Toxic Shock Syndrome Publications (31936)
Toxic Shock Syndrome Publications
Hierarchical logistic regression to determine associations of hospital "early" DNR rates (DNR order placed within 24 hours of admission) with utilization of invasive interventions.
California State Inpatient Database, year 2011.
Patients with DNR orders at high-DNR-rate hospitals were less likely to receive invasive mechanical ventilation for acute respiratory failure or hemodialysis for acute renal failure, but more likely to receive palliative care than DNR patients at low-DNR-rate hospitals. Patients without DNR orders experienced similar rates of invasive interventions regardless of hospital DNR rates.
Hospitals vary widely in the scope of invasive or organ-supporting treatments provided to patients with DNR orders.
The effect of the sepsis intervention was evaluated for all patients, and High and Low Risk subgroups for illness severity. A separate analysis was performed patients on the intervention and non-intervention units (without the electronic surveillance). Sensitivity, specificity, and the positive predictive values were calculated to evaluate the accuracy of the alerting system for detecting sepsis or severe sepsis/ septic shock.
There was positive effect on the intervention units with sepsis electronic surveillance with an adjusted mortality rate of -6.6%. Mortality rates for non-intervention units also improved, but at a lower rate of -2.9%. Additional outcomes improved for patients on both intervention and non-intervention units for home discharge (7.5% vs 1.1%), total length of hospital stay (-0.9% vs -0.3%), and 30 day readmissions (-6.6% vs -1.6%). Patients on the intervention units showed better outcomes compared with non-intervention unit patients, and even more so for High Risk patients. The sensitivity was 95.2%, specificity of 82.0% and PPV of 50.6% for the electronic surveillance alerts.
There was improvement over time across the hospital for patients on the intervention and non-intervention units with more improvement for sicker patients. Patients on intervention units with electronic surveillance has better outcomes; however, due to differences in exclusion criteria and types of units, further study is needed to draw a direct relationship between the electronic surveillance system and outcomes.
5 mg vial added to 250 ml solvent in plastic bag (1 ml = 6 micg) given at 2 mcg/kg intravenous bolus over 1 min followed by 0.01 mcg/kg/min for 24 h. The primary outcome measurements were blood marker of intestinal hypoperfusion in form of intestinal fatty acid binding protein (I-FABP), malondialdehyde (MDA), myloperoxidase enzyme activity (MPO), protein carbonyl (PC), and glutathione peroxidase activity (GPA) measured before start of ANP infusion, 6 h, 12 h, and 24 h after start of infusion. The secondary outcome measurements were the duration of noradrenaline infusion, duration of ICU stay, hospital mortality rate, and complications related to ANP.
In comparison with Group C, Group A showed a significant decrease (P < 0.05) in serum level of MPO, MDA, PC, and I-FABP, with a significant increase (P < 0.05) in serum level of GPA, 6 h, 12 h, and 24 h after the start of ANP infusion. There was significant decrease (P < 0.05) in mean duration of noradrenaline infusion, the length of ICU stay and mortality rate in Group A in comparison with Group C. In Group A, seven patients had mean arterial blood pressure < 65 mmHg but respond to volume resuscitation, three patients serum sodium was 125-130 mmol/L.
In cases of septic shock, concomitant administration of ANP with noradrenaline may have a protective effect against intestinal injury through a decrease in the level of intestinal hypoperfusion owing to its anti-inflammatory and antioxidant effect.
This is a prospective randomized observer-blinded study carried out in surgical Intensive Care Unit (ICU) after approval by Hospital Ethical Committee. After admission to ICU patients were randomly divided into two groups of thirty patients each-Group (C): Control group managed according to the routine protocol of sepsis and Group (E): Edaravone treated SP managed according to the routine protocol of sepsis + edaravone at dose of 30 mg/12 h intravenous infusion for 2 weeks. All patients were monitored for invasive blood pressure, central venous pressure, heart rate, temperature, urine output, total fluid balance, and routine investigation. Blood sample was taken weekly for 2 weeks to measure the following parameters: Nuclear transcription factor kappa B activity (NFKB), mitogen-activated protein kinase (MAPK), heat shock protein 72 (HSP 72) and total antioxidant capacity (TAC).
There was significant decrease (P < 0.05) in serum level of NFKB, MAPK in Group E in comparison with Group C. While serum level of HSP 72 and TAC showed significant increase (P < 0.05) in Group E compared with Group C with better outcome.
SP treatment with edaravone could significantly improve the inflammatory and oxidative states with better patient outcomes.
Blood cultures and ear canal swabs were positive for Burkholderia pseudomallei The temporal lobe cerebritis eventually developed into an abscess, necessitating a cortical mastoidectomy, craniectomy and temporal lobectomy. After the surgical interventions, antibiotic therapy was continued for a further 6 months. The patient remained well and had no signs of recurrence up to 7 months after the initial presentation.
A bronchoalveolar lavage sample was positive via PCR for adenovirus which we suspect exacerbated a pre-existing bacterial pneumonia and led to a severe and non-responsive respiratory failure. His serum adenovirus load was markedly elevated. Treatment was started once the diagnosis of disseminated adenovirus infection was made; however, at that time patient was suffering from refractory hypoxaemia, respiratory acidosis, right heart failure and septic shock. Despite maximal supportive measures our patient ultimately expired over the course of 6 days.
Prospective, observational study.
Intensive care units of a tertiary medical center.
The study comprised 47 patients admitted with new diagnoses of severe sepsis or septic shock.
All patients underwent transthoracic echocardiograms with assessment of MPI at enrollment and 24 hours later. Hemodynamic data and information on sepsis-related mortality were collected. In the primary analysis, the association between change in MPI from enrollment to 24 hours and sepsis-related 90-day mortality was assessed.
Of the 47 patients enrolled, 30 demonstrated an improvement in MPI from 0 to 24 hours ("improved" group), and MPI worsened in the remaining 17 patients ("worsened" group). Despite no significant differences in ejection fraction or severity of illness, the median MPI at enrollment in the "improved" group was higher than baseline values in the "worsened" group (p = 0.005). A worsening MPI over the 24-hour study interval was associated with increased mortality at 90 days (p = 0.04), which remained significant (hazard ratio 3.72; 95% confidence interval 1.12-12.41; p = 0.03) after adjusting for severity of illness (Acute Physiology and Chronic Health Evaluation II score), intravenous fluids, and vasopressor use.
In patients admitted to the intensive care unit with a diagnosis of severe sepsis or septic shock, a worsening MPI during the first 24 hours after intensive care unit admission was associated with higher 90-day mortality.
In this international, randomised, double-blind, double-dummy, phase 3 trial, we recruited patients aged 16 years or older with severe influenza admitted to 97 hospitals from 26 countries. We randomly assigned patients (1:1:1 stratified by symptom onset ≤4 days or 5-6 days) to receive 300 mg or 600 mg intravenous zanamivir, or standard-of-care (75 mg oral oseltamivir) twice a day for 5-10 days; patients were followed up for 28 days. The randomisation schedule, including stratification, was generated using GlaxoSmithKline's RandAll software. Patients, site study staff, and sponsor were masked to study treatment. The primary endpoint was time to clinical response-a composite of vital sign stabilisation and hospital discharge-in the influenza-positive population. The trial was powered to show an improvement of 1·5 days or greater with 600 mg intravenous zanamivir. Pharmacokinetic, safety, and virology endpoints were also assessed. This trial is registered with ClinicalTrials.gov, number NCT01231620.
Between Jan 15, 2011, and Feb 12, 2015, 626 patients were randomly assigned to receive 300 mg intravenous zanamivir (n=201), 600 mg intravenous zanamivir (n=209), or 75 mg oral oseltamivir (n=205) twice a day; 11 patients discontinued the study before receiving any study treatment. 488 (78%) of 626 patients had laboratory-confirmed influenza. Compared with a median time to clinical response of 5·14 days in the 600 mg intravenous zanamivir group, the median time to clinical response was 5·87 days (difference of -0·73 days, 95% CI -1·79 to 0·75; p=0·25) in the 300 mg intravenous zanamivir group and 5·63 days (difference of -0·48 days, 95% CI -2·11 to 0·97; p=0·39) in the oseltamivir group. Four patients with influenza A/H1N1pdm09 in the oseltamivir group developed H275Y resistance mutations. Adverse events were reported in 373 (61%) of treated patients and were similar across treatment groups; the most common adverse events (300 mg intravenous zanamivir, 600 mg intravenous zanamivir, oseltamivir) were diarrhoea (10 [5%], 15 [7%], 14 [7%]), respiratory failure (11 [5%], 14 [7%], 11 [5%]), and constipation (7 [3%], 13 [6%], 10 [5%]). 41 (7%) treated patients died during the study (15 [7%], 15 [7%], 11 [5%]); the most common causes of death were respiratory failure and septic shock.
Time to clinical response to intravenous zanamivir dosed at 600 mg was not superior to oseltamivir or 300 mg intravenous zanamivir. All treatments had a similar safety profile in hospitalised patients with severe influenza.
Enterococci are Gram-positive cocci which are inhabitants of the human gastrointestinal tract. Even though enterococci can cause serious infections in multiple sites, they are a rare cause of pneumonia. We present a case of disseminated strongyloides with vancomycin-resistant enterococcus causing pneumonia. The patient had a complicated course with respiratory failure and septic shock. He died eventually due to his severe infections. After a literature review, we could not find a similar case of coinfection of disseminated strongyloides with vancomycin-resistant enterococcus pneumonia in immune-compromised patients.