This review summarizes current knowledge concerning incidence, risk factors, and mechanisms of perioperative nerve injury, with focus on local anesthetic-induced neurotoxicity. Perioperative nerve injury is a complex phenomenon and can be caused by a number of clinical factors. Anesthetic risk factors for perioperative nerve injury include regional block technique, patient risk factors, and local anesthetic-induced neurotoxicity. Surgery can lead to nerve damage by use of tourniquets or by direct mechanical stress on nerves, such as traction, transection, compression, contusion, ischemia, and stretching. Current literature suggests that the majority of perioperative nerve injuries are unrelated to regional anesthesia. Besides the blockade of sodium channels which is responsible for the anesthetic effect, systemic local anesthetics can have a positive influence on the inflammatory response and the hemostatic system in the perioperative period. However, next to these beneficial effects, local anesthetics exhibit time and dose-dependent toxicity to a variety of tissues, including nerves. There is equivocal experimental evidence that the toxicity varies among local anesthetics. Even though the precise order of events during local anesthetic-induced neurotoxicity is not clear, possible cellular mechanisms have been identified. These include the intrinsic caspase-pathway, PI3K-pathway, and MAPK-pathways. Further research will need to determine whether these pathways are non-specifically activated by local anesthetics, or whether there is a single common precipitating factor.
Background: The majority of patients admitted to the intensive care unit (ICU) experience severe hypotension which is associated with increased morbidity and mortality. At present, prospective studies examining the incidence and severity of hypotension using continuous waveforms are missing. Methods: This study is a prospective observational cohort study in a mixed surgical and non-surgical ICU population. All patients over 18 years were included and continuous arterial pressure waveforms data were collected. Mean arterial pressure (MAP) below 65 mmHg for at least 10 s was defined as hypotension and a MAP below 45 mmHg as severe hypotension. The primary outcome was the incidence of hypotension. Secondary outcomes were the severity of hypotension expressed in time-weighted average (TWA), factors associated with hypotension, the number and duration of hypotensive events. Results: 499 patients were included. The incidence of hypotension (MAP < 65 mmHg) was 75% (376 out of 499) and 9% (46 out of 499) experienced severe hypotension. Median TWA was 0.3 mmHg [0–1.0]. Associated clinical factors were age, male sex, BMI and cardiogenic shock. There were 5 (1–12) events per patients with a median of 52 min (5–170). Conclusions: In a mixed surgical and non-surgical ICU population the incidence of hypotension is remarkably high.
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