Articles: peripheral-nerve-injuries.
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McCombe and Bogod report on their analysis of 55 medicolegal claims relating to obstetric neuraxial anaesthesia and analgesia.
Why is this important?
Not only is neurological injury the second most common reason for obstetric anaesthetic claims (behind inadequate regional anaesthesia resulting in pain during Caesarean section), the average claim cost is greater.
McCombe and Bogod provide a factful exploration of many of the causes of neurological complications.
Which themes emerged from their analysis?
- Consent, particularly around providing inadequate pre-procedure information of the risk of neurological injury1 and the challenges, medical and legal, to achieving informed consent.
- Nerve injury and it's mechanisms: non-anaesthetic causes2, direct trauma, chemical, and compression (abscess, haematoma).
- Complication recognition & management means timely follow-up and assessment, and maintaining a high index of suspicion for abnormalities. Remember the 4 hour rule: blocks should be regressing 4 hours after the last dose.
Important reminders
The level of spinal cord termination varies a lot among individuals, as does the level of Tuffier's line3. Considering the inaccuracy of spinal level identification by anaesthetists, there is a lot of potential to place a needle higher than expected.
Bottom-line: the intrathecal space should be accessed at the lowest possible level, and "the L2/3 interspace should not be an option."
And never allow chlorhexidine to contaminate gloves, the sterile workspace or neuraxial equipment.
summary
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Noting from NAP3 the risk of nerve injury ranges from, temporary injury 1:1,000, prolonged (>6 months) 1:13,000, to severe (including paralysis) 1:250,000. ↩
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'Obstetric palsy' (pelvic nerve compression) estimated by Bromage as occurring in 1:3000 deliveries; arterial obstruction & ischaemia 1:15,000; AV malformations 1:20,000. A prospective French study found postpartum neuropathy in 0.3%, 84% were femoral, and 69% resolved at 6 weeks. ↩
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Although generally accepted as being at the L4/5 interspace, in up to 50% of people the intercristal line might be at or above L2/3! ↩
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A body of evidence indicates that peripheral nerves have an extraordinary yet limited capacity to regenerate after an injury. Peripheral nerve injuries have confounded professionals in this field, from neuroscientists to neurologists, plastic surgeons, and the scientific community. Despite all the efforts, full functional recovery is still seldom. ⋯ Resourcing to nerve guidance conduits, a variety of methods have been experimentally used to bridge peripheral nerve gaps of limited size, up to 30-40 mm in length, in humans. Herein, we aim to summarize the fundamentals related to peripheral nerve anatomy and overview the challenges and scientific evidences related to peripheral nerve injury and repair mechanisms. The most relevant reports dealing with the use of both synthetic and natural-based biomaterials used in tissue engineering strategies when treatment of nerve injuries is envisioned are also discussed in depth, along with the state-of-the-art approaches in this field.
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Exosomes are extracellular microvesicles implicated in intercellular communication with ability to transfer cargo molecules, including protein, lipids, and nucleic acids, at both close and distant target sites. It has been shown that exosomes are implicated in physiological and pathological processes. In recent years, the interest on exosomes' role in many pain states has increased. ⋯ Specific molecular patterns characterize exosomes' cargo according to the cellular origin, epigenetic modifications, environmental state, and stressor factors. Therefore, the identification of specific cargo's profile associated to pain states may lead to recognize specific pathological states and to consider the use of exosomes as biomarkers of diseases. Furthermore, exosomes' ability to transfer information and their presence in many accessible biological fluids suggest a potential use as novel non-invasive therapeutic tools in pain field.
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Background Acute pain is a warning mechanism that exists to prevent tissue damage, however pain can outlast its protective purpose and persist beyond injury, becoming chronic. Chronic Pain is maladaptive and needs addressing as available medicines are only partially effective and cause severe side effects. There are profound differences between acute and chronic pain. ⋯ On one hand the delivery of neuron-derived miR-21 to macrophages for example, polarises these cells towards a pro-inflammatory/pro-nociceptive phenotype; on the other hand, silencing miR-21 expression in sensory neurons prevents both development of neuropathic allodynia and recruitment of macrophages in the DRG. Immune system mechanisms in the central nervous system In the dorsal horn of the spinal cord, growing evidence over the last two decades has delineated signalling pathways that mediate neuron-microglia communication such as P2X4/BDNF/GABAA, P2X7/Cathepsin S/Fractalkine/CX3CR1, and CSF-1/CSF-1R/DAP12 pathway-dependent mechanisms. Conclusions and implications Definition of the modalities by which neuron and immune cells communicate at different locations of the pain pathway under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction and provides opportunities for novel approaches for the treatment of chronic pain.
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Review Case Reports
Management of large peripheral nerve defects with autografting.
A segmental nerve defect from trauma results in significant loss of function of the extremity, and rarely occurs in isolation. Autografting of the nerve defect is the current gold standard. ⋯ Nerve grafting for segmental nerve injuries continues to be an essential and appropriate treatment.