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Epidural abscesses.

Abstract

Until recently epidural abscess was considered a rare, almost theoretical, complication of central nerve block, but anecdotal reports suggest that this is no longer the case. Thus a review of the risk factors, pathogenesis, clinical features and outcome of this condition is appropriate, the primary aim being to make recommendations on best anaesthetic practice to minimize the risk of this serious complication. A search of EMBASE(c), PUBMED(c) and MEDLINE(c) databases from 1966 to September 2004 was performed using several strategies, supplemented by reference list screening. Spontaneous epidural abscess is rare, accounting for 0.2-1.2 cases per 10,000 hospital admissions per year. Estimates of the incidence after central nerve block vary from 1:1,000 to 1:100,000. Risk factors (compromised immunity, spinal column disruption, source of infection) are present in the majority of patients, whether the condition is spontaneous or associated with central nerve block. Presentation is vague, fever and back pain usually preceding neurological deficit. Diagnosis requires a high index of suspicion and modern imaging techniques. Treatment involves early surgical drainage to prevent permanent deficit and high dose parenteral antibiotics chosen with bacteriological advice. Primary prevention depends on proper use of full aseptic precautions. Epidural abscess can be a catastrophic consequence of central nerve block. Early diagnosis will minimize permanent damage, but primary prevention should be the aim. There is a need for a large survey to indicate the true incidence to better inform the risk-benefit ratio for central nerve block.

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BibTeXRIS

S Grewal, G Hocking, J A W Wildsmith. 2006-01-23. Epidural abscesses.. https://doi.org/10.1093/bja%2Fael006

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Local anesthetics.

Local anesthetics are used broadly to prevent or reverse acute pain and treat symptoms of chronic pain. This chapter, on the analgesic aspects of local anesthetics, reviews their broad actions that affect many different molecular targets and disrupt their functions in pain processing. Application of local anesthetics to peripheral nerve primarily results in the blockade of propagating action potentials, through their inhibition of voltage-gated sodium channels. Such inhibition results from drug binding at a site in the channel's inner pore, accessible from the cytoplasmic opening. Binding of drug molecules to these channels depends on their conformation, with the drugs generally having a higher affinity for the open and inactivated channel states that are induced by membrane depolarization. As a result, the effective potency of these drugs for blocking impulses increases during high-frequency repetitive firing and also under slow depolarization, such as occurs at a region of nerve injury, which is often the locus for generation of abnormal, pain-related ectopic impulses. At distal and central terminals the inhibition of voltage-gated calcium channels by local anesthetics will suppress neurogenic inflammation and the release of neurotransmitters. Actions on receptors that contribute to nociceptive transduction, such as TRPV1 and the bradykinin B2 receptor, provide an independent mode of analgesia. In the spinal cord, where local anesthetics are present during epidural or intrathecal anesthesia, inhibition of inotropic receptors, such as those for glutamate, by local anesthetics further interferes with neuronal transmission. Activation of spinal cord mitogen-activated protein (MAP) kinases, which are essential for the hyperalgesia following injury or incision and occur in both neurons and glia, is inhibited by spinal local anesthetics. Many G protein-coupled receptors are susceptible to local anesthetics, with particular sensitivity of those coupled via the Gq alpha-subunit. Local anesthetics are also infused intravenously to yield plasma concentrations far below those that block normal action potentials, yet that are frequently effective at reversing neuropathic pain. Thus, local anesthetics modify a variety of neuronal membrane channels and receptors, leading to what is probably a synergistic mixture of analgesic mechanisms to achieve effective clinical analgesia.

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