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Aim Ventricular fibrillation amplitude spectral area (AMSA) and end-tidal carbon dioxide (ETCO2) are predictors of shock success, understood as restoration of an organized rhythm, and return of spontaneous circulation (ROSC). However, little is known about their combined use. We aimed to assess the prediction accuracy when combined, and to clarify if they are correlated in out of hospital cardiac arrest' victims. Materials and Methods Records acquired by external defibrillators in out-of-hospital cardiac arrest patients of the Lombardia Cardiac Arrest registry were processed. The 1-min pre-shock ETCO2 median value (METCO2) was computed from the capnogram and AMSA (2–48 mV.Hz range) computed applying the Fast Fourier Transform to a 2-second pre-shock filtered ECG interval (0.5−30 Hz). Support Vector Machine (SVM) predictive models based on METCO2, AMSA and their combination were fit; results were given as the area under the curve (AUC) of the receiver operating characteristic (ROC) curves. Results We considered 112 patients with 391 shocks delivered. METCO2 and AMSA were predictors of shock success [AUC (IQR) of the ROC curve: 0.59 (0.56−0.62); 0.68 (0.65−0.72), respectively] and of ROSC [0.56 (0.53−0.59); 0.74 (0.71−0.78),]. Their combination in a SVM model increased the accuracy for predicting shock success [AUC (IQR) of the ROC curve: 0.71 (0.68−0.75)] and ROSC [0.77 (0.73−0.8)]. AMSA and METCO2 were significantly correlated only in patients who achieved ROSC (rho = 0.33 p = 0.03). Conclusions AMSA and ETCO2 predict shock success and ROSC after every shock, and their predictive power increases if combined. Notably, they were correlated only in patients who achieved ROSC.

Introduction: SARS-Cov-2 infection can be asymptomatic, greatly impair respiratory function and, sometimes, affect other organs. Gastro-enteric involvement seems to be not so rare and many patients suffered for abdominal pain, anorexia, nausea and vomiting, diarrhoea or jaundice. Case presentation: Here we report a case of a Covid-19 patient who developed a right colon perforation due to a pseudomembranous colitis without Clostridium Difficile toxins finding associated to a necrotising vasculitis. In this patient a PCR test performed on gastric fluid showed SARS-CoV-2 enteric replication. Discussion: Necrotizing vasculitis is an anatomopathological typical findings in Covid-19. It has been documented in several organs and tissues. In our case, evident foci of necrotizing vasculitis with intravascular obliteration by fibrin thrombi with macrophagic cells infiltration are anatomopathological findings of a CD toxins free pseudomembranous colitis leading to bowel perforation. Conclusions: Bowel perforation due to necrotizing vasculitis leading to pseudomembranous colitis could be a SARS-Cov-2 related clinical finding.

Background Post-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. Methods This was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. Results We enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66–0.82; increased to AUC = 0.79, 95% CI 0.71–0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65–0.81 increased to AUC = 0.80, 95% C.I. 0.69–0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups. Conclusions PTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS. Trial registration The present study was registered in ClinicalTrial.gov with the ID number NCT02430324.

Background: Post-traumatic cerebral infarction (PTCI) is common in patients dying after a traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. Methods: This was a prospective multicenter cohort study of moderate and severe TBI patients admitted to nine Italian intensive care units (ICUs). The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. Findings: We enrolled 143 patients; 47 (32·9%) developed a PTCI for a total of 94. The mean (SD) onset time of a PTCI was 6·2 (11·4). In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC=0·73, 95% C.I. 0·66-0·82; increased to AUC=0·79, 95% CI 0·71-0·83, p=0·0007) and extended model (AUC=0·74, 95% C.I.: 0·65-0·81 increased to AUC=0·80, 95% C.I. 0·69-0·85; p=0·00008). Patients with a PTCI showed higher ICU mortality (10 patients [21·3%] vs one patient [1·0%], p

Guillain-Barré syndrome (GBS) is an acute immune-mediated disorder of the peripheral nervous system and a triggering infectious event is often reported in the weeks before the disease onset. Influenza viruses have been associated with Guillain-Barré syndrome (GBS), both after infection and, in rare cases, after vaccination. However, GBS has rarely reported to be a neurological complication of the recent pandemic influenza A(H1N1) 2009 virus infections. Here we describe the case of a young man, who developed acute severe motor inflammatory demyelinating polyradiculoneuropathy during influenza A(H1N1)2009 infection. Peculiar features are the findings of a mutated haemagglutinin gene (D222E variant), which has never previously been associated with neurological involvement, and the almost simultaneous appearance of respiratory infectious and immune-mediated neurological symptoms. Moreover we review the clinical presentation, laboratory findings and outcome of influenza-related GBS.

BACKGROUND: Improved technology, as well as professional and parental awareness, enable many ventilator-dependent children to live at home. However, the profile of this growing population, the quality and adequacy of home care, and patients' needs still require thorough assessment. OBJECTIVES: To define the characteristics of Italian children receiving long-term home mechanical ventilation (HMV) in Italy. METHODS: A detailed questionnaire was sent to 302 National Health Service hospitals potentially involved in the care of HVM in children (aged

Background Infections caused by multidrug-resistant gram-negative bacteria have caused a resurgence of interest in colistin. To date, information about pharmacokinetics of colistin is very limited in critically ill patients, and no attempts have been made to evaluate its concentration in BAL. Methods In this prospective, open-label study, 13 adult patients with ventilator-associated pneumonia caused by gram-negative bacteria were treated with colistin methanesulfonate (CMS) IV, 2 million International Units (174 mg) q8h, a usually recommended dose, for at least 2 days. Blood samples were collected from each patient at time intervals after the end of infusion. BAL was performed at 2 h. Colistin was measured by a selective, sensitive high-performance liquid chromatography-based method. Pharmacokinetic parameters were determined by noncompartmental analysis. Results Patients received 2.19 ± 0.38 mg/kg (range, 1.58-3.16) of CMS per dose. At steady state, mean ± SD plasma colistin maximum (Cmax) and trough (Ctrough) concentrations were 2.21 ± 1.08 and 1.03 ± 0.69 μg/mL, respectively. Mean ± SD area under the plasma concentration-time curve from 0 to 8 h (AUC0-8), apparent elimination half-life, and apparent volume of distribution were 11.5 ± 6.2 μg × h/mL, 5.9 ± 2.6 h, and 1.5 ± 1.1 L/kg, respectively. Cmax/minimum inhibitory concentration (MIC) ratio and AUC0-24/MIC ratio (MIC = 2 μg/mL) were 1.1 ± 0.5 and 17.3 ± 9.3, respectively. Colistin was undetectable in BAL. Nephrotoxicity was not observed. Conclusions Although the pharmacodynamic parameters that better predict the efficacy of colistin are not known in humans, in critically ill adult patients the IV administration of CMS 2 million International Units (174 mg) q8h results in apparently suboptimal plasma concentrations of colistin, which is undetectable in BAL. A better understanding of the pharmacokinetic-pharmacodynamic relationship of colistin is urgently needed to determine the optimal dosing regimen.

Clinical and radiological patterns from 148 patients with post-traumatic subarachnoid haemorrhage (TSAH) were analysed with specific regard for the amount and distribution of blood in subarachnoid spaces to verify if these variables have any influence on overall outcome. The degree and extent of TSAH were classified according to Fisher's criteria: in 93 patients it was grade 1, in 36 grade 2, in 13 grade 3, and in six grade 4. There was a significant correlation between increasing clinical severity at admission and the amount of subarachnoid bleeding and a direct relation between a favourable outcome and a low Fisher grade. The distribution of subarachnoid blood was not significantly related to clinical condition at admission, whereas the pattern had a significant impact on the outcome. The results of the present study confirm that TSAH is a negative prognostic factor. Whereas the degree of TSAH is mainly related to clinical conditions at admission, the presence of subarachnoid blood clots both in basal cisterns and over the cerebral convexity indicates a poor outcome.