Transient recurrence of chemotherapy‐induced peripheral neuropathy in the immediate postoperative period following gynaecological surgery under general anaesthesia

Summary

Peripheral neuropathy is a well‐described side effect of certain chemotherapeutic agents, including taxanes, and often improves in the weeks following treatment. The recurrence of motor and sensory neuropathies after anaesthesia has not yet been described to our knowledge. We present a case of transient recurrence of chemotherapy‐induced peripheral neuropathy following general anaesthesia. Although an exact mechanism has not yet been described and is likely multifactorial in nature, anaesthetists should be prepared to address this phenomenon in the growing population of patients on chemotherapeutic agents.

1. Introduction

The diagnosis of motor and sensory deficits in the immediate postoperative period poses a considerable challenge due to its broad range of potential causes, including cerebrovascular accidents, perioperative peripheral nerve injuries, electrolyte abnormalities, residual neuromuscular blockade and the lingering effects of volatile anaesthetic exposure. The overall incidence of such events is quite rare; one study analysing data from a national database found that the frequency of non‐fatal stroke among 10,581,621 major non‐cardiac surgeries between 2004 and 2013 was 0.54% [1], while another study using data from a single university hospital over a 10‐year period found that 0.03% of 380,680 patients undergoing anaesthesia suffered a perioperative nerve injury [2].

Despite being a relatively uncommon postoperative complication, postoperative motor and sensory deficits must be promptly identified and treated to minimise long‐term morbidity and mortality. Patients with pre‐existing neuropathies present a particularly challenging scenario due to difficulties in assessing their baseline deficits alongside the potentially confounding effects of general anaesthesia. Peripheral neuropathy is a known sequelae of pathologies such as diabetes mellitus and vitamin deficiencies and is also a side effect of several medications, including some chemotherapeutic agents. The authors present a case detailing transient recurrence of chemotherapy‐induced peripheral neuropathy (CIPN) following general anaesthesia.

2. Report

A 57‐year‐old female patient with a BMI of 24.8 kg.m⁻² presented for laparoscopic bilateral salpingo‐oophorectomy as a risk‐reducing surgery given her history of triple‐negative breast cancer with BRCA2 mutation. Her medical history was otherwise notable for asthma, allergies to polyglactin and chlorhexidine gluconate‐isopropyl alcohol, and her medication list included paracetamol, albuterol sulphate and vitamin supplements. She had completed four cycles of adjuvant chemotherapy with docetaxel and cyclophosphamide, as well as adjuvant radiation therapy for her breast cancer. The last cycle of chemotherapy was approximately 5 months before the scheduled surgery. The patient had pre‐existing neuropathy in both hands from carpal tunnel syndrome, for which she had previously undergone corrective surgeries. Following her chemotherapy treatments, the patient would experience worsening of her existing neuropathies in the form of increased numbness in her hands and feet bilaterally, which she managed to some extent through exercise. On the day of surgery, neither the surgical nor the anaesthesia teams documented any abnormal physical examination findings.

The patient underwent general anaesthesia with a tracheal tube. On induction of anaesthesia, the patient received fentanyl, lidocaine, propofol and rocuronium, and then maintenance with sevoflurane. The patient was positioned in the lithotomy position with her upper extremities tucked appropriately by her side as per the institutional peri‐operative protocols. The anaesthetists administered fentanyl, hydromorphone and ketorolac for analgesia. Neuromuscular blockade was reversed at the conclusion of the procedure with sugammadex. The patient was breathing spontaneously and her trachea was extubated. However, upon arrival to the post‐anaesthesia care unit, she displayed significant weakness in her upper and lower extremities and reported sensory deficits in her limbs. The cranial nerve examination was unremarkable, and her vital signs were normal with no subjective respiratory weakness reported. Although the patient received an appropriate dose of sugammadex in the operating room before extubation, an additional dose was administered in the recovery area to rule out residual neuromuscular blockade as the cause of her weakness. A full electrolyte panel was checked which showed no abnormalities.

The neurology team was consulted and by the time of their assessment about three hours later the patient's weakness had begun to improve. Neurological examination revealed 3/5 (Medical Research Council grade) strength in hip flexion bilaterally, 4/5 strength in knee extension bilaterally and 4/5 strength in her right upper extremity and her left finger flexors and adductors. Sensation to pinprick and temperature was reduced in a stocking‐glove distribution. Deep tendon reflexes were normal. The neurologist concluded that the symptoms were consistent with a recrudescence of chemotherapy‐induced peripheral neuropathy following anaesthesia, deeming further imaging or investigations unnecessary. The patient was monitored overnight in the post‐procedure unit and then discharged the following day after complete resolution of her symptoms.

3. Discussion

This case highlights the wide differential diagnosis of postoperative motor and sensory deficits and a unique case presentation of the recurrence of CIPN being a diagnosis of exclusion. Chemotherapy‐induced peripheral neuropathy is a clinically significant and often debilitating complication of cancer treatment, characterised by damage to the peripheral nerves from chemotherapeutic agents – most commonly taxanes, platinum‐based agents and vinca alkaloids [3]. With the increasing efficacy and use of chemotherapy in oncological care, anaesthetists must possess a comprehensive understanding of associated side effects. Taxanes, such as docetaxel and paclitaxel, are extensively used in both adjuvant and neoadjuvant breast cancer treatment due to compelling evidence supporting their efficacy. Up to 70% of patients receiving taxane therapy develop CIPN [4], and a mounting body of evidence appears to favour docetaxel over paclitaxel for many patients with breast cancer [5]. Typical symptoms and manifestations of CIPN include numbness, tingling, muscle weakness and pain often presenting in a ‘stocking‐glove’ distribution [3]. While symptoms generally improve in the weeks following cessation of therapy [6], pharmacological treatments such as duloxetine, gabapentin, pregabalin and tricyclic antidepressants are commonly used to manage the neuropathic pain associated with CIPN [7, 8]. Moreover, several studies have also demonstrated the benefits of exercise therapy in both treating and preventing CIPN [8, 9]. Anaesthetists frequently provide care for patients on these chemotherapeutic agents, and as such, stand at the forefront of recognising and addressing potential side effects, thereby optimising perioperative decision‐making and patient outcomes.

As previously mentioned, the differential diagnosis for postoperative motor and sensory deficits is broad, and anaesthetists must be meticulous in their work‐up to avoid missing reversible causes. Patients should be kept warm throughout the peri‐operative period to rule out hypothermia as a cause of postoperative deficits. Residual neuromuscular blockade should always be considered when patients present with postoperative respiratory or motor impairments and should be treated with appropriate reversal agents. Anaesthetists should additionally remain vigilant for cerebrovascular accidents in the perioperative period, particularly if focal neurologic deficits are present. The patient in this report had a normal cranial nerve examination and her motor and sensory deficits were bilateral. Electrolyte abnormalities, particularly hypophosphatemia and hypokalaemia, can also present with muscle weakness. Laboratory testing should be employed promptly and deficiencies should be treated with intravenous replacement therapy. Furthermore, clinicians should consider specific peripheral nerve injuries in the context of surgical positioning. For instance, surgery in the lithotomy position, as in this case, has been associated with common peroneal nerve injury and necessitates appropriate preventative measures. Elbows should be carefully padded per institutional protocols to avoid compressive ulnar neuropathies.

To our knowledge, this is the first report of a recurrence of CIPN following general anaesthesia. As such, a potential mechanism behind this phenomenon has not yet been elucidated. Peripheral neuropathy, by nature, waxes and wanes. As previously detailed, there are a multitude of potential factors within the surgical period which may contribute to the occurrence of transient peripheral motor and sensory deficits. Anaesthetists should be exhaustive in their investigation to expeditiously rule out the most serious causes of postoperative deficits. After other organic aetiologies are ruled out, the transient recurrence of CIPN should then be considered. Because of the dynamic nature of the peri‐operative experience, it is less probable that a direct causal relationship between anaesthetic medications and the recurrence of CIPN exists. Nonetheless, postoperative motor and sensory neuropathies can be immensely stressful for patients. It is thus imperative that anaesthetists are aware of this phenomenon and consider discussing with patients before surgery that they may experience a transient recurrence of prior symptoms.