scholarly journals Iatrogenic peripheral nerve injury: a guide to management for the orthopaedic limb surgeon

2021 ◽  
Vol 6 (8) ◽  
pp. 607-617
Author(s):  
Timothy Bage ◽  
Dominic M. Power
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Trauma Surgery ◽  
Limb Lengthening ◽  
Nerve Blocks ◽  
True Incidence ◽  
Direct Injury ◽  
Arthroplasty Surgery

Nerves may be inadvertently injured during trauma surgery due to distorted anatomy, traction applied to a limb, soft tissue retraction, by power tools, instrumentation and from compartment syndrome. Elective orthopaedic surgery has additional risks of joint dislocation for arthroplasty surgery, limb lengthening, thermal injury from cement and direct injury from peripheral nerve blocks. The true incidence is unknown, and many cases are diagnosed as neurapraxia with the expectation of a full and timely recovery without the need for intervention. The incorrect assignation of a neurapraxia diagnosis may delay treatment for a higher grade of injury and in addition fails to recognize that a diagnosis of neurapraxia should be made with caution and a commitment to regular clinical review. Untreated, a neurapraxia can deteriorate and result in axonopathy. The failure to promptly diagnose such a nerve injury and instigate treatment may result in further deterioration and expose the clinician to medicolegal challenge. The focus of this review is to raise awareness of iatrogenic peripheral nerve injuries in orthopaedic limb surgery, the importance of regular clinical examination, the role of investigations, timing and nature of interventions and also to provide a guide to when onward referral to a specialist peripheral nerve injury unit is recommended. Cite this article: EFORT Open Rev 2021;6:607-617. DOI: 10.1302/2058-5241.6.200123

Role of Histamine H3 and H4 Receptors in Mechanical Hyperalgesia following Peripheral Nerve Injury

2007 ◽  
Vol 14 (6) ◽  
pp. 317-325 ◽  
Author(s):  
Fiona M. Smith ◽  
Hila Haskelberg ◽  
David J. Tracey ◽  
Gila Moalem-Taylor
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Mechanical Hyperalgesia

scholarly journals Role of the Excitability Brake Potassium Current I KD in Cold Allodynia Induced by Chronic Peripheral Nerve Injury

2017 ◽  
Vol 37 (12) ◽  
pp. 3109-3126 ◽  
Author(s):  
Alejandro González ◽  
Gonzalo Ugarte ◽  
Carlos Restrepo ◽  
Gaspar Herrera ◽  
Ricardo Piña ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Potassium Current ◽  
Cold Allodynia

scholarly journals Role of IL-10 in Resolution of Inflammation and Functional Recovery after Peripheral Nerve Injury

2015 ◽  
Vol 35 (50) ◽  
pp. 16431-16442 ◽  
Author(s):  
B. Siqueira Mietto ◽  
A. Kroner ◽  
E. I. Girolami ◽  
E. Santos-Nogueira ◽  
J. Zhang ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Functional Recovery ◽  
Peripheral Nerve Injury ◽  
Resolution Of Inflammation

Increase of interleukin-6 mRNA in the spinal cord following peripheral nerve injury in the rat: potential role of IL-6 in neuropathic pain

1998 ◽  
Vol 62 (2) ◽  
pp. 228-235 ◽  
Author(s):  
Janice L Arruda ◽  
Raymond W Colburn ◽  
Amy J Rickman ◽  
Maria D Rutkowski ◽  
Joyce A DeLeo
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Interleukin 6 ◽  
Peripheral Nerve Injury ◽  
Potential Role

FLEXOR TENDON AND PERIPHERAL NERVE REPAIR

Hand Surgery ◽  
2002 ◽  
Vol 07 (01) ◽  
pp. 83-100 ◽  
Author(s):  
Judith A. Bell Krotoski
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Flexor Tendon ◽  
Nerve Repair ◽  
Hand Function ◽  
Tendon Injury ◽  
Finger Movement ◽  
Flexor Tendon Injury ◽  
Direct Injury

Any restoration of hand function following tendon and nerve injury has to include the repair or replacement of the hand's ability to perform a great many tasks. It is hard at first to appreciate fully the loss that occurs with flexor tendon injury. With loss of flexor tendons operating at the fingers or thumb, they cannot be fully closed and the hand is impaired for grasp and release as it interfaces with objects. But, sensibility can also be compromised from tendon injury even without direct injury to nerve, as object recognition in the absence of vision requires finger movement. When peripheral nerve injury is combined with flexor tendon injury, sensibility is directly impaired. There is a loss in the sense of finger or thumb position, pain, temperature, and touch/pressure recognition, in addition to the tendon injury.

scholarly journals SIRT6 inhibition delays peripheral nerve recovery by suppressing migration, phagocytosis and M2-polarization of macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying Zou ◽  
Jiaqi Zhang ◽  
Jiawei Xu ◽  
Lanya Fu ◽  
Yizhou Xu ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Macrophage Polarization ◽  
Nerve Degeneration ◽  
M2 Polarization ◽  
M1 Macrophage ◽  
Nerve Recovery

Abstract Background Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family. Prior evidences suggested that the anti-inflammatory function of SIRT6 after spinal cord and brain injury, and it plays a crucial role in macrophages polarization of adipose tissue and skin. However, the role of SIRT6 in macrophages involved peripheral nerve injury is still unknown. Given the prominent role of macrophages in peripheral nerve recovery, we aim to investigate the role of SIRT6 in the regulation of phenotypes shift and functions in macrophages after peripheral nerve injury. Results In the present study, we first identified a significant increase of SIRT6 expression during nerve degeneration and macrophages phagocytosis. Next, we found nerve recovery was delayed after SIRT6 silencing by injected shRNA lentivirus into the crushed sciatic nerve, which exhibited a reduced expression of myelin-related proteins (e.g., MAG and MBP), severer myoatrophy of target muscles, and inferior nerve conduction compared to the shRNA control injected mice. In vitro, we found that SIRT6 inhibition by being treated with a selective inhibitor OSS_128167 or lentivirus transfection impairs migration and phagocytosis capacity of bone marrow-derived macrophages (BMDM). In addition, SIRT6 expression was discovered to be reduced after M1 polarization, but SIRT6 was enhanced after M2 polarization in the monocyte-macrophage cell line RAW264.7 and BMDM. Moreover, SIRT6 inhibition increased M1 macrophage polarization with a concomitant decrease in M2 polarization both in RAW264.7 and BMDM via activating NF-κB and TNF-α expression, and SIRT6 activation by UBCS039 treatment could shift the macrophages from M1 to M2 phenotype. Conclusion Our findings indicate that SIRT6 inhibition impairs peripheral nerve repair through suppressing the migration, phagocytosis, and M2 polarization of macrophages. Therefore, SIRT6 may become a favorable therapeutic target for peripheral nerve injury.

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