Hair removal with a clipper and microbial colonisation prior to knee arthroplasty: a randomised controlled trial.

Background: Despite the widely reported success of knee arthroplasty, studies show that 1.6-3 % of patients undergo revision within the first postoperative year predominantly due to infection. Preoperative skin preparation may potentially decrease the bacterial load and consequently, the risk of periprosthetic joint infections. The effects of hair removal on prosthetic joint infection are inconsistent. Our primary aim was to investigate if hair removal with a clipper influenced skin colonisation and bacterial composition. Methods: Forty Caucasian male participants who were planned to undergo knee arthroplasty, (mean age 63.8 years), were included. Patients were randomised to hair removal in a within-person study design. As a control, the opposite leg of the patient was used. Swabs were collected prior to hair removal (baseline), immediately after hair removal (Day 0), and with follow-up after one and seven days. Results: The intervention showed significant decrease in mean log colony-forming units per. cm2 from baseline 2.97 to 2.67 (P<0.01) immediately after hair removal and sustained at Day 1 (P=0.01). At Day 7, the mean was non-significant compared to baseline. The control group did not show any decrease of skin microbiota at follow-up on Day 0, 1 or 7.No significant differences within the bacterial composition were found between the intervention and control leg at baseline among the six most prevalent detected bacterial species: Staphylococcus epidermidis, Micrococcus luteus, S. hominis, S. capitis, S. haemolyticus and S. aureus. The study did not find any changes in the bacterial composition over time. Conclusion: Hair removal with a clipper within 24 hours prior to surgery causes a significant non-selective reduction in skin colonisation.

OXYGEN CONSUMPTION AS AN EARLY WARNING SYSTEM IN THE CRITICALLY ILL.

ABSTRACT: Introduction: In this study, we assessed whether changes in oxygen consumption (VO 2 ) and other metabolic parameters could be used as an early warning system for detecting clinical deterioration in mechanically ventilated patients. Methods: This was a prospective cohort study of adult patients requiring mechanical ventilation between February 2016 and March 2019. We looked for changes in VO 2 , carbon dioxide production (VCO 2 ), respiratory quotient (RQ), and end-tidal carbon dioxide (EtCO 2 ), occurring prior to clinical deterioration. Clinical deterioration was predefined as a requirement of vasopressor, an increase in serum lactate by 20% where at least one value was above 3 mmol/L, or a decrease in hemoglobin by 20% in the 4 hours prior to clinical deterioration. Results A total of 141 patients were included. There were no detectable changes in VO 2 , VCO 2 , and EtCO 2 within the 4 hours prior to any clinical deterioration. RQ increased significantly within the 4 hours prior to an increase in lactate as compared with no increase in lactate, but there were no detectable changes prior to other clinical deteriorations. Conclusions RQ has the potential to be an early marker of tissue hypoperfusion or mitochondrial dysfunction. However, future studies are necessary to evaluate the use of RQ as a bedside monitor in critical care settings.

Thermoregulation in post-cardiac arrest patients treated with targeted temperature management.

OBJECTIVE: Evaluate the relationship between heat generation during rewarming in post-cardiac arrest patients receiving targeted temperature management (TTM) as a surrogate of thermoregulatory ability and clinical outcomes. METHODS: This is a prospective observational single-centre study conducted at an urban tertiary-care hospital. We included post-cardiac arrest adults who received TTM via surface cooling device between April 2018 and June 2019. RESULTS: Patient heat generation was calculated by multiplying the inverse of the average machine water temperature with time to rewarm to 37 °C and standardized in two ways to account for target temperature variation: (1) divided by number of degrees between target temperature and 37 °C, and (2) limited to when patient was rewarmed from 36 °C to 37 °C. The primary outcome was poor neurologic status, defined as Cerebral Performance Category (CPC) score 3-5, and the secondary outcome was 30-day survival. Sixty-six patients were included: 45 (68%) had a CPC-score of 3-5 and 23 (35%) were alive at 30 days. Besides initial rhythm and arrest downtime, baseline characteristics were similar between outcomes. Heat generation was not associated with poor neurological outcome (CPC 3-5: 6.6 [IQR: 6.1, 7.4] versus CPC 1-2: 6.6 [IQR: 5.7, 7.6], p = 0.89) or survival at 30 days (non-survivors: 6.6 [IQR: 6.6, 7.4] vs. survivors: 6.6 [IQR: 5.7, 8.0, p = 0.78]). CONCLUSION: Heat generation during rewarming was not associated with neurologic outcomes. However, there was a relationship between poor neurological outcome and higher median water temperatures. Time to rewarm was prolonged in patients with poor neurological outcome.

Ubiquinol (reduced coenzyme Q10) as a metabolic resuscitator in post-cardiac arrest: A randomized, double-blind, placebo-controlled trial.

INTRODUCTION: Ubiquinol (reduced coenzyme Q10) is essential for adequate aerobic metabolism. The objective of this trial was to determine whether ubiquinol administration in patients resuscitated from cardiac arrest could increase physiological coenzyme Q10 levels, improve oxygen consumption, and reduce neurological biomarkers of injury. MATERIALS AND METHODS: This was a randomized, double-blind, placebo-controlled trial in patients successfully resuscitated from cardiac arrest. Patients were randomized to receive enteral ubiquinol (300 mg) or placebo every 12 h for up to 7 days. The primary endpoint was total coenzyme Q10 plasma levels at 24 h after enrollment. Secondary endpoints included neuron specific enolase, S100B, lactate, cellular and global oxygen consumption, neurological status, and in-hospital mortality. RESULTS: Forty-three patients were included in the modified intention-to-treat analysis. Median coenzyme Q10 levels were significantly higher in the ubiquinol group as compared to the placebo group at 24 h (441 [IQR, 215-510] ηg/mL vs. 113 [IQR, 94-208] ηg/mL, P < 0.001). Similar results were observed at 48 and 72 h. There were no differences between the two groups in any of the secondary endpoints. Median neuron specific enolase levels were not different between the two groups at 24 h (16.8 [IQR, 9.5-19.8] ηg/mL vs. 8.2 [IQR, 4.3-19.1] ηg/mL, P = 0.61). CONCLUSIONS: Administration of enteral ubiquinol increased plasma coenzyme Q10 levels in post-cardiac arrest patients as compared to placebo. There were no differences in neurological biomarkers and oxygen consumption between the two groups.

Association Between the Oxygen Consumption: Lactate Ratio and Survival in Critically Ill Patients With Sepsis.

INTRODUCTION: Mitochondrial dysfunction leading to impairment of oxygen extraction, referred to as cytopathic hypoxia, contributes to morbidity in sepsis. Oxygen consumption (VO2) may be a useful measure of the severity of cytopathic hypoxia. We monitored VO2 and carbon dioxide production (VCO2) in septic patients and investigated the association with hospital survival. METHODS: We retrospectively identified adult (≥18 years) septic patients from a larger prospective observational cohort of critically ill patients on mechanical ventilation. A gas-exchange monitor recorded continuous VO2 and VCO2 for up to 48 h. We then tested the association of median VO2, VCO2, respiratory quotient (RQ), and the VO2:lactate ratio with survival. RESULTS: A total of 46 septic patients were included in the analysis, of whom 28 (61%) survived. Overall median VO2 was not associated with survival (3.72 mL/kg/min [IQR: 3.39, 4.92] in survivors and 3.42 mL/kg/min [IQR: 2.97, 5.26] in non-survivors, P = 0.12). The overall median VCO2 and RQ were also not associated with survival. Adjusting for age and the presence of shock did not change these results. The VO2:lactate ratio was associated with survival (adjusted OR 2.17 [95% CI 1.12, 4.22] per unit increase in ratio, P = 0.03). The percent change in median VCO2 was 11.6% [IQR: -8.2, 28.7] in survivors compared with -8.3% [IQR: -18.0, 4.7] in non-survivors (P = 0.03). The percent changes in median VO2 and RQ were not different between groups. CONCLUSION: The VO2:lactate ratio was significantly higher in survivors, while there was no association between median VO2 alone and survival. There was a significant difference in change in VCO2 over time between survivors and non-survivors.

Trends in Survival After Pediatric In-Hospital Cardiac Arrest in the United States.

BACKGROUND: Cardiac arrest in hospitalized children is associated with poor outcomes, but no contemporary study has reported whether the trends in survival have changed over time. In this study, we examined temporal trends in survival for pediatric patients with an in-hospital pulseless cardiac arrest and pediatric patients with a nonpulseless cardiopulmonary resuscitation event from 2000 to 2018. METHODS: This was an observational study of hospitalized pediatric patients (≤18 years of age) who received cardiopulmonary resuscitation from January 2000 to December 2018 and were included in the Get With The Guidelines-Resuscitation registry, a United States-based in-hospital cardiac arrest registry. The primary outcome was survival to hospital discharge, and the secondary outcome was return of spontaneous circulation (binary outcomes). Generalized estimation equations were used to obtain unadjusted trends in outcomes over time. Separate analyses were performed for patients with a pulseless cardiac arrest and patients with a nonpulseless event (bradycardia with poor perfusion) requiring cardiopulmonary resuscitation. A subgroup analysis was conducted for shockable versus nonshockable initial rhythms in pulseless events. RESULTS: A total of 7433 patients with a pulseless cardiac arrest and 5751 patients with a nonpulseless event were included for the analyses. For pulseless cardiac arrests, survival was 19% (95% CI, 11%-29%) in 2000 and 38% (95% CI, 34%-43%) in 2018, with an absolute change of 0.67% (95% CI, 0.40%-0.95%; P<0.001) per year, although the increase in survival appeared to stagnate following 2010. Return of spontaneous circulation also increased over time, with an absolute change of 0.83% (95% CI, 0.53%-1.14%; P<0.001) per year. We found no interaction between survival to hospital discharge and the initial rhythm. For nonpulseless events, survival was 57% (95% CI, 39%-75%) in 2000 and 66% (95% CI, 61%-72%) in 2018, with an absolute change of 0.80% (95% CI, 0.32%-1.27%; P=0.001) per year. CONCLUSIONS: Survival has improved for pediatric events requiring cardiopulmonary resuscitation in the United States, with a 19% absolute increase in survival for in-hospital pulseless cardiac arrests and a 9% absolute increase in survival for nonpulseless events between 2000 and 2018. However, survival from pulseless cardiac arrests appeared to have reached a plateau following 2010.

Sepsis, Endocarditis, and Purulent Arthritis due to a Rare Zoonotic Infection with Streptococcus equi Subspecies zooepidemicus.

Streptococcus equi subspecies zooepidemicus (S. zooepidemicus) is mostly known as an opportunistic pathogen found in horses and as a rare human zoonosis. An 82-year-old male, who had daily contact with horses, was admitted in a septic condition. The patient presented with dyspnea, hemoptysis, impaired general condition, and severe pain in a swollen left shoulder. Synovial fluid from the affected joint and blood cultures showed growth of S. equi subsp. zooepidemicus. Transesophageal echocardiography showed a vegetation on the aortic valve consistent with endocarditis. Arthroscopic revision revealed synovitis and erosion of the rotator cuff. Technetium-99m scintigraphy showed intense increased activity in the left shoulder, suspicious of osteitis. The infection was treated with intravenous antibiotics over a period of five weeks, followed by oral antibiotics for another two months. The patient recovered without permanent sequelae.

Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients.

Pseudomonas aeruginosa is the predominant microorganism in chronic lung infection of cystic fibrosis patients. The chronic lung infection is preceded by intermittent colonization. When the chronic infection becomes established, it is well accepted that the isolated strains differ phenotypically from the intermittent strains. Dominating changes are the switch to mucoidity (alginate overproduction) and loss of epigenetic regulation of virulence such as the Quorum Sensing (QS). To elucidate the dynamics of P. aeruginosa QS systems during long term infection of the CF lung, we have investigated 238 isolates obtained from 152 CF patients at different stages of infection ranging from intermittent to late chronic. Isolates were characterized with regard to QS signal molecules, alginate, rhamnolipid and elastase production and mutant frequency. The genetic basis for change in QS regulation were investigated and identified by sequence analysis of lasR, rhlR, lasI and rhlI. The first QS system to be lost was the one encoded by las system 12 years (median value) after the onset of the lung infection with subsequent loss of the rhl encoded system after 17 years (median value) shown as deficiencies in production of the 3-oxo-C12-HSL and C4-HSL QS signal molecules respectively. The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR. Accumulation of mutations in both lasR and rhlR correlated with development of hypermutability. Interestingly, a higher number of mucoid isolates were found to produce C4-HSL signal molecules and rhamnolipids compared to the non-mucoid isolates. As seen from the present data, we can conclude that P. aeruginosa and particularly the mucoid strains do not lose the QS regulation or the ability to produce rhamnolipids until the late stage of the chronic infection.

Silver against Pseudomonas aeruginosa biofilms.

Silver has been recognized for its antimicrobial properties for centuries. Most studies on the antibacterial efficacy of silver, with particular emphasis on wound healing, have been performed on planktonic bacteria. Our recent studies, however, strongly suggest that colonization of wounds involves bacteria in both the planktonic and biofilm modes of growth. The action of silver on mature in vitro biofilms of Pseudomonas aeruginosa, a primary pathogen of chronic infected wounds, was investigated. The results show that silver is very effective against mature biofilms of P. aeruginosa, but that the silver concentration is important. A concentration of 5-10 mug/mL silver sulfadiazine eradicated the biofilm whereas a lower concentration (1 mug/mL) had no effect. The bactericidal concentration of silver required to eradicate the bacterial biofilm was 10-100 times higher than that used to eradicate planktonic bacteria. These observations strongly indicate that the concentration of silver in currently available wound dressings is much too low for treatment of chronic biofilm wounds. It is suggested that clinicians and manufacturers of the said wound dressings consider whether they are treating wounds primarily colonized either by biofilm-forming or planktonic bacteria.