Head Injury & Peripheral Nerve Injury
Essam Elgamal MS FRCS(SN) Assistant Professor & Consultant Neurosurgery Division
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Head Injury
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Trauma is the most common cause of mortality in people <45 years. Head injury is the highly weighted predictor of outcome.
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Epidemiology
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Incidence:
200-300, hospital admission, per 100,000 population per year
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>50% RTA 20% moderate to severe (GCS 3-13)
has fallen from 50% to below 30% in the last 20 years (safety belts, air bags)
Mortality:
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Pathophysiology
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characterised by stereotypic pattern at a cellular level. Primary injury: damage caused by the initial impact or event. (irreversible) Secondary injury: sometimes later
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Stages of brain damage:
1) primary damage, at the moment of injury,
contusions lacerations Intracranial haemorrhage diffuse axonal injury
2) secondary damage, include
intracranial haemorrhage hypoxic brain damage brain swelling infection (ICP)
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Grading Head injury
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Mild Moderate Severe
GCS:14-15 GCS:9-13 GCS:3-8
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GCS
Eye opening Spontaneous to speech to pain none 4 3 2 1 Verbal response orientated confused words sounds none 5 4 3 2 1 Motor response obeys commands 6 localization 5 flexion 4 abnormal flexion 3 extension 2 none 1
GCS = 15 fully conscious,
Coma = GCS < 9
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Examination
Evidence of skull base fracture: n Raccoon eyes
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Examination
Evidence of skull base fracture: n Raccoon eyes n Battle’s sign
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Examination
Evidence of skull base fracture: n Raccoon eyes n Battle’s sign n CSF rhinorrhoea/ototorrhoea n Brain matter
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Examination
Facial Fracture: n LeFort fracture
- Lefort I: thru floor of maxillary sinus - Lefort II: thru maxillary sinus, pyramidal. - Lefort III: craniofacial dislocation
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Examination
Facial Fracture: n LeFort fracture
- Lefort I: thru floor of maxillary sinus - Lefort II: thru maxillary sinus, pyramidal. - Lefort III: craniofacial dislocation
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Examination
Facial Fracture: n LeFort fracture
- Lefort I: thru floor of maxillary sinus - Lefort II: thru maxillary sinus, pyramidal. - Lefort III: craniofacial dislocation
Orbital rim fracture
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Level of Consciousness (GCS)
Eye opening Spontaneous to speech to pain none 4 3 2 1 Verbal response orientated confused words sounds none 5 4 3 2 1 Motor response obeys commands 6 localization 5 flexion 4 abnormal flexion 3 extension 2 none 1
GCS = 15 fully conscious
Coma = GCS < 9
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Investigation
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CT scan to rule out: (1) Blood - Epidural:
(biconvex, arterial)
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Investigation
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CT scan to rule out: (1) Blood - Subdural:
(crescentic, venous)
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Investigation
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CT scan to rule out: (1) Blood - Intracerebral
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Investigation
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CT scan to rule out: (1) Blood - Combined
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Investigation
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CT scan to rule out: (2) Contusion
(fluffy, in-homogenous)
Diffuse Axonal Injury
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Investigation
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CT scan to rule out: (2) Swelling
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Investigation
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CT scan to rule out: (2) Skull fracture
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Pathophysiology
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CPP = mABP – ICP CBF (autoregulation)
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Pathophysiology
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Pathophysiology
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Pathophysiology
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Pathophysiology
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Transfer of trauma patient
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Hypoxia Hypotension or hypertension Anemia Seizures Infection or hyperthermia Spinal stability
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Management
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Prehospital Care: - Begin with ABC (Airway, Breathing & Circulation)
- The goal is adequate oxygenation & removal of CO2 - Hypotension SBP <90mmg
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Management
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Emergency Center: - Continue ABCs
- Resuscitation - Neurological examination - CT scan, lab chemistries - ICP monitoring
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Management
General principles in ITU:
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Intubate and ventilate patients in coma, multiple injury, or with respiratory compromise to facilitate maintenance of adequate PO2 & control of PCO2 (4.0-4.5 kPa) Muscle relaxnts, reduces intrathoracic and hence intracranial pressure but increrases the risk of nosocomial iinfection. Medazolam is an appropriate sedative and Alfentanil is the opioid of choice. Prophylactic antibiotic is controversial There is no evidence to support prophylactic anticonvulsants after TBI
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Management
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Surgery:
(General Principles)
- Evacuation of large hematomas or contusions
- Debridement of open wounds - Decompressive craniectomy
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Standards, Guidelines, Options on Treatment
Topic Subject 1 Trauma Centres 2 3 4 5 6 7 8 Resuscitation BP & O2 Indications for ICP monitoring ICP treatment threshold Recommendation for ICP technology CPP Hyperventilation Standerds Non Non Non Non Non Non Non Avoid prolonged hyperventilation (aPCO2<25mmH) Non Non Not recommended Non Non Guidelines All regions should have organised trauma care system Non Options Neurosurgical service, trauma surgeon and CT Sedation & paralysis for safe transfer. Mannitol bolus if deteriorating Hypotension (SBP<90mmHg) Maintain MAPabove 90mmHg & CPP Hypoxia (PO2<60mm Hg) above 70mmHg Severe TBI GCS(3-8) Abnormal Moderate TBI Abnormal CT scan. CT Severe injury with normal scan Upper threshold (20-35mmHg) Should be corporated by CPP & Clinical examination Non Intraventricular & Intraparenchymal are suitable Non Above 70mmHg Use hyperventilation fror breif periods Avoid prophylactic Hyperventilation(aPCO2<35mmHg to reduce acute rises in ICP ) Intermittent boluses Prior to ICP monitoringemergency treatment of cerebral herniation in refractory intracranial hypertension in potentially salvagable patient Non Non 100-140% of resting metabolic expediture Parentral or entral by 7th day Non Non Suggested treatment Jujenal feeding preferred
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Mannitol Barbiturates for raised ICP Glucocorticoids Raised ICP Neutritional support
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Prophyalactic anticonvulsants
Not recommended
for high risk of seizures
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Glasgow Outcome Scale 5 4 3 2 1 Good recovery Moderate disability Severe disability Vegitative Death
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Peripheral Nerve Injury
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Peripheral Nervous System
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Cranial nerves (III – XII) Spinal nerves Nerves of the extremities Cervical, Brachial, and Lumbosacral Plexi
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Problem:
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Loss of motor function, sensory function, or both may result from an injury to a peripheral nerve.
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Etiology:
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Trauma: - blunt or - penetrating wound or - acute compression.
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Structure of the nerve
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Pathophysiology:
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Demyelination or axonal degeneration, result in disruption of the sensory and/or motor function of the injured nerve. Recovery occurs with - remyelination and with - axonal regeneration and - reinnervation of the sensory receptors, muscle end plates, or both.
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Clinical:
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depends on the nerve affected: - motor nerve injury results in a loss of muscle function, and - injury to a sensory nerve results in a loss of sensation to the affected dermatome or causalgia pain.
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Seddon-Sunderland Classification Seddon
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Neuropraxia Axonotemesis Neurotemesis
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Seddon-Sunderland Classification
Sunderland - 1st degree (temporary conduction block with demyelination, 2nd degree (Wallerian degeneration, NCS; denervation, The 3rd degree (more severe than second-degree. NCS; denervation
normal NCS and recovery is complete)
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endoneurial tubes remain intact, and, therefore, recovery is complete)
changes with fibrillations. Regeneration at 1 mm/d, endoneurial tubes are not
intact, incomplete recovery)
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Seddon-Sunderland Classification Sunderland - 4th degree (large area of scar, requires surgery to
restore continuity)
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5th degree (complete transection) 6th degree (mixed injury)
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Royal Medical Research Council of Great Britain strength Grading Scale
Grade
0 1 2 3 4 5
Strength
No Contraction Flickers Active movement with gravity Against gravity Against resistance Normal Strength
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Electrodiagnostic studies:
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Treatment
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Medical therapy: - protection of the joints - Physical therapy Surgical therapy: - Reconstruction of nerve continuity - Nerve graft - Nerve transfer
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Treatment
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cont.
Closed injuries: no evidence of recovery surgery is recommended. Open injury: (laceration): Surgical exploration is recommended as soon as possible. Crush injury: exploration may be delayed for 3 months surgical reconstruction with repair or graft is indicated.
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