This growing collection of articles focuses on the evidence and expert guidance relating to the use of personal protective equipment (PPE) and the SARS-CoV-2 / COVID pandemic, with specific focus on PPE use by anaesthesiologists and anaesthetists.
More articles can found found via the PPE topic index.
What we know:
- Hospitals are frequent sources of outbreaks, among both staff, patients and the wider community.
- The quality of PPE evidence is low. Most evidence must be contextualised in consideration of expert opinion, and of the similarities between SARS-CoV-2 and SARS (SARS-CoV-1), MERS and influenza.
- Droplet-vs-airborne spread is a conceptual simplification and not a simple dichotomy. It is best understood as a spectrum of transmission risk.
- Time-exposed may be a more important consideration, especially in indoor, poorly ventilated spaces.
- PPE supply is globally limited, and so a pragmatic approach must be taken to its use, considering individual risk scenarios.
- Training, simulation and fit testing are critical for effective use of PPE.
- There are specific steps in the PPE donning & doffing workflow that are frequently associated with breaches exposing HCWs to infection. These require extra attention.
- Beyond cost, increasingly complex PPE (eg. PAPR, hoods, intubation boxes etc.) also increase the opportunity for PPE failure and exposure if users have not had adequate training in their use, and some PPE has been demonstrated to make intubation more difficult.
- The superiority of N95/P2 respirator masks over standard surgical masks for personal protection is unclear and unproven.
- Remifentanil infusions above 0.20-0.25 μg/kg/min are associated with hyperalgesia (OIH = Opioid Induced Hyperalgesia) and tolerance (AOT = Acute Opioid Tolerance) respectively.
- Some of these effects can be mitigated by multimodal analgesia (notably ketamine), and possibly by gradual weaning of a remifentanil infusion.
- The findings have been predominately identified in rats and volunteer human studies. The clinical and longterm significance is still uncertain.
- Although OIH and AOT arise from different physiological mechanisms, they are clinically difficult (if not impossible) to differentiate.
- The clinical priority for management is prevention.
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