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.

Short tau inversion recovery MRI

This is a unique form of magnetic resonance imaging (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.^{[67, 13, 53]}

Ultrasonography

A study by Endo et al indicated that the reliability of short-axis ultrasonography for assessing digital nerve injuries of the hand is greater than previous research had suggested, while long-axis ultrasonography has reduced efficacy in such evaluations. The report found that of laceration images obtained with long-axis imaging, the injury was demonstrated on 10 images and absent on four. However, all 20 lacerations assessed with short-axis ultrasonography appeared on the image.^[68]

Other Tests

Sensory tests^{[4, 69, 70, 71]}

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, 70, 71]}

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.

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.^{[72, 13]}

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

	Electromyography		Nerve Conduction Study/Nerve Conduction Velocity
	Fibrillations	Voluntary Muscle Unit Action Potential	Sensory and Motor Latency	Compound Motor Action Potential/Sensory Nerve Action Potential
Normal	None	Present	Normal	Normal
Nerve block/neurapraxia	None	None	None across the block, normal above and below	Normal above and below the block
Complete lesion/ axonotmesis, neurotmesis	Present	None	Absent	Absent
Incomplete	Present	Decreased in distribution of injury	Normal 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.^{[72, 73, 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.^{[72, 73, 74, 12]}

Treatment & Management

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Media Gallery

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.

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Table 1. Clinical Progression Based on Degree of Injury

Degree	Severity	Description	Tinel Sign	Progress Distally	Recovery Pattern	Rate of Recovery	Surgery
First	Neurapraxia	Demyelination with restoration in weeks	—	Fast	Complete	Fast (days to 12 wk)	None
Second	Axonotmesis	Disruption of axon with regeneration and full recovery	+	+	Complete	Slow (3 cm/mo)	None
Third		Disruption of axon and endoneurium causing disorganized regeneration	+	+	Varies*	Slow (3 cm/mo)	Varies
Fourth		Disruption of axon, endoneurium, and perineurium, with intact epineurium and no regeneration	+	—	None	None	Yes
Fifth	Neurotmesis	Transection of the nerve	+	—	None	None	Yes
Sixth	Neuroma-in-continuity	Mixture of one or more of the above conditions	Varies 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*

Timing	Degeneration	Regeneration
6 hours	Nucleus becomes displaced and Nissl bodies break up, turning the cell basophilic.^[15]	Axon spikes appear briefly at the proximal end.
1 day	Macrophages 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 days		Mitochondria in the axoplasm for distal transport.
3 days	Degenerative 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 days		RNA production increases in the cell body. Axon sprouting may begin at day 4 in a clean transection.^[21]
1 week	Infiltration 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 weeks	Schwann 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 weeks	The 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 weeks		Remyelination 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

Surgery	Ends Can Approximate	Vascularized Bed	Graft Possible	Proximal Portion Intact	Distal Portion Intact
End-to-end closure	Yes	Yes	Yes	Yes	Yes
Nerve graft	No	Yes	Yes	Yes	Yes
Vascularized graft	No	No	Yes	Yes	Yes
Conduit	No	No	No	Yes	Yes
Nerve transfer	No	No	No	No	Yes

Table 4. Electrodiagnostic Characteristics of Nerve Injury

	Electromyography		Nerve Conduction Study/Nerve Conduction Velocity
	Fibrillations	Voluntary Muscle Unit Action Potential	Sensory and Motor Latency	Compound Motor Action Potential/Sensory Nerve Action Potential
Normal	None	Present	Normal	Normal
Nerve block/neurapraxia	None	None	None across the block, normal above and below	Normal above and below the block
Complete lesion/ axonotmesis, neurotmesis	Present	None	Absent	Absent
Incomplete	Present	Decreased in distribution of injury	Normal or slightly prolonged (spread out)	Reduced

Table 5. Common Donor Sites

Graft Donor Site	Length Obtained	Sensory Deficit
Distal posterior interosseous nerve	15-20 cm	Dorsal wrist joint
Lateral antebrachial cutaneous nerve	15 cm	Lateral forearm surface
Medial antebrachial cutaneous	20 cm	Medial and anterior surface of forearm
Superficial radial	25 cm	Dorsal radial hand surface
Lateral femoral cutaneous	30 cm	Lateral and thigh
Anterior femoral cutaneous	40 cm	Medial and anterior thigh
Sural	40 cm	Lateral foot surface and a portion of the heel
Saphenous	25-40 cm	Medial foot surface

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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 College of Phlebology, Canadian Society of Plastic Surgeons, College of Physicians and Surgeons of Ontario, Plastic Surgery Research Council, American Society of Plastic Surgeons, Royal College of Physicians and Surgeons of Canada, Wound Healing Society, California Society of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Medical Informatics Association, Canadian Medical Association, Canadian Society of Plastic Surgeons, Quebec Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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.

Chief Editor

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

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

Disclosure: Received grant/research funds from Clinical Cell Culture for co-investigator; Received honoraria from Integra Life Sciences for speaking and teaching; Received honoraria from Healogics for board membership; Received honoraria from Anika Therapeutics for consulting; Received honoraria from Food Matters for consulting.

Additional Contributors

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, Missouri State Medical Association

Disclosure: Nothing to disclose.