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1.
Anaesthesiol Intensive Ther ; 54(1): 3-11, 2022.
Article in English | MEDLINE | ID: mdl-35266376

ABSTRACT

BACKGROUND: The Sequential Organ Failure Assessment (SOFA) score has been developed to score the severity of organ dysfunction in critically ill sepsis patients and has been proven to have a high predictive value for intensive care unit (ICU) mortality in severely ill patients. Our goal was to evaluate the prognostic value of the SOFA score as well as trends in SOFA score for ICU mortality in COVID-19 patients. METHODS: All consecutive patients with confirmed COVID-19 pneumonia admitted to the ICU between March 13th, 2020, and October 17th, 2020 were included in this retrospective cohort study. The worst SOFA score was evaluated daily. Multiple logistic regression models were used to evaluate the predictive value of SOFA in ICU mortality. RESULTS: 103 patients were included in this study. 30 patients (29%) died during their ICU stay and 73 (71%) patients were discharged alive. The ICU admission SOFA score was 5.2 ± 3.3 in ICU non-survivors vs. 4.3 ± 2.9 in ICU survivors (P = 0.15). The maximum SOFA score in ICU non-survivors was 11.7 ± 4.7 vs. 7.4 ± 4.3 in ICU survivors. SOFA scores increased the first week in both survivors and non-survivors, but the increase was less pronounced in survivors. In the multiple logistic regression models, neither admission SOFA score nor combination with delta SOFA in the first 48 hours was statistically significantly related to ICU mortality. Only the maximum SOFA score remained significant (OR = 1.23, 95% CI: 1.11-1.37, P < 0.001) in the multiple logistic models with an AUC of 0.91. CONCLUSIONS: Evaluation of SOFA scores in the first 48 hours after ICU admission is not a good prognostic indicator in COVID-19 patients. Only the maximum SOFA score was predictive for ICU mortality.


Subject(s)
COVID-19 , Organ Dysfunction Scores , Critical Illness , Humans , Intensive Care Units , Prognosis , ROC Curve , Retrospective Studies
2.
Anesth Pain Med ; 10(3): e101669, 2020 Jun.
Article in English | MEDLINE | ID: mdl-32944560

ABSTRACT

BACKGROUND: Nowadays, complicated and painful surgical procedures are encouraged to be carried out in an ambulatory setting. OBJECTIVES: The current study aimed to assess 4-week postoperative pain profiles of 4 painful ambulatory surgical procedures. We analyzed the prevalence of and reasons for non-adherence and partial adherence of patients to a predefined treatment schedule after the ambulant surgery. METHODS: The current study analyzed data from a large randomized trial by evaluating the effect of postoperative pain medication on acute postoperative pain at home during the first 4 postoperative days (POD) in patients scheduled for ambulatory hemorrhoid surgery, shoulder or knee arthroscopy, and inguinal hernia repair. Postoperative pain intensity was assessed at POD 0, 1, 2, 3, 4, 7, 14, and 28 via the Numeric Rating Scale (NRS). Adherence was assessed on POD 1, 2, 3, and 4. RESULTS: Median average pain scores were above an NRS of 3 during the first postoperative week after shoulder arthroscopy and even above 4 during the first postoperative week after hemorrhoid surgery. 26% of patients undergoing shoulder arthroscopy and hemorrhoid surgery still had moderate pain 1 week after surgery. Median average pain scores were below an NRS of 3 during the whole study period after inguinal hernia repair and knee arthroscopy. 24.61% of patients did not use the study medication as prescribed, 5.76% of whom were non-adherent, and 18.85% were partially adherent. CONCLUSIONS: Each type of ambulant surgery has its unique postoperative pain profile. New strategies should be developed for pain therapy at home, particularly after the ambulatory arthroscopic shoulder surgery and hemorrhoid surgery. Non-adherence is uncommon if they are provided with a multimodal analgesic home kit together with clear verbal, written instructions, and intensive follow-up.

3.
Crit Care ; 13(1): R5, 2009.
Article in English | MEDLINE | ID: mdl-19166623

ABSTRACT

INTRODUCTION: Intensive insulin therapy (IIT) reduced the incidence of critical illness polyneuropathy and/or myopathy (CIP/CIM) and the need for prolonged mechanical ventilation (MV >or= 14 days) in two randomised controlled trials (RCTs) on the effect of IIT in a surgical intensive care unit (SICU) and medical intensive care unit (MICU). In the present study, we investigated whether these effects are also present in daily clinical practice when IIT is implemented outside of a study protocol. METHODS: We retrospectively studied electrophysiological data from patients in the SICU and MICU, performed because of clinical weakness and/or weaning failure, before and after routine implementation of IIT. CIP/CIM was diagnosed by abundant spontaneous electrical activity on electromyography. Baseline and outcome variables were compared using Student's t-test, Chi-squared or Mann-Whitney U-test when appropriate. The effect of implementing IIT on CIP/CIM and prolonged MV was assessed using univariate analysis and multivariate logistic regression analysis (MVLR), correcting for baseline and ICU risk factors. RESULTS: IIT significantly lowered mean (+/- standard deviation) blood glucose levels (from 144 +/- 20 to 107 +/- 10 mg/dl, p < 0.0001) and significantly reduced the diagnosis of CIP/CIM in the screened long-stay patients (125/168 (74.4%) to 220/452 (48.7%), p < 0.0001). MVLR identified implementing IIT as an independent protective factor (p < 0.0001, odds ratio (OR): 0.25 (95% confidence interval (CI): 0.14 to 0.43)). MVLR confirmed the independent protective effect of IIT on prolonged MV (p = 0.002, OR:0.40 (95% CI: 0.22-0.72)). This effect was statistically only partially explained by the reduction in CIP/CIM. CONCLUSIONS: Implementing IIT in routine daily practice in critically ill patients evoked a similar beneficial effect on neuromuscular function as that observed in two RCTs. IIT significantly improved glycaemic control and significantly and independently reduced the electrophysiological incidence of CIP/CIM. This reduction partially explained the beneficial effect of IIT on prolonged MV.


Subject(s)
Critical Care/methods , Critical Illness/therapy , Insulin/administration & dosage , Neuromuscular Junction/drug effects , Neuromuscular Junction/pathology , Adult , Aged , Female , Humans , Male , Middle Aged , Muscular Diseases/complications , Muscular Diseases/drug therapy , Muscular Diseases/physiopathology , Polyneuropathies/complications , Polyneuropathies/drug therapy , Polyneuropathies/physiopathology , Randomized Controlled Trials as Topic/methods , Retrospective Studies , Risk Factors
4.
Crit Care Med ; 30(11): 2548-52, 2002 Nov.
Article in English | MEDLINE | ID: mdl-12441768

ABSTRACT

OBJECTIVE: Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine. DESIGN: Prospective laboratory investigation using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: Seven adult beagle dogs weighing 8-14 kg. INTERVENTIONS: After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure. MEASUREMENTS AND MAIN RESULTS: Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion. CONCLUSIONS: In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.


Subject(s)
Arginine Vasopressin/adverse effects , Hypertension, Pulmonary/drug therapy , Vasoconstrictor Agents/adverse effects , Ventricular Dysfunction, Right/chemically induced , Ventricular Dysfunction, Right/drug therapy , Acute Disease , Analysis of Variance , Animals , Dogs , Hemodynamics/drug effects , Phenylephrine/pharmacology , Prospective Studies , Stroke Volume/drug effects , Vascular Resistance/drug effects
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