Management of Complications in Sensory Nerve Surgery

4 Management of Complications in Sensory Nerve Surgery

Pierluigi Tos, Alessandro Crosio, and Simona Odella

Abstract

Complications of nerve injuries repair or neurolysis in the hand or elsewhere include no recovery or incomplete sensory recovery, painful neuroma, painful scar neuropathy, and cold intolerance.

All of these can be summarized as painful neuropathy. It is important to identify this condition immediately. The longer the symptoms exist, the worse the resolution obtained is: the neuropathic pain becomes chronic. Furthermore, painful neuropathy can also lead to a complex regional pain syndrome II (CRPS II), a chronic (lasting greater than 6 mo) pain condition with burning pain and allodynia (pain to nonpainful stimuli).

In presence of a symptomatic neuroma or a scar neuropathy, surgical treatment can lead to a good result. But it is important to emphasize that surgical treatment has limited capacity in symptoms reduction when previous attempts have been performed.

Furthermore, in chronic neuropathic condition nonresponsive to surgery, a multidisciplinary approach is indicated.

The role of rehabilitation process following nerve injury and repair, a relearning process, is the key to preventing discomfort and pain after repair. The sensory re-education programs are very important for the recovery of functional sensibility and are essential before and after any surgical attempt in nerve surgery. Dysesthesia and disuse of the hand may occur, and are best treated with an aggressive desensitization and sensory re-education program under the supervision of a hand therapist.

Keywords: pain, neuroma, traction neuropathies, nerve injury, complications

4.1 No Recovery or Incomplete Sensory Recovery

4.1.1 Definition

About one-third of digital nerve repair results are stated as poor in adults. This is true both for primary and secondary, with or without a nerve graft/conduit repair, as reported in the meta-analysis by Paprottka et al.1

Nowadays, there is no surgical repair technique that can guarantee full recovery of tactile discrimination in the hand of an adult patient. In contrast, very young individuals usually reach a complete recovery.

4.1.2 Treatment

If no recovery occurs after nerve surgery, a secondary operation is always possible.² The lack of recovery is sometimes due to rupture of the suture site, sometimes due to a poor trimming of the nerve stumps to “healthy axons.” In other cases, the cause is not clear.

Conduits or nerve grafts may give good results even after a long period.

The end organs of skin include Meissner and Pacinian corpuscles, Ruffini endings, Merkel cells, and free nerve endings. Pacinian and Meissner Corpuscle are quickly adapting fiber receptors that mediate moving touch and vibration. Merkel mediate slow adapting fibers for pressure and constant touch. The Ruffini endings play a role in vibration and proprioception. The free nerve endings are free unmyelinated fibers that are sensitive to touch, temperature, and pain. Pacinian corpuscle receives only one axon and normally do not reinnervate. All other sensory receptors are able to reinnervate.

Sensory reinnervation can occur, differently than motor reinnervation, many years after denervation. In this case, sensory organs may undergo changes that alter the ultimate quality of reinnervation. After a long-lasting period of denervation, the protective sensation can be achieved more by means of free nerve endings than receptors reinnervation.³

The technique indicated to restore the continuity of a sensory nerve depends on the length of the residual gap after the trimming of the two stumps. It is important to suture a proximal stump correctly trimmed without residual interfascicular scar. Furthermore, a direct suture should be performed without tension. It is demonstrated that an excessive tension at the suture site induces impaired activation of Schwann cells, and a higher amount of apoptotic Schwann cells, with a subsequent deteriorated axonal outgrowth and the well-known scarring across the nerve repair.⁴^,⁵^,⁶ If the gap at the end of the nerve stumps resection is between 2 and 4 cm, a nerve conduit can be used to avoid a withdrawal of a healthy nerve as a graft, whereas if the gap is longer than 3 to 4 cm, a nerve graft should be indicated. It seems, without a clear evidence, that in sensory nerves the critical gap is 3 to 4 cm. It has been proven that there is no optimal surgical technique for digital nerve repair up to 3 to 4 cm.¹

4.1.3 Rehabilitation

A specific rehabilitation program to enhance the residual sensibility should be started. MacKinnon and Dellon stated that up to S3+ results are classified as “poor,” but we personally think that an S3 (discrimination between 7 and 15 mm, recovery of pain and touch sensibility without an over-response, as shown in Table 4‑1) should be considered a good result.

Table 4.1 Sensory recovery outcome, the Highet classification, static two-point discrimination (s2PD), moving two-point discrimination (m2PD), and recovery of sensibility

Sensory recovery outcome	Highet	s2PD	m2PD	Recovery sensibility
Failure	S0			No recovery of sensibility in the autonomous zone of the nerve
Poor	S1			Recovery of deep cutaneous pain sensibility with the autonomous zone of the nerve
	S1+			Recovery of superficial pain sensibility
	S2			Recovery of superficial pain and some touch sensibility
	S2+			As in S2, but with over response
	S3	>15 mm	>7 mm	Recovery of pain and touch sensibility with disappearance of over response
Good	S3+	7–15 mm	4–7 mm	As in S3, but with good localization of the stimuli and imperfect recovery of 2PD
Excellent	S4	2–6 mm	2–3 mm	Complete sensory recovery
Source: Modified from S. E. Mackinnon and A. L. Dellon. Surgery of the Peripheral Nerve. New York: Thieme Medical Publishers; 1988.

Tips and Tricks

If the patient presents a hypoesthesia, it could be considered a “normal” result and no other surgery is indicated (S1+, S2).

4.2 Neuropathy

Neuropathy is defined by the IASP (International Association for the Study of Pain) as “pain caused by a lesion or disease of the somatosensory system.”7

Neuropathy is not a single disease with a single origin, but rather a group of symptoms caused by different pathologies ranging from diabetes to nerve compression and nerve injury, with the unifying cause that it is pain developed by a lesion or disease of the somatosensory system.

The core symptoms of neuropathic pain are temperature hyperesthesia (a painful stimulus perceived as more painful than normal), mechanical allodynia (a nonpainful stimulus, perceived as painful), and spontaneous burning pain also known as spikes.

For most of the underlying diseases the cause of the neuropathic component is still unclear, also because they are difficult to study in patients. Injury of the peripheral nerves is more clear in their pathology and a number of experimental animal models exist for the study of the development of neuropathic pain, like the “spared nerve injury model” and the “spinal nerve constriction injury model.”⁸

It remains difficult to assess pain in animals directly, but these models provide indirect clues to the development of neuropathic pain. Using these models, it has been described that the cutaneous denervation following a nerve injury facilitates development of neuropathic pain. This is mediated by collateral sprouting fibers from adjacent uninjured nerves.⁹^,¹⁰^,¹¹

This is probably why upper limb surgeons have maintained the thought of always repairing a nerve, as soon as possible, preventing a denervated area of the skin, diminishing the chances of developing neuropathic pain.

Clinically, the patient with neuropathic pain presents with brush pain, spontaneous burning pain, and severe temperature hyperalgesia. This usually means no garment can be worn on the afflicted area, a cool breeze can be excruciatingly painful, rain becomes a fearful event, and the area cannot be taken under a shower. Treatment of neuropathic pain remains difficult as long as we do not fully understand the mechanisms behind the origins of the pain. Pain medication is often trial and error, and usually neuropathic pain evolves in chronic neuropathic pain.¹² Grace et al demonstrated that prolonged pain is an unrealized and clinically concerning consequence of the abundant use of opioids in chronic pain.¹³ Surgery for neuropathic pain is only successful if a specific cause for the pain is present, but most often it only partly resolves.

4.3 Hyperalgesia/Hyperesthesia

Hyperalgesia can be divided into primary and secondary. The distinction depends on how centralized the symptoms are.

The first case is a condition in which the primary afferent A-delta and C-nociceptors in the injured region begin to respond to normally non-noxious stimuli, respond to noxious stimuli in an amplified fashion, and may also develop spontaneous activity. This is due to genetic and molecular remodeling of the primary nociceptors as well as an “inflammatory soup” of chemicals present in the injured site.

Secondary hyperalgesia describes increased sensitivity in areas of the body that are outside the injured site and are therefore thought to reflect altered CNS function. Such situations indicate that the CNS is operating in a sensitized state. It responds in an amplified fashion resulting in pain evoked also by nonpainful stimuli. Both peripheral and CS play an important role in creating and maintaining neuropathic pain.

When the patient is affected by hyperalgesia or hyperesthesia, the treatment consists of desensitization programs and the use of plaster with local anesthetic drugs to reduce the symptoms.14

4.4 Cold Intolerance

Cold intolerance or sensitivity was initially thought of as a vascular problem¹⁵ but is currently more viewed as one of the neuropathic symptoms (temperature hyperesthesia). It is frequently seen following hand injury and fractures (38%)¹⁶ or for instance surgery for Dupuytren’s disease, up to 63% of patients.¹⁷ However, in approximately 80% of patients with nerve injury, cold intolerance will develop.¹⁸ This mechanism is also seen in rodents.¹⁹ Conditioned pain modulation seems to be reduced in patients with cold intolerance.²⁰ Classically cold intolerance is thought to diminish after a number of years, but recent studies have shown that the symptoms can last for longer periods. Fortunately, only one-fifth of these go on to develop severe or extreme symptoms, and of course this is more predominant in areas with colder climates. For many patients, treatment consists of adaptation and protective strategies when exposed to cold temperatures, like wearing heated gloves and raising the core temperature.²¹

4.5 Painful Neuropathies

4.5.1 Definition

This group of pathological conditions merges painful neuroma and painful scar neuropathy or traction neuropathy. These are the most important complications following peripheral nerve injury, seriously affecting patients’ daily life. The true incidence of symptomatic neuroma is unknown and is estimated at approximately between 2 and 60% of patients involved in peripheral nerve injury.²²^,²³^,²⁴^,²⁵^,²⁶

Interestingly, in digital amputations, only about 7% of the patients develop a painful neuroma.²⁷^,²⁸

A neuroma is part of the normal biological process in a transected and unreconstructed nerve. The axons sprout and grow, but without direction and form the neuroma, if there is no connection to a distal part of the nerve. It is absolutely unclear why a neuroma becomes a painful neuroma.

Two processes are responsible for pain: (1) persistent mechanical or chemical irritation of the axons within the neuroma and (2) the development of spontaneous and disturbing sensory symptoms²⁹ caused by persistent stimulation of the axons within the neuroma and accompanied by the development of spontaneous activity of neurons within the dorsal root ganglion, dorsal horn of the spinal cord, or even more proximal level.³⁰ Neuromas are provoked by axons sprout into the surrounding scar tissue. It seems that an up-regulation of sodium channels, adrenergic, and nicotinic cholinergic receptors leads to abnormal sensitivity and spontaneous activity of injured axons.³¹ During this time a central sensitization in the spinal cord and sensory cortex takes place.

The so-called “scarring neuritis” or “scar neuropathy,” as defined by Elliot,²¹ encompass all the conditions related to formation of perineural and intraneural fibrotic tissue involving neurological symptoms and induced by a nerve injury. Perineural scarring and consequently traction neuropathy has traditionally been associated to the complications of nerve decompression surgery. Nerve tethering in the surgical scar is still the main cause of symptoms related to perineural scarring. The problem of neuropathic pain can be present even only after surgery that “touches” the peripheral nerve, without interrupting the fibers, and causes a perineural scarring reaction. This problem can benefit from a new surgery with the application of antiadherent gels or adipofascial flaps. All these procedures aim to promote the normal sliding of the nerve on the surrounding tissues. It is absolutely not clear why certain patients are more susceptible to neuroma formation than others.

Spontaneous pain, allodynia, hyperalgesia, and cold intolerance are the main symptoms reported by the patient.

The neuroma can be:

●Terminal without possibility to a distal reconnection (i.e., a digital neuroma or the distal nerve trunk is not available for multiple surgery, loss of substance).

●Terminal with the possibility to a connection with a distal nerve stump (i.e., sensory radial nerve branch as a complication of surgery or traumatic transection of a nerve).

●In continuity (after a nerve suture or a trauma):

Without residual function

With a residual function

4.5.2 Diagnosis

The diagnosis of painful neuropathy is based on history and physical examination. The history of a nerve injury is accompanied by pain and typical symptoms with a defined neural anatomic distribution often with cold intolerance. History is crucial to establish the cause of symptoms: is it related to a simple nerve decompression, reconstruction, direct trauma, or posttraumatic scarring? Physical examination and pain type—at rest or elicited by movement or mechanical stimuli—may provide information on lesion type. Pain at rest commonly entails that the scar involves the deep nerve structure. Perineural scarring usually induces nerve tethering, which is exacerbated by movement. Another important information is the presence of a painful Tinel sign. A local anesthetic injection can be helpful to understand if the symptoms are related just to the neuroma or if they have already centralized. Furthermore, instrumental examination—US or magnetic resonance imaging (MRI)—can confirm the diagnosis. It is suggested to pair a simple assessment of pain, such as the visual analog scale (VAS), with a more detailed pain and function questionnaire, such as the DASH or PROMIS. Serial assessment with these forms facilitates tracking progress that is sometimes not apparent to the patients themselves.

Once you have completed the physical examination, diagnostic nerve blocks can be performed to determine what effect decompression or neurectomy might have in that region. Blocks provide patients with an idea of the potential area of altered sensation with nerve resection but do not guarantee operative success. On the other hand, if block doesn’t relieve the pain, it means that no surgical procedure can solve the problem and surgery should be avoided.32

Ultrasound and dynamic US may also be used in experienced hands to diagnose the perineural scar neuropathy or an intraneural neuroma.

It remains unclear why the same pathological anatomy problem can cause pain in some patients and nothing in others.

4.5.3 Principles of Treatment

Every surgical procedure must be preceded by appropriate medical treatment and by pharmacological and physical therapy with dedicated operators for at least 6 months. There is no consensus on surgery timing.³³ As a general rule, surgery is indicated when medical and physical therapies have failed to bring benefit.

Different surgical treatments must be performed depending on the cause of pain. For the painful “scar neuropathy,” treatment consists of a surgical exploration, neurolysis under magnification, and procedures aimed at preventing new scar formation such as flap coverage and application of antiadhesion devices. In case of a terminal neuroma or a neuroma without function, the procedure consists of resection of the neuroma and reconstruction of the nerve trunk with graft if it is possible. In other cases, the terminal nerve stump has to be transferred and covered with well-vascularized soft tissue.

Prevention and Treatment of Terminal Neuroma

Prevention of terminal neuroma formation should be attempted during revision amputation through some surgical precautions as avoiding tension, care in soft tissue management, and accurate debridement. Despite these precautions, a painful stump cannot be excluded because of the arise of a new neuroma in the apex of the cut nerve.³⁴ Actually just the targeted muscle reinnervation is the unique technique that limits the neuroma formation.³⁵ The prevention of neuroma formation in a nerve suture site due to “painful sprouting” can be obtained by “the vein conduit coverage” of the suture site as described by Alligand-Perrin et al.³⁶ This technique is useful for both the first nerve suture and the nerve grafting. We routinely apply this procedure in our department as shown in Fig. 4‑1.