The carbon footprint of the operating room related to infection prevention measures: a scoping review.

BACKGROUND: Infection prevention measures are widely used in operating rooms (ORs). However, the extent to which they are at odds with ambitions to reduce the health sector's carbon footprint remains unclear. AIM: To synthesize the evidence base for the carbon footprint of commonly used infection prevention measures in the OR, namely medical devices and instruments, surgical attire and air treatment systems. METHODS: A scoping review of the international scientific literature was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. The search was performed in PubMed and Google Scholar. Articles published between 2010 and June 2021 on infection prevention measures, their impact on the health sector's carbon footprint, and risk for surgical site infections (SSIs) were included. FINDINGS: Although hospitals strive to reduce their carbon footprint, many infection prevention measures result in increased emissions. Evidence suggests that the use of disposable items instead of reusable items generally increases the carbon footprint, depending on sources of electricity. Controversy exists regarding the correlation between air treatment systems, contamination and the incidence of SSIs. The literature indicates that new air treatment systems consume more energy and do not necessarily reduce SSIs compared with conventional systems. CONCLUSION: Infection prevention measures in ORs can be at odds with sustainability. The use of new air treatment systems and disposable items generally leads to significant greenhouse gas emissions, and does not necessarily reduce the incidence of SSIs. Alternative infection prevention measures with less environmental impact are available. Implementation could be facilitated by embracing environmental impact as an additional dimension of quality of care, which should change current risk-based approaches for the prevention of SSIs.

[Steps for reducing the carbon footprint of the operating room]. / Manieren om de CO2-voetafdruk van de OK te verlagen.

The healthcare sector contributes significantly to global warming due to carbon emissions; this sector is, therefore, partially responsible for the negative effects of climate change on public health. Carbon emissions by the healthcare sector amount to 7% of the total carbon footprint of the Netherlands. It is anticipated that measures to reduce carbon emissions in the operating room (OR) can make an important contribution to reducing carbonemissions in the hospital as a whole. The most important elements contributing to the carbon footprint of the OR are: energy consumption for heating, ventilation and air conditioning (HVAC); the emission of inhalation anaesthetics; the purchase of materials and equipment; and waste production. Direct carbon emissions by the OR can be reduced through the use of sustainable energy and setback of the HVAC outside office hours. Anaesthetists can dramatically reduce the carbon footprint of the OR by choosing for intravenous anaesthetics instead of inhalation anaesthetics. Indirect carbon emissions and waste production by the OR can be reduced through circular procurement, choosing reusable over disposable products and recycling.

Sevoflurane based anaesthesia does not affect already impaired cerebral autoregulation in patients with type 2 diabetes mellitus.

BACKGROUND: The baroreflex regulates arterial blood pressure (BP). During periods when blood pressure changes, cerebral blood flow (CBF) is kept constant by cerebral autoregulation (CA). In patients with diabetes mellitus (DM), low baroreflex sensitivity (BRS) is associated with impaired CA. As sevoflurane-based anaesthesia obliterates BRS, we hypothesised that this could aggravate the already impaired CA in patients with DM resulting in a 'double-hit' on cerebral perfusion leading to increased fluctuations in blood pressure and cerebral perfusion. METHODS: On the day before surgery, we measured CBF velocity (CBFV), heart rate, and BP to determine BRS and CA efficacy (CBFVmean-to-BPmean-phase lead) in 25 patients with DM and in 14 controls. During the operation, BRS and CA efficacy were determined during sevoflurane-based anaesthesia. Patients with DM were divided into a group with high BRS (DMBRS↑) and a group with low BRS (DMBRS↓). Values presented are median (inter-quartile range). RESULTS: Preoperative vs intraoperative BRS was 6.2 (4.5-8.5) vs 1.9 (1.1-2.5, P<0.001) ms mm Hg-1 for controls, 5.8 (4.9-7.6) vs 2.7 (1.5-3.9, P<0.001) ms mm Hg-1 for patients with DMBRS↑, and 1.9 (1.5-2.8) vs 1.1 (0.6-2.5, P=0.31) ms mm Hg-1 for patients with DMBRS↓. Preoperative vs intraoperative CA efficacy was 43° (38-46) vs 43° (38-51, P=0.30), 44° (36-49) vs 41° (32-49, P=0.52), and 34° (28-40) vs 30° (27-38, P=0.64) for controls, DMBRS↑, and DMBRS↓ patients, respectively. CONCLUSIONS: In diabetic patients with low preoperative BRS, preoperative CA efficacy was also impaired. In controls and diabetic patients, CA was unaffected by sevoflurane-based anaesthesia. We therefore conclude that sevoflurane-based anaesthesia does not contribute to a 'double-hit' phenomenon on cerebral perfusion. CLINICAL TRIAL REGISTRATION: NCT 03071432.

Novel method for intraoperative assessment of cerebral autoregulation by paced breathing.

Background: Cerebral autoregulation (CA) is the mechanism that maintains constancy of cerebral blood flow (CBF) despite variations in blood pressure (BP). Patients with attenuated CA have been shown to have an increased incidence of peri-operative stroke. Studies of CA in anaesthetized subjects are rare, because a simple and non-invasive method to quantify the integrity of CA is not available. In this study, we set out to improve non-invasive quantification of CA during surgery. For this purpose, we introduce a novel method to amplify spontaneous BP fluctuations during surgery by imposing mechanical positive pressure ventilation at three different frequencies and quantify CA from the resulting BP oscillations. Methods: Fourteen patients undergoing sevoflurane anaesthesia were included in the study. Continuous non-invasive BP and transcranial Doppler-derived CBF velocity (CBF V ) were obtained before surgery during 3 min of paced breathing at 6, 10, and 15 bpm and during surgery from mechanical positive pressure ventilation at identical frequencies. Data were analysed using frequency domain analysis to obtain CBF V -to-BP phase lead as a continuous measure of CA efficacy. Group averages were calculated. Values are means ( sd ), and P <0.05 was used to indicate statistical significance. Results: Preoperative vs intraoperative CBF V -to-BP phase lead was 43 (9) vs 45 (8)°, 25 (8) vs 24 (10)°, and 4 (6) vs -2 (12)° during 6, 10, and 15 bpm, respectively (all P =NS). Conclusions: During surgery, cerebral autoregulation indices were similar to values determined before surgery. This indicates that CA can be quantified reliably and non-invasively using this novel method and confirms earlier evidence that CA is unaffected by sevoflurane anaesthesia. Clinical trial registration: NCT03071432.

Cerebral oxygenation during changes in vascular resistance and flow in patients on cardiopulmonary bypass - a physiological proof of concept study.

Despite a rise in blood pressure, cerebral oxygenation decreases following phenylephrine administration, and we hypothesised that phenylephrine reduces cerebral oxygenation by activating cerebral α1 receptors. We studied patients on cardiopulmonary bypass during constant flow. Phenylephrine raised mean arterial pressure (α1 -mediated) from mean (SD) 69 (8) mmHg to 79 (8) mmHg; p = 0.001, and vasopressin raised mean arterial pressure (V1 mediated) from 69 (8) mmHg to 83 (6) mmHg; p = 0.001. Both drugs elicited a comparable decrease in cerebral oxygenation from 61 (7)% to 60 (7)%; p = 0.023 and 61 (8)% to 59 (8)%; p = 0.022, respectively. This implies that after phenylephrine or vasopressin administration, cerebral oxygenation declines as a result of cerebral vasoconstriction, due to either both cerebral α1 and V1 receptors being equipotentially activated or to an intrinsic myogenic mechanism of cerebral vasculature in reaction to blood pressure elevation.