Top Tweets for #TypesofNerveInjuries

almost 3 years ago

*"Knowing it, B4 Blocking It" : ABCD of Peripheral Nerves* #PeripheralNerveInjuries #NerveInjuries #Nervefibres #TypesofNerveInjuries #PreventionofNerveInjuries #SHEDapproach #DiagnosisOfPNI *My 10 points:* A. NERVE ANATOMY & PHYSIOLOGY 1. The *Epineurium* is absent around monofascicular Ns.& at Free nerve endings. The tough *Perineurium* acts as a semipermeable barrier to LA. During nerve injury, the *Endoneurial* fluid increases, causing nerve edema - detected by Magnetic resonance neurography (MRN). 2. The *Paraneurium* protects the nerve from stretching/compression during body movements. This *Sweet spot* of the N. can be an ideal site for LA deposition. 3. Most impulses arise at the *Trigger zone* - A junction of the axon hillock with the initial segment. A nerve transmits these electrochemical impulses from one neuron to another by crossing a synapse. The message is converted from electrical to chemical and then back to electrical. 4. The arrangement of the peripheral mantle to inner core fibers in the nerve is responsible for *differential block* by LA. The diffusion of LA from the mantle to the core fibers depends on the concentration gradient. The sequence of blockade includes *B fibers> C fibers = Aδ fibers> Aγ fibers> Aβ fibers> Aα fibers.* B. NERVE INJURY TYPES AND PATHOPHYSIOLOGY 5. *Neurapraxia* is associated with reversible conduction blockade due to localized myelin degeneration (without affecting the axon/ neural tube/connective tissues) due to transient ischemia, mainly due to compression. *Axonotmesis* involves complete interruption of axons (without affecting neural connective tissues), leading to conduction loss in the nerve fiber beyond the zone of injury - Common with crush and stretch injuries. *Neurotmesis*, a most severe form of nerve injury, involves complete transection of the nerve - Observed after massive trauma, sharp injuries, traction or avulsion injuries, & the injection of noxious drugs. 6. Following nerve injury, the nerve undergoes Degeneration followed by regeneration. *Degeneration* proximal to injury site - primary/retrograde Degeneration. Degeneration distal to the injury site -secondary/anterograde/Wallaerian Degeneration. *Regeneration* is not possible when the cell body is damaged, but it is possible with axonal damage. The ER and ribosome responsible for protein synthesis are present in the cell body cytoplasm but absent in the axoplasm. C. PREVENTION OF NERVE INJURIES 7. *Subjective monitoring* (paresthesia, pain on injection, or syringe feel) can be unreliable than *Objective monitoring* (injection port pressure display, PNS, compressed air injection technique (CAIT), real-time visualization under ultrasound, and injection pressure manometers such as BSmart, NerveGuard, and SAFIRA). 8. *Dual guidance* (USG + PNS) helps reduce the risk of nerve injury. In addition, *Triple guidance* (USG + PNS + injection pressure monitoring) further improves RA safety and gives the confidence to administer PNBs without nerve injury. D. TREATMENT OF NERVE INJURIES 9. The *SHED* (Symptoms categorization-History taking-Examination-Diagnostic evaluations) approach can be helpful when approaching nerve injury patients. Available diagnostic tools for PNI include high-resolution US, MRI/MRN, CT scan, and electrophysiological testing. The choice of diagnostic tests depends on the time since nerve injury and the time required to complete post-injury physiological processes (like Degeneration, regeneration, remyelination, and reinnervation). 10. *NCS* detects and *EMG* locates the nerve lesion. Initial NCS is performed only after 1-2 days of injury and can be repeated in 10-14 days if the symptoms persist. EMG study is conducted 2-4 weeks after the injury. After 4 weeks, the beginning of the reinnervation process can interfere with the EMG study.

KartikBSonawane's tweet photo. *"Knowing it, B4 Blocking It" : ABCD of Peripheral Nerves*

#PeripheralNerveInjuries
#NerveInjuries
#Nervefibres
#TypesofNerveInjuries
#PreventionofNerveInjuries
#SHEDapproach
#DiagnosisOfPNI

*My 10 points:*

A. NERVE ANATOMY & PHYSIOLOGY

1. The *Epineurium* is absent around monofascicular Ns.& at Free nerve endings.

The tough *Perineurium* acts as a semipermeable barrier to LA.

During nerve injury, the *Endoneurial* fluid increases, causing nerve edema - detected by Magnetic resonance neurography (MRN).

2. The *Paraneurium* protects the nerve from stretching/compression during body movements.

This *Sweet spot* of the N. can be an ideal site for LA deposition.

3. Most impulses arise at the *Trigger zone* - A junction of the axon hillock with the initial segment.

A nerve transmits these electrochemical impulses from one neuron to another by crossing a synapse.

The message is converted from electrical to chemical and then back to electrical.

4. The arrangement of the peripheral mantle to inner core fibers in the nerve is responsible for *differential block* by LA.

The diffusion of LA from the mantle to the core fibers depends on the concentration gradient.

The sequence of blockade includes *B fibers> C fibers = Aδ fibers> Aγ fibers> Aβ fibers> Aα fibers.*

B. NERVE INJURY TYPES AND PATHOPHYSIOLOGY

5. *Neurapraxia* is associated with reversible conduction blockade due to localized myelin degeneration (without affecting the axon/ neural tube/connective tissues) due to transient ischemia, mainly due to compression.

*Axonotmesis* involves complete interruption of axons (without affecting neural connective tissues), leading to conduction loss in the nerve fiber beyond the zone of injury - Common with crush and stretch injuries.

*Neurotmesis*, a most severe form of nerve injury, involves complete transection of the nerve - Observed after massive trauma, sharp injuries, traction or avulsion injuries, & the injection of noxious drugs.

6. Following nerve injury, the nerve undergoes Degeneration followed by regeneration.

*Degeneration* proximal to injury site - primary/retrograde Degeneration. Degeneration distal to the injury site -secondary/anterograde/Wallaerian Degeneration.

*Regeneration* is not possible when the cell body is damaged, but it is possible with axonal damage. The ER and ribosome responsible for protein synthesis are present in the cell body cytoplasm but absent in the axoplasm.

C. PREVENTION OF NERVE INJURIES

7. *Subjective monitoring* (paresthesia, pain on injection, or syringe feel) can be unreliable than *Objective monitoring* (injection port pressure display, PNS, compressed air injection technique (CAIT), real-time visualization under ultrasound, and injection pressure manometers such as BSmart, NerveGuard, and SAFIRA).

8. *Dual guidance* (USG + PNS) helps reduce the risk of nerve injury. In addition, *Triple guidance* (USG + PNS + injection pressure monitoring) further improves RA safety and gives the confidence to administer PNBs without nerve injury.

D. TREATMENT OF NERVE INJURIES

9. The *SHED* (Symptoms categorization-History taking-Examination-Diagnostic evaluations) approach can be helpful when approaching nerve injury patients.

Available diagnostic tools for PNI include high-resolution US, MRI/MRN, CT scan, and electrophysiological testing.

The choice of diagnostic tests depends on the time since nerve injury and the time required to complete post-injury physiological processes (like Degeneration, regeneration, remyelination, and reinnervation).

10. *NCS* detects and *EMG* locates the nerve lesion.
Initial NCS is performed only after 1-2 days of injury and can be repeated in 10-14 days if the symptoms persist.

EMG study is conducted 2-4 weeks after the injury. After 4 weeks, the beginning of the reinnervation process can interfere with the EMG study.

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