Little is known about the clinical importance of blood pressure variability (BPV) during anesthesia in non-cardiac surgery. We sought to investigate the impact of intraoperative BPV on postoperative mortality in non-cardiac surgery subjects, taking into account patient- and procedure-related variables. This prospective observational study covered 835 randomly selected patients who underwent gastrointestinal (n = 221), gynecological (n = 368) and neurosurgical (n = 246) procedures. Patient’s and procedure’s risks were assessed according to the validated tools and guidelines. Blood pressure (systolic, SBP, and diastolic, DBP) was recorded in five-minute intervals during anesthesia. Mean arterial pressure (MAP) was assessed. Individual coefficients of variation (Cv) were calculated. Postoperative 30-day mortality was considered the outcome. Median SBP_Cv was 11.2% (IQR 8.4–14.6), DBP_Cv was 12.7% (IQR 9.8–16.3) and MAP_Cv was 10.96% (IQR 8.26–13.86). Mortality was 2%. High SBP_Cv (i.e., ≥11.9%) was associated with increased mortality by 4.5 times (OR = 4.55; 95% CI 1.48–13.93; p = 0.008). High DBP_Cv (i.e., ≥22.4%) was associated with increased mortality by nearly 10 times (OR = 9.73; 95% CI 3.26–28.99; p < 0.001). High MAP_Cv (i.e., ≥13.6%) was associated with increased mortality by 3.5 times (OR = 3.44; 95% CI 1.34–8.83; p = 0.01). In logistic regression, it was confirmed that the outcome was dependent on both SBPV and DBPV, after adjustment for perioperative variables, with AUCSBP_Cv = 0.884 (95% CI 0.859–0.906; p < 0.001) and AUCDBP_Cv = 0.897 (95% CI 0.873–0.918; p < 0.001). Therefore, intraoperative BPV may be considered a prognostic factor for the postoperative mortality in non-cardiac surgery, and DBPV seems more accurate in outcome prediction than SBPV.

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The stiff person syndrome (SPS) is an extremely rare neurological disorder with primarily immune-mediated etiology. The cardinal symptoms are progressive, fluctuating axial/proximal limb muscle stiffness and spasms. The diagnosis is based on the clinical picture, electromyography examination and detection of antibodies to glutamic acid decarboxylase (anti-GAD). Adverse effects of medications might preclude its use or increase in dosing, therefore symptomatic and/or immunomodulatory medical therapy might be ineffective in acute exacerbation of the disease. We present a case of a 49-year-old female with exacerbation of SPS, in whom some standard pharmacotherapy could not be introduced (clonazepam, baclofen used in the past) and doses of existing standard medications could not be increased (diazepam, gabapentin, and levetiracetam) due to adverse effects. Moreover, a newly introduced medication (methylprednisolone) also led to a serious adverse effect (severe hyperglycemia). The patient underwent therapeutic plasma exchange (TPE) with good effect and no complications. We review the literature regarding the efficacy and safety profile of TPE in exacerbation of SPS unresponsive to medical therapy. The procedure seems to have a good safety profile as an adjunct therapy for exacerbation of SPS not responding to standard medical therapy in this patient population.

IntroductionIron tests are deranged in sepsis; therefore new biomarkers should be used for diagnosis of iron deficiency (ID)/ID anemia (IDA).Material and methodsDiagnosis of ID/IDA was based on reticulocyte (RET) hemoglobin (Hb) equivalent (RET-He) and Hb concentration, with hepcidin (Hep) determined retrospectively.ResultsThe prevalence of ID and IDA was 7% and 47%, respectively. The AUROCs for RETs number and Hep in prediction of ID/IDA were 0.69 and 0.62, respectively.ConclusionsApproximately half of sepsis patients are iron-deficient. Number of RETs may be a predictor of ID/IDA when RET-He is not available. Hepcidin is a poor IDA predictor.

Prudent administration of fluids helps restore or maintain hemodynamic stability in the setting of perioperative blood loss. However, fluids may arguably exacerbate the existing coagulopathy. We sought to investigate the influence of balanced crystalloid and synthetic gelatine infusions on coagulation and fibrinolysis in healthy volunteers. This prospective randomized crossover study included 25 males aged 18–30 years. Infusions performed included 20 mL/kg of a balanced crystalloid solution (Optilyte®) or 20 mL/kg of gelatine 26.500 Da (Geloplasma®) in a random order over a period of 2 weeks. Laboratory analysis included conventional coagulation parameters and rotational thromboelastometry (ROTEM) assays. We confirmed a decrease in fibrinogen concentration and the number of platelets, and prolongation of PT after infusions. Compared to baseline values, differences in the ROTEM assays’ results after infusions signified the decrease in coagulation factors and fibrinogen concentration, causing impaired fibrin polymerization and clot structure. The ROTEM indicator of clot lysis remained unaffected. In the case of both Optilyte® and Geloplasma®, the results suggested relevant dilution. Gelatine disrupted the process of clot formation more than balanced crystalloid. Infusions of both crystalloid and saline-free colloid solutions causing up to 30% blood dilution cause significant dilution of the coagulation factors, platelets, and fibrinogen. However, balanced crystalloid infusion provides less infusion-induced coagulopathy compared to gelatine.