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Alistair Ross MB FRCS Consultant Orthopaedic Surgeon, Bath, UK Associate Editor The Bone & Joint Journal Cambridge Annual Medico-Legal Conference Peterhouse,Cambridge,2016
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Neurapraxia Axonotmesis Neurotmesis Seddon HJ Three types of nerve injury Brain 1943, 66 (4): 238-283 ἀπραξία : inaction τμησις : a cutting (of)
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Neurapraxia: a non-degenerative lesion of a nerve characterised by a complete or partial failure to propagate an action potential (conduction defect) along the nerve resulting in motor and/or sensory loss.
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Usually caused by compression or ischaemia, resulting in ischaemia of the myelin sheath. Can be reversed if the injurious agent is removed. Nerve remains intact. Wallerian degeneration does not occur.
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Stimulation of the distal segment of the nerve evokes a response. Normal motor action potential expected distal to the site of injury by day 10. Recovers by re-myelination of distal segment Time to recovery: 2-12 weeks
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The assumption that a lesion is a neurapraxia rather than a more severe injury leads to delay in diagnosis and a poorer outcome. A potentially dangerous diagnosis to make particularly in the presence of persistent pain which suggests that the injurious agent is continuing to act. Diagnosis should not be made in the presence of a strong Tinel test which indicates that axons have been ruptured.
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Axonotmesis: disruption of the axon and its myelin sheath. The supporting structures, Schwann cells, endoneurium, perineurium and epineurium, remain intact.
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Usually the result of severe compression or crush. Wallerian degeneration occurs distally and proximally to the closest node of Ranvier. Repair is by a combination of collateral sprouting in lesser injuries and axonal regeneration in more severe injuries. The latter occurs at 1-2mm per day. Time to recovery: 2 to 6 months
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Nerve conduction studies show a loss of conduction in the distal segment 3-4 days after injury (demyelination). Small or absent compound muscle or sensory nerve action potentials (axon loss) EMG studies show fibrillation potentials and sharp waves 2-3 weeks after injury (axon loss). Degree of recovery depends on the age of the patient, the site of injury and the amount of fibrosis that occurs.
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Neurotmesis : the complete disruption of a peripheral nerve by any means.
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Wallerian degeneration occurs distal to the lesion. Nerve conduction studies show a loss of conduction in the distal segment 3-4 days after injury. EMG studies show fibrillation potentials and sharp waves 2-3 weeks after injury. Surgical intervention is required to repair the nerve, whether by direct suture or grafting. Time to recovery 2 to 18 months
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Closed Ischaemia (A/C) Crush / Compression (A/C) Traction Thermal injury Electric shock Vibration Radiation Open Injection Laceration
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…or iatropathic …or iatrogenous …but caused by those treating a patient
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“When a patient enters hospital without a nerve lesion and emerges with one, it is seldom possible to resist an allegation of negligence.” Bonney GLW Iatrogenic injuries of nerves J Bone Joint Surg 1986; 68B: 9-13
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“If there is an incision over the line of a main nerve and if, after operation, there is complete paralysis (including vasomotor and sudomotor paralysis) in the distribution of that nerve, speculation is unnecessary: the nerve has been cut, and there will be no recovery unless it is explored and repaired.” Bonney GLW Iatrogenic injuries of nerves J Bone Joint Surg 1986; 68B: 9-13
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Bonney GLW Iatrogenic injuries of nerves J Bone Joint Surg 1986; 68B: 9-13 “When pressure on a nerve has been followed by partial paralysis in its distribution, but stimulation below the level of the lesion produces a motor response, it is reasonable to assume that there has been a conduction block which will recover.”
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Bonney GLW Iatrogenic injuries of nerves J Bone Joint Surg 1986; 68B: 9-13 “Between these extremes, precise diagnosis is much more difficult.”
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“Failure to make the diagnosis of a nerve injury, and failure to treat that complication of the first surgery, the iatrogenic nerve injury, is as much a cause for concern as the initial injury to the peripheral nerve.” Dellon AL Invited discussion: management strategies for iatrogenic peripheral nerve lesions. Annals of Plastic Surgery 2005,54: 140-42
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Overall incidence unknown NHS Litigation Authority does not specifically record cases under the heading ‘peripheral nerve injury’
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1990 to 1998 722 consecutive cases of peripheral nerve injury 126 iatrogenic (17.5%) Usually resulting from orthopaedic surgery, trauma or hand surgery ‘Lumps and bumps’ surgery Kretschmer T et al Evaluation of iatrogenic lesions in 722 surgically treated cases of peripheral nerve trauma J Neurosurg 94:905–912, 2001
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Adequate outcome data available for 97/126 patients Results: Very good: 24% Good: 46% Unchanged: 26% Worse: 4% Kretschmer T et al Evaluation of iatrogenic lesions in 722 surgically treated cases of peripheral nerve trauma J Neurosurg 94:905–912, 2001
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1991 to 1998 612 cases of iatrogenic PNI 291 subsequently explored 144 the subject of litigation Khan R & Birch R Iatropathic injuries of peripheral nerves J Bone Joint Surg 2001, 83B(7); 1145-1148
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Excision of tumour or cyst 67 Lymph-node biopsy 52 Internal fixation of fracture 48 Varicose vein/arterial surgery 20 Carpal tunnel decompression 18 Shoulder stabilisation 16 Total 231
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Orthopaedics 174 General surgery 70 Vascular surgery 11 Obs / Gynae 9 Plastic surgery 7 Cardiothoracic 5 ENT surgery 5 Anaesthetics 4 Neurosurgery 4 Maxillofacial surgery 2 Total 291
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Defined as a new (within 48 hours) sensory and/or motor deficit in any patient who had been sedated or anaesthetised Injuries as a result of the surgical procedure itself excluded Overall incidence: 0.03% (112 / 380,680 ops) Welch MB et al Perioperative Peripheral Nerve Injuries. A Retrospective Study of 380,680 Cases during a 10-year Period at a Single Institution Anesthesiology 2009; 111:490–7
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Most commonly affected nerves: Ulnar (28%) Brachial plexus (20%) Lumbosacral nerve root (16%) Spinal cord (13%)
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Poor padding and positioning of limbs Needle trauma secondary to regional anaesthesia Haematoma surrounding a nerve Local anaesthetic agents: toxicity and direct damage from intraneural injection
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Pre-existing disease Diabetes Smoking Hypertension Pre-existing neuropathy Perioperative problems Hypovolaemia, dehydration, hypotension, Hypoxaemia, electrolyte disturbance & hypothermia
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Bruner's ten rules for the safe use of tourniquet (Modified by Braithwaite and Klenerman J Med Def Unions 1996;12:14-15)
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Diagnosis is the responsibility of the treating clinician. Nerve repair is the business of a sub-specialist.
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The earlier a peripheral nerve injury is diagnosed and treated the better Ease of recognition of injury Ease with which the nerve stumps can be mobilised and approximated Lack of scarring and distortion of the anatomy Best results achieved by early direct nerve repair
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A delay of two months halves the number of axons crossing a repair and halves their rate of growth. Further deterioration occurs with longer delay. Motor end plate loss progresses even after repair and is near total after one year (for a proximal repair). Central cord changes also progress prior to repair and become less reversible with time. British Orthopaedic Association ‘Blue Book’ 2011
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If complete or partial laceration to nerve identified at operation (whether the result of trauma or iatrogenic injury): Trained nerve surgeon: primary epineural suture. Untrained surgeon: attempt to oppose ends; gentle mobilisation of nerve if necessary; tag nerve end/s with coloured epineural sutures.
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Clear, accurate documentation of the injury and action taken. Prompt discussion with, and referral to, a nerve surgeon. Discussion with/explanation to patient Accurate early postoperative assessment and documentation of neurological deficit
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If patient found to have neurological deficit postoperatively: Clear, accurate documentation of neurological deficit Inform patient of possible nerve injury Discussion with/referral to nerve surgeon
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If patient found to have neurological deficit postoperatively: At this stage it is unclear of the nature of the lesion If the nerve is thought to have been divided (cf Bonney) : re-explore with a view to repair If not, EMG and NCS at three weeks
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Clinical evidence of neurotmesis Failure of recovery from presumed axonotmesis at the predicted time Deterioration of lesion while under observation Persistent, intractable pain
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Establish diagnosis Relieve pain Improve function
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Baseline study (0–7 days) Usually unnecessary Can only determine whether or not a nerve has been injured, not the degree of injury Baseline for later comparison Documents nerve continuity with presence of voluntary motor units on EMG NB. If fibrillation potentials or sharp waves are seen at this stage, this implies pre-existing disease/injury After: Quan.D. & Bird SJ Nerve Conduction Studies and Electromyography in the Evaluation of Peripheral Nerve Injuries The University of Pennsylvania Orthopaedic Journal 12: 45–51, 1999
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Initial study (10–21 days) Distinguishes lesions with predominant demyelination from those with substantial axonal loss Assesses extent of axonal loss (reduced CMAP amplitude and number of motor units recruited with maximum effort) Follow-up study (3–6 months) Documents extent of reinnervation in markedly weak muscles If necessary, intraoperative studies assess presence of axonal regeneration through the injured segment
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Clinical improvement on presentation Prolonged delay in presentation Palliative treatment preferred Pain relief possible by non-operative means (Outstanding claims for compensation)
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Inadequate informed consent Avoidable damage to nerves/nerves Delay in diagnosis / missed diagnosis Delay in referral Delay in treatment Inappropriate treatment
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Now subject to Montgomery Should be discussed in detail if the proposed operation puts a named nerve at more than a remote risk of damage e.g.: Excision of lump from posterior triangle of neck Fracture fixation / removal of metalwork Discectomy / spinal decompression Excision of lump from or close to a nerve Etc. Discussion should be clearly recorded
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“It must be accepted that despite careful surgery nerve injury during operation may occur. Recognition and prompt remedial action after the event are the keys.” British Orthopaedic Association ‘Blue Book’ 2011
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Properly informed consent more important than ever A thorough knowledge of the local anatomy reduces the risk of inadvertent nerve damage Identify any PNI promptly Document neurology accurately Discuss situation with patient Discuss with / refer to an expert early
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Inadequate consent Avoidable damage to trunk / sensory nerves Delay in diagnosis /missed diagnosis Delay in referral to expert Delay in treatment Inappropriate treatment
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