Assessment of main complications of regional anesthesia recorded in an acute pain unit in a tertiary care university hospital: a retrospective cohort

Abstract Background Regional anesthesia has been increasingly used. Despite its low number of complications, they are associated with relevant morbidity. This study aims to evaluate the incidence of complications after neuraxial block and peripheral nerve block. Methods A retrospective cohort study was conducted, and data related to patients submitted to neuraxial block and peripheral nerve block at a tertiary university hospital from January 1, 2011 to December 31, 2017 were analyzed. Results From 10,838 patients referred to Acute Pain Unit, 1093(10.1%) had side effects or complications: 1039 (11.4%) submitted to neuraxial block and 54 (5.2%) to peripheral nerve block. The most common side effects after neuraxial block were sensory (48.5%) or motor deficits (11.8%), nausea or vomiting (17.5%) and pruritus (8.0%); The most common complications: 3 (0.03%) subcutaneous cell tissue hematoma, 3 (0.03%) epidural abscesses and 1 (0.01%) arachnoiditis. 204 of these patients presented sensory or motor deficits at hospital discharge and needed follow-up. Permanent peripheral nerve injury after neuraxial block had an incidence of 7.7:10,000 (0.08%). The most common side effects after peripheral nerve block were sensory deficits (52%) and 21 patients maintained follow-up due to symptoms persistence after hospital discharge. Conclusion Although we found similar incidences of side effects or even lower than those described, major complications after neuraxial block had a higher incidence, particularly epidural abscesses. Despite this, other serious complications, such as spinal hematoma and permanent peripheral nerve injury, are still rare.

Assessment of main complications of regional anesthesia recorded in an acute pain unit in a tertiary care university hospital: a retrospective cohort.

BACKGROUND: Regional anesthesia has been increasingly used. Despite its low number of complications, they are associated with relevant morbidity. This study aims to evaluate the incidence of complications after neuraxial block and peripheral nerve block. METHODS: A retrospective cohort study was conducted, and data related to patients submitted to neuraxial block and peripheral nerve block at a tertiary university hospital from January 1, 2011 to December 31, 2017 were analyzed. RESULTS: From 10,838 patients referred to Acute Pain Unit, 1093(10.1%) had side effects or complications: 1039 (11.4%) submitted to neuraxial block and 54 (5.2%) to peripheral nerve block. The most common side effects after neuraxial block were sensory (48.5%) or motor deficits (11.8%), nausea or vomiting (17.5%) and pruritus (8.0%); The most common complications: 3 (0.03%) subcutaneous cell tissue hematoma, 3 (0.03%) epidural abscesses and 1 (0.01%) arachnoiditis. 204 of these patients presented sensory or motor deficits at hospital discharge and needed follow-up. Permanent peripheral nerve injury after neuraxial block had an incidence of 7.7:10,000 (0.08%). The most common side effects after peripheral nerve block were sensory deficits (52%) and 21 patients maintained follow-up due to symptoms persistence after hospital discharge. CONCLUSION: Although we found similar incidences of side effects or even lower than those described, major complications after neuraxial block had a higher incidence, particularly epidural abscesses. Despite this, other serious complications, such as spinal hematoma and permanent peripheral nerve injury, are still rare.

Nicotinic α7 receptor-induced adenosine release from perisynaptic Schwann cells controls acetylcholine spillover from motor endplates.

Acetylcholine (ACh) spillover from motor endplates occurs after neuronal firing bursts being potentiated by cholinesterase inhibitors (e.g., neostigmine). Nicotinic α7 receptors (α7nAChR) on perisynaptic Schwann cells (PSCs) can control ACh spillover by unknown mechanisms. We hypothesized that adenosine might be the gliotransmitter underlying PSCs-nerve terminal communication. Rat isolated hemidiaphragm preparations were used to measure (1) the outflow of [3 H]ACh, (2) real-time transmitter exocytosis by video-microscopy with the FM4-64 fluorescent dye, and (3) skeletal muscle contractions during high-frequency (50 Hz) nerve stimulation bursts in the presence of a selective α7nAChR agonist, PNU 282987, or upon inhibition of cholinesterase activity with neostigmine. To confirm our prediction that α7nAChR-mediated effects require direct activation of PSCs, we used fluorescence video-microscopy in the real-time mode to measure PNU 282987-induced [Ca2+ ]i transients from Fluo-4 NW loaded PSCs in non-stimulated preparations. The α7nAChR agonist, PNU 282987, decreased nerve-evoked diaphragm tetanic contractions. PNU 282987-induced inhibition was mimicked by neostigmine and results from the reduction of ACh exocytosis measured as decreases in [3 H]ACh release and FM4-64 fluorescent dye unloading. Methyllycaconitine blockage of α7nAChR and the fluoroacetate gliotoxin both prevented inhibition of nerve-evoked ACh release and PSCs [Ca2+ ]i transients triggered by PNU 282987 and neostigmine. Adenosine deamination, inhibition of the ENT1 nucleoside outflow, and blockage of A1 receptors prevented PNU 282987-induced inhibition of transmitter release. Data suggest that α7nAChR controls tetanic-induced ACh spillover from the neuromuscular synapse by promoting adenosine outflow from PSCs via ENT1 transporters and retrograde activation of presynaptic A1 inhibitory receptors.