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INTRODUCTION

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Neurologic injury following regional anesthesia is an uncommon, but dreaded, complication that creates high levels of anxiety in the patient and anesthesiologist.1,2,3 Most deficits will be sensory predominant and limited in duration and severity and can be handled with reassurance and appropriate follow-up. Discerning these cases from the rare complications that require emergent imaging, neurologic or neurosurgical consultation, or treatment is vital. This chapter focuses on recognition of postoperative neurologic complications, recognition of barriers to their recognition and evaluations, and an efficient, structured clinical approach to postanesthesia neurologic complications.

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BARRIERS TO RECOGNITION OF POSTOPERATIVE NEUROLOGIC INJURY

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Neurologic deficits in the postoperative setting may result from perioperative anesthetic procedures, surgical factors or iatrogenic injury, nerve compression occurring in the operative theater or during postoperative recuperation, or recognition of preexisting, but previously unappreciated, neurologic disease. While recognizing a neurologic complication immediately postoperatively would strongly implicate a perioperative complication (surgical, anesthetic, or positioning), there are many barriers to early recognition of perioperative neurologic complications. Postoperative sedation or analgesia may mask the complication.

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Given expected neurologic symptoms postoperatively after regional anesthesia, patients and caregivers may presume that the patient’s symptoms are block related. Patients therefore fail to complain of symptoms that may be unrelated to the block, and caregivers may fail to pursue reported symptoms because they presume they are block related, when in fact they may be distinct in distribution from the expected neurologic deficit. Patients also are unaware of what to expect postoperatively and may presume that postoperative symptoms are normal. Surgical dressings, drains, castings, and postoperative activity restrictions limit a patient’s activity level postoperatively such that a postoperative neurologic deficit may be unrecognized until more normal activity levels can be resumed. Finally, patients often see the postoperative period as a single time epoch (the perioperative blur) instead of individual days where precise recognition of symptom onset would have been useful in fine-tuning the differential diagnosis regarding the cause of a postoperative neurologic complication. In a prospective study of postoperative ulnar neuropathy, some patients in follow-up reported that their symptoms were noted “immediately” following surgery, while the prospective evaluations had clearly documented an onset of signs and symptoms more than 48 hours after surgery, hence exonerating the surgical and anesthesia operative teams and implicating a postoperative convalescence complication.4

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Given these barriers, only 77%–90% of sensorimotor and 20% of sensory nerve injury complications following total hip and knee arthroplasties were recorded during the procedural hospitalization.5,6 Studies that only include early neurologic injury (less than 48 hours postoperatively) likely underestimate risk.7

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Conversely, injuries recognized late often have (or perhaps more likely have) nonanesthetic/operative-related causes, including infection, postoperative inflammation, and consequences of immobilization or compression in the recovery period. The frequency of ulnar neuropathy in surgical cohorts more than 2 days postoperatively, for example, is similar to the frequency in medical ...

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