Anesthesiology
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Review
Presumed β-Lactam Allergy and Cross-reactivity in the Operating Theater: A Practical Approach.
- β-lactam allergy, particularly penicillin allergy is the most common perioperative patient-reported sensitivity, in up to 35% of patients.
- Unneccessary switching to non-β-lactams for surgical prophylaxis is not cost-free, and is contributing to the rise of c. difficile and vancomycin-resistant Enterococcus (VRE).
Patient history of penicillin allergy is of variable quality, and often does not allow the allergy to be ruled-out.
Step 1 – differentiate drug side effects from allergy. Isolated nausea, vomiting or diarrhoea are usually side effects.
Step 2 – identify the type of hypersensitivity.
- Most drug reactions are Type 4 (T-cell mediated), delayed from 2 hours to days after exposure. Mostly benign cutaneous symptoms (eg. rash) that do not necessarily require avoiding future β-lactam exposure, except in the case of Stevens-Johnson syndrome.
- Type 1 (IgE-mediated) hypersensitivities are immediate (minutes to 2 hours) but less common, causing urticaria, angioedema and/or anaphylaxis. Future exposure should be avoided.
- Type 2 (cytotoxic) and Type 3 (immune complex) are much less common, and present with more serious, though delayed, reactions (days to weeks).
Take home: Mild symptoms (eg. rash developing more than 2h after exposure) probably do not require β-lactam avoidance. If there is a history of moderate or severe reaction, then avoiding all β-lactams is wise.
Of interest: Although R1 side-chain similarity is the main contributor to penicillin-cephalosporin cross-reactivity, importantly, 1st generation cephazolin has a different R1 side-chain and has been reported to not cross-react. Other cephalosporins share side-chains with specific penicillins.
Finally, stop giving IV test doses. It makes no sense from a safety point of view and offers no useful information.
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Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. ⋯ Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.
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WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Traumatic brain injury induces cellular proliferation in the hippocampus, which generates new neurons and glial cells during recovery. This process is regulated by N-methyl-D-aspartate-type glutamate receptors, which are inhibited by ketamine. The authors hypothesized that ketamine treatment after traumatic brain injury would reduce hippocampal cell proliferation, leading to worse behavioral outcomes in mice. ⋯ Ketamine alters hippocampal cell proliferation after traumatic brain injury. Surprisingly, these changes were associated with improvement in a neurogenesis-related behavioral recall task, suggesting a possible benefit from ketamine administration after traumatic brain injury in mice. Future studies are needed to determine generalizability and mechanism.