Case report and literature review of chronic neuropathic pain associated with peripheral venous cannulation
Correspondence to: S. Gohil
We report a case of neuropathic pain following peripheral venous cannulation for an elective surgical procedure and discuss the various mechanisms by which this could occur. The mostly likely trigger in this case is phlebitis as the onset of symptoms coincided with the local infection. Neuropathic pain can occur following innocent interventions and its impact on the patient’s quality of life may be reduced by timely recognition and management.
A 42-year-old right-handed male underwent elective craniotomy for stereotactic biopsy of a left frontal lobe tumour. He had a longstanding history of focal seizures (short-lived sensory disturbance in his right upper limb). His pre-operative medications included carbamazepine and levetiracetam for epilepsy, propranolol prophylaxis for migraines and a statin. In the anaesthetic room, aseptic cannulation (70% v/v isopropyl alcohol swab) of the dorsal aspect of the left hand with a 20-G intravenous cannula was uneventful and the patient did not complain of undue pain at the time (as documented in the cannula care pathway). This cannula was used for intravenous induction of anaesthesia; after induction, another cannula was inserted in the dorsum of the right hand for intra-operative access and fluid administration. The intra-operative period and recovery phase were initially uneventful. However, on the first postoperative day, the patient described pain at the site of insertion of the 20-G cannula in the dorsum of the left hand; swelling and reddish discolouration were noticed. He had developed phlebitis and local cellulitis which was managed by immediate removal of the cannula, oral doxycycline and intravenous gentamicin. His discharge from hospital was delayed by two days for this treatment until the phlebitis and cellulitis cleared.
Although the infection subsided, he continued to experience residual discomfort in the area. Six months after surgery, he described pain with a severity of 5 out of 10 at rest on a visual analogue score, aggravated by movement of the left hand, intermittent swelling, redness, sensation of heat and weakness in the left arm. He was then referred to the rheumatology team where a diagnosis of complex regional pain syndrome was proposed, based on clinical signs and symptoms of hyperalgesia, allodynia to cold, vasomotor, sudomotor and trophic changes. Despite treatment with paracetamol, ibuprofen, codeine, tramadol, gabapentinoids, topical capsaicin and physiotherapy, the patient had persistent symptoms at the cannula insertion site. The patient was already taking carbamazepine for seizures, which may have helped, although the evidence that it is effective for neuropathic pain, except trigeminal neuralgia, is weak . Investigations, including magnetic resonance imaging scan of the hand, were normal. He was referred to the pain management clinic a year after developing pain. Three years from the initial insult, he continues to suffer from localised discomfort. Although our patient is a highly motivated individual and has returned to active employment with workplace modifications, the persistent pain has had a significant impact on his quality of life.
Following the surgery, focal seizures in the right upper limb subsided. The frontal lobe brain tumour histology showed a dysembryoplastic neuroepithelial tumour, which has since been managed by clinical and radiological surveillance. As the tumour was restricted to the left frontal lobe it is unlikely that the tumour bears any relation to the subsequent development of pain in the left hand.
Neuropathic pain is due to primary lesion or dysfunction of the nervous system. In our case, it is less likely to be due to direct nerve injury, as the patient did not experience any undue pain at the time of cannula insertion. It is most likely to be secondary to inflammatory changes due to phlebitis. The radial nerve carries a particular anatomic pre-disposition to this complication, probably due to its superficiality and its lack of cushioning from muscle and fatty tissue. Anatomical relationships between upper extremity superficial veins and cutaneous nerves are so intimate that needle–nerve contact during venepuncture must be common . Following nerve injury, the development of ectopic activity may be particularly important for the development of hyperalgesia, allodynia and ongoing pain . This produces a clinical picture of neuropathic pain, which includes features of dysaesthesia, paroxysmal pain, allodynia and pain in the absence of ongoing tissue damage .
The evidence regarding the incidence of neuropathic pain from cannulation is mostly from subjects undergoing blood donation, where cannulation is for a short period of time and more often in the antecubital fossa rather than in the dorsum of the hand. A 1996 study of 419 000 blood donations showed that 1:6300 donors had a nerve injury resulting in radiating pain and loss of muscle power. Many patients recovered in a month and most recovered within six months. Only four were left with a mild, localised residual numbness, but not pain . Over a two-year period in a blood transfusion centre, Berry and Wallis reported six patients with painful nerve injuries after venepuncture in the antecubital fossa, with an annual incidence of 1:25 000 . A summary of studies between 1977 and 1985 reporting venepuncture associated nerve injuries collated 93 cases; more than two thirds reported satisfactory outcome at three months, but approximately 17% were left with permanent sequelae . These case series predominantly represent pain due to direct nerve injury and none reported any association with phlebitis or infection.
Alongside direct nerve injury and phlebitis, thrombophlebitis, soft tissue infection, haematoma and extravasation of fluid may increase the risk of neuropathic pain following cannulation. In our case, the mostly likely trigger for neuropathic pain may be a combination of phlebitis and local soft tissue infection. The early management of infection was timely, but management of neuropathic pain was delayed. This patient was only referred to the pain management clinic one year after the onset of neuropathic pain.
The question of whether poorly managed acute pain can lead to chronic pain has not been completely resolved, but it is believed that some type of stimulus or continuous nociceptive process provides the impetus for chronic pain to develop . Factors other than direct nerve insult may play a role in the development of persistent pain. These include: genetic variables; old age; intense pain in the acute phase; the individual’s psychological pre-disposition (e.g. depression, catastrophising); neuropathic sensory abnormalities; and persistent severe pain at three months [9, 10]. Certainly, there is also evidence to suggest that clinical conditions, such as migraine (from which our patient suffered), fibromyalgia syndrome, irritable bowel, irritable bladder, backache and Raynaud’s syndrome, might also have an underlying genetic pre-disposition to the development of post-surgical pain .
Aseptic precautions at the time of insertion, vigilant observation of cannulae, early recognition and aggressive treatment of infection may reduce the incidence of phlebitis/cellulitis. In the UK, cannula care pathways have highlighted these facts and reduced the incidence of peripheral venous cannula complications . Venepuncture-induced nerve injuries resulting in persistent neuropathic pain are rare, but the true incidence remains unknown and they may be underreported. A small proportion of patients can develop persistent pain. Early identification and management may limit or prevent chronicity.
No external funding and no competing interests declared.