Intraneural Injection Of Local Anesthetic Research Articles

Smart needle electrical bioimpedance to provide information on needle tip relationship to target nerve prior to local anesthetic deposition in peripheral nerve block (USgPNB) procedures.

Ultrasound guided peripheral nerve block (USgPNB) refers to anaesthetic techniques to deposit local anesthetic next to nerves, permitting painful surgery without necessitating general anesthesia. Needle tip position prior to local anesthetic deposition is a key determinant of block success and safety. Nerve puncture and intra-neural injection of local anesthetic can cause permanent nerve injury. Currently ultrasound guidance is not sufficiently sensitive to reliably detect needle to nerve proximity. Feedback with bioimpedance data from the smart needle tip might provide the anesthetist with information as to the relationship between the needle tip and the target nerve prior to local anesthetic deposition. Bioimpedance using a smart needle integrated with a two-electrode impedance sensor has been developed to determine needle to nerve proximity during USgPNB. Having obtained all necessary ethical and regulatory approvals, in vivo data on brachial plexus, vagus, femoral and sciatic nerves were obtained from seven pig models using the smart needle bioimpedance system. The excision and histological analysis of above peripheral nerves and observation of the architecture and structure of nerves by means of histology allow the calculation of the ratios of connective tissue to neural tissue to determine the influence of this variable on absolute impedance. The ratio results give extra clinical data and explain the hetrogeneity of impedance data in the pig models and the hypothesis that connective tissue with intra-neural fat has higher impedance than neural tissue.

Paraparesis after Spinal Anesthesia During Delivery

Traumatic injury to the spinal cord during spinal or epidural anesthesia is usually secondary to either direct needle penetration or intra-neural injection of local anesthetics. Two women were admitted to a rehabilitation department with paraparesis and hypoesthesia after delivery. One had undergone a lower segment cesarean section under spinal anesthesia and the other, a spontaneous delivery under epidural anesthesia. After discharge from the rehabilitation treatment, they both experienced some weakness in the lower limbs. The patho-physiological basis of this complication seems to be either direct damage to the spinal cord by intra-neural injection of local anesthetics, or local ischemia.

Effects of Intraneural Injection of Dexmedetomidine in Combination With Ropivacaine in Rat Sciatic Nerve Block.

Dexmedetomidine is known to have neural protection effect via attenuation of inflammatory responses induced by local anesthetics. We investigated whether intraneural dexmedetomidine is effective for attenuating or preventing neural injury resulting from inadvertent intraneural injection of local anesthetic. Rats were randomly divided, and left sciatic nerve was surgically exposed. The rats received no injection (control group) or intraneural injections of 0.2 mL of normal saline (saline group), 0.2 mL of 0.5% ropivacaine (ropivacaine group), or 0.2 mL of 0.5% ropivacaine and 0.5 μg/kg of dexmedetomidine (ropivacaine plus dexmedetomidine group). Interleukin (IL)-6 and IL-1β messenger RNA (mRNA) levels were detected at 60 minutes after intraneural injection in experiment 1 (5 per group). Sensory and motor functions were assessed until the return of normal sensory and motor functions, and histopathological and ultrastructure analysis were performed at 4 weeks after intraneural injection in experiment 2 (8 per group). Dexmedetomidine with ropivacaine better enhanced sensory and motor blockade than ropivacaine alone. IL-6 (3.2 ± 1.0 vs 5.9 ± 2.1), IL-1β (1.1 ± 0.1 vs 2.2 ± 0.7) levels, scores of axon and myelinated fiber degeneration (1 [0-2] vs 2 [1-3]), and demyelinated fiber percentages (20.1 ± 10.4 vs 48.3 ± 12.7) were lower in the ropivacaine plus dexmedetomidine group than in the ropivacaine group. No animals showed any signs of permanent neurological deficit. Intraneural dexmedetomidine has sensory and motor blockade-enhancing effects, anti-inflammatory properties, and protective effects against neural injury. These findings suggest that dexmedetomidine as an adjuvant has beneficial effects in rat when intraneural injection of local anesthetic occurs.

Pressure of Local Anesthetic Solution While Performing Sciatic Nerve Blockade in Human Subgluteal Area

Intraneural introduction of local anesthetic belongs to the existing complications of peripheral nerves blockades. The damage of peripheral nerves is associated with the damaging effect of the injection needle and with the pressure caused by the introduction of local anesthetic. Purpose: Determine the pressure of the local anesthetic in fascial compartment of the sciatic nerve during his administration in the blockade of the sciatic nerve subgluteal access. Materials and Methods: Submitted blockade of the sciatic nerve subgluteal access in 22 patients with peripheral nerve electrostimulation under ultrasound guidance. To measure interstitial pressure system was used with the inclusion of a probe invasive blood pressure. Results: During the introduction of 1 ml in the fascial compartment of the sciatic nerve, the pressure of 0.77 psi (40 mmHg) was registered. In the course of the further introduction of local anesthetic up to 13 ml, the pressure did not alter validly (p > 0.05) and its average was 40 (35; 45) mmHg or 0.77 (0.68; 0.87) psi. This is the first study that has allowed to determine the pressure of local anesthetic in the fascial compartment of the sciatic nerve at the time of its introduction, the blockade of the sciatic nerve subgluteal access for the first time determined the probable maximum pressure intraneural injection of local anesthetic. The disadvantage of this study is that it is impossible to measure the pressure of administration over 5.8 psi (300 mmHg), and the lack of opportunity to assess the intraneural blood flow in the sciatic nerve during the creation of such pressure.

Safety of intraneural injection of local anesthetic

There is conflicting information in the literature regarding nerve damage following regional anesthesia. Intraneural injection of local anesthetic was described as a safe practice in regional anesthesia. This review focuses on the histopathological and functional assessment of peripheral nerve function following intraneural injection of local anesthetics.

A preliminary assessment of the ability of anesthesiologists to purposefully perform intra- or perineural injection of local anesthetic for sciatic nerve block

Abstract Intraneural injection of local anesthetic (LA) during peripheral nerve block performance has been found to be a rather common occurrence. We examined some of the variables recorded in an ongoing trial of intraneural vs. perineural injection of LA for sciatic nerve block. Patients were randomly assigned to intra- or perineural injection of LA. Ultrasound images were evaluated by attending anesthesiologists and an independent investigator. Expansion of sciatic nerve diameters was measured as a ratio of post-injection over pre-injection values. The incidence of unintended intraneural injection was 10% in this case series. Concordance between operators’ judgment and post-hoc evaluation of intraneural vs. perineural LA deposition was high (Cohen’s kappa = 0.914). The mean maximum change in sciatic nerve diameter was 1.46 (1.14–1.78) after intraneural injection; 1.13 (0.99–1.26) after perineural injection. In the controlled setting of a clinical trial, anesthesiologists showed higher ability to predict intraneural injection of LA using images alone than seen in observational data based on electrical stimulation.

Local Anesthetic Schwann Cell Toxicity Is Time and Concentration Dependent

Peripheral nerve blocks with local anesthetics (LAs) are commonly performed to provide surgical anesthesia or postoperative analgesia. Nerve injury resulting in persistent numbness or weakness is a potentially serious complication. Local anesthetics have previously been shown to damage neuronal and Schwann cells via several mechanisms. We sought to test the hypothesis that LAs are toxic to Schwann cells and that the degree of toxicity is directly related to the concentration of LA and duration of exposure. Intraneural injection of LAs has been shown to produce nerve injury. We sought to test the hypothesis that a prolonged extraneural infusion of LA can also produce injury. Schwann cells cultured from neonatal rat sciatic nerves were incubated with LAs at different concentrations (10, 100, 500, and 1000 μM), and each concentration was assessed for toxicity after 4, 24, 48 and 72 hours of exposure. Local anesthetics tested were lidocaine, mepivacaine, chloroprocaine, ropivacaine, and bupivacaine. Cell death was assessed by lactate dehydrogenase release measured by optical density.In a separate experiment, a microcatheter was placed along the sciatic nerves of Sprague-Dawley rats. Rats were randomly assigned to receive either 0.9% saline (n = 8) or bupivacaine (0.5%, n = 4; 0.75%, n = 4) via the perineural catheters for 72 hours. The rats were then killed, and their nerves sectioned and stained for analysis. Sections were stained for myelin and with an antimacrophage (CD68) antibody. None of the LAs tested produced significant Schwann cell death at very low concentrations (10 μM, or 0.0003%) even after prolonged exposure. With prolonged exposure (48 or 72 hrs) to high concentrations (1000 μM, or 0.03%), all of the LAs tested produced significant Schwann cell death (increased lactate dehydrogenase release relative to control as measured by optical density, 0.384-0.974; all P values < 0.001). Only bupivacaine produced significant cell death (0.482, P < 0.001) after prolonged exposure to low concentrations (100 μM, or 0.003%). At intermediate concentrations (500 μM, or 0.015%), cell death was more widespread with bupivacaine (0.768, P < 0.001) and ropivacaine (0.675, P < 0.001) than the other agents (0.204-0.368; all P values < 0.001). Prolonged extraneural exposure of rat sciatic nerves to bupivacaine caused significant demyelination and infiltration of nerves with inflammatory cells. Local anesthetics induce Schwann cell death in a time- and concentration-dependent manner. Bupivacaine and ropivacaine have greater toxicity at intermediate concentrations, and prolonged exposure to bupivacaine produces significant toxicity even at low concentrations. Brief exposure to high concentrations of bupivacaine damages Schwann cells. Prolonged extraneural infusion of bupivacaine results in nerve injury.

Extraneural versus Intraneural injection of local anesthetic during ultrasound-guided sciatic block

s and Programme: EUROANAESTHESIA 2011: The European Anaesthesiology Congress: Local and Regional Anaesthesia

From basic concepts to emerging technologies in regional anesthesia

The present article details how our understanding of the basic concepts of regional anesthesia has recently evolved. We will appraise current technological advances and question the commensurate nature of the relationship between tradition and innovation. Ultrasound localization has enhanced our understanding of the needle-nerve relationship. Intraneural injection of local anesthetic may occur with greater frequency than previously thought without inevitably leading to neurological complications. The ratio of neural to non-neural tissue varies both between and within nerves and may be an important determinant of neural injury. Ultrasonographic evidence of intraneural injection is subject to observer expertise and the resolution of the ultrasound image. Current ultrasound resolution capability does not reliably permit differentiation between intrafascicular and extrafascicular drug injection. Perineural electrical impedance may be a determinant of current threshold and conceivably distinguish between intraneural and extraneural tissue. Technology that enhances the sonographic image of both procedure needle and target nerve is the focus of current endeavors in ultrasound innovation.There is inconclusive evidence that the use of ultrasound technology has reduced the incidence of local anesthetic toxicity. Lipid emulsion therapy is now an accepted treatment for systemic local anesthetic toxicity. There are new reports on the development of an ultra long-acting local anesthetic agent that would permit lower doses and superannuate catheter-based continuous regional anesthesia techniques. Over the past decade, our understanding of the fundamental concepts of regional anesthesia continues to be challenged by emerging experimental and clinical evidence.

Intraneural Catheterization of the Sciatic Nerve In Humans: A Pilot Study

Imaging studies in humans have shown that intraneural injection of local anesthetic may be relatively frequent. The incidence of intraneural catheterization is unknown. We speculated that early neural blockade after the injection of a small dose of local anesthetic might be a common finding produced by unintended intraneural catheterization. We investigated the clinical effect of a small dose of local anesthetic injected through a stimulating sciatic catheter, and also the placement of the tip of the catheters by computed tomography (CT) scan. In this descriptive study, a dose of 3 to 5 mL of 1.5% mepivacaine was injected through a stimulating sciatic catheter in 45 patients undergoing hallux valgus repair. Patients with early neural blockade at the foot, within 5 minutes after injection, were suspected to have an intraneural placement of the catheter. A CT scan of the thighs was performed in 10 additional patients to assess catheter tip placement. Nine of 45 patients had early neural blockade with the small dose of local anesthetic. Seven patients underwent surgery without further supplementation. There was a statistically significant lower intensity of stimulating current through the catheter in the group of patients with early neural blockade. Of 10 CT scans, 3 showed clear intraneural placement of the catheter. No postoperative sequelae were observed. Intraneural catheterization of the sciatic nerve may be a frequent finding and was not followed by nerve injury under the conditions of our small pilot study.

Intraneural Injection of Local Anesthetics during Ultrasound-guided Peripheral Nerve Block May Lead to Nerve Injury

Clinique du Parc saint Lazare, Beauvais, France. balnasser@wanadoo.frI read with interest the article by Bigeleisen.1In this article, the author presented a prospective study of ultrasound-guided axillary blocks and determined the incidence of nerve puncture, intraneural injection of local anesthetics, and transient or permanent nerve injuries. After reading this well-written article it occurred to me that there are some points that may add to discussion. Damage may be caused to peripheral nerves after regional anesthesia techniques by mechanical, chemical, or ischemic injuries, which may occur alone or in combination.2Iohom et al. 2reported that intraneural injection of ropivacaine in rat sciatic nerve, in a concentration routinely used in clinical practice, caused no deleterious effect on motor function. Hadzic et al. 3reported varying degrees of damage to the neural architecture after high-pressure injection of local anesthetic in dog sciatic nerve. This damage ranged from mechanical disruption and delamination to fragmentation of the myelin sheath and marked cellular infiltration. They also reported severe and persistent motor deficits.3Since the introduction of ultrasound-guided peripheral nerve blocks at my institution, I frequently observe nerve puncture during this procedure. In my experience, the combination of electrical stimulation does not result always in motor response even if the needle tip is positioned intraneurally. In the same condition, I also sometimes observe no pain on intraneural injection. The advantage of ultrasound-guided nerve blocks in my practice is that I can watch the needle’s advancement in real time. Accordingly, in case I suspect nerve puncture, I slightly withdraw the needle and avoid intraneural injection to increase safety. In this study, the author excluded 22 patients from the study because of preoperative abnormalities in their motor and sensory examination. In daily practice, patients may present some degree of neurologic abnormalities before surgery. They may also be at high risk of nerve damage. Furthermore, intraneural injection in these patients may lead to an aggravating condition of their preexisting neuropathy. There are multiple causes and a combination of factors that may lead nerve injury after regional anesthesia techniques.4However, peripheral nerves have a dual blood supply of intrinsic exchange vessels in the endoneurium and an extrinsic plexus of supply vessels in the epineurial space that cross the perineurium to anastomose with intrinsic circulation.2Accordingly, nerve ischemia due to intraneural compression (local anesthetic volume or edema) and/or perineural compression (local anesthetic volume) may cause permanent or transient nerve damage.4Moreover, high-pressure intrafascicular or endoneural injection may also cause neural damage.3Consequently, the combination of ischemia, high-pressure intrafascicular or endoneural injection and local anesthetic toxicity could be deleterious to peripheral nerves.3,4According to my experience, it is difficult to tell from the ultrasound image after apparent intraneural placement of the needle tip, whether the needle is positioned perineurially, epineurially, or endoneurially. The injection of the local anesthetic, even in a small quantity, in one of these positions may not lead to the same outcome. Furthermore, endoneural injection could result in nerve damage by promoting ischemic changes.2For this reason, I believe that avoidance of intraneural placement of the needle tip should be a major concern during ultrasound-guided peripheral nerve blocks. Moreover, performing a peripheral nerve block in real time and under direct vision gives us the possibility to correct the needle position, avoid intraneural injections, and avoid nerve injury.In conclusion, although this study and other reports1,2suggested that nerve puncture and intraneural injection of low to moderate volumes of local anesthetic do not inevitably lead to neurologic injury, the role of ultrasound-guided peripheral nerve blocks is to increase safety. Even if we hypothesize that intraneural injections do not lead to neurologic damage, they present no advantage over perineural injections in rapidity of installation or in success rate after ultrasound-guided techniques. Finally, practitioners who have already experienced neurologic problems after regional anesthesia techniques always remember the difficulties encountered during the long way of patient care.Clinique du Parc saint Lazare, Beauvais, France. balnasser@wanadoo.fr

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Introduction: The success and complications associated with interscalene brachial plexus block (IBPB) anesthesia for shoulder surgery have been reviewed in recent retrospective reports with wide variability in results and differing conclusions. Numerous prior case reports have documented significant complications related to IBPB anesthesia. Those same reports generally conclude that the success of IBPB is less than optimal. Further, those reports conclude that IBPB should not be performed on patients who are heavily sedated or under general anesthesia because of the risk of undetectable intraneural injection of local anesthetic. This prospective study was undertaken to study the safety and efficacy of IBPB performed on patients after induction of general anesthesia. Methods: Following IRB approval, 500 consecutive consenting patients undergoing a variety of open and arthroscopic shoulder surgeries were enrolled in this study. For inclusion, the IBPB had to be performed by an anesthesiologist skilled and experienced in IBPB after the patient had been administered general anesthesia. Blocks were performed with an insulated needle, and a nerve stimulator was utilized to determine appropriate needle placement. Stimulation of the biceps brachia muscle, without stimulation of the phrenic nerve, with the current produced by the nerve stimulator set below 0.5 milliamps was required. Bupivicaine 0.5% with epinephrine 1:200,000 (40 ml) was instilled. Aspiration was performed after every 5 ml of injected fluid to ensure the absence of blood in the aspirate. Corticosteroid (Kenalog 25 mg) was randomly added to the anesthetic injection in some patients, while others received anesthetic without steroid. Adverse events were noted and followed, and the success and duration of each block was documented. Results: Mean time required for the performance of the blocks (positioning and preparation of the head/neck, needle placement, and instillation of meds) was 5.5 minutes. Mean current for nerve stimulation was 0.30 milliamps. The block was successful in 490 (98%) of the 500 cases. Overall mean block duration for all patients was 26 hours. Mean duration of analgesia for blocks performed without steroid was 20 hours. Mean duration for blocks performed with steroid was 28 hours. Immediate post-operative adverse side effects occurred in 54 patients (11%), including: Horner’s syndrome in 37 patients, mild subjective dyspnea due to phrenic nerve dysfunction in 7, severe subjective dyspnea in 3, and hoarseness due to recurrent laryngeal nerve dysfunction in 7. No patient suffered a pneumothorax. No treatment was required for the side effects of the IBPB. One block was aborted after instillation of 20 ml of Bupivicaine (without steroid) due to aspiration of blood during the routine intrablock aspiration check. That patient experienced 19 hours of post-injection analgesia. Nine patients noted persistent hypesthesia and/or paresthesia in the distal portion of the upper extremity after resolution of the analgesic effect of the IBPB. These symptoms resolved in less than one week in 4 patients. The remaining 5 patients had hypesthesis/paresthesia lasting longer than 2 weeks, but all noted spontaneous resolution between 2 weeks and 3 months post-IBPB. No patient had lasting sensory symptoms and no patient experienced persistent motor deficits. Conclusion: IBPB performed on patients under general anesthesia was found to be safe (no serious or permanent complications) and effective (98% success). It provided a satisfactory duration of effective analgesia (26 hours). Minor short-lasting adverse side effects occurred in 11% of patients, and temporary minor neurologic adverse events occurred in 2%. If noted, the author indicates something of value received. The codes are identified as follows: a, research or institutional support; b, miscellaneous funding; c, royalties; d, stock options; e, consultant or employee. *The Food and Drug Administration has not cleared the drug and/or medical device for the use described in this presentation (ie, the drug or medical device is being discussed for an “off-label” use). If noted, the author indicates something of value received. The codes are identified as follows: a, research or institutional support; b, miscellaneous funding; c, royalties; d, stock options; e, consultant or employee. *The Food and Drug Administration has not cleared the drug and/or medical device for the use described in this presentation (ie, the drug or medical device is being discussed for an “off-label” use).

Neurologic and histologic outcome after intraneural injections of lidocaine in canine sciatic nerves

Inadvertent intraneural injection of local anesthetics may result in neurologic injury. We hypothesized that an intraneural injection may be associated with higher injection pressures and an increase in the risk of neurologic injury. The study was conducted in accordance with the principles of laboratory animal care, and was approved by the Laboratory Animal Care and Use Committee. Fifteen dogs of mixed breed (16-21 kg) were studied. After general endotracheal anesthesia, the sciatic nerves (n= 30) were exposed bilaterally. Under direct vision, a 25-gauge, long-beveled needle (30 degrees) was placed either epineurally (n= 10) or intraneurally (n= 20), and 4 ml of preservative-free lidocaine 20 mg/ml was injected using an automated infusion pump (4 ml/min). Injection pressure data were acquired using an in-line manometer coupled to a computer via an analog-to-digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. One week later, the dogs were killed, the sciatic nerves excised and histologic examination was performed by pathologists blind to the purpose of the study. All perineural injections resulted in low pressures (< or = 5 psi). In contrast, eight of 20 intraneural injections resulted in high pressures (20-38 psi) at the beginning of the injection. Twelve intraneural injections, however, resulted in pressures of less than 12 psi. Neurologic function returned to baseline within 3 h after perineural injections and within 24 h after intraneural injections, when the measured injection pressures were less than 12 psi. Neurologic deficits persisted throughout the study period after all eight intraneural injections that resulted in high injection pressures. Histologic examination of the affected nerves revealed fascicular axonolysis and cellular infiltration. The data in our canine model of intraneural injection suggest that intraneural injections do not always lead to nerve injury. High injection pressures during intraneural injection may be indicative of intrafascicular injection and may predict the development of neurologic injury.

Nerve Puncture and Apparent Intraneural Injection during Ultrasound-guided Axillary Block Does Not Invariably Result in Neurologic Injury

Nerve puncture by the block needle and intraneural injection of local anesthetic are thought to be major risk factors leading to neurologic injury after peripheral nerve blocks. In this study, the author sought to determine the needle-nerve relation and location of the injectate during ultrasound-guided axillary plexus block. Using ultrasound-guided axillary plexus block (10-MHz linear transducer, SonoSite, Bothel, WA; 22-gauge B-bevel needle, Becton Dickinson, Franklin Parks, NJ), the incidence of apparent nerve puncture and intraneural injection of local anesthetic was prospectively studied in 26 patients. To determine the onset, success rate, and any residual neurologic deficit, qualitative sensory and quantitative motor testing were performed before and 5 and 20 min after block placement. At a follow-up 6 months after the blocks, the patients were examined for any neurologic deficit. Twenty-two of 26 patients had nerve puncture of at least one nerve, and 21 of 26 patients had intraneural injection of at least one nerve. In the entire cohort, 72 of a total of 104 nerves had intraneural injection. Sensory and motor testing before and 6 months after the nerve injections were unchanged. Under the conditions of this study, puncturing of the peripheral nerves and apparent intraneural injection during axillary plexus block did not lead to a neurologic injury.

Regional Anesthesia, Intraneural Injection, and Nerve Injury

Regional Anesthesia, Intraneural Injection, and Nerve Injury

Combination of intraneural injection and high injection pressure leads to fascicular injury and neurologic deficits in dogs

Unintentional intraneural injection of local anesthetics may cause mechanical injury and pressure ischemia of the nerve fascicles. One study in small animals showed that intraneural injection may be associated with higher injection pressures. However, the pressure heralding an intraneural injection and the clinical consequences of such injections remain controversial. Our hypothesis is that an intraneural injection is associated with higher pressures and an increase in the risk of neurologic injury as compared with perineural injection. Seven dogs of mixed breed (15-18 kg) were studied. After general endotracheal anesthesia, the sciatic nerves were exposed bilaterally. Under direct microscopic guidance, a 25-gauge needle was placed either perineurally (into the epineurium) or intraneurally (within the perineurium), and 4 mL of lidocaine 2% (1:250,000 epinephrine) was injected by using an automated infusion pump (4 mL/min). Injection pressure data were acquired by using an in-line manometer coupled to a computer via an analog digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. On the 7th day, the dogs were killed, the sciatic nerves were excised, and histologic examination was performed by pathologists blinded to the purpose of the study. Whereas all perineural injections resulted in pressures < or =4 psi, the majority of intraneural injections were associated with high pressures (25-45 psi) at the beginning of the injection. Normal motor function returned 3 hours after all injections associated with low injection pressures (< or =11 psi), whereas persistent motor deficits were observed in all 4 animals having high injection pressures (> or =25 psi). Histologic examination showed destruction of neural architecture and degeneration of axons in all 4 sciatic nerves receiving high-pressure injections. High injection pressures at the onset of injection may indicate an intraneural needle placement and lead to severe fascicular injury and persistent neurologic deficits. If these results are applicable to clinical practice, avoiding excessive injection pressure during nerve block administration may help to reduce the risk of neurologic injury.

Sympathetic reflex activity and neuroeffector transmission change after chronic nerve lesions

Unintentional intraneural injection of local anesthetics may cause mechanical injury and pressure ischemia of the nerve fascicles. One study in small animals showed that intraneural injection may be associated with higher injection pressures. However, the pressure heralding an intraneural injection and the clinical consequences of such injections remain controversial. Our hypothesis is that an intraneural injection is associated with higher pressures and an increase in the risk of neurologic injury as compared with perineural injection.Seven dogs of mixed breed (15–18 kg) were studied. After general endotracheal anesthesia, the sciatic nerves were exposed bilaterally. Under direct microscopic guidance, a 25-gauge needle was placed either perineurally (into the epineurium) or intraneurally (within the perineurium), and 4 mL of lidocaine 2% (1:250,000 epinephrine) was injected by using an automated infusion pump (4 mL/min). Injection pressure data were acquired by using an in-line manometer coupled to a computer via an analog digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. On the 7th day, the dogs were killed, the sciatic nerves were excised, and histologic examination was performed by pathologists blinded to the purpose of the study.Whereas all perineural injections resulted in pressures ≤4 psi, the majority of intraneural injections were associated with high pressures (25–45 psi) at the beginning of the injection. Normal motor function returned 3 hours after all injections associated with low injection pressures (≤11 psi), whereas persistent motor deficits were observed in all 4 animals having high injection pressures (≥25 psi). Histologic examination showed destruction of neural architecture and degeneration of axons in all 4 sciatic nerves receiving high-pressure injections.High injection pressures at the onset of injection may indicate an intraneural needle placement and lead to severe fascicular injury and persistent neurologic deficits. If these results are applicable to clinical practice, avoiding excessive injection pressure during nerve block administration may help to reduce the risk of neurologic injury.