n = 41, 8.7%) and stumbling (n = 26, 5.5%) were the most common causes of canyoning accidents. A large proportion of injuries were documented for the lower extremities (n = 133, 47.5%), followed by the upper extremities (n = 65, 23.2%) and the spine (n = 44, 15.7%). Death was mainly caused by drowning. Overall mortality was 1.9% (n = 9), and the absolute risk was 0.02 deaths per 1000 hrs of canyoning. Many uninjured persons required evacuation (n = 116, 24.6%), which resulted in a substantial expense and workload for emergency medical services. Increased safety precautions are required to reduce accidents while jumping and rappelling and fatalities caused by drowning.