Hand Nerve Injury Repair Workup

  • Author: Subhas Gupta, MD, PhD, CM, FRCSC, FACS; Chief Editor: Joseph A Molnar, MD, PhD, FACS   more...
 
Updated: Oct 7, 2011
 

Laboratory Studies

Serum albumin test

  • The reason for ordering this test is to determine if the nutritional status of the patient is adequate to allow reconstructive surgery. If the values returned are less than normal, healing may be impaired and surgical repair compromised.
  • Generally, proceeding is acceptable when albumin levels are greater than or equal to 2.5 g/dL.
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Imaging Studies

Short tau inversion recovery MRI

  • This is a unique form of MRI that returns pictures that can highlight nerve trauma, although it is less sensitive than other diagnostic tests for determining the degree and location of injury.
  • The short tau inversion recovery MRI works by placing a phased array of surface coils on the body, thus allowing imaging of a smaller area with a more precise picture.
  • Both T1- and T2-weighted images can be used to view nerve pathology, which alters the nerve signal from its normally isodense state. T2-weighted images allow the hyperintense signal of nerve injury to be more apparent because of the ability to suppress the fat signal.
  • This type of test is indicated in patients with nonclassic symptoms, in those with ambiguous findings such as occur in patients with diabetes, for scar and nerve inflammation imaging after the addition of gadolinium, to visualize neuromas, and to determine the length of damaged nerve present.
  • This technology is not yet consistent enough to play a major role in diagnosis, but it can serve as a useful adjunct to other tests.[65, 13, 53]
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Other Tests

Sensory tests[4, 66, 67, 68]

  • Tinel test: The patient should feel a sensation when the tip of the severed nerve is tapped.
  • Two-point discrimination: Both moving (M2PD) and static (S2PD) are performed with the patient's eyes closed. Results should be consistent enough to exclude the patient guessing. This examination should be very thorough if a partial injury is suggested. S2PD is excellent if less than or equal to 6 mm, and M2PD is considered excellent if less than or equal to 3 mm. A lack of 2PD is poor.
  • Semmes-Weinstein test: This uses monofilaments, which allow the application of stimuli using constant force so that administration error is reduced. Findings should be similar to those from S2PD and M2PD.

Motor tests[4, 67, 68]

  • Grip and pinch strength: This is usually tested by having the patient squeeze a measuring device that can determine the amount of force the patient produces. Results may be compared to the unaffected hand to grade the deficiency. Testing intrinsic and extrinsic muscles separately can be helpful.
  • Muscle bulk: This test looks for atrophy of large muscles such as the first interosseous muscle.

Williams test: Denervated skin responds differently to stimuli. This allows clear demarcation of the affected area in the hand when the injured hand is placed in water. Innervated skin wrinkles when submerged, but denervated skin does not.

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Diagnostic Procedures

Electrodiagnostic techniques have been refined and help a great deal in testing and diagnosing neuromuscular lesions. The 2 most common tests are the nerve conduction study (NCS) or nerve conduction velocity test and electromyography (EMG). EMG is often understood to refer to both tests.[69, 13]

Table 4. Electrodiagnostic Characteristics of Nerve Injury (Open Table in a new window)

ElectromyographyNerve Conduction Study/Nerve Conduction Velocity
FibrillationsVoluntary Muscle Unit Action PotentialSensory and Motor LatencyCompound Motor Action Potential/Sensory Nerve Action Potential
NormalNonePresentNormalNormal
Nerve block/neurapraxiaNoneNoneNone across the block, normal above and belowNormal above and below the block
Complete lesion/ axonotmesis, neurotmesisPresentNoneAbsentAbsent
IncompletePresentDecreased in distribution of injuryNormal or slightly prolonged (spread out)Reduced

NCSs use a percutaneous current to stimulate muscle and sensory nerves. This can result in a compound motor action potential or sensory nerve action potential, respectively. An active pickup generates the current that travels along the nerve and is read by another pickup a set distance away in either the efferent or afferent directions. This measures how fast the nerve conducted the stimulus (v = d/t). The current is gradually increased until a maximum response is obtained. This provides the basis for comparison of results over time. The distal ends of transected nerves have an NCS result that gradually falls over 7-9 days postinjury. This test can also help detect complete and partial nerve blocks.[69, 70, 13]

EMG tests record the depolarization potentials of active and spontaneous muscle movement. This is recorded as a muscle unit action potential. Resting muscle is normally electrically silent. Muscle distal to an injury may appear normal for several days after the injury until wallerian degeneration has advanced far enough for the muscle to become denervated and fibrillations to start. This often requires 14-21 days; thus, the best time for EMG diagnosis is 3-4 weeks after injury. Denervated muscle displays positive sharp waves and fibrillations, in that order.[69, 70, 71, 12]

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Contributor Information and Disclosures
Author

Subhas Gupta, MD, PhD, CM, FRCSC, FACS  Chief of Surgical Services, Professor of Surgery, Chairman, Department of Plastic Surgery, Director of Plastic Surgery Residency, Director of Comprehensive Wound Service, Department of Plastic Surgery, Loma Linda University School of Medicine

Subhas Gupta, MD, PhD, CM, FRCSC, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American Burn Association, American College of Phlebology, American College of Surgeons, American Medical Association, American Medical Informatics Association, American Society of Plastic Surgeons, California Society of Plastic Surgeons, Canadian Medical Association, Canadian Society of Plastic Surgeons, Canadian Society of Plastic Surgeons, College of Physicians and Surgeons of Ontario, Plastic Surgery Research Council, Quebec Medical Association, Royal College of Physicians and Surgeons of Canada, and Wound Healing Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Anthony E Sudekum, MD  Consulting Staff, Department of Plastic Surgery, St John's Mercy Health Center of St Louis

Anthony E Sudekum, MD is a member of the following medical societies: American College of Surgeons, American Society for Surgery of the Hand, and Missouri State Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

David W Chang, MD, FACS  Associate Professor, Department of Plastic Surgery, MD Anderson Cancer Center, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Nicolas (Nick) G Slenkovich, MD  Director, Colorado Plastic Surgery Center

Nicolas (Nick) G Slenkovich, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Society of Aesthetic Plastic Surgery, American Society of Plastic Surgeons, and Colorado Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Joseph A Molnar, MD, PhD, FACS  Director, Wound Care Center, Associate Director of Burn Unit, Associate Professor, Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine

Joseph A Molnar, MD, PhD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, American Society of Plastic Surgeons, North Carolina Medical Society, Peripheral Nerve Society, Undersea and Hyperbaric Medical Society, and Wound Healing Society

Disclosure: KCI, Inc. Honoraria Speaking and teaching; Integra Life Sciences Honoraria Speaking and teaching; Clincal Cell Culture Grant/research funds Co-investigator; KCI, Inc Wake Forest University receives royalties Other

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Hand nerve injury repair. Crushed median nerve at the elbow.
Hand nerve injury repair. Epineural repair of median nerve.
Hand nerve injury repair. Partial transection of ulnar nerve in the forearm.
Hand nerve injury repair. Posttraumatic neuroma.
Hand nerve injury repair. Excision of posttraumatic neuroma.
Hand nerve injury repair. Algorithm for the treatment of nerve injuries.
Table 1. Clinical Progression Based on Degree of Injury
DegreeSeverityDescriptionTinel SignProgress DistallyRecovery PatternRate of RecoverySurgery
FirstNeurapraxiaDemyelination with restoration in weeks—FastCompleteFast (days to 12 wk)None
SecondAxonotmesisDisruption of axon with regeneration and full recovery++CompleteSlow (3 cm/mo)None
ThirdDisruption of axon and endoneurium causing disorganized regeneration++Varies*Slow (3 cm/mo)Varies
FourthDisruption of axon, endoneurium, and perineurium, with intact epineurium and no regeneration+—NoneNoneYes
FifthNeurotmesisTransection of the nerve+—NoneNoneYes
SixthNeuroma-in-continuityMixture of one or more of the above conditionsVaries by fascicle, depending on injury
*Recovery is at least as good as nerve repair but varies from excellent to poor, depending on the degree of endoneurial scarring and the amount of sensory and motor axonal misdirection within the injured fascicle.
Table 2. Pathophysiology of Degeneration and Regeneration*
TimingDegenerationRegeneration
6 hoursNucleus becomes displaced and Nissl bodies break up, turning the cell basophilic.[15] Axon spikes appear briefly at the proximal end.
1 dayMacrophages begin entering the site of degeneration. This stimulates Schwann cell proliferation[19] Nerve function drops off with rupture of the blood-nerve barrier.[20] Distal stump begins to swell. Growth cones that contain a cytoskeleton form at the end of axon sprouts. Cell bodies of severed axons begin to enlarge as the cells become activated. The nucleus must become hypochromatic before elongation can occur.[21]
2 daysMitochondria in the axoplasm for distal transport.
3 daysDegenerative process involves all myelinated axons. Perineurial cells become enlarged and active. Axons shrink, and myelin begins to disintegrate. This is cleaned up by macrophages and Schwann cells and can take as many as 3 months.[14] Schwann cell proliferation peaks.[19]
4 daysRNA production increases in the cell body. Axon sprouting may begin at day 4 in a clean transection.[21]
1 weekInfiltration of inflammatory cells and RBCs occurs, along with myelin fragmentation.Schwann cells are activated and dividing. Growth cones can occasionally be seen within a Schwann cell, depending on the injury type. Swelling of axoplasm occurs in myelinated fibers, caused by mitochondria.
2 weeksSchwann cell proliferation has peaked, and endoneurial clearance is proceeding. As the contents of the tubes are removed, they shrink; if collagen is laid down, the reduced size can become permanent.[19, 22, 23] Schwann cells near regenerating axons stop myelin destruction and surround axons.[24]
3 weeksThe distal portion of the axon is finishing the degenerative processes, and the myelin is fragmenting.[21] The axon is surrounded completely by myelin, and the organelle count in the Schwann cell drops. Most of the regenerating axons are found outside the degenerating endoneurial tubes.[24] Metabolic changes in the axon peak.[20] Axon sprouting usually starts and can cross the anastomoses.[21]
4 weeksRemyelination starts, and perineurial cells decrease in size once the nerve is remyelinated.
*Times can vary extensively with the type and extent of damage.[25, 24, 14]
Table 3. Selection of Operative Procedure
SurgeryEnds Can ApproximateVascularized BedGraft PossibleProximal Portion IntactDistal Portion Intact
End-to-end closureYesYesYesYesYes
Nerve graftNoYesYesYesYes
Vascularized graftNoNoYesYesYes
ConduitNoNoNoYesYes
Nerve transferNoNoNoNoYes
Table 4. Electrodiagnostic Characteristics of Nerve Injury
ElectromyographyNerve Conduction Study/Nerve Conduction Velocity
FibrillationsVoluntary Muscle Unit Action PotentialSensory and Motor LatencyCompound Motor Action Potential/Sensory Nerve Action Potential
NormalNonePresentNormalNormal
Nerve block/neurapraxiaNoneNoneNone across the block, normal above and belowNormal above and below the block
Complete lesion/ axonotmesis, neurotmesisPresentNoneAbsentAbsent
IncompletePresentDecreased in distribution of injuryNormal or slightly prolonged (spread out)Reduced
Table 5. Common Donor Sites
Graft Donor SiteLength ObtainedSensory Deficit
Distal posterior interosseous nerve15-20 cmDorsal wrist joint
Lateral antebrachial cutaneous nerve15 cmLateral forearm surface
Medial antebrachial cutaneous20 cmMedial and anterior surface of forearm
Superficial radial25 cmDorsal radial hand surface
Lateral femoral cutaneous30 cmLateral and thigh
Anterior femoral cutaneous40 cmMedial and anterior thigh
Sural40 cmLateral foot surface and a portion of the heel
Saphenous25-40 cmMedial foot surface
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