Open Traumatic Injuries of Peripheral Nerves

What are open traumatic injuries of peripheral nerves?

These are nerve injuries associated with an open wound and may result in motor and/or sensory deficits.

Peripheral nerves carry signals from the brain and spinal cord to the muscles (movement) and from the skin/joints back to the brain (sensation). In an open injury, a nerve may:

• be partially cut (partial transection),
• be completely cut (complete transection),
• or remain in continuity but sustain severe internal damage (crush/scarring) that blocks conduction.

Distinguishing transection from an in-continuity injury is crucial, because the former requires surgical reconstruction, while the latter often begins with observation and objective documentation of regeneration.

Which mechanisms cause these injuries—and why does the type of transection matter?

The mechanism of injury provides strong clues about whether the nerve is transected and whether the injury is sharp or blunt/high-energy.

Clinically, open nerve injuries most commonly result from:

• Penetrating injury (e.g., a sharp object or glass/metal fragments): often causes a sharp transection.
• Through-and-through / high-energy injury: more often produces crush and indirect forces, with the nerve remaining “in continuity.”

A sharp transection typically has clearer injury margins and is therefore better suited for primary repair. By contrast, a blunt/crush-type transection is often associated with extensive internal injury along the nerve, making delayed reconstruction preferable once viable tissue has clearly “declared itself” over time.

What are the main types of nerve injury (neurapraxia–axonotmesis–neurotmesis)?

This classification explains why some injuries recover spontaneously while others require surgical repair.

In clinical practice, we use a “functional” framework to understand the severity of injury:

• Neurapraxia (mild, reversible conduction block): the nerve is not cut, and function typically returns with time.
• Axonotmesis: the axons are injured, but the nerve’s connective-tissue scaffolding is preserved to some degree; regeneration is possible, often slowly.
• Neurotmesis (complete transection): the nerve is “cut,” and spontaneous recovery is not expected without microsurgical repair.

Practical rule: a complete neurologic deficit after an open injury raises strong concern for transection and warrants timely specialist evaluation.

What symptoms are typical, and what should I watch for?

Symptoms depend on which nerve is affected and whether the injury involves motor function, sensation, or both.

Common findings include:

• Weakness or inability to perform specific movements (e.g., finger/wrist extension, ankle dorsiflexion).
• Numbness or loss of sensation in a defined skin territory.
• Shooting/burning pain or allodynia (pain from light touch).
• Loss of fine motor control (especially in the hand/fingers).

Symptoms that require urgent attention:

• Progressive weakness or spreading numbness/sensory loss.
• Signs of vascular injury (cold, pale limb; severe pain; absent pulses).
• Severe pain with swelling/tightness (concern for compartment syndrome).
• Signs of wound infection (fever, increasing redness, purulent drainage).

What is the immediate management in the acute setting?

The goal is to stabilize the patient, manage the wound safely, and promptly identify a possible nerve transection.

In the acute phase, priorities include:

• Bleeding control and assessment of vascular integrity.
• Wound cleansing/care and infection prevention (as appropriate: antibiotics, tetanus prophylaxis).
• Neurologic examination before and after any intervention (motor–sensory–pain).
• Immobilization when there is associated tendon/bone injury or when limb protection is required.
• Referral to a specialized team when transection is suspected or when there is a significant neurologic deficit.

Early documentation of neurologic function (motor/sensory findings) is essential, both for selecting the correct treatment strategy and for accurately tracking recovery over time.

How is the clinical diagnosis made (neurologic exam and “nerve mapping”)?

The clinical exam is the cornerstone: it identifies which nerve is affected and how severe the deficit is.

Assessment typically includes:

• Motor testing: targeted muscles corresponding to specific nerves/branches.
• Sensory testing: mapping cutaneous nerve territories (light touch and pinprick).
• Reflex testing when indicated.
• Wound assessment: trajectory of injury relative to known nerve anatomy.

In an open injury, a complete motor/sensory deficit in the distribution of a specific nerve increases the likelihood of partial or complete transection and guides the need for surgical exploration.

What is the role of electrophysiologic testing, and when is it useful?

Electrophysiologic studies help document axonal regeneration, but timing is critical for meaningful interpretation.

Electromyography (EMG) combined with nerve conduction studies can:

• document whether there is conduction across the injury site,
• identify signs of denervation and track reinnervation,
• support decisions about delayed surgical exploration, especially when clinical recovery is absent.

Very early testing (within the first days) may not yet reveal the full extent of denervation. For that reason, timing is individualized based on the clinical picture + time since injury.

When is urgent management/surgical exploration required?

In an acute open injury (sharp laceration) with a complete neurologic deficit, early exploration may allow immediate reconstruction.

Common indications for urgent surgical exploration include:

• Injury from a sharp object with a complete neurologic deficit consistent with transection.
• An open wound with visible injury/exposure of neural structures.
• Combined tendon/vascular/bony injury requiring surgery, where simultaneous nerve assessment is appropriate.
• Limb-threatening complications (vascular injury, compartment syndrome).

If exploration confirms a partial or complete sharp transection, the goal is primary reconstruction. If the injury reflects blunt crush/traction, reassessment and planning for delayed reconstruction is often preferred.

When is primary end-to-end repair performed, and what is the goal?

Primary repair is ideal when the transection is sharp and a tension-free coaptation can be achieved.

Primary reconstruction is generally recommended when:

• the transection is sharp (knife or similar),
• the nerve ends are viable with minimal trimming required,
• coaptation can be achieved with direct approximation of the nerve ends without tension.

Repair is performed using microsurgical techniques, aiming for: precise alignment, minimal tissue trauma, and stable, tension-free repair with as few sutures as necessary.

When is delayed reconstruction preferred, and what does it involve?

In blunt/crush transection, delaying reconstruction for several weeks allows viable tissue to “declare itself” and improves decision-making.

Immediate neurorrhaphy after a blunt, high-energy injury can be suboptimal, because internal nerve damage often extends beyond the visibly injured segment. In such cases, neuromas can develop at the cut ends (stumps) even later on, as axons attempt to regenerate. These neuromas may disrupt normal conduction even after a technically successful repair.

A two-stage strategy is often preferred:

• Initial exploration: wound debridement, identification of nerve ends, and protection/marking of the transected nerve stumps.
• Secondary reconstruction after a few weeks: trimming back the stumps until healthy nerve tissue is reached, followed by delayed end-to-end repair when feasible or reconstruction using a graft.

Treatment planning is individualized, taking into account the mechanism of injury, neurologic deficits, associated injuries, wound status, and any early clinical signs of nerve regeneration.

When is a graft or “conduit” needed, and what should I expect?

When excision of nonviable tissue creates a “meaningful gap” between nerve ends (inability to approximate without tension), reconstruction requires a nerve graft or, in selected cases, a conduit.

After removal of the damaged segment/neuroma, a gap often remains between the nerve ends. If the ends cannot be approximated without tension, reconstruction may include:

• Autologous nerve graft (autograft): the most reliable option when the gap is significant. Purely sensory donor nerves are commonly used (e.g., the sural nerve), with acceptable donor-site morbidity.
• Reconstruction conduit: may be used for very small gaps and in selected small-caliber, primarily sensory nerves. Indications remain limited and case-dependent.

After reconstruction, axonal regeneration is slow and requires substantial time. In parallel, physical and occupational therapy protects joints, preserves range of motion, and strengthens functional recovery while reinnervation proceeds.