PERIPHERAL NERVE

INJURY

Wahyudi
 INTRODUCTION

PERIPHERAL NERVE INJURY HAS BEEN

RECOGNIZED AS A POTENTIAL COMPLICATION OF
REGIONAL ANESTHESIA
THE REPORTED FREQUENCIES OF NERVE INJURY
RANGING FROM 0,1 % - 5,6 % AND THAT MANY
OF THE INJURIES COULD BE ATTRIBUTED TO
MECHANICAL TRAUMA OR LOCAL ANESTHETIC
TOXICITY
 WOOLLEY AND VANDAM, RECOMMENDED THAT
AN ATRAUMATIC TECHNIC WITH THE USE A SMALL
GAUGE NEEDLES AND AVOIDANCE OF
HEMATOMA FORMATION BE THE PRIMARY GOAL
FURTHERMORE, THEY SUGGESTED THAT THE
PATIENT BE CAREFULLY PREPARED WITH
SEDATIVE , SO THAT DISAGREEABLE EXPERIENCE
OF NERVE INJECTION IS NOR RECOLLECTION TOO
CLEAR
 SEVERAL BASIC SCIENCE AND CLINICAL
INVESTIGATIONS HAVE EXAMINED THE ISSUE OF
PERIPHERAL NERVE INJURY TO IDNETIFY RISK
FACTORS ASSOCIATED WITH POSTOPERATIVE
NEUROLOGIC DISFUNCTION
 RISK FACTORS
PATIENT RISK FACTORS :
PREEXISTING NEUROLOGIC DYSFUNCTION
MALE GENDER
ADVANCCED AGE
EXTREMES OF BODY HABITUS
PREEXISTING DIABETES MELITUS
 ANESTHETIC RISK FACORS :
NEEDLE OR CATHETER INDUCED TRAUMA
ISCHEMIC INJURY
PERINEURAL EDEMA
LOCAL ANESTHETIC TOXICITY
 SURGICAL RISK FACTORS :
SURGICAL TRAUMA OR STRETCH
TOURNIQUET ISCHEMIA
INFLAMMATION
INFECTION
HEMATOMA
PATIENT POSITIONING
 DEFINITION

PERIOPERATIVE NERVE INJURY MAY BE DEFINED

AS THE PRESENCE OF :
1. PAIN
2. PARESTHESIA
3. SENSORY OR MOTOR DEFICIT
4. OTHER NERVE DYSFUNCTION
 A PERSISTENT NEUROLOGIC DEFICIT OCCURING
AFTER REGIONAL ANESTHESIA REFERS TO
SENSORY OR MOTOR ABNORMALITY THAT LAST
BEYOND THE EXPECTED DURATION OF
ADMINISTERD LOCAL ANESTHETIC
ALTHOUGH, ThE MAJORITY Of PERIOPERATIVE
NEUROLOGIC DEFICITS ARE TRANSIENT AND
SELF-LIMITED, THOSE REMAINING UNCHANGED
AFTER 12 MONTHS ARE CONSIDERED
PERMANENT
 SCOPE

BACKGROUND
NEUROLOGIC COMPLICATIONS RELATED TO
REGIONAL ANESTHETIC TEHNIQUES OCCURED
IN 0,03 % - 0,04 % PATIENTS
OF THE ALL NEUROLOGIC COMPLICATIONS :
1. A 70 % OCCURED DURING SPINAL
ANESTHHESIA
2. A 18 % DURING EPIDURAL ANESTHESIA
3. A 12 % DURING PERIPHERAL NERVE
BLOCKADE
 ADDITIONAL COMPLICATIONS THAT OCCURRED
DURING PERIPHERAL NERVE BLOCKADE
INCLUDE :
1. CARDIAC ARREST ( 0,01 % )
2. RADICULOPATHY ( 0,02 )
3. SEIZURES ( 0,08 % )
4. DEATH ( 0,005 % )
ALL NEUROLOGIC COMPLICATIONS OCCURRED
WITHIN 48 HOURS OF SURGERY AND
RESOLVED WITHIN 3 MONTHS ( 85 % OF
PATIENTS
 IN 12 % CASES OF RADICULOPATHY AFTER SPINAL
ANETHESIA AND IN ALL ( 100 % ) CASSES OF
RADICULOPATHY FOLLOWING EPIDURAL OR
PERIPHERAL NERVE BLOCKADE, NEEDLE
PLACEMENT WAS ASSOCIATED WITH EITHER A
PARESTHESIA DURING NEEDLE/CATHETER
INSERTION OR PAIN UPON INJECTION
IN ALL CASES, THE RADICULOPATHY HAD SAME
TOPOGRAPHY AS THE ASSOCIATED PARESTHESIA
DURING BLOCK PLACEMENT
 THE AUTHORS CONCLUDED THAT NEEDLE
TRAUMA AND LOCAL ANESTHETIC
NEUROTOXICITY WERE THE PRIMARY ETIOLOGIES
OF MOST NEUROLOGIC COMPLICATIONS
ALTHOUGH THESE STUDIES FOUND THAT THE
INCIDENCE OF SEVERE COMPLICATIONS IS
EXTREMELY LOW, THAT CONTINUED VIGILANCE
IN PATIENT UNDERGOING REGIONAL ANESTHESIA
IS NOT WARRANTED, BUT CRITICAL IN
MINIMIZING PERIOPERATIVE NERVE INJURIES
 CLOSED ANALYSIS :
THE MOST FREQUENT SITES FOR ANESTHESIA-
RELATED NERVE INJURY WERE :
1. THE ULNAR NERVE ( 28 % )
2. THE BRACHIAL PLEXUS ( 20 % )
3. THE LUMBO-SACRAL NERVE ROOTS ( 16 % )
4. THE SPINAL CORD ( 13 % )
 THE ULNAR NERVE INJURIES, WHICH WERE
PREDOMINANTLY ASSOCIATED WITH GENERAL
ANESTHESIA ( 85 % )
OF ALL BRACHIAL PLEXUS INJURY, 31 %
EXPERIENCED A PARESTHESIA EITHER DURING
NEEDLE PLACEMENT OR WITH INJECTION OF
LOCAL ANESTHETIC
 IT AS BEEN SUGGESTED THAT NEUROLOGIC
DEFICIT THAT ARISE WITHIN THE FIRST 2 HOURS
OF SURGERY MOST LIKLEY REPRESENT ;
1. AN EXTRA OR INTRANEURAL HEMATOMA
2. INTRANEURAL EDEMA
3. A LESION INVOLVING A SUFFICIENT NUMBER OF
THE NERVE
 COMPLICATIONS DISTRIBUTION OCCURRING
DURING PERIPHERAL NERVE BLOCKADE :
1. AXILLARY BLOCKS ( 44 % )
2. INTRAVENOUS REGIONAL ANESTHESIA ( 21 % )
3. INTERSCALENE BLOCKS ( 19 % )
4. SUPRACLAVICULAR BLOCKS ( 7 % )
 PATHOPHYSIOLOGY

PATHOGENESIS OF PERIPHERAL NERVE INJURY.

1. DISTAL TO THE SITE OF INJURY :
ONCE INJURY OCCURS, THOSE COMPONENTS
DISTALT TO THE SITE OF INJRY WILL DEGENERATE (
WALLERIAN DEGENERATION ) AND BE DESTROYED
BY PHAGOSITOSIS AND THIS PROCESS MAY
REQUIRE UP TO 4 WEEKS FOR COMPLETION
MORPHOLOGIC CHANGES WILL BEGIN TO OCCUR
WITHIN THE FIRST 72 HORS AND DURING THIS
TIME THE NERVE MAY RETAIN A VARIABLE DEGREE
OF FUNCTIONALITY WHILE DISTAL AXONAL BEGIN
TO SHRINK
 AT APPROXIMATELY ONE WEEK POST INJURY,
MACROPHAGES HAVE REACHED THE SITE OF
INJURY AND CLEARING ALL DEBRIS WITHIN 2
4 WEEKS
SCHWANN CELL BY MITOSIS OCCURS
SIMULTANEOUS WITH THIS PROCESS,
INCREASING THE NUMBER OF CELLS TO FILL
THE AREA ONCE OCCUPIED BY THE DISTAL
AXON AND MYELIN SHEATH
2. PROXIMAL TO THE SITE OF INJURY :
THE REACTION PROXIMAL TO THE SITE OF
INJURY IS REFERRED TO PRIMARY RETROGRADE
DEGENERATION
RETROGRADE DEGENERATION PROCEEDS FOR
AT LEASST 1 INTTERNODAL SPACE
THE MORE PROXIMAL THE SITE OF INJURY THE
MORE PRONOUNCED THE CHANGES WITHIN
THE AXONAL CELL BODY
 IF PRESENT, THIS WILL GENERALLY OCCUR
WITHIN THE FIRST 5 7 DAYS, WITH DEATH OR
RECOVERY OVER THE NEXT 4 6 WEEKS
AXONAL REGENERATION MAY BEGIN WITHIN
THE FIRST 24 HOURS AFTER INJURY

CLASSIFICATION OF PERIPHERAL NERVE

INJURY :
THE CLASSIFICATION OF PERIPHERAL NERVE
INJURIES WAS INITIALLY INTRODUCED BY
SEDDON IN 1943
 THIS CLASSIFICATION WAS GENERALLY
ACCEPTED, BUT RARELY USED BECAUSE POOR
ASSOCIATION WITH CLINICALL USEFULNESS
FOLLOWING THE DESCRIPTION OF SEDDON,
SUNDERLAND DEVELOPED ONE OF THE MOST
WIDELY USED OF CLASSIFICATION OF
PERIPHERAL NERVE INJURIES
 SEDDON CLASSIFICATION OF PERIPHERAL
NERVE INJURY

1. NEURAPRAXIA :
A MINOR CONTUSION OR COMPRESSION OF
PERIPHERAL NERVE WITH PRESERVATION OF THE
AXIS CYLINER. MINOR EDEMA WITHIN THE CELL
BODY OR FOCAL DISRUPTION OF THE MYELIN
SHEATH MAY RESULT IN TRANSIENT DISRUPTION
OF NERVE CONDUCTION AND GENERALLY
RECOVERS AND RESOLVES WITHIN DAYS TO
WEEKS
2. AXONOTMESIS :
A MORE SIGNIFICANT INURY WITH BREAKDOWN
OF THE AXON AND SUBSEQUENT WALLERIAN
DEGENERATION. HOWEVER, ENDONEURAL TUBE
STRUCTURE AND SHWANN CELLS ARE WELL
PRESERVED, THUS ALLOWING SPONTANEOUS
REGENERATION AND GOOD FUNCTIONAL
RECOVERY OVER TIME
3. NEUROTMESIS :
A SEVERE INJURY SECONDARY TO AN AVULSION
OR CRUSH INJURY WITH COMPLETE AXONAL
TRANSECTION. ALL STRUCTURE ARE
COMPLETELY DISRUPTED. THE PERINEURIUM
AND EPINEURIUM ARE ALSO DISRUPTED TO
VARYING DEGREES. IN GENERAL, SIGNIFICANT
FUNCTIONAL RECOVERY IS UNLIKELY
 SUNDERLAND CLASSIFICATION OF NERVE
INJURY

TYPE I :
FOCALLY INTERUPTED AT SITE OF INJURY
NO WALLERIAN DEGENERATION
MAINTAINED ENDONEURAL INTEGRITY
VARIABLE LOSS OF FUNCTION ( MOTOR >
SENSORY )
COMPLETE RESTORATION WITHIN DAYS TO
WEEKS
 TYPE II :

INTERUPTED DISTALLY FROM SITE OF INJURY

WALLERIAN DEGENERATION PROCESSES
MAINTAINED ENDONEURIAL INTEGRITY
TRANSIENT LOSS OF MOTOR, SENSORY AND
SYMPATHETIC FUUNCTION
REGENERATION AND FUNCTIONAL RECOVERY
WITHIN WEEKS TO MONTH
 TYPE III :

INTERUPTED DISTALLY FROM SITE OF INJURY

WALLERIAN DEGENERATION PROCESSES
DISRPTED WITH SCARRING OF ENDONEURIUM
PROLONGED MOTOR, SENSORY ND SYMPATHETIC
DEFICITS
PARTIAL REGENERATION AND COMPLETE RETURN
OF FUNCTION DOES NOT OCCUR
 TYPE IV :

INTERRUPTED DISTALLY FROM SITE OF INJURY

WALLERIAN DEGENERATION PROCESSES
DISRUPTED OF PERINEURIUM ALSO
SEVERE LOSS OF MOTOR, SENSORY AND
SYMPATHETIC FUNCTION
PERMANENT DEFICITS WITHOUT SURGERY
 TYPE V :

INTERRUPTED DISTALLY FROM SITE OF INJURY

WALLERIAN DEGENERATION PROCESSES
SEVERE EPINEURIUM DISRUPTED
SEVERE LOSS OF MOTOR, SENSORY AND
SYMPATHETIC FUNCTION
PERMANENT DEFICITS EVEN WITH SURGERY
 RISK FFACTORS

1. PATIENT RISK FACTORS :

MALE GANDER
INCREASING AGE
EXTREMES OF BODY HABITUS
PEEXISTING DIABETES MELITUS
NEUROLOGIC DEFICITS
THE PERFORMANCE OF NEURAXIAL OR
PERIPHERAL TECHNIQUES IN PATIENTS WITH
PREEXITING NEUROLOGIC DISORDER, MAY
THEORITICALLY PLACE THEM AT INCREASED RISK
OF A DOUBLE CRUSH PHENOMENON
2. SURGICAL RISK FACTORS :

DIRECT INTRAOPERATIVE TRAUMA OR STRETCH

VASCULAR COMPROMISE
PERIOPERATIVE INFECTION
HEMATOMA FORMATION
PROLONGED TORNIQUETT ISCHEMIA
IMPROPERLY APPLIED CASTS OR DRESSING
3. ANESTHETIC RISK FACTORS :

NEEDLE OR CATHETER INDUCED

MECHANICAL TRAUMA :
IN VITRO , NEURONAL INJURY OCCURRED MORE
FREQUENTLY WITH LONG-BEVEL WHEN
COMPARED TO SHORT-BEVEL
NERVE INJURY WAS DEFINED AS :
1. THE SEPARATION OR CURLING OF NERVE
FIBERS
2. THE HERNIATION OF FIBERSS THROUGH THE
PERINEURIUM
3. CUT NEURAL FIBERS
 THE ORIENTATION OF THE BEVEL ( PARALLEL OR
TRANSVERSE TO THE NERVE ) WAS OF LITTLE
IMPOORTANCE REGARDING THE FREQUENCY OF
INJURY
MORE SEVERE INJURY WERE ENCOUNTERED
WHEN LONG-BEVEL WERE INSEERTED
TRANSVERSELY TO NERVE FIBERS VERSUS
PARALLEL INSERTION
INVESTIATOR CONCLUDED, THHAT LONG-BEVEL
NEEDLES IN THE PARALLEL TO NERVE FIBERS
PRODUCED LESS INTRANEURAL DAMAGE THAN
TRANSVERSELY
 IN ADDITION, THAT NEURAL REPAIR MAY BE
ACCELERATED AND MORE ORGANIZED WITH
LONG-BEVEL INJURIES AND LONGTERM
CONSEQUENCES MAY BE LESS OF A CONCERN
WHEN LONG-BEVEL NEEDLES ARE USED AND
MAY BE MORE COMFORTABLE FOR PATIENTS
 PARESTHESIA INDUCED NEEDLE INJURY.

MANY ANESTHESIOLOGISTS INTENTIONALLY ELICIT

A PARESTHESIA DURING THE PERFORMANCE OF
PERIPHERAL NERVE BLOCK
THIS MAY HAVE ORIGINATED IN PART, FROM THE
DICTUM NO PARESTHEISIA , NO
ANESTHESIA
ALTHOUGH THE ELICITATION OF A PARESTHESIA
MAY REPRESENT DIRECT NEEDLE TRAUMA AND
THEORITICALLY INCREASE THE RISK OF
NEUROLOGIC INJURY, THERE ARE NO PROSPECTIVE
STUDIES THAT ARE ABLE TO DEFINITIVELY
SUPPORT THESE CLAIMS
 THEORITICALLY, SUPPLEMENTARY INJECTIONS
BEFORE REGIONAL BLOCK, MAY SIGNIFICANTLY
INCREASE THE RISK OF NEURAL INJURY BECAUSE
OF THE ABSENCE OF WARNING SIGNS SUCH
PARESTHESIA
INVESTIGATIONS IN WHICH LOCAL ANESTHETIC
WAS NOT INJECTED ONTO PARESTHESIA, HAVE
RESULTED IN SIGNIFICANT LOWER NEUROLOGIC
COMPLICATION RATES
 SELANDER CONCLUDED, FOLLOWING CATHETER
PLACEMENTT AND NEGATIVE ASPIRATION, LOCAL
ANESTHETIC WAS INJECTED THROUGH THE
CANULA WITH NO REPORT OF PAIN OR PRESSURE
PARESTHESIA, THERE WERE NO NEUROLOGIC
SQUELAE POSTOPERATIVELY
MOORE SUUGGESTED THAT A PROPERLY
ELICITED PARESTHESIA DOES NOT INDICATED
THAT : (1) THE BEVEL OF NEEDLE HAS
PUNCTURED THE EPINEURIUM, (2) THE NERVE
HAS BEEN IMPALED, (3) NEURAL FIBRES HAVE
BEEN CUT OR (4) AN INTRANEURAL INJECTION
 MOORES FURTHER EMPHASIZES THAT NO
STATISTICALL SINIFICANNT CLINICAL DATA HAVE
BEEN PUBLISHED THAT DEMONSTRATE THAT
ELICIED PARESTHESIAS DURING REGIONAL
BLOCKADE RESULT IN THE TEMPORARY OR
PERMANENT LOOS OF NEURAL FUNCTION
ALL POSTOPERATIVE NEUROLOGIC SEQUELAE
INVOLVED DIMINISHED SENSATION WITHIN THE
DISTAL EXTREMITY AND HAD RESOLVED WITHIN 7
MONTHS
 THE AUTHORS POSTULATED THAT SUBCLINIAL
HEMATOMA MIGHT CONTRIBUTE TO THE
DEVELOPMENT OF TRANSIENT POSTOPERATIVVE
NEUROLOGIC SYMPTOMS
 ISCHEMIC INJURY CAUSED BY EPINEPHRINE

EPINEPHRINE IS A COMMON ADJUVANT OFTEN

ADDED TO LOCAL ANESTHETICS DURING
PERIPHERAL NERVE BLOCKADE
IN CONCENTRATION OF 1 : 200.000, EPINEPHRINE
IS NOT ONNLY PROLONGS THE DURATION OF
BLOCKADE, BUT REDUCES VASCULAR UPTAKE
WITHIN THE ANESTETIZED AREA
THIS ADRENERGIC EFFECT AVOIDS RAPID
REDISTRIBUTION OF THESE DRUGS TO THE
SYSTEMIC CIRCULATION, WHERE THEY MAY
CAUSE POTENTIALLY TOXIC REACTION
 RECENT INVESTIGATIONS HAVE FOCUSED ON THE
ROLE OF EPINEPHRINE AND NEURAL BLOOD FLOW
IN THE PATHOGENESIS OF NERVE FIBER INJURY
IT HAS LONG BEEN RECOGNIZED THAT THE
FUNCTIONAL INTEGRITY OF PERIPHERAL NERVES
IS DEPENDENT ON THEIR MICROCIRCLATION
 THE BLOOD SUPPLAY TO PERIPHERAL NERVES
CONSISTS :
1. AN INTRINSIC SUPPLY OF VESSELS WITHIN THE
ENDONEURIUM
2. AN EXTRINSIC SUPPLY OF LARGER VESSELS.
WHERE THE
VASCULATURE RUNS LONGITUDINALLY ALONG THE
NERVE
WITHIN THE PERINEURAL AND CROSSES
PERINEURIUM TO
ANASTOMOSEE WITH THE INTRINSIC CIRCULATION
 THE EPINEURIAL CIRCULATION IS CRITICAL
COMPONENT OF THE NEURAL CIRCULATION,
REDUCES IN 50 % NEURAL BLOOD FLOW CAN
CAUSE DEMYELINATION OF INTRINSIC NERVE
FIBERS
IN ADDITION, THIS EXTRINSIC CIRCULATION THAT
IS UNDER ADRENERGIC CONTROL, AND THUS
HIGHLY RESPONSIVE TO EPINEPHRINE-
CONTAINING SOLUTION
 THE RISK OF NERVE INJURY MAY BE LIMITED TO
ONLY THOSE INDIVIDUALS WITH UNDERLYING
TOXIC ( CHEMOTHERPY ) OR METABOLIC
NEUROPATHIES, SO TO MINIMIZE THE
CONCENTRATION OF EPINEPHRINE USED DURING
PERIPHERAL BLOCKADE
ISCHEMIC NERVE INJURY MAY ALSO OCCUR
FOLLOWING THE INTRAFASCICULAR
( INTRANEURONAL ) INJECTION OF LOCAL
ANESTHETICS
 INTRAFASCICULAR INJECTIONS MAY RESULT IN
1. COMPRESSIVE NERVE MAY EXCEED CAPILLLARY
PERFUSION
PRESSUR AND INTERFERING WITH THE
ENDONEURIAL
MICROCIRCULATION
2. AN ELEVATED PRESSURES MAY ALSO ALTER
PERMEABILIITY
OF THE BLOOD-NERVE BARRIER AND DISRUPT
THE
INTERNAL MILIEU OF THE ENDONEURIUM
 THIS RESULT IN AXONAL DEGENERATION AND
PATHOLOGIC DAMAGE TO PERIPHERAL NERVE
FIBER
FIBROBLAST PROLIFERATION HAS ALSO BEEN
OBSERVED AT THE SITE OF INJURY,
CONTRIBUTING TO LATE-OCCURING CHANGES IN
PERINEURAL THICKNESS AND ENDONEURIAL
FIBROSIS
 CHEMICAL INJURY BY LOCAL ANESTHETIC
TXICITY

THE USE LOCAL ANESTHETICS WITH AN

INAPPROPRIATELY HIGH CONCENTRATION,
PROLONGED EXPOSURE TIMES AND INTRANEURAL
INJECTION ARE ENCOUNTERED SEVERE
DEGENERATIVE CHANGES MAY OCCUR AND
LEADING NEUROLOGIC SEQUELAE
NERVE CONDUCTION DEFFICITS MAY RESULT
FROM DIRET TOXIC OR ISCHEMIC EFFECT OR
FROM INDIRECT EFFECTS THAT ALTER
PERMEABILITY AND MICROENVIRONTMENT OF
THHE NERVE
 THE AUTHORS, IT HAS BEEN SUGGESTED THAT
THE REGIONAL ANESTHESIA INDUCED
PERIOPERATIVE NERVE INJURY, MAY BE THE
RESULT OF A COMBINED MECHANICAL AND
CHEMICAL INSULT
SELANDER AT AL, CONCLUDED THAT
NEUROLOGIC INJURY FOLLOWING PERIPHERAL
NERVE BLOCKADE MIGHT BE MULTI FACTORIAL,
INVOLVING TRAUMATIC, TOXIC AND ISCHEMIC
VARIABLES
THE ROLE OF NERVE STIMULATION.

THE USE OF NERVE STIMULATION WHILE PERFORMING

REGIONAL ANESTHETIC TECHNIQUES WAS
INTRODUCE BY GREENLATT AND DENSON IN 1962
AN ADVOCATES OF THE TECHNIQUE HAVE REPORTED
SEVERAL ADVANTAGES INCLUDING :
1. A HIGH SUCCESS RATE
2. THE ABILITY TO PERFORM PROCEDURES ON
SEDATED OR
UNCOOPERATIVE PATIENTS
3. THE AVOIDANCCE OF PARESTHESIAS
4. THE AVOIDANCE OF ARTERIAL PUNCTURE
 NEUROLOGIC COMPLICATION ASSOCIATED WITH
NERVE STIMULATOR USE RANGE FROM 0 8 %
COMPLETE RECOVERY OF NEUROLOGIC FUNCTION
WAS OBSERVED WITHIN 3 MONTHS
 DIAGNOSTIC EVALUATION.

ALTHOUGH MOST NEUROLOGIC COMPLICATIONS

RESOLVE COMPLETELY WITHIN SEVERAL DAYS OR
WEEKS, NEURAL INJURIES NECESSITATE FURTHER
NEUROLOGIC CONSULTATION AND INVESTIGATION
NEUROLOGIC PREOPERATIVE ASSESSMENT
DOCUMENTED TO ALLOW THE EARLY DIAGNOSIS
OF NEUROLOGIC DYSFUNCTION
POSTOPERATIVELY
 KNOWLEDGE BASELINE NEUROLOGIC STATUS
PRIOR TO REGIONAL ANESTHESIA IS A CRITICAL
ELEMENT THAT IS OFTEN MISSING
THEREFORE, MANY EXPERTS SUGGEST THAT A
BRIEF NEUROLOGIC EXAMINATION BE
PERFORMED PRIOR TO THE PERFORMANCE OF
REGIONAL ANESTHETIC TECHNIQUE TO
DOCUMENT THE PRESENCE OF PREEXISTING
DEFICITS
 HISTORICAL FEATURES THAT ARE IMPORTANT TO
IDENTIFY INCLUDE :
1. THE ONSET OF SYMPTOMS
2. THE TYPE AND QUALITY OF SYMPTOMPS ( SENSORY,
MOTOR, SYMPATHETIC )
3. THE PATHOGENESIS ( CONSTANT, FLUCTUATING,
PROGRESSIVE )
4. MEDICAL HISTORY ( PREEXISTINGG NEUROLOGIC
DISORDERS, DIABETES, PERIPHERAL VASCULAR
DISEASE )
 5. SURGICAL EVENT (PROLONGED TOURNIQUET,
TRAUMA,
STRETCH, VASCULAR INJURY )
FINALLY, A DETAILED NEUROLOGIC EXAMINATION
BY A NEUROLOGIST OR NEUROSURGEON SHOULD
OCCUR SOON AFTER THE IDENTIFICATION OF AN
UNEXPECTED DIFICIT
EARLY IMAGING TECHNIQUES ( CT, MRI ) MAY BE
RECOMMENDED
PREVENTION

TO AVOID REGIONAL ANESTHETIC TECHNIQUE IN

ASLEEP OR HEAVILY SEDATED
TO AVOID PAIN WITH INJECTION OF LOCAL
ANESTHETIC
POTENTIAL RISKS FACTOR ( GERIATRIC, SPINAL
STENOSIS, NEUROPATHY DIABETIC ) SHOULD BE
CAREFULLY CONSIDERED
 PATIENT WITH PREEXISTING NEURAL
COMPROMISE MAY NOT JUSTIFY THE POTENTIAL
BENEFIT
HOWEVER, IF THE CLINICAL RISK IS DEEMED
APPROPRIATE FOR CLINICAL MANEUVERS, SUCH
REDUCING THE LOCAL ANESTHETIC DOSE OR
CONCENTRATION OR MINIMIZING THE
CONCENTRATION OF EPINEPHRINE ADDITIVES
MAY BE PRUDENT
TREATMENT AND REHABILITATION

CONSERVATIVE MEASURES AND CAREFUL

OBSERVATION ARE APPROPRIATE DURING THE
INITIAL PHASES OF RECOVERY
THE CRITICALLY IMPORTANT THAT DIRECTABLE
CAUSES OF NERVE INJURY BE INVESTIGATED AND
EXCLUDED DURING THE IMMADIATE
POSTOPERATIVE PERIOD
NEUROLOGIC REFERRAL AND CONSULTATION IS
CONSIDERED IMPORTANT TO PROVIDE SERIAL
CLINICAL AND ELECROPHYSIOLOGIC
EXAMINATIONS TO MONITOR THE PROGRESSION
OR RESOLUTION OF SYMPTOMS
 UNDER ALL CIRCUMSTAANCES, PHYSICAL
THERAPY SHOULD BE INSTITUTED SOON AFTER
THE INJURY TO MAINTAIN STRENGTH IN THE
UNAFFECTED MUSCLES AS WELL AS JOINT
RANGGE OF MOTION
PATIENT WITHH PERSISTENT ( 6 - 8 WEEKS )
SYMPTOMS OR PROGRESSIVE NEUROLOGIC
DEFICITS SHOULD UNDERGO NEUROSURGICAL
EVALUATION
 THE GOAL OF SURGERY MAY BE :
1. HALT THE PROGRESSION OF SENSORY-MOTOR
DEFICITS
2. PROVIDE RELIEF OF PAIN AND OTHER
NEUROLOGIC
SYMPTOMS
3. RESTORE FUNCTIONAL CAPACITY
 SUGGESTED MANAGEMENTT OF
POSTOPERATIVE NERVE DYSFUNCTION

EARLY INTERVENTION :
- RULE OUT CORRECTABLE CAUSES THAT MAY
REQUIRE
SURGICAL INTERVENTION WITHIN 72 HOURS
- CONSIDER ELECTROPHYSIOLOGIC TESTING TO
ESTABLISH
BASELINE FUNCTION
 PERSISTENT OR PROGRESSIVE NEUROLOGIC
DEFICITS
1. INSTITUTE SERIAL CLINICAL AND ELECTRO-
PPHYSIOLOGIC
EXAMINATION
2. IF NO IMPROVEMENT, CONSIDER SURGICAL
EXPLORATION
AND NEUROLYSIS
PRESCRIBE PHYSICAL THERAPY
- MAINTAIN STRENGTH AND JOINT MOBILITY
 EARLY SURGERY INTERVENTION IS RARELY
INDICATED IN PERIOPERATIVE NERVE INJURIES
SURGERY WITHIN 72 HOURS IS INDICATED
( HEMATOMA, COMPARTEMENT SYNDROME,
PSEUDOANEURYSMA, IATROGENIC SUTURIN OF
NEURAL STRUCTURE, NEURAL LACERATION ) AND
IS OFTEN CRITICAL IN THE TREATMENT TO
FACILITATE THE END-TO-END ANASTOMOSIS AND
REPAIR OF NEURAL STRUCTURE
 IN CONTRAST, BLUNT INJURED NERVE IS BEST
REPAIRED AFTER A DALAY OF SEVERAL WEEKS,
BY THE TIME THE NEUROMAS WILL BE OBVIOUS
AND ALLOWING A COMPLETE RESECTION
FOR THE FOCAL ( NEEDLE OR MECHANIC
TRAUMA, INTRANEURAL INJECTION ) OR DIFFUSE (
STRETCH, COMPRESSION, ISCHEMIA,
NEUROTOXICITY ) NEURAL INSULTS ARE MORE
LIKELY OCCUR, SO MUST BE CLOSE OBSERVATION
WITH SERIAL CLINICAL AND ELECTROPHYSILOGIC
EXAMINATTIONS
 HOWEVER, IN CASES WITH NO EVIDENCE OF
CLINICAL OR ELECTROPHYSIOLOGIC RECOVERY,
SURGICAL EXPLORATION AND NEUROLYSIS
SHOULD BE CONSIDERED
IT IS RECOMMENDED THAT PATIENS WITH FOCAL
LESSION BE SURGICALLY EXPLORED AT 2 3
MONTHS, WHEREAS WITH DIFFUSE INJURIES
EXPLORED AT 3 5 MONTHS TIME
 SUMMARY

PERIPHERAL NERVE INJURIES ARE RARE,

ALTHOUGH POTENTIALLY CATASTROPHIC
PERIOPERATTIVE COMPLICATION
PATIENT, SURGICAL AND ANESTHETIC RISK
FATORS HAVE ALL BEEN IDENTIFIED, AS
POENTIAL ETIOLOGIES
PATIENTS WITHH SEVERAL RISK FACTORS MAY BE
AT GREATEST RISK OF DEVELOPING
POSTOPERATIVE NEUROLOGIC COMPLICATIONS
SELESAI